Gastroenterology Today Autumn 2016

Volume 26 No. 2

Autumn 2016

Gastroenterology Today

In this issue IBS: The case for self care Managing Chronic Diarrhoea in Primary Care Posters

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CONTENTS

pepsia without it CONTENTS 5

EDITORS COMMENT

urate predictor gastric preneoplasia 7 FEATUREof I BS: The Case for Self Care

13 FEATURE M anaging Chronic Diarrhoea in Primary Care: symptomatic patients How Should Chronic Diarrhoea Be Managed At GP Level?

y risk factors for gastric cancer 14 NEWS

18 BSG POSTERS se further investigations 28

COMPANY NEWS

about the GastroPanel® blood test

COVER STORY www.gastropanel.com

Routine Testing for Dysbiosis In recent years studies on intestinal microbiota have increased our understanding ealthcare.co.uk www.biohithealthcare.com of the importance of gut bacteria in health and disease considerably. It is well recognised that a “normobiosis” in a healthy state does not differ significantly from one adult to the next but under certain conditions this balance can become disrupted leading to Dysbiosis, where the microbiota does differ from that of a normal, healthy state.

Clinicians studying microbiota using a variety of techniques in the past have helped build our understanding of the role of the microbiota today. We now know for example that dysbiosis can be associated with many gastrointestinal diseases and functional disorders (FGID) including IBS, IBD, Obesity and Diabetes. In fact, studies have shown that only 30% of patients with FGID have a normal microbiota profile and a reduction in the abundance of buturateproducing bacteria such as Faecalibacterium prausnitzii is characteristic of the microbiota in both IBD and IBS patients.

Use the GA-map™ dysbiosis test to: • Analyse microbiota in IBS/IBD patients • Monitor changes in microbiota during treatment (e.g. diet, supplements, drugs, faecal transplant) • Assist with targeted bacteriotherapy in FGID

This issue edited by: Dr A Poullis c/o Media Publishing Company Media House 48 High Street SWANLEY, Kent BR8 8BQ ADVERTISING & CIRCULATION: Media Publishing Company Media House, 48 High Street SWANLEY, Kent, BR8 8BQ Tel: 01322 660434 Fax: 01322 666539 E: info@mediapublishingcompany.com www.MediaPublishingCompany.com PUBLISHING DATES: February, June and October.

COPYRIGHT: Media Publishing Company Media House 48 High Street SWANLEY, Kent, BR8 8BQ PUBLISHERS STATEMENT: The views and opinions expressed in this issue are not necessarily those of the Publisher, the Editors or Media Publishing Company.

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GASTROENTEROLOGY TODAY - AUTUMN 2016

GA-Map™ Dysbiosis Test This new validated technology identifies and grades dysbiosis in symptomatic patients in a routine setting. From a single stool sample more than 300 species of bacteria are detected using 16S rRNA DNA analysis by our laboratory in Oslo.

The GA-Map Dysbiosis Test is a routine, standardised, accessible diagnostic tool that gives clinicians and patients a comprehensive report that not only shows the relative abundance of the most important bacteria, but an overall Dysbiosis Index score comparing the results to a control population as well.

Gastroenterology Today

3

For distal ulcerative colitis1,2

An oral treatment that delivers like a rectal?

What a relief.

When you’ve just been diagnosed with ulcerative colitis, rectal therapy isn’t always the most welcome of prospects.

Thankfully, Salofalk Granules, with their nifty dual release mechanism, allow continuous mesalazine release throughout the entire colon.1 Which means they work rather well, even for those with distal disease.2

Where it works is why it works

4 hrs 20 mins

9 hrs 30 mins

24 hrs

Prescribing Information (Please refer to full SPC before prescribing): Salofalk gastro-resistant prolonged-release granules Presentation: Stick-formed or round, greyish white gastro-resistant prolongedrelease granules in sachets containing 500mg, 1000mg, 1.5g or 3g mesalazine per sachet. Indications: Treatment of acute episodes and the maintenance of remission of ulcerative colitis. Dosage: Adults: Once daily 1 sachet of 3g granules, 1 or 2 sachets of 1.5g granules or 3 sachets of 1000mg or 500mg granules (equivalent to 1.5 – 3.0g mesalazine daily) preferably to be taken in the morning, according to the individual clinical requirement. It is also possible to take the prescribed daily dose in three divided doses (1 sachet of 500mg granules three times daily or 1 sachet of 1000mg granules three times daily) if this is more convenient. Maintenance: 0.5g mesalazine three times daily (in the morning, at midday and in the evening) corresponding to a total dose of 1.5g mesalazine per day. For patients known to be at increased risk for relapse for medical reasons or due to difficulties to adhere to application of three daily doses the dosing schedule can be adapted to 3.0g mesalazine given as a single daily dose, preferably in the morning. Children: There is only limited documentation for an effect in children (age 6-18 years). Children 6 years of age and older: Active disease: To be determined individually, starting with 30-50mg/kg/day once daily preferably in the morning or in divided doses.

Maximum dose: 75mg/kg/day. The total dose should not exceed the maximum adult dose. Maintenance treatment: To be determined individually, starting with 15-30mg/kg/day in divided doses. The total dose should not exceed the recommended adult dose. It is generally recommended that half the adult dose may be given to children up to a body weight of 40kg; and the normal adult dose to those above 40kg. Method of administration: The granules should be taken on the tongue and swallowed, without chewing, with plenty of liquid.

Contra-indications: Hypersensitivity to salicylates or any of the excipients.

Severe impairment of renal or hepatic function. Warnings/Precautions: Blood tests (differential blood count; liver function parameters such as ALT or AST; serum creatinine) and urinary status (dip sticks) should be determined prior

Spread of Salofalk Granules in the gut shown using gamma-scintigraphy

to and during treatment at the discretion of the treating physician. Caution is recommended in patients with impaired hepatic function. Should not be used in patients with impaired renal function. Mesalazine-induced renal toxicity should be considered if renal function deteriorates during treatment.

Patients with pulmonary disease, in particular asthma, should be very carefully monitored. Patients with a history of adverse drug reactions to preparations containing sulphasalazine should be kept under close medical surveillance on commencement of treatment. Should Salofalk cause acute intolerance reactions such as abdominal cramps, acute abdominal pain, fever, severe headache and rash, therapy should be discontinued immediately. For patients with phenylketonuria - Salofalk granules contain aspartame as a sweetening agent equivalent to 0.56mg phenylalanine (500mg granules), 1.12mg phenylalanine (1000mg granules), 1.68mg phenylalanine (1.5g granules) and 3.36mg phenylalanine (3g granules). Salofalk granules contain sucrose: 0.02mg (500mg granules), 0.04mg (1000mg granules), 0.06mg (1.5g granules) and 0.12mg (3g granules). Interactions: Specific interaction studies have not been performed. Lactulose or similar preparations that lower stool pH: possible reduction of mesalazine release from granules due to decreased pH caused by bacterial metabolism of lactulose. In patients who are concomitantly treated with azathioprine, 6-mercaptopurine or thioguanine a possible increase in the myelosuppressive effects of azathioprine, 6-mercaptopurine or thioguanine should be taken into account. There is weak evidence that mesalazine might decrease the anticoagulant effect of warfarin. Use in pregnancy and lactation: There are no adequate data. Do not use during pregnancy unless the potential benefit outweighs the possible risks. Limited experience in the lactation period. Use during breast-feeding only if the potential benefit outweighs the possible risks; if the infant develops diarrhoea, breast-feeding should be discontinued. Undesirable effects: Headache, dizziness, periand myocarditis, abdominal pain, diarrhoea, flatulence, nausea, vomiting, aplastic anaemia, agranulocytosis, pancytopenia, neutropenia, leukopenia, thrombocytopenia, peripheral neuropathy, allergic and fibrotic lung

Mesalazine, the Dr Falk way

reactions (including dyspnoea, cough, bronchospasm, alveolitis, pulmonary eosinophilia, lung infiltration, pneumonitis), acute pancreatitis, impairment of renal function including acute and chronic interstitial nephritis and renal insufficiency, alopecia, myalgia, arthralgia, hypersensitivity reactions such as allergic exanthema, drug fever, lupus erythematosus syndrome, pancolitis, changes in hepatic function parameters, hepatitis, cholestatic hepatitis and oligospermia (reversible). Legal category: POM. Basic cost: Salofalk 500mg granules, pack size 100 sachets – £28.74; €41.55. Salofalk 1000mg granules, pack size 50 sachets – £28.74; €38.28. Salofalk 1.5g Granules, pack size 60 sachets – £48.85; €56.05. Salofalk 3g Granules pack size 60 sachets – £97.70; €129.07 (UK - NHS price; IE - PtW). Product licence number: Salofalk 500mg granules – PL08637/0007; PA573/3/1. Salofalk 1000mg granules – PL08637/0008; PA573/3/2. Salofalk 1.5g granules PL08637/0016; PA573/3/7. Salofalk 3g granules PL08637/0025; PA573/3/6. Product licence holder: Dr Falk Pharma GmbH, Leinenweberstr.5, D-79108 Freiburg, Germany.

Date of preparation: June 2014 Further information is available on request.

Adverse events should be reported. Reporting forms and information can be found at http:// www.mhra.gov.uk/yellowcard (UK residents) or at http://www.hpra.ie/EN/Safety--Quality/Online-Forms.aspx (residents of the Republic of Ireland). Adverse events should also be reported to Dr Falk Pharma UK Ltd. References: 1. Brunner M et al. Aliment Pharmacol Ther 2003; 17: 1163–9.

2. Leifeld L et al. Aliment Pharmacol Ther 2011; 34: 1115–22.

Date of preparation: March 2016

DrF 16/026

EDITORS COMMENT

EDITORS COMMENT Benign lower gastrointestinal disease A hugely important part of the gastroenterology workload is in the diagnosis and management of malignant gastrointestinal disease. However, the majority of our patients do not have malignant disease and there is a risk of benign disease been relegated and seen as less important. With relatively new NICE GI cancer guidelines there is increasing pressure on diagnostic services and this could potentially have a negative impact on the diagnostics in benign disease.

Wider adoption of non-invasive diagnostics has a key place in guiding the timely investigation of patients in whom we are not suspecting cancer but who may have serious benign disease. At present non-invasive tests are limited to widely used blood tests and less widely used stool tests. Faecal calprotectin was first recommended for use by NICE in 2013 but although it has had a steady increase in use it is still not nationally available and is underused. With increasing evidence of poor outcomes in delayed diagnosis of inflammatory bowel disease (IBD) and strong evidence of the increased cost of delayed and emergency presentations of newly presenting cases of IBD it is essential that all involved in the initial assessment and diagnosis of lower GI symptoms utilise this test.

