Specialist Forum May26

Vol. 26 • No. 5 • May 2026

www.specialistforum.co.za

Under pressure: Immunity, infection and inflammation

Forum

Allergology

Winter sniffles?

Allergy or virus – know the difference

Allergology Bilastine targets allergic rhinitis and urticaria symptoms

Infectious diseases Double trouble winter: Flu and RSV team up early in 2026

Otolaryngology Rhinosinusitis: From acute episodes to chronic complexity

News & views for medical professionals

Forum

Amplify your brand with accredited webinars that work Partner with Specialist Forum to host expert-led webinars featuring South Africa’s leading KOLs – and let us handle the logistics.  Invitations sent to ±28 000 HCPs or a focused target audience  Full webinar marketing and CPD accreditation  Professional hosting, recording, and on-demand replay  Published synopsis article in Specialist Forum  Optional print advert next to your article  HCP leads list of those opting in to hear from you  Banner adverts included – branded and unbranded

Contact Angi Latimer on 083 999 3123 or send an email to angela.latimer@media24.com to book your expert webinar package.

Remember to join our WhatsApp channel for updates and insights!

Simply click on this link: https://bit.ly/4stYQNG Let’s put your brand at the centre of clinical conversations.

CONTENTS

Contents Editor’s note: Breath, skin, and the allergic body: Navigating the immune frontier

5

Adopting AI responsibly

7

End-of-life law in South Africa: The DignitySA challenge and what it could mean for patients, practitioners and insurers

9

FIDSSA 2026 Congress set to unite global infectious disease experts in Cape Town

10 Measure, manage, repeat: Hypertension control starts here

9

15

4

13 Navigating MS diagnosis together

26

15 Nicotine hooks deep, making quitting hard 17 Online CPD: Winter sniffles?

Allergy or virus – know the difference 18 Bilastine redefines modern non-sedating allergy control 21 Atopic dermatitis flares with seasonal extremes 23 Winter skin SOS: When dryness becomes a diagnosis, not just a nuisance

30

25 Cold or flu? Understanding the symptoms behind URTIs 26 Double trouble winter: Flu and RSV team up early in 2026 30 Rhinosinusitis: From acute episodes to chronic complexity

32 Online CPD: Local ARISE insights on real-world IDegAsp efficacy 34 Webinar report: Initiating menopause hormone therapy – Back to basics EDITORIAL EDITOR: Deneshree Varaden Deneshree.Varaden@media24.com CONTRIBUTING EDITOR: René Bosman SUB EDITOR: Gill Abrahams LAYOUT & DESIGN: Allison McCallum ADVERTISING ADVERTISING EXECUTIVE Angi Latimer | 083 999 3123 Angela.Latimer@media24.com DISTRIBUTION & SUBSCRIPTIONS Rae Morrison Rae.Morrison@media24.com PUBLISHING TEAM General Manager: Dev Naidoo Head of Content & Digital Strategy: Varushka Padayachi Production Manager: Angela Silver Group Art Director: David Kyslinger MEDIA24 MEDIA CEO: Minette Ferreira CFO: Lana Goliath

MEDIA24 CORPORATE CEO MEDIA24: Raj Lalbahadur CFO MEDIA24: Nelmarie Beyers B2B JOHANNESBURG OFFICE Building 13, The Woodlands Office Park, 20 Woodlands Drive, Woodmead, Sandton PO Box 784698, Sandton 2146 Tel: +27 11 867 6111

25

28 Cough: Causes, duration, diagnosis, management explained

Published by Media24 B2B www.medicalacademic.co.za PRINTING Printed by Novus Print, Cape Town COVER PRICE Specialist Forum per issue R80,00 VAT Incl.

ISSN: 2218-8282 Cover photograph: Getty Images/evemilla

Disclaimer: Please take note that the products featured in this journal are available in South Africa. Products may be marketed under a different name or might not be registered in your country. For more information, contact your local representative.

All content in Specialist Forum is sourced independently and under no circumstances should articles be considered promotional unless specified with a postscript.

Articles are created with the assistance of artificial intelligence (AI) tools to aid in research and drafting. The content has been reviewed and edited by a human expert for quality and reliability.

Please note that all advertising is intended for healthcare professionals only.

Unless previously agreed in writing, Specialist Forum owns all rights to all contributions, whether image or text.

SOURCES: Getty Images, supplied images, editorial staff.

While precautions have been taken to ensure the accuracy of its contents and information given to readers, neither the editor, publisher, or its agents can accept responsibility for damages or injury which may arise therefrom.

All rights reserved. © Specialist Forum. No part of this publication may be reproduced, stored in a retrieval system or transmitted in any form or by any means, photocopying, electronic, mechanical or otherwise without the prior written permission of the copyright owners.

Specialist Forum May 2026 | Vol. 26 No. 5

3

EDITOR’S NOTE

Photo credit: GettyImages/Sebastian Kaulitzki/Science Photo Library

Breath, skin, and the allergic body:

Navigating the immune frontier The May issue of Specialist Forum is anchored by a unifying theme: Allergy and its far-reaching consequences. Allergic disease spans the respiratory tract, the skin, and the systemic immune axis – and its burden continues to increase across South Africa and globally.

A

llergic rhinitis (AR) provides the clinical centerpiece of this edition. It remains among the most prevalent immunemediated conditions in both primary and specialist practice yet is chronically underdiagnosed and undertreated.

Two articles examine its management. The CPD article offers a structured framework from allergen avoidance and nasal irrigation through to combination intranasal pharmacotherapy and immunotherapy for refractory disease.

The second article focuses on bilastine, a modern non-sedating H1-antihistamine with strong evidence for symptom control in AR and chronic urticaria, without meaningful impairment of cognition or driving ability – a clinically significant distinction in a workingage population.

The dermatological impact of allergic disease is highlighted in an update on atopic dermatitis, aligned with the first paediatric-specific guidelines from the American Academy of Dermatology, outlining management approaches ranging from emollients and topical corticosteroids to biologic therapies for moderate-to-severe disease.

A companion article on winter-related xerosis cutis explores the progression from dry skin to asteatotic eczema – particularly in elderly patients – and reinforces proactive emollient use as a firstline strategy.

The respiratory theme continues with articles on cough evaluation, rhinosinusitis, and distinguishing the common cold from influenza.

The rhinosinusitis review explores emerging perspectives on its association with obstructive sleep apnoea and the gut-sinus microbiome axis. In the cough infographic, we highlight 10 facts to better understand its causes, classification, and clinical significance.

Don’t miss the interview with Dr Alan, pulmonologist and clinical head of the Internal Medicine Unit at Chris Hani Baragwanath 4

Specialist Forum May 2026 | Vol. 26 No. 5

Academic Hospital in Johannesburg. The article looks at the cocirculation of influenza and respiratory syncytial virus in South Africa this winter underscores vaccination as the cornerstone of prevention for vulnerable populations, including those with chronic lung disease, HIV, and tuberculosis.

Beyond allergy and respiratory disease, this issue covers several topics of broader clinical relevance. Our health awareness features focus on Multiple Sclerosis Awareness Day (30 May) and World No Tobacco Day (31 May). Multiple sclerosis is explored through the updated McDonald diagnostic criteria and the barriers to equitable neurological care across sub-Saharan Africa. The World No Tobacco Day feature examines nicotine replacement therapy as an accessible smoking cessation strategy under the theme, Unmasking the appeal – countering nicotine and tobacco addiction.

Our second CPD article focuses on a real-world evaluation of insulin degludec/aspart (IDegAsp) in South African patients with type 2 diabetes demonstrates meaningful glycaemic improvement and reduced hypoglycaemia in routine practice.

The DignitySA legal challenge to South Africa’s prohibition on medical assistance in dying is also reviewed for its clinical, ethical, and medico-legal implications. This issue further previews the 11th Federation of Infectious Diseases Societies of Southern Africa Congress taking place in Cape Town this June.

These articles reflect our commitment to translating scientific evidence into clinically actionable insight – equipping practitioners to deliver confident, patient-centred care. As always, we welcome your feedback, perspectives, and contributions. SF

Deneshree Varaden Editor, Specialist Forum

MEDICOLEGAL

Photo credit: GettyImages/Shinsei Motions

Prof Martin Brand, Medical Adviser at Medical Protection

Adopting AI responsibly In 2018, Elaine Herzberg became the first recorded case of a pedestrian killed by a self-driving autonomous car while pushing her bicycle across a road in Tempe, United States. But who was responsible for the accident? Herzberg herself?

The ‘safety driver’? The car? Uber? The safety managers at Uber? Engineers at Uber? Arizona government officials who allowed Uber to test their cars in Tempe?

All of them? None of them? In 2023 the safety driver who was allocated to the car pleaded guilty to a reduced charge of endangerment and was sentenced three years of supervised probation.

A

I applications are becoming increasingly widespread in healthcare. As an administrative tool, AI scribe technology is supporting clinicians to keep accurate patient records in real time, and AI-driven x-ray and screening tools are supporting early diagnoses. The technology has the potential to be transformative to patient outcomes and almost every day in the news around the world we are hearing how AI is detecting diseases like cancer earlier from scans, predicting patient deterioration in hospitals, accelerating the discovery of new drugs, and enabling more personalised treatment plans for patients. However, as with any technology, it is not infallible.

Who is liable in AI-related healthcare malpractice claims is still murky territory. Is it the AI software developer for defective design, or false representation of accuracy or inadequate warnings could face a product liability claim? The clinician or hospital could be found liable for incorrect implementation, training or oversight of AI systems? Third-party vendors which have products integrated with the original AI system? Furthermore, courts are also not clear on how to view AI – as a medical device, a service or simply as a clinical tool?

It is interesting to look at how some AI-related legal cases and studies in the healthcare arena have played out in other jurisdictions, for example: S In September 2024, Pieces technology sold a clinicianassisted AI product which worked within a USA hospital’s electronic healthcare record programme to generate progress notes, discharge summaries and multidisciplinary care plans with the aim of ‘returning time to medicine’ by reducing the administrative and documentation burden of doctors, nurses, and hospital administrative staff. They claimed the AI system hallucination rate (the rate by which AI systems generate false or misleading information and present it as factual) was less than 0.001%. The Texas State Regulators found this to be an underestimation and proceeded with a successful enforcement action in court.

S In an external validation study, the Epic Sepsis Model, which was integrated into patient electronic healthcare records in hundreds of hospitals in the USA to predict the early onset of sepsis, was able to assign higher risk scores to patients who developed sepsis only about 63% of the time, and only identified Specialist Forum May 2026 | Vol. 26 No. 5

5

MEDICOLEGAL 7% of patients whose sepsis diagnosis was missed by a clinician.

Both themes leave the clinician exposed to significant risk.

Meanwhile, the company claimed an accuracy rate of 76-83% Furthermore, HCPs should be aware of aforementioned issues S A systematic review of 86 studies evaluating commercial like errors and hallucinations, and the uncertainty around liability. radiology AI algorithms found that 81% of the algorithms Alongside this, they must be wary of their under or over-reliance showed decreased performance during on the technology and how use of AI may erode external validation, with 24% showing their skills over time. substantial declines.

Steps to consider to help reduce Treat AI as a S A review into AI bias from the British Journal medicolegal risk: of Radiology found various areas in the S When choosing an AI product, ensure that it decision-support development of clinical AI tools which may is appropriate for the specific task you are tool, not as a be prone to bias. It also found that from data using it for and check for external validation replacement collection to data preparation and annotation, tests of the product. and from model development and deployment S Treat AI as a decision-support tool, not as for your clinical to evaluation, the earlier the bias is introduced a replacement for your clinical judgement, judgement — your into the data, or the more types of bias in line with HPSCA guidance. Always patients must be are involved, the worse the final model will consider how the AI correlates with your informed and give perform with external data validation. clinical findings and question generated When assessing the potential legal risks of AI results in the same way that you would any voluntary consent and how they may impact a clinician using AI, investigation result. there are many important factors to consider.

S Where AI systems are used within an A key consideration, ‘The black box’ problem, organisation, ensure that appropriate initial results where deep learning models are unexplainable as they and ongoing training is provided for all users. are either hidden or incomprehensible to humans (making them S Review whether metrics such as false positives/negatives and unverifiable and open to significant bias). hallucination rates are available and double check or audit some Additionally, the developmental data set used to programme the AI of the results. Alternatively, ensure that the organisation is tool may not include all relevant patient populations or characteristics, doing so and you are kept up to date with any updates, changes creating an inherent and perpetuating bias specifically towards or concerns raised. minority, under-resourced or disadvantaged groups.

S Importantly, your patients must be informed if AI was used in their management and give their voluntary consent which should be recorded. To obtain informed consent also involves clinicians being able to explain to patients how the AI reaches its outputs and how data is stored.

S Keep in mind that a patient has the right to refuse AI-assisted care without the refusal impacting their care.

AI represents an incredible opportunity to advance medical care and make significant leaps in improving patient care.

At Medical Protection, we want to help ensure practitioners and their patients reap the potential benefits of AI and we provide advice and support which helps practitioners mitigate any emergent medicolegal risks.

We have developed the AI Safer Practice Framework to help practitioners to safely and responsibly integrate AI into their practice. The Framework is divided into two parts – INFORMED and RECORDS – and is structured around these acronyms to ensure it is practical and memorable.

Medical Protection Society members can also access the ‘Managing the risks of AI in medicine’ course on The Learning Hub, as a benefit of membership. The course introduces the AI Safer Practice Framework to help healthcare practitioners integrate AI into practice safely, ethically, and effectively. The interactive course can be accessed any time: https://prism.medicalprotection. org/course/view.php?id=1834

REFERENCE: 1. Borg W, Sinnott-Armstrong JS, Conitzer V. Moral AI: And How We Get There. Random House. 2024 [Online]. Available at: https://books.google. co.za/books?id=5wi-EAAAQBAJ&printsec=frontcover&source=gbs_ge_ summary_r&cad=0#v=onepage&q&f=false SF

6

Specialist Forum May 2026 | Vol. 26 No. 5

MEDICOLEGAL

Photo credit: GettyImages/Mininyx Doodle

Natasha Naidoo, director – Fairbridges with Sibusiso Madisha, Candidate Attorney – Fairbridges

End-of-life law in South Africa The DignitySA challenge and what it could mean for patients, practitioners and insurers

South African law draws a clear distinction between medical care that may shorten life and medical actions that are intended to end life. Healthcare practitioners may lawfully stop treatment in circumstances where treatment may be futile or the burden of treatment outweighs benefit, or if the patient refuses treatment, even if death follows.

However, the law prohibits healthcare practitioners from actively helping a person to die, even if that person is a mentally capable consenting patient who has no prospect of recovery.

O

n the 10 April 2026, Dignity SA NPC (DignitySA) brought an application in the Gauteng Division of the High Court, Pretoria.

The application challenges the common‑law prohibition on what DignitySA refers to as ‘medical assistance in dying’ (MAiD) and prays for an order to declare the prohibition unconstitutional.

The current legal position

South African case law and professional guidelines draw a distinction between assisted suicide and voluntary euthanasia.