Faecal calprotectin is the most established non-invasive biomarker for investigating “benign” lower GI symptoms but there is no doubt that non-endoscopic diagnostics is set to grow. Studies on cytology and biomarker analysis on non-invasively collected colonic mucous have shown the potential to diagnose IBD non-invasively raising the possibility of a reduced need for endoscopy (possibly leading to a reduction in endoscopy waiting times….).

Dr A Poullis St George’s Hospital, London Member of NHS England Faecal Calprotectin Working Group

GASTROENTEROLOGY TODAY - AUTUMN 2016

“With relatively new NICE GI cancer guidelines there is increasing pressure on diagnostic services and this could potentially have a negative impact on the diagnostics in benign disease.”

5

FEATURE

Happy with her selfie When the symptoms of Crohn’s disease are already harming her self-esteem, steroid-related side-effects can make things even worse.1 Budenofalk is different - it offers the efficacy of a systemic steroid, but the side-effect level is more like mesalazine.2,3

Now that’s something to smile about.

Eudragit L/S coating modified release formulation meaning the drug is released in the terminal ileum and caecum4

50x

greater receptor affinity than prednisolone meaning a lower effective steroid dose is required5,6

90%

pre-systemic clearance meaning the potential risk of side-effects is limited2

Corticosteroids, the Dr Falk way

GASTROENTEROLOGY TODAY - AUTUMN 2016

Prescribing Information (Please refer to full SPC before prescribing) Presentation: Budenofalk® 9 mg gastro-resistant granules, each sachet contains 9mg budesonide, 828mg sucrose, 36mg lactose monohydrate and 900mg sorbitol. Budenofalk® 3mg gastro-resistant capsules, each containing 3mg budesonide, 240mg sucrose and 12mg lactose monohydrate. Indications: (granules and capsules) Induction of remission of mild to moderate active Crohn’s disease affecting the ileum and/or the ascending colon.

Extraintestinal symptoms unlikely to respond. Induction of remission of active collagenous colitis. Autoimmune hepatitis (capsules only). Dosage: Adults: Granules: One sachet daily, in the morning, half an hour before food, taken with liquid without chewing or crushing granules. Capsules: For Crohn’s disease and collagenous colitis, three capsules once daily, in the morning, half an hour before food and taken with liquid. One capsule three times daily if more convenient. Both formulations: limit treatment to 8 weeks. Treatment should not be stopped abruptly but withdrawn gradually. For autoimmune hepatitis, one capsule three times daily. Combine with azathioprine in suitable cases. For maintenance of remission: one capsule twice daily (morning and evening).

Revert to 3 capsules daily in the event of elevated transaminases ALAT and/or ASAT. Continue treatment for maintenance of remission of autoimmune hepatitis for 24 months. Children: Not recommended in children younger than 12 years. Safety and efficacy in adolescents aged 12 -18 years has not been established. See SmPC sections 4.8 and 5.1 for data. No specific dose recommendations in renal/hepatic impairment.

Contraindications: hypersensitivity to budesonide or any of the ingredients. Hepatic cirrhosis. Warnings/ Precautions: Transfer of patients from other steroid therapy may result in symptoms relating to the lowering of systemic steroid levels. Use with caution in patients with tuberculosis, hypertension, diabetes mellitus, osteoporosis, peptic ulcer, glaucoma, cataracts or family history of glaucoma or diabetes, or any other condition in which glucocorticoids may have undesirable effects. Not appropriate for use in upper GI Crohn’s disease or for extraintestinal symptoms e.g., of the eyes, skin, joints. Long term, high dose use may result in systemic effects of corticosteroids such as Cushing’s syndrome, adrenal suppression, growth retardation, decreased bone mineral density, cataract, glaucoma and rarely, psychiatric/behavioural effects. Infection: suppression of the inflammatory response and immune function increases susceptibility to infections and their severity, with risk of deterioration of bacterial, fungal, amoebic and viral infections. The clinical presentation of infections may be atypical and the presentation of serious infections e.g. septicaemia and tuberculosis, may be masked.

Chickenpox can be fatal in immunosuppressed patients. Those without definite medical history of this infection should avoid close personal contact with chickenpox or herpes zoster and seek medical attention if exposed.

Passive immunisation is needed by exposed non-immune patients receiving (or who have received within the previous 3 months) systemic corticosteroids, within 10 days of exposure to chickenpox. Urgent specialist care is required if chickenpox is confirmed; corticosteroids should not be stopped and dosage may need to be increased. Measles: Immunosuppressed patients who come into contact with measles should receive normal immunoglobulin as soon as possible after exposure. Live vaccines should not be given to patients with chronic corticosteroid use/impaired immune responsiveness. Antibody response to other vaccines may be diminished. Patients with liver function disorders: increased systemic bioavailability of budesonide expected where there is severe impairment. Other: Corticosteroids may suppress the HPA axis and reduce the stress response. Supplementary systemic glucocorticoid treatment is recommended in patients subject to surgery or other stress. Concomitant treatment with ketoconazole or other CYP3A4 inhibitors should be avoided. Do not use in patients with rare hereditary problems of galactose or fructose intolerance, glucose – galactose malabsorption, sucrase – isomaltase insufficiency or Lapp lactase deficiency or congenital lactase deficiency. In autoimmune hepatitis evaluate transaminase levels every 2 weeks for the first month and then every 3 months.

Can lead to positive results in doping tests. Interactions: Concomitant administration of cardiac glycosides may

6

potentiate the activity of the glycoside (due to increased excretion of potassium); simultaneous treatment with saluretics may exacerbate the hypokalaemia. Avoid concomitant administration with ketoconazole, grapefruit juice or other CYP3A4 inhibitors (e.g. ritonavir, itraconazole and clarithromycin) because they may markedly increase the plasma concentrations of budesonide. CYP3A4 inducers (e.g. carbamazepine and rifampicin) may reduce systemic and local (gut mucosa) exposure, necessitating dose adjustment of budesonide. CYP3A4 substrates may compete with budesonide leading to possible increases in plasma concentrations of either budesonide or substrate, depending on their relative affinities for this enzyme. Elevated plasma concentrations and enhanced effects of corticosteroids have been reported with oestrogens or oral contraceptives, although not with oral low dose contraceptives. Cimetidine has a small (non-significant) effect on the kinetic effects of budesonide. Omeprazole has no effect on the pharmacokinetics of budesonide. Steroid-binding compounds (e.g. cholestyramine) and antacids may reduce the efficacy of budesonide, therefore they should be given at least 2 hours apart. Use in pregnancy and lactation: Budenofalk should be avoided during pregnancy unless essential. Avoid breastfeeding during Budenofalk treatment. Undesirable effects: Cushing’s syndrome e.g., moon-face, truncal obesity, reduced glucose tolerance, diabetes mellitus, hypertension, sodium retention with oedema, increased excretion of potassium, inactivity or atrophy of the adrenal cortex, red striae, steroid acne, disturbance of sex hormone secretion (e.g. amenorrhoea, hirsutism, impotence). Growth retardation in children, glaucoma, cataracts, stomach complaints, constipation, gastroduodenal ulcers, pancreatitis, increase in risk of infections, muscle and joint pain and weakness and twitching, osteoporosis, aseptic necrosis of bone, headache, pseudotumor cerebri (including papilloedema) in adolescents, depression, irritability and euphoria, a range of psychiatric/behavioural effects, allergic exanthema, petechiae, ecchymosis, contact dermatitis, delayed wound healing, increased risk of thrombosis, vasculitis (after withdrawal from long-term treatment), tiredness and malaise, dizziness, nausea, vomiting, hyperacusis. Occasionally side effects characteristic of systemic corticosteroid therapy may occur although clinical studies have shown that the frequency of these side effects is lower with Budenofalk (approximately half) than with oral equivalent doses of prednisolone. Other adverse effects include exacerbation or reappearance of extraintestinal manifestations when switching treatment from systemically acting glucocorticosteroids. Legal category: POM. UK NHS Cost: (granules) packs of 60 sachets £135; (capsules) packs of 100 capsules £75.05. Ireland cost (PtW): (granules) packs of 60 sachets: €165.80; (capsules) packs of 100 capsules: €78.96. Product licence holder: Dr Falk Pharma GmbH, Leinenweberstr.5, D-79108 Freiburg, Germany. Product licence number: (granules) PL08637/0020 (UK) PA573/2/3 (IE) (capsules) PL08637/0002 (UK) PA573/2/1 (IE). Date of preparation: May 2015.

Further information is available on request.

Adverse events should be reported. Reporting forms and information can be found at www.mhra.gov.uk/yellowcard (UK residents) or at http://www.hpra.ie/homepage/about-us/report-an-issue (residents of the Republic of Ireland). Adverse events should also be reported to Dr Falk Pharma UK Ltd. References: 1. McDermott E et al. Inflamm Bowel Dis 2015; 21(2): 353-60. 2. De Cassan C et al. Dig Des 2012; 30(4): 368-75. 3. Bar-Meir S et al. Gastroenterol 1998; 115(4): 835-40. 4. Data on file, Dr Falk Pharma.

5. Möllman HW et al. In: Möllman HW, May B. Glucocortcoid Therapy in Chronic Inflammatory Bowel Disease.

Dordrecht: Kluwer 1996. 6. He Y et al. Cell Res 2014; 24(6): 713-26.

Date of preparation: December 2015

DrF15/143

FEATURE

IBS: THE CASE FOR SELF CARE

By Dr Nick Read Nick Read is a retired

Although there is no single definitive cause for IBS, patients often exhibit

gastroenterologist, physiologist

a combination of abnormalities involving both the gut and the brain1.

and nutritionist. During his

An increase in bowel sensitivity, which may be caused by either an

academic career, he held

upset in the patient’s gut and/or their life often occurs in combination

university chairs in Gastrointestinal

with an alteration in gut motility and a mild inflammation. It may also be

Physiology, Human Nutrition and

associated with changes in gut bacteria, a leaky gut and stimulation

Integrated Medicine, published

of the gut immune system. This releases neurotransmitters which may

over 500 original papers and

affect the activity of the emotional centres of the brain, which then

reviews and 11 books. These

dysregulates the autonomic nervous system and affects the gut; a

include the popular monograph,

vicious cycle. So are there many different causes for IBS that need to

‘Sick and Tired; healing the

be teased out by more research? Or might this represent a resetting of

illnesses, doctors cannot cure,’

the physiological systems that regulate the bowel.

(Phoenix, 2006), which serves as a guide to help people understand and manage illnesses, like IBS, that have no clear cause or pathology. Since retiring, Dr Read has

The sensitive bowel

maintained a private practice in psychotherapy, but devotes the majority of his time to The IBS Network (www.theibsnetwork.org), the national

The nearest we get to a marker for IBS is ‘a sensitive bowel’, that reacts

charity for people with Irritable Bowel Syndrome.

to whatever stimulates it, most commonly ‘food and mood’. The food components include fats, hot spices, coffee, alcohol and a host of poorly absorbed sugars that may either retain fluid in the gut resulting

What’s it all about?

In our current age, illness tends to be treated by doctors, skilled operatives who have undergone many years of intensive training in medical sciences and clinical practice. This is based on the assumption that only experts, well versed in the science of medicine, can understand what is going on in their patients’ bodies and put it right. All too often, medical practice ignores what might be going on in the patient’s mind, and even ignores the patient. The disease is the object. First make a diagnosis by carrying out an appropriate test and then give a specific treatment and as if by some kind of sorcery, the patient gets better. But not all illness is like that.

IBS is a syndrome, a ‘diagnosis by committee’ that confers an identity upon a selection of unexplained bowel symptoms. There is no definitive Although successive Rome committees have stressed the importance of a positive diagnosis, for practical purposes, most doctors regard IBS as ‘a diagnosis of exclusion’, a collection of colonic symptoms for which no cause can be found. Hence, they apply screening tests to rule

bloating, flatulence and pain. The latter have been characterised by the term FODMAPs which stands for Fermentable Oligosaccharides, Disaccharides, Monosaccharides and Polyols2. ‘Mood’ involves an increase in emotional tension caused by current events or thoughts that carry particular significance for that individual.

A hypersensitive gut may be instigated ‘bottom up’ by changes that occur in the gut or ‘top down’ by events or situations in a person’s world, most often their social environment.

Post-infectious IBS. One of the most common risk factors for the development of IBS is an attack of gastroenteritis3. IBS does not occur in everybody who gets gastroenteritis, but is more likely in those who are anxious or depressed at the time of the attack or have experienced some upsetting life situation or event. Post infectious IBS initiates a cascade of immunological and microbiological changes in the gut.

Antibiotics. The prescription of broad spectrum antibiotics may decimate the colonic microflora, leading to overgrowth of more harmful species, which might induce changes in permeability and immune activation.

out the most common life threatening ‘diseases’ that might cause the same symptoms: Coeliac Disease, Crohn’s Disease, Colitis and Bowel

Small Intestinal Bacterial Overgrowth. In the USA, Small Intestinal

Cancer.

Bacterial Overgrowth (SIBO) is regarded as one of the most common mechanisms underlying IBS though many gastroenterologists suspect

Above all, IBS is an individual ailment; a personal state of unwellness

this may be over-diagnosed by a misinterpretation of breath tests.

or dysphoria that involves the mind, the gut and many other parts of

However, recent research has indicated that some organisms that cause

the body. It is the interaction between an individual’s susceptibility

gastroenteritis may release a toxin (cytolethal distending toxin; CDT) that

(either genetic or historic) and their environment. Getting better involves

partially paralyses the gut. Antibodies to CDT cross react with those

changing either or both. It comes and goes and is shaped according to

for the protein vinculin that increases cell binding and stimulates gut

what happens. One person’s IBS is not the same as another’s.

motility4.

GASTROENTEROLOGY TODAY - AUTUMN 2016

pathology, no specific cause and no cure or single effective treatment.

in diarrhoea or are fermented in the colon releasing gas and causing

7

FEATURE Alcohol. Binge drinking can encourage the growth of gram negative coliforms that break down the alcohol to acetaldehyde5. Acetaldehyde makes the gut more permeable, allowing invasion by endotoxin which excites the immune system and causes inflammation, not only in the gut wall but throughout the body.

to prevent or treat IBS. Some studies have shown promise, but supplements have to be taken every day and there is no convincing data to suggest that any one strain of probiotic is better than any other.

The European Food Standards Agency still prohibits companies from making health claims about probiotics.

Trauma and the pace of life. Many people relate the onset of their IBS to some personal trauma or grief, the collapse of a love affair, the loss of a job, the death of a child, sexual abuse or conflict trauma. Their systems are sensitised. Everything upsets them, they are hyper-aroused, pushed beyond their limits of tolerance. Brain imaging techniques have indicated that at those times, the emotional centres in the brain stem are hyperactive together with centres that regulate the physiological systems of the body including bowel function, while the part of the brain that is self aware and keeps the body under control (the medial prefrontal cortex), goes off line6. Emotions and body regulation are out of control, unable to cope with the pace and demands of modern life.

Prebiotics are poorly absorbed complex sugars that provide the nutrient to support the growth of beneficial bacteria. Some may be fermented and cause bloating, but there is evidence that transgalactooligosaccharides encourage the growth of non gas-producing bifidobacteria spp and reduce bloating9.

What can we do about it?

If IBS is the disruption of a range of interconnected physiological mechanisms that control the gut, how can we help our patients break the vicious cycle and rectify these? There are many options.

They include: enhancing the microbiome with diet and prebiotics or probiotics, using supplements or drugs to reduce the leakiness of the gut, suppressing immune activation, reducing inflammation and sensitivity, altering gut motility, reducing the release of neurotransmitters, or suppressing activation of the emotional and visceral centres of the brain with therapies that relax and induce a state of mindfulness.

Medical treatments For many years, prescription of antispasmodics and bowel regulators has been the standard pharmacological approach for IBS. These are moderately effective for some symptoms but may make others worse. For example, antispasmodics can induce constipation, laxatives may cause more pain, anti-diarrhoeal medication may lead to constipation and pain.

Antidepressants, even when given in low doses, may produce a global suppression of IBS symptoms, but at the expense of a degree of drowsiness, depersonalisation and in older people, a greater predisposition to dementia7.

GASTROENTEROLOGY TODAY - AUTUMN 2016

Simethicone is said to be useful for the treatment of bloating but the data is unconvincing.

Many patients with IBS-D have evidence of bile acid malabsorption8, presumably due to rapid small bowel transit. These can respond well to bile acid sequestrants such as colestyramine or colesevelam.

Finally, it has to be said that in randomised controlled trials of treatment for IBS, the placebo responsiveness is often very high, especially for pain Supplements Bulking agents such as ispaghula, psyllium and methylcellulose are all sources of soluble fibre and can be useful to treat constipation. They may however induce bloating, though this is said to reduce if you persist with the treatment.

Probiotics can briefly replenish the microbiome and have been used

8

Glutamine is an amino acid that is said to reduce permeability. Early studies in IBS look promising10.

Diet Exclusion of FODMAPs can reduce symptoms of bloating and pain and diarrhoea in as many as 70% of people but they also reduce populations of beneficial bifidobacteria spp2. This problem is compounded by the difficulty in reintroducing some of the excluded foods. A preliminary study has indicated that restriction of onions and pulses is as effective as the complete low FODMAP diet2.

So who is the expert?

Is it the doctor, who has studied the gut immune system, the colonic microbiome, the enteric nervous system and the brain gut axis? Or is it the patient, who alone understands the context of the illness, when it began, what brings it on, what takes it away and what it means? This is the difference between knowledge and knowing. Tests will not help the doctor know his patients or the patients know themselves, but perhaps a collaboration between the two will help to create an understanding that can work. No healthcare professional can make people with IBS better. Their task is more to co-create the opportunity and shared understanding within which patients can find solutions to ‘help themselves better’.

For IBS and other ‘medically unexplained’ illnesses, we need to see things in a different way. After a time and a few tests, people often come to realise there may be nothing medically wrong with them. But in the meantime, they may have entered into a dependant relationship with their doctor, which has eroded their self efficacy. A powerless patient is a patient for life.

Nevertheless, people can get over their IBS, but they do so by accepting their limitations, taking control and making the best of it.

Knowledge is power. People can learn to live with their IBS better by understanding their illness, what sets it off, what takes it away and what it means. This allows them to accept themselves and be less ashamed of having an illness like IBS. If doctors are ever to really help people with IBS, they need to understand what the illness might represent. Some people can feel bullied by their IBS, others see it as a source of considerable shame, others feel trapped by it, confined to their homes, too frightened to take the risk. IBS is not just in the gut, it is so often related to fear and powerlessness, but acted out and represented in the gut. Everybody has their IBS story.

FEATURE

GASTROENTEROLOGY TODAY - AUTUMN 2016

9

FEATURE How can you leave your IBS? There are no cures for life or IBS; but there are many different routes to well being. Professional uncertainty is exemplified by the varied and often contradictory treatments that claim efficacy for IBS. But do these treatments work because they capture the patient’s imagination and belief?

IBS fluctuates, getting worse at some times and better at others. So it is important for people with IBS to recognise what sets it off and what can calm it down and adjust their lives accordingly. Keeping a diary of flare ups of symptoms and noting any changes in their diet, sleep, sexual activity, life situation or lifestyle can often reveal what provokes attacks of IBS. But it may not be the actual event that is important, it is often what it means and the context in which it occurs. For example, an intolerance to certain foods is not necessarily related to their chemical composition, but may be triggered by the context in which they are eaten and the memory that is evoked. Stress can often make people sensitive to certain foods. People do better when they can take charge of their own diet, understand why their symptoms fluctuate and learn to select and prepare the kind of foods that soothe their symptoms.

Exercise, if pursued with a vengeance, may become a stress. Trying to sleep might liberate disturbing thoughts that have been suppressed by the days activities. Once people can see what provokes their symptoms, they can work out what to do to control these.

Illnesses of the individual require individual treatments, but only the patient can know the true meaning of the symptoms, what instigates them and what can help and why. An illness provoked by a particular situation requires a solution that addresses the meaning, but it may take time and space for contemplation before that can be realised.

Being mindful Mindfulness is a form of meditation that helps people become aware of the sensations that occur in their bodies in the present without fretting about the past or worrying about what might happen. It brings the bodily conscious part of the brain back on line, so that the emotions and symptoms are under control11. Mindfulness helps people deal with what has happened or is happening and enables them to carry out everyday tasks in a relaxed and focussed manner. Some people find it more helpful to go to classes where they can learn techniques to facilitate mindfulness, such as tapping on acupuncture points (Emotional Freedom Technique), Eye Movement Desensitisation and Reprocessing (EMDR), therapeutic massage, yoga, pilates and several complementary therapies.

GASTROENTEROLOGY TODAY - AUTUMN 2016

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But being mindful doesn’t mean sitting in a darkened room with jostiks and candles and chanting mantras; you can practice mindfulness while you are cooking, writing, drawing, fishing, singing, dancing, running, walking, swimming even washing or cleaning your teeth. You just need to get ‘in the zone’. Regular exercise is an important route to physical and emotional well-being, promoting self awareness, rebalancing the autonomic nervous system and stimulating the release of endorphins.

Facilitating Self Help The classical medical model for treating disease does not work well for IBS. Drugs are often ineffective and cause too many side effects. Diets almost inevitably fail in the long term. These disappointing outcomes may occur because the patient is a passive recipient and not actively engaged. There are no cures for life or IBS; just many different routes to well being. So as healthcare professionals, we must remain humble and not tell our patients what to do. Instead we should listen, show we understand, pick up cues, be a focus of identification to adjust the way

they think, supply the information to help them understand their illness and encourage the skills to escape the cycle of despair and bring their own healing brain on line to find their own solutions.