Assisted suicide refers to circumstances in which a patient is provided with the means to end their own life, typically by selfadministering prescribed medication. Voluntary euthanasia, by contrast, involves a medical practitioner administering a lethal intervention at the patient’s request with the intention of causing death.

Under the common law, the intentional killing of another person constitutes murder and patient consent does not render such conduct lawful. The Health Professions Council of South Africa (HPCSA)’s Guidelines for the Withholding and Withdrawing of Treatment (Booklet 7) classifies euthanasia and assisted suicide as unethical conduct and inconsistent with South African law.

The Supreme Court of Appeal in Minister of Justice and Correctional Services v Estate Stransham-Ford (531/2015) 2016 ZASCA 197 distinguished between assisted suicide and voluntary euthanasia, on the one hand, and the lawful refusal or withdrawal

of medical treatment, on the other. The court confirmed that a competent patient may refuse treatment, and that healthcare practitioners may withhold or withdraw treatment where it no longer serves a therapeutic or palliative purpose, even if death ensues.

South African law allows healthcare practitioners to relieve pain and symptoms even in circumstances where such treatment may shorten the patient’s life. The purpose of such treatment is to ease suffering and not to cause death. A healthcare practitioner is allowed to withhold or withdraw medical treatment if such treatment no longer benefits the patient or no longer improves comfort.

Healthcare practitioners are required to respect a competent patient’s refusal of treatment, request to stop life‑sustaining treatment, including artificial nutrition or hydration, and a patient’s decision to voluntarily stop eating and drinking. These practices are lawful and regarded as ethically acceptable because the intention is not to cause death but to respect the patient’s choice and autonomy.

DignitySA’s application

DignitySA states that its application is made in its own interest and on behalf of those with terminal or permanent medical conditions, healthcare professionals and workers, and in the public interest. It defines MAiD broadly as physician assisted suicide and physician Specialist Forum May 2026 | Vol. 26 No. 5

7

MEDICOLEGAL administered euthanasia, both of which are prohibited in terms of South African law.

DignitySA refers to several case studies of people who, according to DignitySA, suffer from or have, in the past, suffered irremediable pain and the steps they took to end their lives such as refusing medical treatment or ending their own lives by not seeking medical help.

One of the grounds on which DignitySA has founded its application is that the law treats similar situations differently without a rational basis. It contends that a competent patient may refuse treatment or request that treatment be withdrawn even if death follows. Further, it states that a healthcare practitioner may lawfully provide symptom‑relieving medication that shortens life as a side effect. However, the same patient may not make such a request even in circumstances where the request is informed and voluntary.

It is argued that the prohibition on MAiD infringes on individuals’ Constitutional rights such as dignity, life, equality and freedom and security. It states that the Constitution protects bodily and psychological integrity and that competent adults have the right to decide how to respond to serious and incurable illness. Preventing a person from acting on a settled decision about their body and future therefore undermines this right.

It states further that the Constitution protects everyone’s inherent dignity and that this dignity includes respect for personal autonomy. As such, forcing a person to continue living in circumstances they experience as intolerable, against their wishes amounts to a failure to respect that person’s autonomous individuality.

SAVRS 2026 CONGRESS

13-15 JUNE THE CAPITAL ZIMBALI, KZN

Our Speakers

Prof Noemi Lois Dr Matias Iglicki www.savrs.co.za

8

Specialist Forum May 2026 | Vol. 26 No. 5

It contends that the law operates unevenly in that some people can bring about death by refusing treatment or stopping eating and drinking while others cannot do so because of the nature of their illness or disability. Wealthier individuals may travel overseas, while others cannot. DignitySA argues that this results in unequal operation of the law.

Further, it is argued that the right to life is linked to dignity and autonomy and that the prohibition may pressure some people to end their lives earlier than they wish, while they are still physically able to do so, which undermines the value the Constitution places on human life. DignitySA further argues that a patient forced to continue to endure unbearable suffering, against their will, is not being treated as a human being with dignity.

At the same time, concerns are often raised regarding the protection of vulnerable patients, the adequacy of safeguards, and the ethical obligations of healthcare practitioners, particularly within a resource-constrained healthcare system.

A comparison of South African end-of-life-laws is made with other constitutional democracies within the global context where medical assistance in dying is legal. It further states that South Africa already possesses the institutional, ethical, and professional infrastructure necessary to implement a regulated system to accommodate medical assistance in dying.

What the case could mean if the order is granted

If the court grants the order in favour of DignitySA, the legal position will not change immediately upon the granting of such an order.

Any declaration of constitutional invalidity by the High Court would require confirmation by the Constitutional Court. A court may suspend the order of invalidity to allow Parliament an opportunity to enact appropriate legislation, and the Constitutional Court may confirm, vary or set aside such suspension. During this period, the current prohibition on assisted suicide and voluntary euthanasia would remain in place.

Should legislation ultimately be introduced to regulate medical assistance in dying, it would mark a significant shift in South Africa’s legal and ethical framework governing end-of-life care.

Patients who meet the prescribed requirements may, in time, be able to lawfully request such assistance, subject to the framework enacted by Parliament. This would require corresponding amendments to professional guidelines, including those of the Health Professions Council of South Africa, and the development of clear clinical protocols and safeguards.

For healthcare facilities, practitioners, insurers, underwriters and brokers, the implications extend beyond the immediate legal position. A change in the law would necessitate careful consideration of clinical governance structures, ethical decisionmaking frameworks, professional liability exposure, policy wording, underwriting risk and claims assessment. It raises complex questions regarding how end-of-life decisions are documented, how patient consent is established and verified, how practitioners are supported within a regulated system, and how insurers classify and respond to deaths occurring in these circumstances.

In the interim, the position remains unchanged. Medical assistance in dying, assisted suicide and voluntary euthanasia are unlawful in South Africa, and healthcare practitioners may only withhold or withdraw treatment where it is no longer clinically indicated or is refused by a competent patient. SF

Photo credit: GettyImages/quantic69

INFECTIOUS DISEASES

FIDSSA 2026 Congress set to unite global infectious disease experts in Cape Town

The 11th Federation of Infectious Diseases Societies of Southern Africa (FIDSSA) Congress will take place from 18 to 20 June 2026 at the Cape Town International Convention Centre, bringing together leading voices in infectious diseases, microbiology, virology, and infection prevention and control. Hosted in the heart of the vibrant Mother City, the event is expected to continue FIDSSA’s tradition as one of the region’s most influential scientific gatherings.

F

IDSSA represents a collaborative network of Southern African societies focused on adult and paediatric infectious diseases, clinical microbiology, virology, and infection prevention. Its broader community includes Young FIDSSA and the South African Association of Clinical Microbiologists and Pathologists, and this year will also welcome colleagues from the Southern African Society of Travel Medicine, reflecting an expanding interdisciplinary approach to infectious disease challenges.

FIDSSA Congresses have long served as a key platform where clinicians, researchers, scientists, policymakers, and industry leaders converge to share knowledge and translate research into practice.

The 2026 programme is being curated as a world-class scientific agenda featuring emerging regional disease trends, cuttingedge research, and practical strategies to address the evolving infectious disease burden in Southern Africa and beyond.

Delegates can expect a comprehensive programme that includes keynote lectures, interactive panel discussions, hands-on workshops, abstract presentations, and poster sessions.

The congress will also provide opportunities for early-career researchers and established experts to exchange ideas, present novel findings, and build collaborative networks that strengthen regional and global responses to infectious diseases.

Among the plenary speakers is Prof Mo Archary (University of KwaZulu-Natal and Africa Health Research Institute), an expert in paediatric infectious diseases with a focus on TB and HIV outcomes, including long-acting therapeutic strategies. His work spans both clinical and implementation science, with involvement in global guideline development through WHO. Also featured is Prof Marc Blockman (University of Cape Town and Groote Schuur Hospital), a leading authority in clinical pharmacology and evidence-based medicine. His extensive leadership in South Africa’s Essential Drugs Programme and regulatory advisory committees reflects a strong commitment to rational medicine use and healthcare policy.

Prof Nelesh Govender (University of the Witwatersrand and National Institute of Communicable Diseases) will contribute expertise in fungal and bacterial epidemiology and antimicrobial resistance, with a focus on public health interventions in

resource-limited settings. His work supports WHO initiatives on antimicrobial resistance globally.

Other prominent speakers include Dr Ranmini Kularatne, a clinical microbiologist with international expertise in STI and infectious disease surveillance, Prof Marc Mendelson, a leading voice in antimicrobial resistance and antibiotic stewardship, and Prof Sikhulile Moyo, renowned for his contributions to pathogen genomics and viral evolution, including landmark HIV research and global recognition for his scientific impact.

Further contributions will come from Prof Mohlopheni Marakalala, whose research focuses on tuberculosis immunopathogenesis and host-directed therapies, Prof Nicolette du Plessis, a paediatric infectious disease specialist and FIDSSA President, Prof Megan Shaw, an expert in RNA virus biology and antiviral drug discovery, and Prof David Jay Weber from the University of North Carolina, a global leader in infection prevention and healthcare epidemiology.

With record-breaking attendance at the previous congress, FIDSSA 2026 is expected to further strengthen its role as a premier scientific meeting on the continent. The event will not only highlight advances in infectious disease research but also foster collaboration across disciplines and borders, reinforcing a shared commitment to improving patient care and public health outcomes in Southern Africa and globally.

To register, click here or scan the QR code. SF

11th FIDSSA Congress 18-20 June Cape Town Specialist Forum May 2026 | Vol. 26 No. 5

9

HEALTH AWARENESS

Photo credit: GettyImages/diego_cervo

Measure, manage, repeat Hypertension control starts here

May Measure Month (01 May-31 July), launched by the International Society of Hypertension, is a global blood pressure (BP) screening campaign aimed at increasing awareness of hypertension and encouraging adults aged ≥18-years to have their BP regularly checked. It also supports individuals with elevated readings by providing lifestyle and dietary advice and promoting appropriate follow-up to reduce long-term risk of cardiovascular disease (CVD), the leading cause of death globally.1,2

R

unning alongside this, Salt Awareness Week (11-17 May) highlights the role of excess salt intake in elevating BP. Global average salt intake is more than twice the World Health Organization (WHO) recommendation, at ~10.8g per day.

The 2026 theme, Salt It Out, focuses on reducing hidden dietary salt and encouraging healthier eating habits to support better BP control and overall CV health.2

Hypertension: The numbers are rising faster than awareness, and the risk factors are stacking up quietly in the background

According to Nweke et al., between 1990 and 2019, the prevalence of hypertension among adults doubled, reaching ~33% globally, with a disproportionate burden in low- and middle-income countries, where ~78% of affected adults reside.3 In Africa, prevalence is estimated at ~30.8%, with persistently lower awareness and control rates compared to high-income countries. In South Africa, ~48.2% of adults have hypertension, and ~33% are unaware of their condition, highlighting major gaps in detection and management.³ The systematic review and meta-analysis by Nweke et al. synthesised evidence on hypertension risk factors in South Africa using epidemiological modelling to improve risk stratification and prediction.

Age (>65-years) was a dominant non-modifiable predictor, with risk increasing significantly in older adults due to vascular ageing 10 Specialist Forum May 2026 | Vol. 26 No. 5

and arterial stiffening. It should be noted that South Africans develop hypertension earlier compared to high-income settings.3 Diabetes showed a strong, consistent association with hypertension through metabolic and vascular mechanisms.

Ethnicity, particularly mixed-race populations, was linked to higher risk, reflecting complex interactions between genetics, lifestyle, and socio-economic disadvantage.3 Socioeconomic status and education demonstrated inverse relationships with hypertension through stress pathways, health literacy, and access to care. Body mass index (BMI) and smoking contributed to risk but with less consistent predictive strength across studies.3

Less theory, more cuffs: making hypertension screening count

Nweke et al. translate epidemiological risk into practical action, recommending:3 S Routine BP screening for adults ≥50-years with diabetes at every clinical encounter S Earlier follow-up in higher-risk mixed-race populations S Strengthened integration of hypertension and diabetes care pathways to improve detection, management, and continuity of care.

At community level, they call for targeted outreach in high-risk groups and expanded use of task-shifting through primary care and community health workers to improve early identification and long-term control.3

HEALTH AWARENESS Tight targets, smarter teams, better BP control – the 2025 ACC/AHA guidelines in a nutshell

The 2025 American College of Cardiology (ACC) and American Heart Association (AHA) guideline reinforces hypertension as the leading modifiable risk factor for CVD, including coronary artery disease (CAD), stroke, heart failure (HF), atrial fibrillation (AFib), chronic kidney disease (CKD), dementia, and premature mortality.

The guideline recommends a universal BP target of <130/80mmHg for most adults, with individualised adjustments for pregnancy, limited life expectancy, or institutional care.4 Hypertension is classified as normal (<120/80mmHg), elevated (120-129/<80mmHg), stage 1 (130-139/80-89mmHg), and stage 2 (≥140/90mmHg). Lifestyle modification remains foundational, including weight management, Dietary Approaches to Stop Hypertension (DASH)-style diet, sodium reduction, increased physical activity, stress control, and limiting alcohol intake.4 Pharmacotherapy is recommended for all adults with BP ≥140/90mmHg, and for selected patients with BP ≥130/80mmHg based on CV risk (≥7.5% 10-year risk), diabetes, CKD, prior stroke, or established CV disease. If risk is lower, a three- to six-month trial of lifestyle change is recommended before starting medication.4 For stage 2 hypertension, combination therapy using two firstline agents in a single-pill formulation is preferred to improve adherence and speed up control. Home BP (HBP) monitoring, combined with structured multidisciplinary care, is strongly recommended, while cuffless wearable devices are not yet considered reliable.4 The guideline also emphasises system-level interventions, including team-based care involving physicians, nurses, pharmacists, and community health workers, alongside partnerships with communities to improve screening and control rates. Severe hypertension (>180/120mmHg) without acute endorgan damage should be managed promptly in outpatient settings with medication initiation or intensification.4

Hypertension rarely plays solo: Why most patients need a smart combination

According to the ACC/AHA, pharmacotherapy is central to hypertension management, as BP is regulated by multiple interacting physiological systems. As a result, most patients require two or more antihypertensive agents to achieve adequate control. Historically, treatment followed a stepwise approach, beginning with monotherapy and escalating doses or adding agents as needed.4 Current recommendations prioritise thiazide-type diuretics, longacting dihydropyridine calcium channel blockers (CCBs), and either ACE inhibitors (ACEi) or angiotensin receptor blockers (ARBs) as first-line therapy to reduce CV risk.4 For adults with stage 2 hypertension (≥140/90mmHg), initiation with two first-line agents from different classes – preferably as a single-pill combination – is recommended to improve BP control and adherence.4 In stage 1 hypertension (130-139/80-89mmHg), starting with a single first-line agent is appropriate, with subsequent titration or addition of therapies if needed. Importantly, the combined use of ACEi, ARBs, and/or direct renin inhibitors is not recommended due to an increased risk of adverse outcomes.4

Thiazide-type diuretics

Agents: Chlorthalidone, hydrochlorothiazide, indapamide Recommendations: Chlorthalidone is preferred due to longer half-life and greater potency. Monitor for electrolyte disturbances (hyponatraemia, hypokalaemia), and increases in glucose, uric acid, and calcium. Use caution in patients with a history of gout.