Health services are becoming overwhelmed by the burden of long term medical illnesses. There is a need for education and services that facilitate self care. This involves reliable information, support and easy access to advice. It inspires self efficacy, enables communication with health professionals and creates the insight and emotional space to make the necessary changes to escape from the prison of IBS. It puts the patient in charge and avoids dependency by encouraging health confidence.

Patients find out more about the food they can eat by cooking the meals they like, they use creative activity to become more calm and self aware and they learn how to regulate their emotions and engage productively with others. This is more effectively conducted in small groups, co-ordinated by group leaders, either ‘expert’ patients or health care professionals but both trained to facilitate understanding of IBS and self help.

Charities can play an essential role in this model of care. The IBS Network - the UK’s national charity for IBS, has the IBS Self Care Programme which is a fully comprehensive information resource (www.theibsnetwork.org/the-self-care-plan). The charity provides a range of services which include blogs, an online forum and a monthly e-newsletter. For members, the charity also offers a personalised oneto-one service via email, access to a telephone helpline, a quarterly magazine, Can’t Wait Card, IBS friendly recipes and Symptom Tracker.

New training programmes are also being rolled out for Healthcare professionals and Expert Patients to be trained to run IBS support groups across the UK. Working together, patients and healthcare professionals can ‘make a difference’ for people with IBS. For more information, please visit: https://www.theibsnetwork.org/ Or email: info@theibsnetwork.org References 1. Spiller RC (2011), Irritable bowel syndrome: gender, infection, lifestyle or what else?.

Digestive Diseases. 29(2):215-21.

2. Gibson, P, Varney, J, Malakar, S and Muir J. (2015). Food and Functional Bowel Disease.

Gastroenterology ;148:1158–1174 3. Marshall JK, Thabane M, Garg AX et al (2010). Eight year prognosis of postinfectious irritable bowel syndrome following waterborne bacterial dysentery. Gut; 59: 605-611.

4. Pimentel M, Morales W, Rezaie A 2015, Development and Validation of a Biomarker for Diarrhea-Predominant Irritable Bowel Syndrome in Human Subjects. DOI: 10.1371/ journal.pone.0126438.

5. Purohita V, Bode JC, Bode C et al (2008) Alcohol, Intestinal Bacterial Growth, Intestinal Permeability to Endotoxin, and Medical Consequences: Summary of a Symposium Alcohol. 42: 349–361.

6. Van der Kolk B, (2014). The Body Keeps the Score; mind, body in the transformation of trauma. London. Allen Lane.

7. Gray SL, Anderson ML, Dublin S et al (2015) Cumulative Use of Strong Anticholinergics and Incident Dementia: A Prospective Cohort Study. JAMA Intern Med. 175:401-407.

8. Wedlake L, A’Hern R, Russell D et al (2009) Systematic review: the prevalence of idiopathic bile acid malabsorption as diagnosed by SeHCAT scanning in patients with diarrhoea-predominant irritable bowel syndrome. Aliment Pharmacol Ther; 30: 707–717.

9. Silk DB, Davis A, Vulevic J, et al (2009). Clinical trial: the effects of a transgalactooligosaccharide prebiotic on faecal microbiota and symptoms in irritable bowel syndrome. Aliment Pharmacol Ther. 29: 508-518.

10. Zhou Q and Verne GN (2011). New insights into visceral hypersensitivity—clinical implications in IBS. Nature Reviews Gastroenterology and Hepatology, 8, 349-355.

11. Zernicke KA, Campbell TS, Blustein PK, et al (2013). Mindfulness-based stress reduction for the treatment of irritable bowel syndrome symptoms: a randomized wait-list controlled trial. Int J Behav Med.20:385-96.

Tillotts acquires Entocort CR for Crohn’s disease ®

Life feels good when Crohn’s is under control

FEATURE

1,2

For the induction of remission in adults with mild to moderate Crohn’s disease affecting the ileum and/or the ascending colon3 Budesonide 9mg daily is recommended by the BSG for isolated ileocaecal disease with moderate disease activity4

GASTROENTEROLOGY TODAY - AUTUMN 2016

ENTOCORT CR 3mg Capsules (budesonide) - Prescribing Information Please consult the Summary of Product Characteristics (SmPC) for full prescribing Information Presentation: Hard gelatin capsules for oral administration with an opaque, light grey body and an opaque, pink cap marked CIR 3mg in black radial print. Contains 3mg budesonide. Indications: The induction of remission in patients with mild to moderate Crohn’s disease affecting the ileum and/or the ascending colon. Dosage and administration: Adults: 9mg once daily in the morning for up to eight weeks. Full effect achieved in 2-4 weeks. When treatment is to be discontinued, dose should normally be reduced in final 2-4 weeks.

Paediatric population: Not recommended. Older people: No special dose adjustment recommended. Swallow whole with water. Do not chew. Contraindications: Hypersensitivity to the active substance or any of the excipients. Warnings and Precautions: Side effects typical of corticosteroids may occur. Systemic effects may include glaucoma and when prescribed at high doses for prolonged periods, Cushing’s syndrome, adrenal suppression, growth retardation, decreased bone mineral density and cataract. Caution in patients with infection, hypertension, diabetes mellitus, osteoporosis, peptic ulcer, glaucoma or cataracts or with a family history of diabetes or glaucoma. Particular care in patients with existing or previous history of severe affective disorders in them or their first degree relatives. Caution when transferring from glucocorticoid of high systemic effect to Entocort CR. Chicken pox and measles may have a more serious course in patients on oral steroids. They may also suppress the HPA axis and reduce the stress response. Reduced liver function may increase systemic exposure. When treatment is discontinued, reduce dose over last 2-4

weeks. Concomitant use of ketoconazole should be avoided. Excessive grapefruit juice may increase systemic exposure and should be avoided.

Patients with fructose intolerance, glucose-galactose malabsorption or sucrose-isomaltase insufficiency should not take Entocort CR. Monitor height of children who use prolonged glucocorticoid therapy for risk of growth suppression. Interactions: Concomitant colestyramine may reduce Entocort CR uptake. Concomitant oestrogen and contraceptive steroids may increase effects. CYP3A4 inhibitors may increase systemic exposure. CYP3A4 inducers may reduce systemic exposure. Fertility, pregnancy and lactation: Only to be used during pregnancy when the potential benefits to the mother outweigh the risks for the foetus.

May be used during breast feeding. Adverse reactions: Anaphylactic reaction, Cushingoid features, growth retardation, hypokalaemia, behavioural changes such as nervousness, insomnia and mood swings, tremor, blurred vision, glaucoma, palpitations, dyspepsia, skin reactions (urticaria, exanthema), muscle cramps, menstrual disorders.

Prescribers should consult the summary of product characteristics in relation to other adverse reactions. Marketing Authorisation Numbers, Package Quantities and basic NHS price: PL 45329/0003. Packs of 100 capsules: £99.00. Legal category: POM. Marketing Authorisation Holder: Tillotts Pharma GmbH, Wambacher Strasse 80, 79618 Rheinfelden, Germany. Date of preparation of PI: April 2016

Adverse events should be reported.

Reporting forms and information can be found at https://yellowcard.mhra.gov.uk. Adverse events should also be reported to Tillotts Pharma UK Ltd. Tel: 01522 813500.

References: 1. Greenberg GR et al. N Engl J Med 1994; 331: 836-41.

2. Rezaie A et al. Cochrane Database Syst Rev 2015;6:CD000296.

3. Entocort® CR 3mg Capsules – Summary of Product Characteristics.

4. Mowat C et al. Gut 2011; 60:571-607.

Date of preparation: September 2016. UK/EN/0002/0915(1)a.

11

NEWS

GASTROENTEROLOGY TODAY - AUTUMN 2016

12

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FEATURE

MANAGING CHRONIC DIARRHOEA IN PRIMARY CARE: HOW SHOULD CHRONIC DIARRHOEA BE MANAGED AT GP LEVEL? Author: Chris Probert Professor of Gastroenterology, University of Liverpool

Gastric complaints, in one way or another account for a large

may actually be misdiagnosed and have Inflammatory Bowel Disease

proportion of a GP’s workload and chronic diarrhoea, defined

instead.

as occurring for more than four weeks, is considered to be a common condition (one study reported a prevalence of 14% in

In the meantime, although not life threatening, the patient is dealing

elderly people).

with an extremely unpleasant condition which can impact on every area of their life including their employment prospects, social life

Chronic diarrhoea can be a symptom of something as benign as

and relationships. They may be back and forth to their doctor or they

gastroenteritis, or as life threatening as cancer, with many other

may give up and not bother at all, simply learning to live with chronic

conditions in-between. No wonder that, as a stand-alone condition,

diarrhoea and all the restrictions it imposes upon them.

it can often be surprisingly complex to diagnose and therefore treat correctly, especially at a Primary Care level.

This situation should never be considered acceptable and efforts should be made to continue to try to work out the cause of the chronic

From a GP perspective there are clear patient pathways, for example,

diarrhoea. However as we said earlier there are a myriad of possibilities,

for people who suffer with chronic diarrhoea due to specific conditions

and unless the GP has a specialist knowledge it is possible he or she

such as diabetes or for red flag symptoms such as a rectal mass,

may not know about them.

unexplained rectal bleeding or unexplained weight loss. Likewise Crohn’s Disease or ulcerative colitis, once suspected and referred on,

One of the first places to look, especially in the over fifties, would

are relatively simply to diagnose with a scope and a biopsy.

be their current medication. Statins, PPIs, diabetes medication can all cause havoc with the bowel. Likewise certain conditions such as

It is also standard procedure that any patient over 45 who shows a red

diabetes can be the culprit.

flag symptom such as a rectal mass, unexplained weight loss or rectal bleeding is fast-tracked for a colonoscopy to rule in or out bowel cancer.

It is perfectly feasible too, that something may have been missed at referral. If the surgeon carrying out the endoscopy is being told that a patient has suspected Crohn’s Disease or UC he may just look for

are found to be the cause of the chronic diarrhoea? Usually the patient

those conditions and not consider others. Microscopic Colitis, which

is sent back as undiagnosed to the GP who then has the task of

can only be diagnosed by multiple biopsies is a relatively common but

deciding whether to continue on a diagnostic pathway or whether to

often missed cause of watery diarrhoea in the over fifties. However once

treat the diarrhoea symptomatically until it clears up.

diagnosed, it can be usually successfully treated with budesonide.

Sometimes the GP may refer the patient back to hospital for repeat

Another commonly missed cause of chronic watery diarrhoea is Bile

tests, adding pressure to an already stretched endoscopy service, but

Salt Malabsorption, which can be caused by damage from surgery, or

usually and understandably, particularly if the patient is under forty five,

radiation, or from serious conditions such as Type II diabetes, Crohn’s

the GP will consider Irritable Bowel Syndrome as a diagnosis. In this

Disease, chronic pancreatitis or peptic ulcer. Research carried out

case they may steer the patient towards lifestyle or dietary changes, or

at Imperial College London found that a third of all patients who are

even consider a low dose of anti-depressants. But what should GPs do

currently being treated for Irritable Bowel Syndrome where diarrhoea is

when this does not work?

the predominant symptom, have bile salt malabsorption.

IBS can be seen as a default diagnosis when other common disorders

Put together, these missed opportunities for diagnosis and treatment

have been ruled out, without any effect being made to ensure the

can add up to a reduced quality of life for the patient, extra burden on

diagnosis is correct. One study, published in the Journal of United

the GP’s and the NHS not to mention the economy as a whole. Clearer

European Gastroenterology in 2014 reported that 1 in 10 patients who

pathways for diagnosis and treatment of chronic diarrhoea at GP level

are told that they are suffering from irritable bowel syndrome (IBS)

could certainly lead to improvements in all these areas.

GASTROENTEROLOGY TODAY - AUTUMN 2016

Yet what if, after referral and the usual tests, none of these conditions

13

NEWS Associate Director for Educational Quality

Engaging global communities in research learning Massive Open Online Courses (MOOCs) are a relatively new way to learn. They make learning accessible and engaging to people all over the world. Insight Monthly looks at how the NIHR Clinical Research Network (CRN) has utilised this pioneering delivery model to bring clinical research learning to

Standards, in close collaboration with the Digital Learning team at Leeds University, the MOOC was initially launched on the 2 November 2015. It is designed to provide around 4 hours of learning a week over a 4 week period as learners follow the process of scientific discovery from a number of perspectives. Fiona O’Neill is a strong advocate for the model: “MOOCs have become popular over the last few years as a way of delivering learning open

more than 12,000 people across the globe.

to anyone who has an internet connection.

Enabling understanding of clinical research

a flexible learning environment so that learners

and its role in improving healthcare is a core objective in the Network. In 2015 the Network’s Workforce, Learning and Organisational Development team partnered with the Digital Learning team at Leeds University to develop a MOOC; ‘Improving Healthcare through Clinical Research’. The MOOC is free, and available to anyone wanting to learn about clinical research.

Developed by Fiona O’Neill, Head of Multi_Ad_2016_ScheBo_17/09/2016 Workforce and Learning, and Allan Gaw,12:02

Courses are deliberately designed to provide can study at their own pace and connect with other learners and educators, should they wish to do so. The MOOC model provides an ideal platform to achieve our goal of reaching a wide community of learners and to provide engaging and interesting content pitched at an introductory level.”

The course is built around the concept of discovery and the ethical and scientific principles that inform every aspect of the process of developing new treatments in healthcare. Short videos, involving different members of research teams, patients and educators, are complemented by activities and opportunities for further reading.

Allan Gaw has years of experience

GASTROENTEROLOGY TODAY - AUTUMN 2016

in clinical research, is an educator for the MOOC, and

medicine and will be the engine that drives it forward. However, for this to happen we continually need new, committed researchers and new willing research participants. There are many misconceptions about how modern research is conducted and any serious attempt to grow and develop this aspect of medicine must address these through the provision of high quality and accessible educational and training opportunities. Thus, the challenge is one of communication and education, and it is a challenge on a large scale.

“To explore new educational possibilities in this area, we decided to tackle this challenge by harnessing the power of modern educational technology to offer a MOOC. The aim of this enterprise was to educate and inform the public, patients and healthcare professionals about clinical research. Most education is local and contained — 10 people in a tutorial group, 30 in a classroom, 200 in a lecture theatre. When we step on to a global platform to deliver education in this or in any field, new opportunities present themselves for the first time, along with equally new challenges… it is a remarkable medium for education — the MOOC has allowed me to teach more people in a few weeks than I had taught in a lifetime in academia.”

features in some of the videos as part of the course material.

He explains some of the challenges of engaging people in research and why a MOOC is a good

Interesting and creative content is a crucial pull factor for MOOCs. So how do you begin to develop a MOOC for such a diverse audience?

Fiona and Allan worked together to create the course, as well as being course educators and featuring in some of the course materials.

Fiona explains how they went about it:

solution: “Research involving people is at the heart of modern

14

“The aim of this enterprise was to educate and inform the public, patients and healthcare professionals about clinical research”

“Existing MOOCs were studied first and an initial plan was developed according to the FutureLearn template. A storyboard was then developed and expanded to included scripts

NEWS for all the video segments. Relevant resources for further reading were

Join the Calprotectin

sourced and self-assessment activities were created. Collaboration with colleagues across the Network, including people bringing patient and carer experience and perspectives, shaped the content and the choice of case studies. Filming took place over the summer of 2015 and Network staff worked closely with the University’s Digital Learning team throughout the editing process, reviewing all materials as they were rendered and refined.”

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Isabelle Abbey-Vital, Research Involvement Officer from Parkinson’s UK, first heard about the MOOC through social media. Isabelle has since developed links with the Clinical Research Network to ensure promotion about the MOOC to Parkinson’s UK members. Parkinson’s UK have commented on how the MOOC has been a valuable tool for its members: “Our Parkinson’s UK Research Support Network has over 2,000 members who are keen to learn about Parkinson’s research and how they can get involved. Our members play a central role in driving the research priorities of the charity, ensuring the needs of people affected

by Parkinson’s are reflected in the types of research we fund, and in the

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GASTROENTEROLOGY TODAY - AUTUMN 2016

Of the 12,000 people that have signed up to the MOOC, the majority of learners are from the UK. That said, the course did have international reach with over 80 countries represented in the learning community.

And the MOOC has enabled a real sense of positive engagement, building a diverse learning community which draws attention to the importance of research. One example of positive engagement is from charities which have been able to provide their members with a tangible resource to learn about how research can benefit their health conditions.

wider Parkinson’s research community.

Gastro-Today_Quart-Ad-Oct16_14Sep16.indd 1

15/09/2016 12:12:13

15

NEWS “As part of our research strategy, we are committed to providing the best tools and resources for our members to be informed about research and empowering them to get involved and take part.

“We are pleased to share the Clinical Research Network’s Massive Open Online Course with our members. This online training course represents a fantastic opportunity for people affected by Parkinson’s to increase their understanding of how new treatments are developed and tested, which can result in improving the care they receive. Having the course available online, allows our members, who are unable to travel, to still engage with research regardless of where they live.”

Sixty year old Graham Ellis is a member of Parkinson’s UK and was diagnosed with Parkinson’s disease in June 2011. Graham registered to undertake the MOOC after receiving an email from the Parkinsons UK communications team about the course.

Graham is a fan of MOOCs and has completed several MOOCs previously, including the ‘Good Brain, Bad Brain and Parkinson’s’ course.

involved and active in research extremely

“The MOOC has given us traction into

motivational. Graham has been actively

other online and digital communities where

involved in questionnaire-based research, and

our Patient and Public Involvement and

is currently participating in a four year study

Engagement strategy goal of ‘getting people

looking into Parkinson’s and dementia. He is

talking about research strikes a real chord with

also a blood donor for future Parkinson’s and

patients and research nurses. So, instead of

the mitochondria research. He says:

talking about ‘active involvement’, we show it in practice. MOOC has also given us opportunities

“MOOC will help increase my understanding

to fit in with existing digital campaigns such

and knowledge of chosen subjects. Not just

as #whywedoresearch which has had

Parkinsons and other health studies, but unrelated

reciprocal benefit of raising the NIHR profile and

areas of interest. It gives me motivation, I’m

increasing awareness. This fits with the PPIE

not one for crosswords or sudoku, these short

Goals of ‘reaching out and connecting’.”

courses keep my mind active. You can make the content suit your circumstances, you decide

Derek’s recent blogs about the MOOC and

on the complexity. Generally [MOOCs] are short

digital engagement can be viewed here

courses usually around four weeks. You are not committed to anything, you can leave the course

A recent discussion on Twitter (TweetChat)

anytime, even on day one.”

about ‘What MOOC means to me’, brought

The MOOC has been well received by patients

to understand more about how the MOOC

and the public wanting to learn more about research. Involving patients and the public in research is something very close to Derek Stewart’s, OBE heart. As a survivor of throat cancer, Derek has championed research for many years and is the Associate Director for

The ‘Improving Healthcare through Clinical Research’ MOOC has increased Grahams understanding and knowledge of research.

He is supportive of research and finds being

Patient and Public Involvement for the Network.

Derek is supportive of the MOOC and regularly promotes its benefits to patients through his blog and through social media:

together members of the public who wanted can help them. It also raised some talking points about how a MOOC could be targeted and used in schools and colleges, which highlighted a real enthusiasm for the MOOC to be available to a wider audience.

Callum 18 is a student who completed the MOOC. He provided his perspective for FutureLearn ‘Learner Stories.’ It describes the value of learning about research discovery and how it helped him to develop his academic journey towards a career in medicine. Callum’s story also demonstrates that MOOC is an accessible platform for younger learners and reinforces suggestion that promoting the MOOC to schools and colleges could be an avenue to pursue in the future.

The MOOC has now run for two consecutive years and, although the 2016 course has been completed, the resources and materials

GASTROENTEROLOGY TODAY - AUTUMN 2016

remain accessible to learners. Fiona O’Neill reflects on the course to date: “The level of positive engagement with the course and the evaluation data all point to a highly effective course that was accessible and valued by learners. As a consequence MOOCs and similar models that promote flexible and collaborative learning will play an important role in our approach to learning in the Clinical Research Network moving forward.”

The next ‘Improving Healthcare through Clinical Research’ MOOC will be available in November 2016. For further information, visit www.futurelearn.com/courses/clinical-research

16

The only licensed treatment for the reduction in recurrence of overt hepatic encephalopathy (OHE)1

NEWS

At home they are still at risk; ...TARGAXAN® rifaximin-a reduces the risk of recurrence of overt hepatic encephalopathy.1

Long-term secondary prophylaxis in hepatic encephalopathy (HE)2 TARGAXAN® 550 mg film-coated tablets.

Presentation: Film-coated tablet containing rifaximin 550 mg.

Uses: Targaxan is indicated for the reduction in recurrence of episodes of overt hepatic encephalopathy in patients m 18 years of age.

Dosage and administration: Adults 18 years of age and over: 550 mg twice daily, with a glass of water, with or without food for up to 6 months. Treatment beyond 6 months should be based on risk benefit balance including those associated with the progression of the patients hepatic dysfunction. No dosage changes are necessary in the elderly or those with hepatic insufficiency. Use with caution in patients with renal impairment.

Contraindications: Contraindicated in hypersensitivity to rifaximin, rifamycin-derivatives or to any of the excipients and in cases of intestinal obstruction.