ACEi

Agents: Benazepril, captopril, enalapril, fosinopril, lisinopril, moexipril, perindopril, quinapril, ramipril, trandolapril Recommendations: Avoid combination with ARBs or direct renin inhibitors. Monitor for hyperkalaemia and renal function, especially in CKD. Contraindicated in pregnancy, bilateral renal artery stenosis, and history of ACEi-induced angioedema.

ARBs

Agents: Azilsartan, candesartan, eprosartan, irbesartan, losartan, olmesartan, telmisartan, valsartan Recommendations: Do not combine with ACEi or renin inhibitors.

Monitor for hyperkalaemia and renal impairment. May be used after ACEi-induced angioedema (after washout). Avoid in pregnancy.

CCBs – dihydropyridines

Agents: Amlodipine, felodipine, isradipine, nicardipine SR, nifedipine LA, nisoldipine Recommendations: Effective antihypertensives, may cause dose-related peripheral oedema, particularly in women.

Alternative agents

CCBs – non-dihydropyridines Agents: Diltiazem, verapamil Recommendations: Avoid with beta blockers due to risk of bradycardia and heart block. Contraindicated in HF with reduced ejection fraction. Be aware of CYP3A4 drug interactions.

Loop diuretics Agents: Bumetanide, furosemide, torsemide Recommendations: Preferred in HF and moderate-to-severe CKD (glomerular filtration rate [GFR] <30ml/min). Torsemide preferred for hypertension due to longer action. Consider in patients intolerant to thiazides (eg hyponatraemia).

When three drugs aren’t enough

In adults with resistant hypertension, a thorough evaluation for secondary causes is recommended, including a careful review of medications that may interfere with BP control, as this can help simplify and optimise treatment.4 For patients who remain uncontrolled despite optimal firstline therapy – typically a combination of an ACEi or ARB, a CCB, and a thiazide-like diuretic (chlorthalidone or indapamide) – the addition of a mineralocorticoid receptor antagonist (MRA) is recommended, provided renal function is adequate (estimated GFR ≥45 mL/min/1.73 m²).4 If MRAs are not tolerated or contraindicated, alternative agents such as amiloride, beta blockers, alpha blockers, central sympatholytics, endothelin receptor antagonists, or direct vasodilators may be considered.4 In selected patients with persistent hypertension despite optimal Specialist Forum May 2026 | Vol. 26 No. 5

11

HEALTH AWARENESS therapy or those unable to tolerate additional medication, renal denervation may be considered as an adjunct to pharmacological and lifestyle treatment. This approach requires multidisciplinary evaluation and shared decision-making, balancing potential benefits against procedural risks.4

Three hypertension guidelines, three slightly different rulebooks

The European Society of Cardiology (ESC) and the European Society of Hypertension (ESH) published separate guidelines for the management of arterial hypertension, in 2024 and 2023 respectively. In table 1, we look at a comparison between the three guidelines.5,6,7

Conclusion

Hypertension is a silent, progressive driver of CVD, yet it is one of the most modifiable risk factors in clinical practice. May Measure Month and Salt Awareness Week highlight the importance of early detection, lifestyle change, and population-level prevention, particularly in high-risk settings such as South Africa. Evidence from Nweke et al. reinforces the need for targeted screening and integrated care, while contemporary ACC/AHA guidance supports tighter BP targets, combination therapy, and multidisciplinary management. Ultimately, improving outcomes depends on moving from awareness to action – measuring BP, reducing dietary salt, and closing the gap between diagnosis and control.

References are available on request. SF

Table 1: Comparison of the 2023 ESH guidelines, 2024 ESC and 2025 ACC/AHA Area of Comparison

2025 ACC/AHA guidelines

2024 ESC Guidelines

2023 ESH guidelines

BP monitors

Validated automated cuff device, appropriate cuff size

Validated upper-arm cuff BP device, appropriate cuff size

Validated upper-arm cuff BP device, appropriate cuff size

Office BP (OBP) methodology

Multiple readings per visit, adequate rest period

3 readings per visit, 5 min rest

3 readings per visit, 5 min rest

>10mmHg

>15-20mmHg

Inter-arm office SBP >15mmHg (recommended for difference requiring evaluation evaluation) Out-of-office BP measurements

Recommended for confirmation of Recommended diagnosis

Strongly encouraged

BP measurement in AFib

Auscultation preferred in AFib

Auscultation

Oscillometric/auscultation

Screening

Regular screening for adults, riskbased approach

Annually >40-years (untreated with elevated BP), at least every 3 years <40-years

Regular BP measurements: >40years, <40-years if high CV risk, screening interval not set

Diagnosis/confirmation

Confirmed elevated readings on separate visits, out-of-office BP for confirmation

OBP + ambulatory BP (ABP) and/ or HBP, repeated OBP if ABP/HBP unfeasible

OBP at least 2 visits (4- weeks apart) unless severe hypertension, ABP/HBP add prognostic value

Classification

Normal, elevated, hypertension stage 1, stage 2

Non-elevated and elevated hypertension

Optimal, normal, high- normal, hypertension grades 1-3 and stages 1-3

CV risk estimation

Predicting Risk of Cardiovascular Disease EVENTs (PREVENT) equations (10-year total CVD risk), risk-based treatment approach

High risk conditions, Systematic Coronary Risk Evaluation 2 (SCORE2), SCORE2-older persons (OP), risk modifiers

High risk conditions; SCORE2, SCORE2-OP, risk modifiers

Patient selection for drug treatment

Risk-based approach using PREVENT equations, consider CVD risk factors

≥130/80mmHg + CVD, diabetes, familial hypercholesterolaemia, CKD, hypertension-mediated organ damage, 10-yr CV risk ≥10%, ≥130/80mmHg + 10-yr CV risk 5%-<10% with upclassification via non-traditional risk modifiers ≥140/90mmHg

≥130/80mmHg + CAD, ≥140/90mmHg, ≥160mmHg if ≥80-years

Secondary hypertension

Detailed evaluation for secondary causes, screen for primary aldosteronism in resistant hypertension

Screening for primary aldosteronism in all hypertensives

Disease-guided diagnostic evaluation upon clinical suspicion

Pharmacological treatment steps

Risk and patient-guided approach, • Low-dose dual combination with any combination therapy preferred two from RAS blocker/CCB/thiazide/ (see below) thiazide-like

• Low-dose dual combination with RAS blocker + CCB or thiazide/ thiazide-like diuretic

• RAS blocker + CCB + thiazide/ thiazide-like Pharmacological treatment – Lower-risk patients, patientmonotherapy indications specific considerations

• Increase to full dose

• Increase to full dose

• RAS blocker + CCB + thiazide/ thiazide-like

• 130-139/80-89mmHg

• ≤150/95mmHg + low CV risk

• Symptomatic orthostatic hypotension

• 130-139/80-89mmHg + high CV risk

• Frail and/or old

• Frail and/or old On-treatment BP target

<130/80mmHg for most adults

• 120-129/70-79mmHg

• <130/80mmHg in most hypertensives up to 79-years • 140-150mmHg if ≥80-years

12 Specialist Forum May 2026 | Vol. 26 No. 5

Photo credit: GettyImages/wildpixel

HEALTH AWARENESS

Navigating MS diagnosis together Multiple sclerosis (MS) affects millions of people worldwide, yet it remains frequently misdiagnosed, with error rates estimated at approximately 20%. This diagnostic uncertainty can delay treatment and worsen long-term outcomes.

In response, World MS Day, observed annually on 30 May, adopts the 2026 theme My MS Diagnosis: Navigating MS Together, emphasising the importance of early, accurate diagnosis and equitable access to care. As global prevalence continues to rise, there is an urgent need for healthcare systems that are not only clinically effective, but also responsive, informed, and patient-centred.1,2,3 Understanding the disease process

MS is a chronic autoimmune disorder characterised by immunemediated damage to the central nervous system (CNS). In this condition, the immune system mistakenly targets the myelin sheath – the protective layer surrounding nerve fibres – disrupting the transmission of electrical signals. The result is neuroinflammation, demyelination, and axonal injury, processes that ultimately contribute to progressive neurological disability over time.1,4 Repeated cycles of inflammation and partial repair lead to the formation of sclerotic plaques within the CNS. Clinically, this manifests as a broad and often unpredictable spectrum of symptoms, including visual disturbances, motor weakness, sensory deficits, and impaired coordination.¹ Importantly, ongoing neurodegeneration contributes to cognitive decline and irreversible disability, positioning MS as one of the leading causes of neurological disability in young adults, particularly among women.¹

The growing global footprint

Epidemiological data highlight the increasing burden of MS worldwide. Over the past three decades, global prevalence has risen by ~26%. A 2024 report estimated that 1.89 million individuals were living with MS in 2021, corresponding to 23.9 cases per 100 000 population.¹ In Southern Africa, incidence rates were reported at nine per

100 000 in 2020, with projections suggesting an increase to >20 per 100 000 across Africa by 2050. These trends reflect not only improved detection but also a genuine increase in disease burden, underscoring the need for strengthened healthcare infrastructure and long-term planning.1,4

MS across the lifespan

MS most commonly presents between the ages of 20 and 40 years, although paediatric cases do occur. About 3%-10% of individuals present before age 16, and fewer than 1% before age 10. Initial presentation often takes the form of a clinically isolated syndrome, frequently involving the optic nerve, brainstem, or spinal cord.5,6 Relapses typically develop over hours to days, stabilise, and then gradually improve. However, even when clinical recovery appears complete, subclinical damage often persists. Magnetic resonance imaging (MRI) demonstrates that for every clinical relapse, there are ~10 silent lesions, indicating a much higher underlying disease burden. Over time, incomplete recovery and cumulative damage lead to progressive disability as neuronal reserve declines.7 Disease progression varies. Relapsing-remitting MS is the most common form, while secondary progressive MS develops in ~15%20% of patients over time. Primary progressive MS, characterised by gradual decline from onset, is less common but often more disabling. Paediatric MS differs in presentation, with 98% of Specialist Forum May 2026 | Vol. 26 No. 5

13

HEALTH AWARENESS children experiencing a relapsing-remitting course and more frequent relapses than adults.6,8

Risk factors and pathogenesis

widely and is influenced by factors such as disease course, relapse frequency, lesion burden, and recovery between episodes.8 Favourable prognostic indicators include female sex, sensory symptoms, and long intervals between relapses, while poorer outcomes are associated with progressive disease, frequent relapses, and early disability accumulation.⁸

MS arises from a complex interplay between genetic susceptibility, environmental exposures, and immune dysregulation. Heritability is estimated between 35% and 75%, with a strong association linked to the human leukocyte The African context: Barriers to care antigen region. However, no single causative gene In sub-Saharan Africa, MS care is constrained 7 has been identified. by significant systemic challenges. Limited More than 62 000 Environmental factors also play a critical specialist availability – estimated at just 0.03 new cases are role. Vitamin D deficiency has been strongly neurologists per 100 000 people – contrasts implicated, supported by geographical patterns sharply with far higher ratios in high-income diagnosed every showing increasing prevalence with distance regions. Access to diagnostic tools such as year (~169 per from the equator.⁷ Infectious agents, smoking, MRI is also severely limited, with only 0.7 day), with an and possibly central nervous system trauma have scanners per million people reported in 2017.12 also been associated with increased risk and Access to treatment remains a major barrier, estimated 16 000 7 disease severity. with high costs placing disease-modifying deaths annually Two main hypotheses attempt to explain therapies out of reach for many patients. attributed to MS disease initiation. The ‘outside-in’ model These disparities highlight the need for proposes that immune activation begins in the targeted interventions to improve awareness, periphery before targeting the CNS, while the infrastructure, and affordability.12 ‘inside-out’ model suggests that primary CNS dysfunction triggers secondary immune responses.7 Looking ahead: Bridging the gaps Improving MS care in Africa will require coordinated, multi-level Advances in diagnosis strategies. Integrating MS into national health policies, expanding Diagnostic criteria for MS have evolved significantly, with the access to affordable treatments, and strengthening healthcare 2024 revision of the McDonald criteria aiming to improve early infrastructure are essential steps. Regional collaboration and detection while maintaining diagnostic accuracy. A notable pooled procurement strategies may help reduce medication costs, update is the inclusion of the optic nerve as a fifth anatomical while telemedicine and rehabilitation services can extend care to site for demonstrating dissemination in space, allowing additional underserved populations.12 diagnostic tools such as optical coherence tomography and visual Equally important is investment in education and training, evoked potentials.9 alongside the development of patient support networks that Criteria have also been streamlined, enabling diagnosis based provide both practical and emotional support. These initiatives on fewer requirements in certain contexts. Dissemination in time are key to reducing stigma, improving disease understanding, and is no longer mandatory in specific scenarios when characteristic enhancing quality of life for people living with MS.¹³ imaging or cerebrospinal fluid findings are present. These changes facilitate earlier diagnosis, which is critical for timely initiation Conclusion of therapy.9 The 2026 World MS Day theme, My MS Diagnosis: Navigating MS Together, underscores the importance of shared responsibility Treatment approaches and symptom management in addressing the growing burden of MS. While advances in Management of MS focuses on three key areas: Treating diagnostics and treatment offer hope, significant disparities in acute relapses, alleviating symptoms, and modifying disease access to care persist. Achieving meaningful progress will require progression. Disease-modifying therapies are central to treatment a combination of early diagnosis, equitable access to treatment, and should be initiated promptly following diagnosis to reduce and sustained global and regional collaboration. Only through 7 inflammatory activity and delay progression. these efforts can MS care evolve into a system that truly supports Spasticity, affecting ~80% of patients, represents a major every individual living with the disease. therapeutic challenge. It results from CNS damage leading to References are available on request. SF increased muscle tone, spasms, and pain. Management follows a stepwise approach, beginning with non-pharmacological strategies such as physiotherapy and progressing to pharmacological interventions.10,11

Prognosis and disease course

MS follows several clinical trajectories, with relapsing-remitting disease accounting for 70%-80% of cases. Other forms include primary progressive, secondary progressive, and less common variants such as progressive-relapsing disease. Prognosis varies 14 Specialist Forum May 2026 | Vol. 26 No. 5

Multiple Sclerosis Awareness Day

30 May

HEALTH AWARENESS

Photo credit: GettyImages/Jikaboom

Nicotine hooks deep, making quitting hard

Cigarette smoking is one of the most significant – and preventable – causes of death globally. Each year, it claims more lives than HIV, alcohol use, drug-related harm, road traffic accidents, and firearm-related injuries combined. By 2030, tobacco use is projected to cause more than eight million deaths annually, with the greatest burden falling on low- and middle-income countries. World No Tobacco Day 2026, themed Unmasking the appeal – countering nicotine and tobacco addiction, highlights the tactics used by the tobacco industry to sustain addiction and calls for stronger regulation, while empowering the public – particularly the youth – to resist and quit.1,2

T

obacco use remains highly prevalent in South Africa.