Warnings and precautions for use: The potential association of rifaximin treatment with Clostridium difficile associated diarrhoea and pseudomembranous colitis cannot be ruled out. The administration of rifaximin with other rifamycins is not recommended.

Rifaximin may cause a reddish discolouration of the urine. Use with caution in patients with severe (Child-Pugh C) hepatic impairment and in patients

with MELD (Model for End-Stage Liver Disease) score > 25. In hepatic impaired patients, rifaximin may decrease the exposure of concomitantly administered CYP3A4 substrates (e.g. warfarin, antiepileptics, antiarrhythmics, oral contraceptives). Ciclosporin may increase the rifaximin Cmax.

Pregnancy and lactation: Rifaximin is not recommended during pregnancy. The benefits of rifaximin treatment should be assessed against the need to continue breastfeeding.

Side effects: Common effects reported in clinical trials are dizziness, headache, depression, dyspnoea, upper abdominal pain, abdominal distension, diarrhoea, nausea, vomiting, ascites, rashes, pruritus, muscle spasms, arthralgia and peripheral oedema. Other effects that have been reported include: Clostridial infections, urinary tract infections, candidiasis, pneumonia cellulitis, upper respiratory tract infection and rhinitis.

Blood disorders (e.g. anaemia, thrombocytopenia).

Anaphylactic reactions, angioedemas, hypersensitivity.

Anorexia, hyperkalaemia and dehydration. Confusion, sleep disorders, balance disorders, convulsions, hypoesthesia, memory impairment and attention disorders. Hypotension, hypertension and fainting. Hot flushes. Breathing difficulty, pleural effusion, COPD. Gastrointestinal disorders and skin reactions. Liver function test abnormalities. Dysuria, pollakiuria and proteinuria. Oedema. Pyrexia. INR abnormalities.

Licensing and legal category: Legal category: POM.

Cost: Basic NHS price £259.23 for 56 tablets.

MA number: PL 20011/0020.

For further information contact: Norgine Pharmaceuticals Limited, Norgine House, Moorhall Road, Harefield, Middlesex, UB9 6NS. Telephone: +44(0)1895 826606 E-mail: medinfo@norgine.com Ref: UK/XIF5/1215/0159 Date of preparation: Dec 2015 Adverse events should be reported.

Reporting forms and information can be found at www.mhra.gov.uk/yellowcard. Adverse events should also be reported to Medical Information at Norgine Pharmaceuticals Ltd on 01895 826606 References: 1. Available from: http://www.nice.org.uk/guidance/ ta337 [Accessed April 2016].

2. Mullen KD, et al. Clin Gastroenterol Hepatol Product under licence from Alfa Wassermann S.p.A. TARGAXAN is a registered trademark of the Alfa Wassermann group of companies, licensed to the Norgine group of companies.

NORGINE and the sail logo are registered trademarks of the Norgine group of companies.

UK/XIF5/0416/0201.

Date of preparation: April 2016.

GASTROENTEROLOGY TODAY - AUTUMN 2016

REFER TO FULL SUMMARY OF PRODUCT CHARACTERISTICS (SmPC) BEFORE PRESCRIBING

17

POSTERS

Audit: Measurement and Anal Turnaround Times in the Endosco Edmondson MJ, Thompson J, Morris J, Scarborough A, Hoare J

Department of Gastroenterology, St. Mary’s Hospital, Imperial College London, U

Introduction The turnaround is a predictable sequence of events between endoscopic procedures with the aim of returning the room to its ready state. It was identified as a potential source of delay at St. Mary’s hospital endoscopy suite, contributing to lengthy endoscopic lists.

Targeting the turnaround time (TAT) has been shown to effectively reduce list times in surgery1 and medical laboratories2. It has also been identified in endoscopy simulation models as having “a significant influence on patient throughput, procedure room utilisation, and endoscopist ultilisation”3 There is no current guideline for how long a turnaround should take or how it should be performed.

Primary Aim •

Measure the average turnaround time at St. Mary’s Hospital (SMH) endoscopy unit and qualitatively assess reasons for delays

1st Cycle (June St. Mary’s Hospital n = 28 Mean TAT = 25m 14s

Table 1. showing number of turnarounds measured and av

Findings: • Commonly identified procedural bottle cannulation • Common delaying factors include avail printer issues (28%) • Endoscopist interruption (E.I) is a pote as any person not involved with the tu communicating with the endoscopist) Action plan: • Partial implementation of nurse led ca • Introduce measurement of endoscopis

Endoscopist Complete report

Secondary Aim •

Identify and compare factors leading to TAT delay at SMH and Charing Cross Hospital (CCH), both tertiary centres based in London

Method

GASTROENTEROLOGY TODAY - AUTUMN 2016

18

Clinical observers were used to record TAT and reasons for delay during endoscopy lists. A TAT was defined as from the point of scope removal from the previous patient to insertion of scope for the next.

Consen patien

Technical assistant

Replace and ready equipme Handover nurse

Take patient out of room an

Figure 1. demonstrating staff roles during a turnaround, with procedural bottle necks highlighted in red Endoscopist led cannulation

Discussion

We have shown nurse led cannulation to be one of the factors contributing to a faster TAT. Endoscopist interruption has also, in combination with endoscopist led cannulation, been shown to lead to a significantly longer TAT. Reductions in TAT at SMH in the second cycle may have been due to reduced printer and scope availability issues associated with having moved into a new suite. However, it is impossible to suggest with the available data whether nurse led cannulation has played a significant role in this decrease. In ‘ideal’ situations with the absence of endoscopist interruption, nurse lead cannulation and no technical issues, there is still large variation in TAT. This suggests further, as yet unknown factors are influencing the TAT.

Endoscopist Interruption

Figure 2. demonstrating factors contributing to longer turnaround times (TAT)

Longer TAT Endoscopist led consent

POSTERS

lysis of opy Suite

United Kingdom 2nd Cycle (March – May 2015)

e 2014)

St. Mary’s Hospital (New suite) n = 44 Mean TAT = 20m 49s

Charing Cross Hospital Not measured in 1st cycle

verage time taken. TAT = Turnaround Time

Table 2. showing number of turnarounds measured and average time taken. TAT = Turnaround Time

e necks are patient consent and

lability of scopes (25%) and

ential factor for delays (defined urn-around procedure

annulation st interruption in 2nd cycle

nt nt

Findings: • Reduced mean TAT at SMH by 4 minutes 25 seconds • Reduced incidence of printer issues (0%) and scope availability problems (5%) • There were significantly more nurse led cannulations in the fastest 20 TAT as compared to the slowest 20 TAT (p = 0.01) • Endoscopist interruption (E.I) occurred in 24% of the total turnarounds measured Nurse led cannulation

+/Cannulation

St. Mary’s Hospital

Charing Cross Hospital

n = 17

n = 10

Mean TAT = 18m 23s* Mean TAT = 19m 58s** E.I = 2 (12%) n = 14

E.I = 1 (10%) n = 12

E.I = 8 (57%)

E.I = 3 (25%)

n = 13

n = 21

Endoscopist led cannulation Mean TAT = 24m 55s* Mean TAT = 18m 21s**

ent for next procedure < 8 mins

No cannula required

nd perform hand over

Table 3. Demonstrating the number of turnarounds in which nurses and endoscopists performed cannulation. The average turnaround time and the associated rate of Endoscopist Interruption (E.I) for each group is also shown. * = p<0.05, ** = p > 0.05

< 8 mins

Next steps…

Unknown factors

1. A 3rd cycle with a focus on eliciting unknown factors influencing TAT 2. Full implementation of nurse led cannulation 3. Address endoscopist interruption • •

References

This would require discussion amongst staff as to how this can be done safely and effectively Focus should be on avoiding lengthy unrelated discussions, allowing time for communications essential to patient care outside of the endoscopy suite, without impacting greatly on the TAT

1) Adams R, Warner P, 2004 Decreasing Turnaround Time between general surgery cases: A six sigma initiative 2) Bluth E, Lambert D 1992 Improvement in ‘Stat’ Laboratory Turnaround Time, Arch Intern Med 3) Berg B, Denton B et al 2009 A Discrete Event Simulation Model to Evaluate Operational Performance of a Colonoscopy Suite

GASTROENTEROLOGY TODAY - AUTUMN 2016

r

Charing Cross Hospital n = 43 Mean TAT = 20m 08s

19

POSTERS

MACHINE LEARNING CREATES A SIMPLE ENDOS IMPROVES DYSPLASIA DETECTION IN BARRETT’ ENDOSCOPISTS

Authors: Vinay Sehgal 1, Avi Rosenfeld 2, David Graham 1, Raf Bisscops 3, Krish Ragunath 4, Matthew Banks 1, Rehan Haidry 1, Institution: 1 - Department of Gastroenterology, University College London Hospitals (UCLH) NHS Foundation Trust, London, Unit Jerusalem, Israel; 3 - Department of Gastroenterology, University Hospitals Leuven, Belgium; 4 - Department of Gastro Contact: Dr Vinay Sehgal Email: v.sehgal@ucl.ac.uk Phone: +44 207 6799 084

INTRODUCTION

METHODS

• Barrett’s oesophagus (BE) is the pre-cursor for oesophageal adenocarcinoma.

• Video recordings were collected from pa and dysplastic (D-BE) BE undergoing en • A strict protocol was used to record area • Endoscopic surveillance is performed to detect biopsy was taken to confirm the histolog dysplasia in BE as it is likely to be amenable to • In a blinded manner, videos were shown curative treatment. Current surveillance relies interpreted them based on their mucosa on white-light endoscopy to obtain 4-quadrant patterns, presence of nodularity, ulcerati biopsies through every 2cm of the BE segment. diagnosis (Figure 2). Acetic acid (ACA) w This samples less than 5% of the BE • The WEKA package was used to create epithelium and is likely to miss dysplasia.

• Non-expert endoscopists (registrars in tr experience were asked to visit a website videos both before and after web-based • i-Scan (PENTAX HOYA, Japan), has been from expert opinion (Figure 3). developed to improve lesion recognition in the • Accuracy, sensitivity and specificity valu gastrointestinal tract (GIT). i-Scan uses post(Table 1). Students t-test was used and processing light filtering to provide real-time Figure 2 – Endoscopic images demonstrating mucosal patterns analysis and enhancement of the mucosa and (A) – Regular oval pits, M1, (B) – villous/gyrus ridged pits, M2, (C microvasculature. ulceration, M3, (D) – nodularity in a segment of BE. • Machine learning (ML) is a branch of artificial intelligence that generates simple rules, known as a decision tree (DT). Using a DT generated from recognised expert endoscopists, we hypothesised this could be used to improve dysplasia detection in non-expert endoscopists.

Figure 1 – schematic of website accessed by non-experts endoscopists

GASTROENTEROLOGY TODAY - AUTUMN 2016

20

A

B

C

Figure 3 - Decision tree constructed from expert o

IS BARRETT’S S YES

MUCOSAL PATTERN M1/M2

NO DYSPLASIA

M3

DYSPLASIA

POSTERS

SCOPIC CLASSIFICATION SYSTEM THAT ’S OESOPHAGUS AMONGST NON-EXPERT

Laurence Lovat 1 ted Kingdom; 2 - Department of Industrial Engineering, Jerusalem College of Technology, oenterology, Queen’s Medical Centre, Nottingham, United Kingdom

RESULTS

atients with non-dysplastic (ND-BE) ndoscopy with i-Scan at UCLH. as of interest after which a matched gical diagnosis. n to 3 expert endoscopists who al (M) and microvasculature (V) ion as well as overall suspected was used in some cases. e a DT for dysplasia prediction. raining) and medical students with no e (Figure 1) and score these same d training used the DT constructed

ues were calculated pre/post-training p<0.05 was statistically significant.

• Videos from 40 patients (11 before and after ACA) were collected (23 ND-BE, 17 D-BE).

• Experts’ average accuracy for dysplasia prediction was 96% using the DT. • Mean sensitivity was 93% and specificity 99%.

• Neither vascular pattern or ACA proved helpful.

• Untrained, students tended to have a high sensitivity but poor specificity. Trainees did the opposite.

• Web-based training significantly improved sensitivity for dysplasia detection amongst trainees, with minimal loss of specificity. (Table 1). Specificity rose sharply in students without loss of sensitivity and significant improvement in overall detection. Neither group reached the accuracy of the experts.

Table 1 – accuracy, sensitivity and specificity in both groups pre and post training

s including nodularity and ulceration using i-Scan.

C) – irregular featureless mucosa with surface

C

Medical Students

Both groups

(n=13)

(n=9)

(n=22)

Before training (%)

65

53

60

After training (%)

68

63

66

0.07

0.0005

0.0005

Before training

71

83

76

After training

83

84

83

0.00002

0.44

0.00079

Before training

60

31

48

After training

57

49

54

0.20

0.00008

0.02

Accuracy

D

p-value Sensitivity

p-value Specificity

opinion to train non-expert endoscopists

NO

DYSPLASIA MUCOSAL PATTERNS M1: regular, oval pits M2: villous/gyrus ridged pits M3: irregular (or featureless) distorted pits

CONCLUSION • ML is able to define rules learnt from expert opinion.

These generate a simple algorithm to accurately predict dysplasia.

• Once taught to non-experts, the algorithm yields a significantly higher rate of dysplasia detection. This opens the door to standardised training and assessment of competence for those who perform endoscopy in BE. It may shorten the learning curve and might also be used to compare competence of trainees with recognised experts.

GASTROENTEROLOGY TODAY - AUTUMN 2016

p-value

SEGMENT FLAT?

A

Registrars

21

POSTERS

SPECIALIST CENTRE PATIENT VOLUME DOE FOR TREATMENT OF BARRETT’S DYSPLA

G. Lipman* 1, 2, A. Gupta2, M. Banks1, 2, R. Sweis2, J. M. Dunn3, D. Morris2, H. Smart4, P. Bhandari5, R. P. Wi Boger13, N. Kapoor14, B. S. Mahon15, J. Hoare16, R. Narayanasamy17, D. O'Toole17, Y. Ang18, A. Vei 1Division

of Surgery & Interventional Science, University College London, 2University College Hospital NHS Foundation Trust Alexandra Hospital, Portsmouth, 6Central Manchester University Hospitals NHS Foundation Trust, Manchester, 7GRI, Glasg Bournemouth, 11Royal Infirmary Edinburgh, Edinburgh, 12Gloucestershire Hospital NHS Trust, Gloucestershire, 13Southampton U 16St Mary's Hospital, London, United Kingdom, 17St James Hospital, Dublin, Ireland, 18Salford Royal Foundation NHS Trust, M Newcastle , 21County Durham Hospital, County Durham, 22Nottingham University Hospital NHS Tr

Introduction

Aims and Methods

• Endoscopic mucosal resection (EMR) • All visible lesions were entirely removed followed by Radiofrequency ablation EMR. Patients then underwent RFA eve (RFA) is first line treatment for months until all visible BE was ablated. mucosal Barrett’s oesophagus (BE) • Biopsies were taken at 12 months to asse treatment success with repeat biopsies e related neoplasia.

6-12 months thereafter.

• The UK Registry collects data from patients at 28 sites undergoing RFA/ • Centres were grouped by total numbers treated; EMR. We examine differences in • Low volume <50 patients outcomes between sites by patient • Medium volume 50-100 patients volume.

Registry Treatment Protocol

• High volume >100 patients • Only outcomes of those who had comple treatment were analysed.

• Further analysis was performed by grou • The first 20 cases at all sites • Cases 21-40 at all sites • Cases 41 and above at all sites !

GASTROENTEROLOGY TODAY - AUTUMN 2016

22

Figure 1: HALO RFA protocol for patients with Barrett’s related neoplasia. EMR was carried out at any stage of the protocol for new visible lesions and nodular disease

Figure 2: Circumferential Ablation with HALO 360 of BE segment (left) and Focal Ablation with HALO 90 right

Sex$(M)!

Age! Initial$Length$(M)!

Prior$EMR! Rescue$EMR! Entry$Histology!

O$IMC! O$High$Grade$Dysplasia!

O$Low$Grade$Dysplasia!

Average$number$of$RFA$ Treatments!

Median$time$to$protocol$ completion$(months)!

CROIM! CROD! Dysplasia$recurrence$!

Time$in$follow$up$(months)! !

Low$ Volume! n=116!

87.1%$ 69.5$ 5.2$ 60.3%$ 9.5%$ $ 28.1%$ 69.3%$ 2.6%$ 2.2$

Medium$ Volume! n=145!

80%$ 68.4$ 5.2$ 55.9%$ 0%$ $ 24.1%$ 66.9%$ 9.0%$ 2.5$

High$ Volume! n=420!

81.7%$ 67.2$ 5.7$ 50%$ 10%$ $ 41.3%$ 70.5%$ 5.7%$ 2.7$

11.7$

11.6$

12.1$

72.4%$ 80.2%$ 10.8%$ 13.3$ $

82.1%$ 88.3%$ 10.9%$ 13.6$ $

80.0%$ 85.7%$ 14%$ 15.0$ $

Table 1: Outcomes by Centre Volume

Acknowledgement:This project was supported by the National Institute for Health Research University College London Hospitals Biomed Departtment of Health.

POSTERS

ES NOT IMPACT ON ENDOSCOPIC OUTCOMES ASIA. RESULTS FROM THE UK REGISTRY

illert6, G. Fullarton7, A. J. Morris7, M. Di Pietro8, P. Mundre9, C. Gordon10, I. Penman11, H. Barr12, P. Patel13, P. itch19, D. Nylander20, A. Dhar21, K. Ragunath22, A. Leahy23, M. Fullard23, R. Haidry1, 2, L. B. Lovat1, 2

t, 3Guy’s and St Thomas’ NHS Foundation Trust, London, 4Royal Liverpool University Hospital, Liverpool, 5Queen gow, 8Addenbrookes Hospital, Cambridge, 9Bradford Royal Infirmary, Bradford, 10Royal Bournemouth Hospital, University Hospital, Southampton, 14Aintree University Hospital, Liverpool, 15Queen Elizabeth Hospital, Birmingham, Manchester, 19Wolverhampton NHS Trust, Wolverhampton, 20Newcastle upon Tyne Hospitals NHS Foundation Trust, rust, Nottingham, 23West Hertfordshire Hospitals NHS Trust, Watford, United Kingdom !

d by ery 3

ess every

s

Sex!(M)!

Age! Initial!Length!(M)!

Prior!EMR! Rescue!EMR! Entry!Histology! '!IMC! '!HGD! '!LGD! Average!no.!of!RFA!Treatments!

Average!time!to!completion!of! protocol!(months)!

CR'IM! CR'D! Dysplasia!recurrence!after!12! months!

Time!in!follow'up!post!protocol!

Cases!1'20!! n=317!

84.5%!

68.4!

5.5!

55.2%!

7.3%! !

27.2%!

69.9%!

2.8%!

2.5!

12.1!

Cases!21'40!! n=165!

77.6%!

66.7!

5.4!

50.3%!

5.5%! !

23.2%!

66.5%!

10.4%!

2.6!

12.9!

Cases!>40!! n=199!

82.4%!

67.8!

4.7!

51.8%!

1.5%! !

21.1%!

71.4%!

7.5%!

2.5!

10.9!

Signif!

71.3%!

79.8%!

15%!

78.2%!

89.1%!

12.8%!

83.9%!

91.0%!

11.6%!

0.004!

0.001!

NS!

21.1!

16.5!

13.4!

<0.001!

NS! NS! 0.068!

NS! 0.016!

0.023!

Table 2: Outcomes by Case Order

NS! 0.003!

Results

eted

uping:

Significance!

<0.001$ NS$ NS$ NS$ NS$ NS$ $

• Endotherapy for Barrett’s dysplasia is highly effective whatever the centre volume.

• The rescue EMR rate in medium volume centres is unexplained.

• Despite lower IM recurrence in high volume centres, dysplasia recurrence rates are not significantly different.

• Caseload volume of a centre in the UK Registry does not appear to affect outcome.

• Increasing experience of endotherapy for BE associated neoplasia is associated with better outcomes.

GASTROENTEROLOGY TODAY - AUTUMN 2016

NS$ 0.047$ NS$ NS$ 0.002$ 0.06$

• 681 patients completed treatment at 24 centres (median follow up 26months) • 420 at high volume (n=5), 145 at medium volume (n=4) & 116 at low volume centres (n=15).

• Patients were marginally older in low volume centres compared with high volume centres.

• CR-D & CR-IM at 12 months are no different between the groups by centre volume (CR-D 80-88%, CR-IM 72-82%).

• Dysplasia recurrence is no different between the groups by centre volume (Log Rank p=0.12).

• Rescue EMR was performed less frequently in medium volume centres (0% vs high 5.3% and low volume 10%, p=001).

• Increasing experience is associated with significantly less rescue EMR, faster protocol completion and improved CR-D and CR-IM rates.

Conclusions

dical Research Centre. The views expressed in this publication are those of the authors and not necessarily those of the

23

POSTERS

PATIENT AND PROFESSIONA BEHAVIOUR IN INFLAMM

John-Patrick Mulligan1 Kay Greveson2 Tom S

University College London Medical School, U Centre for Gastroenterology, Royal Free Hospital Lon 1

2

INTRODUCTION

IBD PATIENTS AND HEALTHC

Travellers with inflammatory bowel disease (IBD) are at greater risk of travel-related morbidity1. ECCO recommend patients seek expert advice prior to travel, including information on vaccination and obtaining antibiotics for self-treatment of travellers’ diarrhoea2. Wasan et al report only 3.5% of patients on immunosuppression therapy were counselled on avoiding particular live vaccines3 and 30% of gastroenterologists would erroneously recommend live vaccines4.