According to the 2024 Global Adult Tobacco Survey, 29.4% (12.7 million) of individuals aged ≥15-years reported tobacco use in 2021, including 41.7% of men and 17.9% of women.³ Smoking remains the dominant form, affecting 25.8% (11.1 million) adults, with 21.2% (9.1 million) reporting daily smoking.3 Smokeless tobacco products, such as snuff and chewing tobacco, are used by 4.3% (1.8 million), while awareness of electronic cigarettes has reached 36.1%, with 6.2% having ever used them and 2.2% currently using them.³ Exposure to secondhand smoke is also widespread. Among indoor workers, 11.2% report exposure in the workplace, while 18%

are exposed at home. Public exposure remains particularly high in bars, taverns, and nightclubs (74.4%), with lower but notable exposure reported in universities, restaurants, cafes, government buildings, healthcare facilities, and public transport.³

Health risks associated with tobacco use

Tobacco smoke contains more than 4000 toxic chemical compounds, many of which enter the bloodstream and are distributed throughout the body.

These substances contribute to DNA damage, abnormal cell growth, and tumour formation. Among the most harmful are carbon monoxide, cyanide, formaldehyde, arsenic, cadmium, and Specialist Forum May 2026 | Vol. 26 No. 5

15

HEALTH AWARENESS tobacco-specific nitrosamines – key carcinogenic agents linked to neurobiological systems, including dopaminergic, serotonergic, and cancer development.¹ noradrenergic pathways, further reinforcing addiction.⁵ The health burden is substantial. Smoking damages nearly every organ and is strongly associated with cancer, cardiovascular Nicotine replacement therapy: an disease, and chronic lung disease. It is responsible for ~90% of evidence-based solution lung cancer deaths and 80% of deaths from chronic obstructive Nicotine replacement therapy (NRT) provides a structured pulmonary disease. Smokers have a mortality risk around three approach to smoking cessation by delivering controlled doses of times higher than non-smokers, with risk increasing according to nicotine without the harmful chemicals found in tobacco smoke. both duration and intensity of smoking.¹ This helps reduce withdrawal symptoms while allowing individuals Secondhand smoke exposure also to gradually break both the chemical dependence carries significant risk. It contributes to and behavioural habit of smoking.6 cardiovascular (CV) disease, stroke, lung NRT is available in several forms, including Tobacco addiction cancer, and respiratory illness in nonpatches, gum, and oromucosal sprays, allowing smokers, including children. Even brief for individualised treatment based on patient drives disease, exposure can have harmful CV effects, while preference and level of dependence. These mental distress, long-term exposure may increase CV risk by products deliver nicotine more slowly and at and inequality, up to 30%.¹ lower concentrations than cigarettes, reducing Electronic cigarettes, although often the risk of addiction reinforcement while yet effective, perceived as safer alternatives, still alleviating cravings.6-12 evidence-based expose users and bystanders to nicotine, The evidence supporting NRT is strong. A large tools like NRT can carcinogens, heavy metals, and other Cochrane review involving >64 000 participants toxic substances. They are therefore not found that NRT increases long-term smoking improve long-term considered safe, particularly for children, cessation rates by ~50% to 60% compared with quit success rates adolescents, and pregnant women.¹ placebo or no treatment.¹³ Combination therapy – such as using a nicotine Tobacco use, patch with a fast-acting form like gum or spray – mental health and behaviour has been shown to further improve quit rates by approximately Beyond physical health, tobacco use is associated with broader 27%. Higher-dose patches and initiating therapy prior to the quit behavioural and mental health risks. Findings from the South date may also enhance outcomes.14 African National Health and Nutrition Examination Survey show NRT is generally safe and well tolerated. Most side effects are that daily tobacco users are significantly more likely to experience mild and localised, such as skin irritation with patches or oral psychological distress and post-traumatic stress disorder discomfort with gum. Serious adverse events are rare, making NRT compared with non-users. Tobacco use is also strongly associated a practical and accessible option for many individuals attempting with problematic alcohol consumption, regardless of whether use to quit.15 4 is past, occasional, or daily.

In addition, tobacco users are more likely to exhibit unhealthy Conclusion lifestyle behaviours. These include inadequate fruit intake, higher Tobacco use continues to impose a substantial burden on public consumption of salty foods, and poorer hygiene practices such as health in South Africa and globally. It contributes to chronic inconsistent handwashing before meals. Interestingly, tobacco use disease, worsens mental health outcomes, and is closely linked was inversely associated with physical inactivity. Overall, these to multiple unhealthy behaviours. Although many smokers are findings suggest that tobacco use clusters with multiple unhealthy motivated to quit, nicotine’s addictive properties make sustained 4 behaviours, compounding its overall impact on health. cessation difficult without support. Nicotine replacement therapy offers an effective, evidence-based strategy to improve quit Why quitting is difficult success by reducing withdrawal symptoms and supporting Despite high levels of awareness, quitting smoking remains behavioural change. Expanding access to cessation support, challenging. Data show that 65.7% of smokers are considering alongside stronger public health interventions, remains essential to quitting, and 40.5% have attempted to quit in the past year. reducing the long-term impact of tobacco use.

However, only 42.9% report receiving advice to quit from a References are available on request. SF healthcare provider.³ Nicotine addiction is driven by a combination of physical, psychological, and behavioural dependence. Once inhaled, nicotine is rapidly absorbed into the bloodstream and reaches the brain within seconds. There, it binds to nicotinic acetylcholine receptors, stimulating the release of dopamine in reward pathways and reinforcing continued use.1,5 Over time, this creates a cycle of dependence characterised by cravings, withdrawal symptoms, and habitual behaviours linked to daily routines or stress. Nicotine also interacts with multiple

World No Tobacco Day

31 May

16 Specialist Forum May 2026 | Vol. 26 No. 5

Photo credit: GettyImages/Westend61

ONLINE CPD

Winter sniffles? Allergy or virus –

know the difference

H

istorically, AR was first described as ‘hay fever’ in the 18th century, based on the mistaken belief that fresh hay triggered symptoms. This was later refined when pollen was identified as the primary cause of seasonal allergic rhinitis (SAR), leading to the broader concept of ‘allergy’.² Today, AR is recognised as a multifactorial condition influenced by environmental exposures and genetic susceptibility. Common triggers include pollens, house dust mites, mould, and animal dander. Climate change is increasingly contributing to disease burden, with rising temperatures and carbon dioxide levels prolonging pollen seasons and enhancing allergen potency.¹ Clinically, AR is characterised by nasal symptoms such as sneezing, itching, rhinorrhoea, and congestion, often accompanied by ocular symptoms like red, itchy, and watery eyes. Physical signs, including allergic shiners and a transverse nasal crease, are particularly evident in children.1,2 The condition is classified as intermittent or persistent, depending on symptom frequency and duration, and may present as seasonal, perennial, or a combination of both. Seasonal disease typically causes acute symptoms such as sneezing and watery eyes, whereas perennial AR is more commonly associated with chronic nasal obstruction and post-nasal drip.2,3 The underlying pathophysiology involves an early-phase allergic response occurring within minutes of allergen exposure, during which mast cells release histamine and other mediators.

This leads to acute symptoms such as sneezing and mucus production. A late-phase response follows several hours later, characterised by infiltration of inflammatory cells and sustained nasal congestion. In some individuals, non-IgE-mediated mechanisms contribute to ongoing hypersensitivity, making the nasal mucosa reactive to irritants such as cold air or smoke.³ AR can significantly impact quality of life, particularly in moderate-to-severe cases. Symptoms may disrupt sleep, impair concentration, and cause fatigue and headaches. If left untreated, AR increases the risk of complications, including sinusitis,

Allergic rhinitis (AR), commonly known as hay fever, is a chronic inflammatory condition of the nasopharynx driven by immunoglobulin E (IgE)-mediated responses to inhaled allergens.

It is highly prevalent, affecting 20%-30% of adults and up to 40% of children, and is closely linked to asthma. Up to 80% of individuals with asthma have coexisting AR, while 20%-30% of those with AR have asthma, highlighting the importance of integrated management to improve overall respiratory outcomes.1,2 recurrent ear infections in children, and worsening asthma control.

Cold weather can further exacerbate symptoms by increasing airway reactivity and inflammation, contributing to persistent symptoms during winter months.4,5,6 Diagnosis is primarily clinical, based on a detailed history and physical examination. Confirmation may involve serum-specific IgE testing or skin prick testing, particularly in cases where symptoms are severe, persistent, or unresponsive to empiric therapy.³ However, AR is frequently misdiagnosed, with conditions such as non-allergic rhinitis, infections, anatomical abnormalities, or paediatric disorders mimicking its presentation. Accurate differentiation from colds and influenza is especially important during winter, as overlapping symptoms can lead to inappropriate management.7,8,9 Management of AR requires a comprehensive approach combining allergen avoidance, pharmacotherapy, and, where appropriate, immunotherapy. Environmental control measures – such as reducing exposure to dust mites, maintaining optimal indoor humidity, and limiting contact with allergens – form the foundation of care.10 Pharmacological treatment includes second-generation antihistamines, intranasal corticosteroids (INCS), and leukotriene receptor antagonists. INCS remain the most effective therapy for controlling nasal inflammation and congestion.10 For patients with persistent or moderate-to-severe symptoms, combination therapy has emerged as a highly effective strategy.

Intranasal corticosteroid and antihistamine combinations provide faster and more comprehensive symptom relief than monotherapy, improving overall disease control. Allergen immunotherapy may be considered in selected patients, particularly those with refractory or severe disease.

In summary, AR is a common yet often underestimated condition with significant clinical and quality-of-life implications. Its strong association with asthma, potential for misdiagnosis, and increasing environmental burden underscore the need for early recognition and targeted management. A structured, patient-centred approach can significantly improve symptom control and long-term outcomes.

To access the article and quiz, click here. SF Specialist Forum May 2026 | Vol. 26 No. 5

17

ALLERGOLOGY

Photo credit: GettyImages/PeopleImages

Bilastine redefines modern

non-sedating allergy control Allergic rhinitis (AR) is a common condition affecting between 25% of children and 40% of adults globally. AR is typically classified as either seasonal (intermittent) or perennial (chronic), with ~20% of patients experiencing seasonal disease, 40% perennial symptoms, and the remaining 40% exhibiting a mixed pattern.1,2

A

ccording to the AR and its Impact on Asthma (ARIA) guidelines, the diagnosis of AR relies on characteristic clinical symptoms together with supportive laboratory evidence of allergic sensitisation or inflammation. Clinically, patients should present with at least two symptoms lasting for more than one hour on most days, including watery rhinorrhoea, paroxysmal sneezing, nasal obstruction, and nasal pruritus, with or without associated conjunctivitis.1 Beyond nasal complaints, AR is frequently associated with extranasal manifestations including allergic conjunctivitis, dry cough, Eustachian tube dysfunction, and chronic sinusitis. Emerging evidence also highlights a clinically meaningful link between rhinitis – particularly AR – and urticaria, an inflammatory skin disorder characterised by transient wheals, angioedema, or both, occurring without systemic symptoms.2,3 A meta-analysis showed a significant bidirectional association between rhinitis and urticaria, with co-occurrence rates of 17.6% and 31.3% respectively and an overall more than two-fold increased risk of overlap (odd ratio 2.67).3 This observed epidemiological overlap is further supported by shared underlying immunopathological mechanisms that link both conditions within a broader allergic and immune dysregulation spectrum.4 AR and chronic spontaneous urticaria are increasingly recognised as part of a shared immunoglobulin E (IgE)-mediated and immune dysregulation spectrum, driven by overlapping pathways involving genetic susceptibility, autoimmune activation (including IgE- and IgG/IgM-mediated mechanisms), and, in some cases, coagulation cascade involvement, all converging on mast cell activation.3,4

Allergy triggers are everywhere

Building on their shared mast-cell-driven pathology, AR and urticaria are also closely linked by overlapping external triggers 18 Specialist Forum May 2026 | Vol. 26 No. 5

that precipitate or amplify disease activity. Both conditions are commonly triggered by environmental allergens, infections, medications, and physical or environmental stimuli.1,4 In AR, IgE-mediated type I hypersensitivity reactions are central, with common allergen sources including foods (such as peanuts, shellfish, eggs, wheat, soy, and cow’s milk), animal dander, and house dust mites. Indoor exposures – particularly house dust mites, cockroaches, and pet dander – are among the strongest risk factors, with additional contribution from the ‘hygiene hypothesis’, which suggests that reduced microbial exposure may impair immune maturation and favour allergic sensitisation.1,4 In house dust mite-driven disease, key allergens can disrupt normal immune regulation by amplifying IgE production, impairing surfactant-mediated allergen clearance, and weakening epithelial tight junction integrity, thereby increasing airway permeability and inflammation.¹ A similar trigger spectrum is seen in urticaria, where acute disease (<6-weeks) is most often associated with infections, foods, or drugs, while chronic urticaria (>6-weeks) is divided into chronic spontaneous urticaria (CSU) – in which no clear trigger is identified – and chronic inducible urticaria (CIndU), where specific and reproducible stimuli can be identified.4 CSU is multifactorial, arising from genetic susceptibility and immune dysregulation, with IgE- or IgG/IgM-mediated autoimmune pathways, systemic disease associations, and sometimes coagulation cascade activation all contributing to mast cell degranulation.4 In contrast, CIndU is directly provoked by defined triggers such as pressure, cold, heat, vibration, or sunlight, as well as nonphysical stimuli including contact exposures, water, or cholinergic responses to heat or exercise, with diagnosis confirmed through provocation testing.4 These findings underscore a strong bidirectional relationship between upper airway and cutaneous allergic disease. Clinicians

FOR HEALTHCARE PROFESSIONALS ONLY

Rapid Onset of Action*2

Well-Documented Efficacy*2,3

Non-sedating Antihistamine3,4

Ilaxten® is effective within 1 h after administration and has a long duration of action2 (lasts for 24 hrs).4

Ilaxten® effective in relieving symptoms such as sneezing, nasal discharge, nasal itching, nasal congestion, ocular itching, tearing and ocular redness.4

Based on the brain H1-receptor occupancy, Ilaxten® can be distinguished as a non-brainpenetrating antihistamine.3

h, hour; hrs, hours; H1, histamine 1 Single center, double-blind, randomised, placebo- controlled, balanced four-treatment, four-period crossover phase II study performed outside of the pollen season in individuals with asymptomatic Seasonal Allergic Rhinitis.2 Seventy-five allergic volunteers were challenged in the Vienna Challege Chamber (VCC) with grass pollen on two consecutive days of allergen provocation; 6 h on day 1 and 4 h day 2. Bilastine 20 mg, cetirizine 10 mg, fexofenadine 120 mg, or placebo were taken orally 2 h after the start of provocation on day 1 only.

Primary objectives: Total nasal symptom scores.

Secondary objectives: The speed of onset of action and the duration of action of each active medication were assessed. The global symptom scores, nasal secretions, and eye symptoms were assessed on both day 1 and day 2. *

Indications and Dosage Therapeutic Indications

Ilaxten® is indicated for the symptomatic treatment of seasonal allergic rhinitis (SAR), perennial allergic rhinitis (PAR) and idiopathic chronic urticaria (ICU) in adults and adolescents (12 years and over).4

Posology

Ilaxten® 20 mg once daily should be taken one hour before or two hours after intake of food or fruit juice.4

• The adverse drug reactions (ADRs) most commonly reported by patients receiving 20 mg ILAXTEN® were headache, somnolence, dizziness and fatigue.4 • Coadministration of ILAXTEN® and P-glycoprotein inhibitors should be avoided in patients with moderate or severe renal impairment.4 References: 1. Marple BF, Fornadley JA, Patel AA, et al. Keys to successful management of patients with allergic rhinitis: focus on patient confidence, compliance, and satisfaction. Otolaryngol Head Neck Surg.

2007;136(6suppl):s107-s124. 2. Horak F, Zieglmayer P, Zieglmayer R, Lemell P. The effects of bilastine compared with cetirizine, fexofenadine, and placebo on allergen-induced nasal and ocular symptoms in patients exposed to aeroallergen in the Vienna Challenge Chamber. Inflamm Res. 2010;59(5):391-398. 3. Kawauchi H, Yanai K, Wang DY, Itahashi K, Okubo K. Antihistamines for Allergic Rhinitis Treatment from the Viewpoint of Nonsedative Properties. Int J Mol Sci. 2019;20(1):213. Published 2019 Jan 8. 4. Ilaxten (Bilastine 20 mg tablets), Professional Information (PI), Menarini South Africa (Pty) Ltd., April 2022.

S2 ILAXTEN® 20. Reg. No: 52/5.7.1/0120. COMPOSITION: Each 20 mg tablet contains 20 mg bilastine. Sugar free. PHARMACEUTICAL FORM: Oval, biconvex, scored, white tablets.

INDICATIONS: Symptomatic treatment of seasonal allergic rhinitis (SAR), perennial allergic rhinitis (PAR) and idiopathic chronic urticaria (ICU) in adults and adolescents (12 years and over). PHARMACOLOGICAL CLASSIFICATION: A 5.7.1 Antihistaminics For full prescribing information, please refer to the approved professional information.

HOLDER OF CERTIFICATE OF REGISTRATION: Menarini South Africa (Pty) Ltd., Reg No. 2022/831217/07. Waterside Place, Unit 02D, South Gate Office Park, Carl Cronje Drive, Tygervalley, Cape Town, 7530. Tel: +27 21 109 6444 Menarini South Africa is a Menarini Group company. Visit the website www.menarini.com

ILAXTEN® PI Scan for more information

Bilastine 20 mg

ZA-ILA-8-2025

Patients with allergic rhinitis want rapid-onset and long-lasting symptom relief without side effects from treatment.1

ALLERGOLOGY should be aware of this overlap and consider evaluating for concomitant nasal and skin symptoms to improve comprehensive patient management.3

From sneezes and itches to science-driven relief

Trigger avoidance and education are strongly recommended in the management of AR and urticaria. Treatment of AR combines symptom control with strategies aimed at modifying the underlying allergic response. Symptomatic therapies remain the cornerstone of treatment and include antihistamines, intranasal or oral corticosteroids, leukotriene receptor antagonists, and nasal decongestants.1 Second-generation oral antihistamines (AH) such as bilastine are preferred due to their improved safety and reduced sedative effects compared to older first-generation agents. Intranasal AH provide targeted delivery directly to inflamed nasal mucosa.1 Most patients with urticaria require a stepwise pharmacological approach. First-line therapy consists of daily second-generation H1 AH, which selectively block peripheral H1 receptors and are less sedating than first-generation agents, improving pruritus, wheal formation, and lesion duration. If response is inadequate, the dose can be increased up to fourfold.4

Bilastine in focus: Everyday allergy relief without sedation

Bilastine is a second-generation, highly selective H1-AH developed for the symptomatic treatment of seasonal and perennial AR as well as chronic idiopathic urticaria in adults and adolescents aged ≥12-years.5 As concerns around the sedative and performance-impairing effects of older AH have increased, growing attention has been placed on therapies that effectively control symptoms without compromising alertness, concentration, psychomotor function, or daily performance. Multiple studies evaluating bilastine’s cognitive, psychomotor, and driving safety profile consistently demonstrated that bilastine does not impair cognitive performance or everyday functioning.6,7,8 The first study, conducted by Valk et al., was a randomised, double-blind, placebo-controlled, three-way crossover trial designed to evaluate whether a single oral dose of bilastine 20mg impairs cognitive and psychomotor performance relevant to flying.6 Twenty-four healthy adult volunteers participated, each receiving bilastine 20mg, hydroxyzine 50mg (a sedating antihistamine used as a positive control), and placebo in balanced sequence, with a washout period of at least seven days between treatments. The study was conducted inside a hypobaric chamber maintained at a simulated cabin altitude of 8000 feet (75.2 kPa) to replicate realworld aviation conditions.6 Participants underwent a Vigilance and Tracking task together with a Multiple-Attribute Task battery at one-, two-, three-, five-, and six-hours post-dose. The findings were clear: bilastine 20mg produced no significant impairment in vigilance, tracking accuracy, complex task performance, or subjective sleepiness compared with placebo. In contrast, hydroxyzine 50mg caused marked and prolonged impairment, with tracking performance deteriorating by up to 89% from baseline and significant effects persisting for as long as six hours post-dose.6 Further evidence supporting bilastine’s suitability for everyday functioning was provided by Kawauchi et al., who reviewed bilastine’s psychomotor and subjective effects – including its interaction with 20 Specialist Forum May 2026 | Vol. 26 No. 5

alcohol – through a series of randomised, double-blind, crossover, placebo- and positive-controlled Phase I clinical trials.7 A key methodological feature of this research was the use of positron emission tomography imaging with the radiotracer [¹¹C] doxepin to directly measure brain H1 receptor occupancy (H1RO), a validated biomarker of antihistamine sedative potential. Based on H1RO values, antihistamines may be classified as non-sedating (H1RO <20%), less-sedating (20-50%), or sedating (≥50%).7 Multiple psychomotor outcomes were evaluated, including the Fine Motoric Test, Critical Flicker-Fusion Frequency, the d2 Cancellation Test, Simple Reaction Time, and the Standard Deviation of Lateral Position (SDLP), a recognised marker of driving performance. Bilastine at therapeutic doses of 20mg and 40mg did not impair psychomotor or driving performance and demonstrated no clinically meaningful interaction with alcohol at the 20mg dose.7 Impairment was only observed at the supratherapeutic dose of 80mg. The study also highlighted bilastine’s high H1 receptor affinity compared with fexofenadine, its minimal cytochrome P450 metabolism, and clinical efficacy comparable to cetirizine and desloratadine.7 Additional real-world evidence was provided by De Monte et al. in a Phase IV, prospective, single-centre, open-label interventional trial evaluating the effect of seven consecutive days of bilastine 20mg on driving performance in patients (mean age 38.4-years) with AR and/or chronic urticaria. Participants were assessed using a high-speed Formula 1 driving simulator before and after treatment at speeds of 50km/h, 150km/h, and 250km/h.8 After seven days of treatment, the mean SDLP significantly decreased (improved) by 0.041 ± 0.047m (p=0.002), indicating no negative effect on lane-keeping performance. Reaction times and speed maintenance similarly remained unaffected across all tested velocities, including 250km/h. No safety concerns were identified, and bilastine was well tolerated throughout the study period.

The investigators concluded that bilastine 20mg posed no risk to driving performance, even under extreme high-speed conditions.8 Taken together, these findings position bilastine as an effective second-generation antihistamine that delivers reliable symptom control in allergic rhinitis and chronic urticaria without compromising alertness, psychomotor performance, driving ability, or everyday functioning.6,7,8

Conclusion

AR and urticaria represent closely linked allergic disorders that share overlapping immunopathological mechanisms, common environmental triggers, and a significant bidirectional clinical association. Their impact extends beyond isolated nasal or cutaneous symptoms, frequently affecting sleep, quality of life, and daily functioning. Effective management therefore requires an integrated approach combining trigger avoidance, patient education, and evidence-based pharmacotherapy targeting the underlying histamine-driven inflammatory response. Within this therapeutic landscape, second-generation AH such as bilastine offer targeted H1 receptor blockade with proven efficacy in symptom control while maintaining cognitive clarity, psychomotor function, and driving safety. Collectively, the evidence supports bilastine as a modern therapeutic option that enables effective allergy relief without sedation or functional impairment.

References are available on request. SF

DERMATOLOGY

Photo credit: GettyImages/Prostock-Studio

Atopic dermatitis flares

with seasonal extremes

W

Both cold and warm temperatures have been linked to increased itch, skin flares, impaired skin barrier function, higher outpatient visits, the development of atopic dermatitis (AD), and asthma exacerbations. AD is a chronic, relapsing, pruritic inflammatory skin disease characterised by epidermal barrier dysfunction, immune dysregulation, and microbial imbalance. The condition affects ~10%-30% of children and 2%-10% of adults in developed countries, with prevalence rates having increased two- to three-fold over recent decades.1,2

ith a rapidly expanding therapeutic armamentarium and newly published paediatric-specific guidelines from the American Academy of Dermatology (AAD), clinicians now have clearer, evidence-based direction for managing this burdensome condition across the lifespan. This article outlines key treatment recommendations, stratified by age group, and contextualised for the South African setting.3,4,5

infection. Dilute bleach baths – approximately half a cup of household bleach in a standard 40-gallon bathtub, once or twice weekly – may be considered in recurrently infected patients to reduce bacterial burden, though evidence remains mixed. Patient and caregiver education on the chronic nature of AD, correct treatment application, and the importance of maintenance therapy are integral to long-term success.2,3

Foundational care: Principles that apply across all ages

Paediatric atopic dermatitis: A new era of guidance

Before pharmacological intervention, foundational skin care forms the non-negotiable basis of AD management for all patients.

Emollients should be applied at least twice daily – ideally within three minutes of a lukewarm bath or shower – to reduce transepidermal water loss and support barrier repair.2 Ointments are the most occlusive and least irritating formulation and are generally preferred. Trigger avoidance is equally essential: patients and caregivers should eliminate known irritants including fragrances, alkaline soaps, wool, polyester fabrics, and harsh laundry products, opting instead for mild detergents and soft cotton clothing.2 Staphylococcus aureus colonises more than 90% of patients with AD, worsening inflammation and increasing the risk of secondary

The AAD published its first-ever guidelines specifically for the prevention and management of paediatric AD in April 2026 – a landmark development recognising that children require ageappropriate, safety-conscious, and evidence-driven treatment strategies distinct from those designed for adults. The guidelines encompass 26 evidence-based recommendations across topical, phototherapy, and systemic therapies, classified by recommendation strength.5

Topical therapies in children

Moisturisers carry a strong recommendation as a core component of paediatric AD management to reduce skin dryness and disease severity. Regular and liberal emollient use from an early age is Specialist Forum May 2026 | Vol. 26 No. 5

21

DERMATOLOGY supported by evidence suggesting that barrier protection may therapy. Similarly, psoralen plus ultraviolet (UV) A phototherapy reduce the risk of AD occurrence in children aged six-months carries a conditional recommendation against use in children, to three-years.5 while conventional phototherapy may be considered for severe, Topical corticosteroids (TCS) carry a strong recommendation widespread disease.5 as first-line anti-inflammatory agents for both flare control and In the South African context, access to biologic therapies in the maintenance in most paediatric patients, favoured in part for their public sector remains a significant challenge due to cost and limited affordability and accessibility.5 specialist availability. Practical, cost-conscious strategies – including TCS potency should be selected according to disease severity optimised TCS and TCI use, structured caregiver education, and the and body site: Low-potency agents such as 1% hydrocortisone provision of affordable emollient alternatives such as petroleum jelly – acetate are appropriate for mild flares on non-sensitive areas, while remain central to equitable paediatric care.3 moderate- to potent-strength agents may be required for more severe presentations under close supervision.3 Adult atopic dermatitis: Building Sensitive areas such as the face, eyelids, and on a growing evidence base flexures require particular caution; potent TCS In adults, management follows a stepwise should be avoided at these sites, with topical approach based on disease severity. Topical In resource-limited calcineurin inhibitors (TCI) preferred instead. therapies remain the cornerstone for mildsettings, optimised TCIs also carry a strong recommendation in to-moderate disease, with TCS as first-line topical therapy, 3,5 paediatric AD. agents for acute flares, applied to inflamed skin patient education, Pimecrolimus 1% cream is indicated in South before emollients and tapered to intermittent Africa for children aged ≥2-years with mildmaintenance dosing – typically twice weekly – and affordable to-moderate disease, while tacrolimus 0.03% once control is achieved. TCIs and newer emollients remain ointment is indicated for moderate-to-severe non-steroidal topicals serve as effective steroidthe cornerstone of disease in children from two-years of age, sparing alternatives, particularly for sensitive and tacrolimus 0.1% ointment is reserved for anatomical sites.3 equitable atopic 3 adolescents aged ≥16-years.

The 2025 AAD focused update to adult AD dermatitis care Applied twice daily from the first signs of guidelines introduced strong recommendations, a flare until resolution, TCIs are the preferred based on high-certainty evidence, for two new option for sensitive anatomical sites and topical therapies (tapinarof and roflumilast, not provide a valuable steroid-sparing strategy. Unlike TCS, they available in South Africa yet). For moderate-to-severe disease do not cause skin atrophy, and long-term surveillance has not inadequately controlled by topicals or conventional systemic demonstrated an increased malignancy risk. Transient applicationagents, the AAD’s 2025 update added two further biologic agents site burning is the most common adverse effect and typically (lebrikizumab and nemolizumab, not available in South Africa yet), resolves within a few days of use.3 to its adult guidance.5 For dosing accuracy in children, the fingertip unit (FTU) method For adults who cannot access or tolerate biologics, conventional is recommended: One FTU represents the amount of cream systemic immunosuppressants remain in use. Cyclosporine is squeezed from the tip to the skin crease of an adult’s index finger, approved for moderate-to-severe AD in patients aged ≥16-years, with the number of units required varying by child age and body typically in intermittent courses of up to 16-weeks, with area. Caregivers should be instructed on correct application mandatory monitoring of blood pressure, renal function, and lipid amounts, frequency, and site-specific precautions to reduce levels throughout treatment, concurrent phototherapy should premature discontinuation and steroid-related concerns. Newer be avoided.2 non-steroidal topical agents are also strongly recommended in the Azathioprine, mycophenolate mofetil, and methotrexate may 2,3,5 updated paediatric guidelines. be used in selected cases under specialist supervision, while narrowband UVB phototherapy remains a useful option when Systemic therapies for moderate-totopical therapies are insufficient and systemic agents are not severe paediatric disease yet warranted.2 When topical therapies are insufficient for children with moderateto-severe AD, escalation to systemic biologic therapy is strongly Conclusion recommended, used in conjunction with topical therapy to reduce The treatment of AD across the age spectrum is entering a new disease severity, decrease flare frequency, and improve itch. era of precision and evidence-based guidance. For children, the Dupilumab, which targets the interleukin (IL)-4 receptor alpha AAD’s first dedicated paediatric guidelines affirm the central role subunit to block both IL-4 and IL-13 signalling, holds the broadest of emollients and TCS while expanding the strongly recommended age approval, extending down to six months of age.2,5 toolkit to include TCIs, novel topical agents, biologics, and oral Oral Janus kinase (JAK) inhibitors carry strong JAK inhibitors – with systemic CS reserved for exceptional recommendations for moderate-to-severe paediatric AD, with circumstances only. In the South African context, successful age-specific eligibility determined by product labelling and management requires balancing emerging therapeutic advances specialist judgment. Systemic CS, by contrast, carry a strong with practical realities of cost and access, underpinned by recommendation against routine use in children; they should be structured patient and caregiver education at every level of care. reserved exclusively for sudden, severe flares as short-term bridge References are available on request. SF 22 Specialist Forum May 2026 | Vol. 26 No. 5

Photo credit: Alamy/Pulsar Imagens

DERMATOLOGY

Winter skin SOS

When dryness becomes a diagnosis, not just a nuisance

As temperatures drop across South Africa and heaters are switched on in homes and offices, dermatologists are urging the public and primary care clinicians to pay closer attention to one of the most prevalent, yet frequently overlooked skin conditions: dry skin, clinically known as xerosis cutis. Affecting between 29% and 85% of the general population – and increasing to as high as 99% in older adults and nursing home residents – xerosis is far more than a cosmetic inconvenience. Left unmanaged, it can progress to painful cracking, inflammation, and a chronic form of eczema that significantly reduces quality of life.

T

he link between cold weather and dry skin is well established, but the mechanism is often misunderstood. It is not just the outdoor cold that strips the skin of moisture – indoor heating plays an equally significant role.

Cold weather and indoor heating reduce humidity, making areas such as the lower legs and back particularly susceptible to dryness and dry skin eczema. The result is a seasonal environment that is almost perfectly engineered to compromise the skin’s natural moisture barrier, explained Dr Hetesh Pitamber, dermatologist and member of both the Dermatological Society of South Africa and the Dermatological Surgical Society of South Africa.

The elderly are disproportionately affected, and the reasons are physiological. Skin naturally loses moisture with age, he noted – a process compounded by reduced sebum production, thinner skin, and declining collagen density. It is for this reason that xerosis is most common in individuals aged ≥65-years, and that prevalence rates in nursing home populations can approach near-universal levels.

Gender also plays a role. Women – particularly those who are postmenopausal – are more prone to dry skin than men, due to hormonal changes that accelerate moisture loss and reduce both sebum and collagen production. Men, by contrast, generally benefit from naturally higher sebum output and structurally thicker skin, offering a degree of built-in protection.

From flaking to eczema: Recognising the stages

Dry skin exists on a clinical spectrum, and recognising where a patient sits on that spectrum is key to choosing the right treatment approach. Dr Pitamber described three distinct stages. Mild dry skin presents as slightly scaly or flaky skin with a sensation of tightness, but without significant symptoms such as itching.

Moderate dry skin involves visible scaling and flaking accompanied by itching and burning – symptoms that are beginning to interfere with daily comfort. Severe dry skin, at the far end of the spectrum, presents with extreme dryness, crack formation, inflammation, and significant, often persistent, itching.

Specialist Forum May 2026 | Vol. 26 No. 5

23

DERMATOLOGY Beyond severe xerosis lies asteatotic eczema – also known as dry skin eczema – a condition in which the skin’s surface develops a characteristic cracked, ‘crazy paving’ appearance, with fissures that can sting, bleed, and become susceptible to secondary infection. Itching is also common and may progress to dry skin eczema, Dr Pitamber warned, underscoring why early intervention matters.

The role of primary care – and when to refer

was clear: A GP should refer a patient when emollients and topical treatments fail to provide relief, and the patient remains symptomatic despite conventional therapy.

Persistent xerosis that does not respond to standard moisturising regimens may indicate an underlying dermatological condition or a more severe disease stage requiring specialist management, including the possible use of topical corticosteroids or other prescription treatments.

Prevention: Small habits,

For most patients, dry skin can and should significant Impact be managed in a primary care setting. The Beyond treatment, Dr Pitamber outlined a set Dermatologists cornerstone of treatment is the prompt of practical, evidence-informed preventative warn xerosis cutis application of an effective emollient measures that patients can adopt to protect peaks in winter, immediately after bathing – a step that helps their skin through the colder months. The advice lock in residual moisture before it evaporates is accessible and actionable – but requires urging early from the skin’s surface. consistency to be effective. moisturising to Dr Pitamber specified that emollients At the top of the list is changing bathing prevent cracking, should ideally contain a combination of key habits. Long, hot showers – a tempting eczema, and active ingredients: Ceramides, which help indulgence in winter – are among the most restore and reinforce the skin’s natural lipid damaging habits for skin moisture, as hot water infection risk barrier, glycerine, a powerful humectant that strips away the natural oils that keep the skin draws moisture into the skin, cetomacrogol, barrier intact. Patients should opt for shorter, an emulsifying agent that improves the lukewarm showers and apply a moisturiser spreadability and skin-feel of moisturising formulations; and immediately afterwards, while the skin is still slightly damp. optionally urea, particularly useful in cases of thickened or Gentle skincare practices matter equally. Over-washing, significantly scaling skin. scrubbing, and excessive exfoliation all compromise the skin’s 2026 PainSA Congress - New media print advert - Reg now open.pdf 1 2026/03/26 09:00 When should a GP escalate care? Dr Pitamber’s guidance protective oils and should be avoided. Patients should choose mild, fragrance-free cleansers where possible. Indoors, the use of a humidifier during winter months can meaningfully counteract the moisture-depleting effects of central heating.

2026 PainSA Congress Systemic hydration also plays a role. Staying well hydrated in supports skin function from within, and Dr Pitamber suggested PAIN that an omega-3 supplement may be worth considering for nd th patients prone to dryness, given omega-3 fatty acids’ established role in supporting skin barrier integrity and reducing inflammation.

22 - 24 May

Ubuntu at the Indaba

Indaba Conference Centre, Fourways, Johannesburg

C

M

HPCSA Accredited

CEU points: 16 Ethics points: 3

Y

Registrations

CM

open

MY

CY

CMY

K

Scan to view website

CONGRESS ORGANISER 011 894 1278 Innovators in Event Excellence

painsacongress@velocityvision.co.za

24 Specialist Forum May 2026 | Vol. 26 No. 5

A condition worth taking seriously

Despite its ubiquity, xerosis cutis is frequently dismissed as a minor, self-resolving issue – an assumption that carries real clinical risk, particularly in vulnerable populations. In older adults, severe dry skin and the itch-scratch cycle it provokes can disrupt sleep, increase fall risk, and significantly impair quality of life.

When eczematous change develops, the skin becomes breached and susceptible to bacterial infection, adding another layer of medical complexity.

Conclusion

South Africa’s cooler winter months create ideal conditions for xerosis to flourish – and with an ageing population and high rates of chronic disease, the burden of skin complications in high-risk groups is likely to grow. Clinicians are encouraged to proactively assess skin health in older patients, educate on emollient use early in the season, and not underestimate the downstream consequences of untreated dry skin. The message from Dr Pitamber is both simple and urgent: moisturise early, moisturise well, and do not wait for cracks to form before acting.

References are available on request. SF

Photo credit: GettyImages/SimpleImages

INFECTIOUS DISEASES

Cold or flu? Understanding the

symptoms behind URTIs Acute upper respiratory tract viral infections (URTIs) are among the most common illnesses worldwide, affecting adults several times each year and schoolchildren even more frequently. Although the common cold and influenza (flu) share many overlapping symptoms, they are caused by different viruses and can differ substantially in severity, duration, and complications.1

M

ore than 200 viruses are associated with URTIs, with rhinoviruses responsible for most common colds, while influenza viruses cause seasonal flu. Because laboratory confirmation is not routinely performed in primary care, diagnosis is usually based on symptoms alone.1 Understanding how these symptoms develop is important, since most treatments target symptom relief rather than the virus itself. Research shows that many URTI symptoms arise not from direct viral damage, but from the body’s immune and inflammatory response to infection.1,2 Table 1: Symptoms of the common cold vs influenza Symptom

Common cold

Influenza (flu)

Onset

Gradual

Sudden

Fever

Rare in adults

Common

Chills

Uncommon

Fairly common

Headache

Mild or occasional Common and often severe

Muscle aches

Mild

Common and pronounced

Fatigue

Mild

Moderate to severe

Sneezing

Common

Sometimes

Runny/stuffy nose

Very common

Sometimes

Sore throat

Common

Common

Cough

Mild to moderate

Common, often severe

Appetite loss

Uncommon

Common

Complications

Usually mild

May lead to pneumonia or hospitalisation

The symptoms of URTIs are largely driven by inflammatory mediators and cytokines released by the immune system in response to viral infection. Macrophages recognise invading viruses through toll-like receptors and trigger the release of cytokines such as interleukin-1 and interleukin-6. These substances recruit immune cells, stimulate inflammation, and contribute to systemic symptoms such as fever, fatigue, malaise, and muscle aches.1 One of the earliest symptoms of a URTI is often a scratchy or irritated throat. This may occur because viral infection initially involves the nasopharynx before spreading through the upper airway.

Inflammatory mediators such as bradykinin and prostaglandins stimulate sensory nerves in the throat, producing irritation and pain.

Sneezing frequently follows and is triggered when inflammation stimulates trigeminal nerves in the nasal passages. Histamine may

contribute to this reflex, explaining why some antihistamines help reduce sneezing.1 Rhinorrhoea, or a runny nose, is another hallmark of the common cold. Early watery secretions are largely produced by glandular stimulation through parasympathetic nerve pathways.

As inflammation progresses, plasma proteins and immune cells leak into nasal secretions, making them thicker. The colour of mucus may change from clear to yellow or green during the course of illness.

Importantly, this colour change reflects the presence of inflammatory cells such as neutrophils rather than indicating a bacterial infection.1 Nasal congestion tends to develop later in the illness and results from dilation of blood vessels within the nasal lining.

Inflammatory mediators increase blood flow and swelling in the nasal passages, narrowing airflow and producing the sensation of blockage. Congestion around the openings of the sinuses may also contribute to sinus pressure and facial pain.1 Cough is particularly common in influenza and may persist for weeks after other symptoms resolve. Unlike sneezing, which is mediated by trigeminal nerves, cough is triggered through the vagus nerve and usually indicates irritation extending below the larynx.

Viral infections can make cough receptors hypersensitive, meaning even mild stimuli such as cold air may trigger persistent coughing.1 Systemic symptoms such as fever, chills, fatigue, headache, and muscle aches are strongly linked to cytokine activity. Fever develops when cytokines alter the hypothalamic temperature set point, triggering shivering and vasoconstriction. Muscle aches are thought to arise from cytokine-induced production of prostaglandin E2 within skeletal muscle, sensitising pain receptors.1 Psychological and behavioural changes are also common during URTIs. Fatigue, reduced concentration, irritability, sleep disturbances, and reduced appetite are increasingly recognised as part of the ‘sickness behaviour’ generated by cytokines acting on the brain. These responses may actually help recovery by conserving energy and supporting immune function.1 Although the common cold and influenza often overlap clinically, influenza typically presents more abruptly and severely, with fever, cough, and body aches being key distinguishing features.

Recognising these differences remains important, particularly during influenza outbreaks, where early diagnosis may guide antiviral treatment and public health interventions.1 References are available on request. SF Specialist Forum May 2026 | Vol. 26 No. 5

25

INFECTIOUS DISEASES

Photo credit: GettyImages/jeffbergen

Double trouble winter Flu and RSV team up early in 2026

South Africa is bracing for a particularly challenging winter respiratory season after the National Institute for Communicable Diseases (NICD) reported an unusually early and simultaneous onset of both the influenza and respiratory syncytial virus (RSV) seasons in 2026. The co-circulation of two highly contagious respiratory pathogens – affecting many of the same high-risk populations through the same modes of transmission – has prompted urgent calls from clinicians for heightened vigilance, proactive testing, and a significant push for vaccination across the country.

D

r Alan Peter, pulmonologist and clinical head of the Internal Medicine unit at Chris Hani Baragwanath Academic Hospital in Johannesburg, warns that the occurrence of two epidemics at the same time, with the same modes of transmission, is a cause for concern and may warrant a return to stringent protective measures such as masks. He pointed out that the absence of an influenza epidemic during the Covid-19 pandemic was directly attributable to widespread mask-wearing.

Two viruses, one dangerous window

Both influenza and RSV typically peak during the southern hemisphere’s winter months of May, June, and July. While healthy adults face relatively low individual risk – with <1% of infected individuals requiring hospitalisation – the picture changes dramatically for vulnerable populations. The frail, the elderly, the immunocompromised, and those living with chronic conditions such as heart disease, diabetes, chronic kidney disease, and chronic lung disease face significantly elevated risks of severe illness and death.

This season, two strains of influenza A are circulating concurrently: H3N2 and H1N1(pdm09) – the pandemic strain of 26 Specialist Forum May 2026 | Vol. 26 No. 5

swine flu that first emerged in 2009, causing an estimated 284 000 deaths globally. Dr Peter noted that the influenza season in Europe, which typically foreshadows trends in Southern Africa, started earlier than usual and is proving more contagious than previous years – though not necessarily more deadly. By that, one means that it spreads more quickly and is more contagious, but not necessarily more deadly, he clarified.

The current influenza vaccine has been updated to cover both circulating H1N1(pdm09) and H3N2 variants, and Dr Peter expressed confidence in its efficacy – provided there is sufficient uptake. Vaccination this year should be as efficacious as in previous years, provided there is uptake by the population, especially those who are at greater risk, he said.

RSV: A particular threat to those with lung disease

While influenza tends to be more virulent across the general population, RSV poses a disproportionate threat to those with preexisting lung conditions. RSV affects more people with underlying lung disease than influenza, which is more virulent amongst people without lung disease, Dr Peter explained.

Both viruses can trigger asthma exacerbations, but RSV’s impact

INFECTIOUS DISEASES on patients with chronic respiratory conditions – including posttuberculosis bronchiectasis – is particularly severe. Among RSV patients admitted to intensive care units (ICU) in the United States, between 10% and 31% require ICU-level care, with 3% to 17% needing mechanical ventilation.

The risk of invasive mechanical ventilation or death from RSV was found to be 1.39 times higher than from Covid-19, and 2.08 times higher than from influenza. Overall RSV mortality sits around 1%, but in susceptible individuals, winter excess mortality attributable to RSV may reach 25% above influenza-related deaths.

Race, history, and inequality: South Africa’s compounded risk

only shortens illness duration and must be administered within 48-hours of symptom onset to be effective – a window that is frequently missed. Its use is most justifiable in immunocompromised patients with confirmed influenza infection.

Healthcare systems under pressure

With both viruses circulating simultaneously, hospitals – and particularly ICUs – face a testing period. Dr Peter acknowledged that South Africa’s health system has benefited from the infrastructure investments and operational lessons learned during the Covid-19 pandemic but warned that ICU capacity remains a ‘critically limited resource’. Triage and admission decisions will Two epidemics at ultimately rest with clinical teams, balancing the same time, with patient prognosis against resource availability, the same modes and guided by patients’ pre-stated wishes and advance directives. of transmission, He also called for healthcare personnel is a cause for themselves to be vaccinated – a measure that concern and may carries its own challenges. A 2018 study found that vaccination uptake among healthcare warrant a return to workers stood at just 33%, a figure Dr Peter stringent protective described as deeply concerning.

South Africa’s specific demographic context amplifies the danger. Dr Peter highlighted that people of African heritage face a 2.3-fold higher rate of hospitalisation compared to their European counterparts – a disparity he links to a disproportionate burden of chronic lung disease.

The racial difference may reflect the fact that Afro-Africans carry a much greater burden of chronic lung disease due to measures such higher HIV prevalence, previous tuberculosis as masks with secondary lung damage, and a higher A vaccination crisis hidden in plain sight percentage of smoking in the population, he Perhaps the most sobering dimension of explained. Adults >75-years also face markedly this story is South Africa’s persistently low elevated hospitalisation risk. vaccination coverage. Despite annual influenza deaths in the This intersection of infectious disease burden, socioeconomic country estimated between 7000 and 12 000, only 3% to 5% of inequality, and structural health vulnerabilities means that a dualthe population receives the influenza vaccine in any given year. virus season could have outsized consequences for South Africa’s Alarmingly, only 18% of elderly South Africans – among the most marginalised communities. highest-risk group – have been vaccinated.

Dr Peter was emphatic about the need for a multi-pronged Spotting the difference: Clinical clues response. Vaccination is central and the most cost-effective when diagnostics are scarce method of preventing thousands of deaths, he said, adding In settings where access to laboratory testing is limited, Dr Peter that pneumococcal vaccination should accompany influenza offered practical clinical guidance for distinguishing between the vaccination, given that viral respiratory infections frequently pave two viruses. Influenza typically presents with a sudden onset of the way for secondary bacterial pneumonia – a complication seen fever, non-productive cough, and muscle pain, often accompanied in 2.5% of patients with chronic disease. by fatigue, sore throat, nausea, nasal congestion, and headache. In Education is critical for vaccination, personal barrier use, and older patients, influenza may manifest atypically – with confusion, handwashing. Confidence needs to be built through education, anorexia, weakness, and dizziness – without the classic fever which will reduce complacency, and efforts must be made to and myalgia. improve access to vaccination for vulnerable patients through local RSV, by contrast, more commonly presents with cough, clinics, he added. wheezing, and shortness of breath, particularly in patients with For those with chronic lung disease, Dr Peter also urged a history of lung disease or asthma. A sudden onset of fever and engagement with the RSV vaccination programme, alongside lack of wheezing may suggest influenza infection, Dr Peter noted, maternal RSV vaccination – a key preventive strategy for adding that vaccination history can serve as an important clinical protecting newborns and infants who face the highest RSV-related clue: A history of prior influenza vaccination would make RSV the mortality risk among young children. most likely pathogen in a vaccinated patient.

Regardless of the clinical impression, he stressed that definitive The bottom line diagnosis requires reverse transcription polymerase chain reaction As South Africa enters what could be one of its most challenging testing on respiratory samples in all patients presenting with respiratory seasons in recent memory, the message from typical viral symptoms. In every patient who presents with typical pulmonologists is clear: vaccinate early, test broadly, identify viral symptoms – nasal congestion, runny nose, sore throat, often high-risk patients promptly, and prepare healthcare infrastructure together with fatigue, loss of appetite, and fever – influenza and for a surge that may already be underway. The tools exist – but RSV should be tested, he said. only concerted action, equitable access, and public education will Regarding antiviral therapy, Dr Peter cautioned that oseltamivir determine how many lives are saved before winter is over. SF Specialist Forum May 2026 | Vol. 26 No. 5

27

PULMONOLOGY

Photo credit: GettyImages/PeopleImages

Cough: Causes, duration, diagnosis,

management explained Cough is a common respiratory symptom and one of the leading reasons for medical consultations worldwide. Although it serves a protective role in clearing the airways, persistent or severe cough may indicate underlying disease. Here are 10 facts to better understand its causes, classification, and clinical significance.

1. Cough is a protective reflex It clears secretions, irritants, and foreign material from the airways via a coordinated inspiratorycompressive-expulsive cycle.

2. It is one of the most common medical symptoms Cough is a leading cause of outpatient and emergency department visits worldwide.

3. Duration defines the diagnostic approach Acute: < 3-weeks Subacute: 3- to 8-weeks Chronic: >8-weeks (adults)/>4-weeks (children)

4. Acute cough is usually infectious Most cases are due to viral upper or lower respiratory tract infections, but serious causes include pneumonia, asthma exacerbation, and pulmonary embolism.

28 Specialist Forum May 2026 | Vol. 26 No. 5

PULMONOLOGY 5. Chronic cough has multiple common causes Top contributors include upper airway cough syndrome, asthma, gastroesophageal reflux disease, chronic bronchitis, and eosinophilic bronchitis.

6. Postinfectious cough is common in the subacute phase Often follows viral illness and results from persistent airway or sinus inflammation.

8. Cough hypersensitivity can drive chronic symptoms

7. Chronic cough significantly affects quality of life It is associated with sleep disturbance, fatigue, anxiety, depression, and social isolation.

Even low-level stimuli (air pollution, reflux, smoke) can trigger persistent coughing due to sensitised cough reflex pathways.

9. Red flags require urgent evaluation Haemoptysis, dyspnoea, hypoxia, weight loss, fever, abnormal vitals, or immunosuppression may indicate serious disease.

10. A structured diagnostic approach is essential History, physical examination, and targeted testing help avoid unnecessary antibiotics and identify treatable underlying causes.

Reference Das S, Goldin J, Alhajjaj MS. Cough: Evaluation and Management. [Updated 2026 Jan 31]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK493221/ Specialist Forum May 2026 | Vol. 26 No. 5

29

OTOLARYNGOLOGY

Photo credit: GettyImages/Moyo Studio

Rhinosinusitis: From acute episodes to

chronic complexity Rhinosinusitis (RS) is common during winter months, largely due to increased viral respiratory infections, indoor crowding, and environmental factors such as cold, dry air that predispose to nasal mucosal irritation and impaired sinus drainage. It is one of the most prevalent and clinically significant conditions in otolaryngology, affecting millions of people worldwide.1

D

efined as symptomatic inflammation of the paranasal sinuses and nasal cavity mucosa, it can be caused by viruses, bacteria, fungi, and allergens, which may act alone, in combination, or sequentially. Far from being a simple or self-limiting condition, RS encompasses a broad clinical spectrum – from acute episodes lasting <4-weeks to subacute disease persisting between four- and twelveweeks, and chronic RS (CRS) lasting >12-weeks.1 Among its most challenging forms is recurrent acute RS (RARS), defined as ≥4 episodes of acute RS per year, each lasting at least ten days, with complete, symptom-free intervals in between. Understanding the full clinical picture – including its complications, its relationship with obstructive sleep apnoea (OSA), and the emerging role of the gut microbiome – is essential for improving patient outcomes.2,3,4

Diagnosing rhinosinusitis: Criteria and clinical presentation Accurate diagnosis remains foundational to appropriate management.

The RS Task Force established a framework that groups diagnostic indicators into major and minor criteria, requiring either two major criteria or one major plus two minor criteria for diagnosis.1 Major criteria include purulence on nasal examination, nasal obstruction or blockage, nasal discharge or discoloured postnasal drainage, hyposmia or anosmia, fever, facial pain or pressure, and facial congestion or fullness. Minor criteria encompass ear pain or fullness, cough, dental pain, fatigue, halitosis, and headache.1 This structured diagnostic approach helps clinicians distinguish rhinosinusitis from other causes of upper respiratory symptoms, particularly in cases where symptom overlap creates diagnostic uncertainty.1

The united airway: CRS and obstructive sleep apnoea

Beyond immediate infectious complications, CRS exerts a broader systemic burden that has increasingly been understood through the lens of the ‘united airway’ model. This framework conceptualises the nasal cavity, sinuses, and lower airways as 30 Specialist Forum May 2026 | Vol. 26 No. 5

a functionally integrated unit, in which disease at one level can propagate and perpetuate dysfunction elsewhere.3 Large-scale epidemiological data illustrate the substantial overlap between both conditions. A TriNetX database analysis identified more than 1.8 million CRS patients and ~480 000 OSA patients, with ~94 000 individuals carrying both diagnoses.3 Patients with comorbid CRS and OSA demonstrate higher rates of systemic comorbidities including hypertension, diabetes, and obesity, and are nearly twice as likely to require endoscopic sinus surgery compared to those with CRS alone (odds ratio 1.91).3 A longitudinal study from Taiwan further demonstrated that a diagnosis of OSA was associated with a hazard ratio of 3.18 for the subsequent development of CRS, suggesting a bidirectional risk between these two conditions. In a particularly striking example, World Trade Center responders exposed to caustic dust showed an OSA prevalence of ~75%, with CRS symptom severity predicting OSA presence.3 Multiple pathophysiological mechanisms explain this bidirectional relationship. Mechanically, nasal obstruction increases upstream airway resistance and can precipitate pharyngeal collapse during inspiration – a process well-described by the Starling resistor model.3 Mouth breathing secondary to nasal obstruction alters mandibular position and narrows the retroglossal space, further increasing the risk of upper airway collapse during sleep. At the neurophysiological level, chronic nasal inflammation can blunt the sensitivity of trigeminal afferents, impairing the nasopharyngeal reflex that normally activates the genioglossus muscle to maintain airway patency during sleep.

This ‘de-afferentation’ reduces the compensatory pharyngeal dilator response, increasing vulnerability to collapse.3 Inflammatory mechanisms further cement the connection.

Intermittent hypoxia from OSA activates nuclear factor kappalight-chain-enhancer of activated B cells (NF-κB) and upregulates pro-inflammatory cytokines including tumour necrosis factor alpha

OTOLARYNGOLOGY (TNF-α), interleukin (IL)-6, and IL-8, which are detectable in nasal lavage and correlate with disease severity.3 In patients with CRS with nasal polyps and moderate-to-severe OSA, broad upregulation of type 1, type 2, and type 3 inflammatory markers has been observed in polyp tissue, suggesting a pan-inflammatory state that may make CRS more refractory to treatment.3 Notably, continuous positive airway pressure (CPAP) adherence is only ~50% in the long term, in part because untreated nasal pathology elevates required CPAP pressures. Addressing nasal disease through surgery or topical therapy has been shown to reduce required CPAP by an average of 2-3cm H2O.3

The gut-sinus axis: A new frontier in CRS pathogenesis

Alongside these well-established mechanisms, an emerging body of evidence points to the gut microbiome as a previously underappreciated driver of sinonasal inflammation. The proposed ‘gut-sinus axis’ is a bidirectional biological link between intestinal microbial composition and mucosal immune function at distant sites, including the sinonasal tract – analogous to the better-characterised gut-lung and gut-skin axes.4 The healthy gut microbiome is dominated by genera including bacteroides, clostridium, bifidobacterium, faecalibacterium, and roseburia, which ferment dietary fibre to produce short-chain fatty acids (SCFAs) such as acetate, propionate, and butyrate.4 These metabolites play critical roles in supporting mucin production, maintaining epithelial tight junction integrity, inhibiting NF-κB signalling, and promoting regulatory T-cell (Treg) differentiation via G-protein-coupled receptors (G-protein coupled receptor [GPR]41, GPR43, GPR109A).4 When gut dysbiosis disrupts SCFA production, systemic immune tone shifts toward a pro-inflammatory state, with elevated circulating IL-6, IL-17, and TNF-α – cytokines directly implicated in CRS pathogenesis.4 A systematic review drawing on human, Mendelian randomisation, and animal studies identified a consistent pattern of gut dysbiosis in CRS patients: Depletion of SCFA-producing genera including Faecalibacterium, Roseburia, Akkermansia, and Bifidobacterium, alongside relative enrichment of potentially proinflammatory taxa such as Enterobacteriaceae.4 Reduced Faecalibacterium was specifically associated with eosinophilic CRS and correlated with greater radiological disease severity on CT imaging. Mendelian randomisation analyses provided genetic support for causality, with variants in taxa from the Ruminococcaceae and Lachnospiraceae families associated with increased susceptibility to CRS with nasal polyps.4 Animal models have further illuminated the mechanisms. Highfibre diets and SCFA supplementation consistently attenuated allergic airway inflammation, while antibiotic-induced dysbiosis exacerbated airway inflammatory responses – effects partly reversible with SCFA administration.4 On the interventional front, a randomised controlled study by De Boeck et al. (2025) found that chewable Lacticaseibacillus rhamnosus GG reduced nasal inflammation and improved symptom scores compared to placebo.4 Ried et al. (2022) demonstrated in adults with seasonal allergic rhinitis that a multi-strain probiotic for eight weeks reduced sneezing and nasal congestion. Endam et al. (2020) observed that fourteen-day sinus irrigations with a Lactococcus lactis-containing

solution produced post-treatment increases in gut Dolosigranulum and improvements in sinonasal symptoms and mucosal scores in refractory CRS patients. While encouraging, effect sizes varied.4

Toward a holistic, multi-system approach to CRS

The cumulative evidence reviewed here reveals that rhinosinusitis cannot be fully understood or managed in isolation. It is a condition shaped by local anatomy, microbial ecosystems in both the nasal cavity and the gut, systemic immune dysregulation, and its bidirectional relationship with sleep-disordered breathing.

A persistent headache or worsening sinusitis demands urgent evaluation for orbital or intracranial extension, given the high mortality associated with intracranial complications.2 For patients with CRS, screening for OSA using validated tools such as STOP-Bang or SNOT-22 should be routine, while CPAPintolerant patients should undergo nasal endoscopy and imaging for underlying sinonasal disease.3 Medical optimisation – beginning with intranasal corticosteroids and high-volume saline irrigations – remains foundational, with biologics such as dupilumab offering rapid improvement in sleep quality and inflammatory burden in severe CRS with nasal polyps.3 Looking ahead, microbiome-targeted therapies and neurophysiological restoration strategies represent a promising but still-evolving frontier. As the connections between the gut, the airway, and sleep continue to unfold, a systems-based approach to rhinosinusitis will be indispensable in reducing the burden of this far-reaching disease.4 References are available on request. SF

Specialist Forum May 2026 | Vol. 26 No. 5

31

ONLINE CPD

Photo credit: Getty Images/ RECVISUAL

Local ARISE insights on real-world IDegAsp efficacy

Diabetes is a chronic metabolic disorder characterised by persistent hyperglycaemia, broadly classified into type 1 diabetes (autoimmune β-cell destruction) and type 2 diabetes (T2DM), which is driven by insulin resistance and progressive βcell dysfunction. Over time, monotherapy becomes insufficient to maintain glycaemic control in T2DM, as β-cell decline reduces treatment effectiveness, necessitating timely intensification strategies to achieve and sustain optimal outcomes.

7 Key messages 1. T2DM is progressive, and declining β-cell function limits the long-term effectiveness of monotherapy, making timely treatment intensification essential to maintain glycaemic control.

2. Sustained glycaemic control is crucial to reduce microvascular complications and improve insulin sensitivity, emphasising the importance of proactive, individualised management.

3. Basal insulin alone may become insufficient as T2DM advances, particularly for controlling postprandial glucose excursions, requiring escalation of therapy.

4. IDegAsp combines basal and prandial insulin in a single formulation, reducing injection burden, eliminating reconstitution, and simplifying treatment regimens.

5. Real-world ARISE data, including South African findings, demonstrate clinically meaningful reductions in HbA1c and fasting plasma glucose with IDegAsp. 6. IDegAsp is associated with reduced total insulin requirements and lower rates of hypoglycaemia, including nocturnal and non-severe episodes, while maintaining stable body weight.

7. Across diverse populations and treatment histories, IDegAsp consistently improves outcomes and reduces healthcare resource utilisation, supporting its use in routine clinical practice.

32 Specialist Forum May 2026 | Vol. 26 No. 5

M

aintaining good glycaemic control is essential, as it improves insulin sensitivity, reduces glucose toxicity, and is strongly associated with a lower risk of microvascular complications such as nephropathy, retinopathy, and neuropathy. Basal insulin is typically the first injectable therapy initiated; however, as disease progresses, it may not adequately address postprandial glucose excursions.

Treatment intensification options include adding prandial insulin, introducing glucagon-like peptide-1 receptor agonists, (GLP-1RA) or switching to fixed-dose combination (FDC) insulin regimens.

Optimising insulin therapy with FDC IDegAsp

IDegAsp, a co-formulation of insulin degludec (basal) and insulin aspart (prandial), provides a simplified approach by combining both components in a single injection. It delivers a stable, long-acting basal profile alongside rapid prandial glucose control. Advantages include fewer injections, no need for reconstitution, dosing convenience, and a relatively low risk of hypoglycaemia, all of which support improved adherence and practical use in clinical settings.

ONLINE CPD BOOSTing glycaemic control: South African ARISE shows IDegAsp in action

Evidence from the BOOST clinical trial programme demonstrated that IDegAsp, administered once or twice daily in treat-to-target studies, achieves effective glycaemic control with simpler titration compared to basal-bolus regimens. In stepwise intensification studies, IDegAsp produced comparable HbA1c reductions to basalbolus therapy, with fewer nocturnal hypoglycaemic episodes and reduced insulin requirements.

A Research Study, Looking at How Insulin Degludec/Insulin Aspart Works in People With Type 2 Diabetes in Local Clinical Practice (ARISE) evaluated the real-world effectiveness of IDegAsp across multiple countries, including South Africa. In the South African cohort, patients were typically long-standing diabetics with suboptimal baseline glycaemic control. Following initiation of IDegAsp, significant reductions in HbA1c and fasting plasma glucose were observed, along with an increased proportion of patients achieving glycaemic targets.

Insulin dosing was optimised during treatment, with reductions in total daily insulin as well as both basal and prandial components.

Hypoglycaemia rates declined, including nocturnal and nonsevere episodes, with no severe hypoglycaemic events reported.

Body weight remained stable, and healthcare resource utilisation improved, with fewer outpatient visits, hospitalisations, and missed workdays.

High completion rates and low discontinuation due to adverse events further support tolerability and adherence.

How do the global ARISE findings compare with South African real-world experience?

The South African findings closely mirror the global ARISE population, demonstrating consistent improvements in glycaemic control, insulin dosing, and hypoglycaemia outcomes across diverse healthcare settings and prior treatment regimens.

In both cohorts, IDegAsp use resulted in meaningful HbA1c reductions, improved fasting plasma glucose, and reduced insulin requirements. These parallel outcomes reinforce the reproducibility of IDegAsp effectiveness in real-world clinical practice, regardless of geographic or demographic differences.

Conclusion

ARISE demonstrates that IDegAsp provides effective, real-world glycaemic control with a favourable safety profile, reduced insulin requirements, and improved hypoglycaemia outcomes. The consistency between South African and global data highlights its practicality across diverse patient populations and clinical settings.

To access the article and quiz, click here. SF This article was sponsored by Novo Nordisk®. This material is intended for distribution to health care professionals only.

Novo Nordisk (Pty) Ltd. Reg. No.: 1959/000833/07. 90 Grayston Drive, Sandown, Sandton, 2031, Gauteng, South Africa. Tel: (011) 202 0500. www.novonordisk.com. ZA26RZG00004 March 2026.

Stay informed with Novo Nordisk scientific updates, product information & medical news!

Experience the freedom* with a 2-in-1 insulin co-formulation providing basal and mealtime control1-5

Targets both FPG and PPG for HbA1c control1,3,6,7

Ryzodeg® offers lower rates of nocturnal hypoglycaemia3,6,7

Once- or twice-daily dosing with main meal(s)1

Upgrade your T2D patients to Ryzodeg®1 From basal only

1:1 Scan here to view the Ryzodeg® API

Convert unit to unit at the same total insulin daily dose

Scan the QR code to access resources

that supports your patients’ use of Ryzodeg®: • How-to video for Ryzodeg®

• Ryzodeg® patient booklet

• Diabetes diary

# Image is for illustrative purposes only. * with flexibility in dose timing when dosed with main meal(s).

FPG: fasting plasma glucose; PPG: post-prandial plasma glucose; HbA1c: glycated haemoglobin.

• And more helpful content

References: 1. Ryzodeg® Professional Information August 2022. 2. Vijan S, et al. J Gen Intern Med. 2005;20(5):479–482. 3. Fulcher G, et al. Comparison of InsulinDegludec/Insulin Aspart and Biphasic Insulin Aspart 30 in Uncontrolled, Insulin-Treated Type 2 Diabetes: A Phase 3a, Randomized, Treatto-Target Trial. Diabetes Care. 2014;37:2085-89. 4. Haahr H, et al. Clin Pharmacokinet. 2017;56(4):339–354. 5. Mehta R, et al. Diabetes Obes Metab. 2020;22(22):1961-1973. 6. The Society for Endocrinology, Metabolism & Diabetes in South Africa. Type 2 Diabetes Guidelines Expert Committee. The 2017 SEMDSA Guidelines for the management of Type 2 Diabetes. JEMDSA 2017. 7. Glastras SJ, et al. J Clin Med 2020;9:1091. 8. Chen SP, et al. Malays Fam Physician 2023;18:31.

S3 Ryzodeg®. Insulin degludec/Insulin aspart (70 % soluble insulin degludec and 30 % soluble insulin aspart) 100 units/ml. Reg. No.: 47/21.1/0165. For full prescribing information, refer to the Professional Information approved by the Medicines Regulatory Authority.

Novo Nordisk (Pty) Ltd. Reg. No.: 1959/000833/07. 90 Grayston Drive, Sandown, Sandton, 2031, Gauteng, South Africa. Tel: (011) 202 0500. Fax: (011) 807 7989. www.novonordisk.com. ZA26RZG00008 February 2026.

Specialist Forum May 2026 | Vol. 26 No. 5

33

WEBINAR REPORT

Photo credit: Getty Images/Carol Yepes

Initiating menopause hormone therapy

Back to basics Menopause is inevitable if we age as women – but how we manage it is entirely within our control. With this pragmatic and engaging opening, Dr Trudy Smith set the tone for a wide-ranging webinar that unpacked the science, clinical nuances, and real-world challenges of menopause management.

D

rawing on her extensive experience in gynaecology and menopause care, Dr Smith began by reframing menopause as a clearly defined clinical milestone – the final menstrual period – rather than a vague or symptomatic state.

She emphasised that menopause is a retrospective diagnosis, confirmed after 12-months of amenorrhoea, and that routine blood testing is rarely required. Importantly, she distinguished between early menopause (40- to 45-years) and premature ovarian insufficiency (<40-years), noting the roles of genetics, environment, and geography.

A key framework underpinning the discussion was the Stages of Reproductive Aging Workshop (STRAW) +10 staging system, which standardises the phases of reproductive ageing. Clinically, irregular menstrual cycles and increasing intervals of amenorrhoea signal progression through the menopausal transition, allowing clinicians to make informed diagnoses without over-reliance on investigations.

Dr Smith highlighted the wide spectrum of menopausal symptoms, with vasomotor symptoms – hot flushes and night sweats – being the most prominent. However, she stressed that menopause extends far beyond flushing.

Symptoms such as anxiety, irritability, sleep disturbance, cognitive complaints (brain fog), vaginal dryness, low libido, and fatigue are common and often under-recognised. She also pointed out that symptom profiles vary across populations, influenced by ethnicity, diet, and lifestyle factors.

The central role of menopausal hormone therapy was explored in depth. Dr Smith was unequivocal that the primary indication for MHT is the treatment of vasomotor symptoms, with oestrogen being the most effective intervention.

While additional benefits include bone preservation, potential colorectal cancer risk reduction, and cardiovascular (CV) protection when initiated early, she cautioned against prescribing MHT solely for these purposes in asymptomatic women.

A critical concept discussed was the timing hypothesis. Initiating MHT within 10-years of menopause or <60-years confers more favourable CV outcomes, whereas delayed initiation may increase the risk of thrombotic events and stroke. This reinforces

the importance of early engagement and timely clinical decision-making.

Dr Smith also addressed the ongoing confusion around hormone formulations.

She strongly cautioned against compounded bioidentical hormones, citing concerns about inconsistent dosing, lack of regulation, and potential Dr Trudy Smith harm, including endometrial cancer.

In contrast, she advocated for the use of regulated, licensed preparations of estradiol and appropriate progestogens.

Endometrial protection was emphasised as non-negotiable in women with an intact uterus, with clear guidance on minimum effective progesterone dosing. She also differentiated systemic from local therapies, noting that vaginal oestrogen is highly effective for genitourinary symptoms and can significantly improve quality of life.

Importantly, risk was contextualised. While certain combined MHT regimens are associated with a small increase in breast cancer risk, this must be weighed against other modifiable factors such as obesity and alcohol use. Not all hormone therapies carry the same risk, and careful selection is essential.

The session concluded with a strong emphasis on individualised care. Management should be tailored to each patient’s symptoms, risks, and preferences, supported by lifestyle interventions such as exercise, nutrition, and cognitive engagement.

Overall, Dr Smith delivered a clinically relevant and balanced perspective, equipping practitioners to navigate the complexities of menopause with confidence and clarity.

This webinar was sponsored by Novo Nordisk and is accredited for one CEU. After watching the replay, available at https://bit.ly/4wxh6Zo, email john. woodford@newmedia.co.za to request allocation of your CPD point to your HPCSA profile. Please include the webinar name and your HPCSA number. Kindly note it may take up to four weeks for the point to reflect on your portfolio.

Allocation of points remains at the discretion of the HPCSA. SF

Access the webinar

34 Specialist Forum May 2026 | Vol. 26 No. 5

Identical to her estrogen1

Post-menopause, Regular Cycles 6, 7

Post-menopause, Bleed-Free4

References: 1. Estrofem® approved professional information. 2. Novofem® approved professional information. 3. Trisequens® approved professional information. 4. Activelle® approved professional information. 5. Kliogest® approved professional information. 6. Keil D, Rakov V, Molemans B. Current experiences with low-dose estradiol sequentially combined with norethisterone acetate as an effective therapeutic regimen for climacteric symptoms. Geburtsh Frauenheilk 2002;62:991-995. 7. Saure A, Hirvonen E, Milsom I, et al. A randomized, double-blind, multicentre study comparing the clinical effects of two sequential estradiol-progestin combinations containing either desogestrel or norethisterone acetate in climacteric women with estrogen deficiency symptoms.

Maturitas.1996;24(1-2):111-8. 8. Vagifem® 10 µg tablet approved professional information. 9. Simon J, Nachtigall L, Gut R, et al. Effective treatment of vaginal atrophy with an ultra-low-dose estradiol tablet. Obstet Gynecol 2008;112(5):1053-60. 10. Minkin MJ, Maamari R, Reiter S. Postmenopausal vaginal atrophy: evaluation of treatment with local estrogen therapy. International Journal of Women’s Health 2014;6:281-288. 11. Dugal R, Hesla K, Sørdal T, et al. Comparison of usefulness of estradiol vaginal tablets and estriol vagitories for the treatment of vaginal atrophy. Acta Obstet Gynecol Scand 2000;79:293-297. ® ® ® ® S2S2Vagifem μgvaginal vaginaltablet tablet Reg. 47/21.8.1/0166, S4 Estrofem 1 mg No.: 34/21.8.1/0159, Estrofem Reg. No.: Novofem Reg. No.: ® Vagifem® 10 10 μg Reg. No.:No.: 47/21.8.1/0166, S4 Estrofem 1 mg Reg. No.:Reg. 34/21.8.1/0159, S4 Estrofem®S4 Reg. No.: J/21.8.1/214, S4 J/21.8.1/214, Novofem® Reg.S4 No.: 37/21.8.2/0297, ® ® ® ® 37/21.8.2/0297, S4 Trisequens Reg. S4 No.: J/21.8.2/212, S4 33/21.8.2/0532, Activelle® Reg.S4No.: 33/21.8.2/0532, S4 KliogestApplicant Reg. No.: Y/21.8.2/230.

Applicant address: Novo Drive, Nordisk (Pty) No.: J/21.8.2/212, Activelle Reg. No.: Kliogest Reg. No.: Y/21.8.2/230. address: Novo Nordisk (Pty) Ltd. 90 Grayston Sandown, S4 Trisequens® Reg. Sandton, 2031, Gauteng, South Africa.

Tel: (011) 202 0500.

NovoSouth Nordisk (Pty)Tel: Ltd,(011) 1959/000833/07.

ZA25ACTV00004.

04_2025.

Ltd. 90 Grayston Drive, Sandown, Sandton, 2031, Gauteng, Africa.

202 0500. Novo Nordisk (Pty) Ltd, 1959/000833/07. ZA25AV00003. 04_2025.

Scan for abbreviated professional information. For full prescribing information, refer to professional information approved by the medicines regulatory authority.

Stay connected with the latest in medical education by joining our WhatsApp channel!

News

ionals rofess ical p d e m r ws fo & vie

Forum

Join thousands of healthcare professionals and be the first to know what’s new.

What you’ll get:  Updates on upcoming webinars and medical advancements  CPD content to enhance your skills  Timely webinar reminders so you never miss out Joining is quick and easy – click the link below to become part of our community. https://bit.ly/4stYQNG