METHODS

GASTROENTEROLOGY TODAY - AUTUMN 2016

24

We explored both patient and gastroenterology health care professionals’ (HCP) perceptions of IBD and travel: whether disease affected travel, interventions people took to travel, and whether ECCO guidelines were being followed. IBD patients attending our IBD clinic during November 2013 were asked to complete a questionnaire collecting demographic, disease specific and travel related information. Using N-ECCO and RCN IBD nurse network databases, HCP were asked to complete an online questionnaire collecting information on perceptions of IBD and travel, confidence at providing travel advice, and the content of that advice.

HEALTHCARE PROFESSIONALS (HCPS)

Do you feel confident to give travel advice?

100%

70%

50%

30%

0% Yes

No

Do you feel confident to give advice on Traveller's diarrhoea?

100%

90%

50% 10% 0% Yes

RESULTS 136 IBD patients (67[49%] Crohn’s disease, 60[44%] male, median age 38 years [range 1885]) and 105 HCP (98/105[93%] nurse specialists, 6/105[6%] consultant, 1/105[1%] registrar) responded. 85%[106/136] patients report feeling adequately prepared for travel, although only 24%[32/136] seek travel medical advice of any

No

Do you feel confident to give vaccine advice?

100%

50%

0%

54%

Yes

46%

No

POSTERS

ALS PERCEPTIONS OF TRAVEL MATORY BOWEL DISEASE

Shepherd2 Mark Hamilton2 Charles Murray2

University College London, United Kingdom ndon NHS Foundation Trust, London, United Kingdom

CARE PROFESSIONALS (HCPS)

IBD PATIENTS

CONCLUSION

Do you seek medical advice prior to travel?

100%

50%

76%

24%

0% Yes

No

Were you prescribed antibiotics for Traveller's diarrhoea?

Patients’ travel is affected by IBD, however, few seek expert medical advice prior to travel. HCP agree IBD affects travel and a majority are confident giving limited advice. It is concerning 52% of immunosuppressed patients are unaware they should avoid live vaccines, and only 54% of HCP are confident giving advice on vaccinations. Results support the need for further travel specific research and better education in both groups.

50%

0%

4% Yes

No

Are you aware of the need to avoid live vaccines?

100%

50%

0%

REFERENCES: 1. Soonwala et al. Inflamm Bowel Dis,2012;18(11):2079-85.

48%

52%

Yes

No

2. Rahier et al. Journal of Crohn’s & Colitis,2009;3(2):47-91.

3. Wasan et al. Inflamm Bowel Dis,2014;20(2):246-50.

4. Wasan et al. Inflamm Bowel Dis,2011;17(12):2536-60.

GASTROENTEROLOGY TODAY - AUTUMN 2016

96%

100%

kind and only 11%[15/136] from the IBD team; all despite 60%[82/136] reporting their IBD affected travel. Despite recommendations, only 4%[5/136] had been prescribed antibiotics for selfmedication of travellers’ diarrhoea. 52%[36/69] of immunosuppressed patients are unaware they should avoid live vaccines. 39%[53/136] patients buy travel insurance covering IBD, 70%[37/53] of which pay a premium. 70%[74/105] HCP felt IBD might limit travel in patients. 70%[74/105] HCP are confident giving travel advice, but 51%[38/74] refer them to a travel clinic. 90%[94/105] are confident giving advice on travellers’ diarrhoea, but only 54%[57/105] on vaccinations and 40%[42/105] on insurance.

25

POSTERS

Poylp detec+on rate and associa+on with midazolam dose Jason Boyd, Lennard YW Lee, Thomas Chapman, Charlo6e Harper, Sandro Lanzon-­‐Miller Department of Gastroenterology, Milton Keynes NHS FoundaFon Trust, United Kingdom

Introduc+on

Midazolam is a short acFng benzodiazepine that is commonly used for sedaFon during colonoscopy.

There is no standard dose of midazolam; however, BriFsh Society of Gastroenterology guidelines suggest a maximum of 5mg with lower doses for elderly paFents.

Bowel preparaFon and endoscopist are factors that have been clearly associated with improved polyp detecFon during colonoscopy. Anecdotally, colonoscopy in paFents who are extremely agitated limits views and leads to a more difficult procedure.

Data exploring the relaFonship between midazolam dose and ability to detect colonic polyps is limited.

Methods

GASTROENTEROLOGY TODAY - AUTUMN 2016

26

n (%)

6200 paFents were included for analysis. The median age was 62 years and 49.4% were male.

The mean midazolam dose was 1.9mg. 16.2% of paFents had a low dose of midazolam (<2mg), 74.5% a standard dose (2mg) and 9.3% a high dose (>2mg).

In the low dose cohort the polyp detecFon rate (PDR) was 20.8%. In the standard dose cohort PDR was 26.9% and in the high dose cohort PDR was 16.4%. Rates of agitaFon were significantly higher in paFents who received higher doses of midazolam.

When paFents with poor bowel preparaFon were excluded PDR was 21.4% in the low dose cohort vs 27.1% in the standard dose.

A retrospecFve cohort study of all paFents who had undergone a colonoscopy at Milton Keynes Hospital between January 2010 and December 2012.

PaFents were idenFfied from the Endoscopy Unit database and their records were reviewed.

PaFent details, midazolam dose and diagnosis on colonoscopy were extracted into a standardized form.

Midazolam dose

Results

<2mg

2mg

1004 (16.2) 4618

(74.5)

>2mg 578 (9.3)

Pa+ents with polyps

2008

1241

95

PDR

20.8%

26.9%

<16.4%

Conclusion

In this study we demonstrate that a 2mg dose of midazolam is associated with a higher polpy detec+on rate than lower doses.

Midazolam has been previously demonstrated to inhibit peristalsis in animal studies by prevenFng release of 5-­‐HT and this is the probable mechanism for our findings.

LimitaFons arise from the retrospecFve nature of this study, however, even following straFficaFon of paFents by adequacy of bowel preparaFon, PDR remained lower in the low dose midazolam group.

Further confirmatory prospecFve studies are warranted.

POSTERS

DEVELOPING THE RECORDED IMAGE QUALITY INDEX (RIQI) TOOL – MEASURING RECORDED IMAGE QUALITY, DEGREE OF REPRESENTATION AND UTILITY. Samuel D, Berrill J, Hurley J, Lee B, Hawkes E, Hawkes, Yosief S, Hawkes N. Department of Gastroenterology, Cwm Taf University Health Board, Llantrisant, UK.

IntroducHon –Endoscopic images saved on the Electronic ReporHng System are the only visible representaHon of completeness of examinaHon and pathological findings. Together with the endoscopy report these become the only reference for other clinicians not present at the original endoscopy on which to base further decisions.

Aim – To develop a systemaHc scoring system for quality of images recorded at endoscopy and to validate this Recorded Image Quality Index (RIQI) scoring system.

Table 1: The RIQI – 4 assessment tool

Conclusions – The RIQI tool provides a method for assessing the quality of image capture across ten procedures with scores in 4 domains. The RIQI score correlates well with clinical uHlity of the images, with acceptable inter-­‐rater reliability. It shows potenHal both as an audit and training tool to improve performance in this area of endoscopic pracHce.

GASTROENTEROLOGY TODAY - AUTUMN 2016

Methods – We searched the HICCS Endoscopic ReporHng System for all colonoscopists performing regular colonoscopy (n=11). All procedures performed between July and December 2015 were idenHfied (screening cases were excluded). All images and the endoscopy report for the first 10 cases with pathological findings for each colonoscopist were obtained, ordered into folders and data anonymised. A RIQI score sheet was devised assessing 4 domains (RepresentaHon (REP), Image Labelling (LAB), Caecal landmarks (CL) and Image Quality (QUAL)) and raHng the uHlity (U) of the informaHon set further decision-­‐making. 110 image sets were scored by 3 independent assessors. Cohen’s kappa values for intra observer variaHon were calculated each domain. CorrelaHon between domain and uHlity scores was calculated using Cohen’s kappa values for inter-­‐rater agreement (IRA); these informed the score weighHng in the final RIQI tool.

27

COMPANY NEWS

A FIT SAMPLE New Faecal Immunochemical Test Systems could Improve Sample Integrity for Faecal Haemoglobin

Using a low level cut-off of 10 µg of Hb/ g faeces, the negative predictive value (NPV) for cancer is very high (100% in the hallmark study by McDonald et al4). Similarly high NPVs of 94%, are seen for higher risk adenomas (HRA) and Inflammatory Bowel Disease (IBD).

The NICE NG12 guidelines on cancer recognition and referral were issued in 2015. They have reintroduced Faecal Occult Blood Tests (FOBT) back into the diagnostic

Further studies in the UK have also shown a high degree of NPV when using FIT with cut-offs at this f-Hb concentration.5,6,7

pathway for those low risk patients with suspected lower gastrointestinal cancers.

This has put a strain on pathology departments to provide a test for the

The HM-JACKarc specimen collection device [Fig.1], contains a proprietary buffer which can stabilise f-Hb in samples for up to 14 days at ambient temperature (up to 25 °C) or up to 120 days in the fridge (4°C). This was confirmed in a study by Carroll et al8 investigating the performance characteristics of four FIT methods.7

presence of blood in faeces.

It presents a challenge, given that in response to the former 2005 guidelines, many pathology departments discontinued their FOBT, which were, at that time, the traditional guaiac-based tests (gFOBT) For some, the decision that now has to be made to satisfy NG12, is which test to implement. Technology has moved on to more analytically and clinically sensitive methods such as the quantitative Faecal Immunochemical Test for haemoglobin (FIT) on systems like HM-JACKarc.

Fig 1. Buffer in the HM-JACKarc specimen collection device stabilises f-Hb

However, the second major challenge has been the logistics of getting a quality sample from the patient to the laboratory

With the move to a more sensitive

for analysis. In part, this is dependent

technology based on an immunoassay

on the technology to be employed for the

specific for human haemoglobin, it is

detection of faecal haemoglobin (f-Hb). In

important to protect the haemoglobin in the

the days of guaiac-based faecal testing,

faecal sample from degradation.

samples were sent in traditional bluecapped “stool pots”. This was clearly wrong, since haemoglobin in native faeces GASTROENTEROLOGY TODAY - AUTUMN 2016

28

Brown and Fraser1 performed a similar

is very unstable (Brown and Fraser1).

study to Young et al2. However, they used

The moiety being examined in gFOBT is

both qualitative and quantitative FIT

the haem component of the haemoglobin

methods to analyse five haemoglobin-

molecule. Young et al demonstrated that,

spiked faecal samples, with daily sampling

with gFOBT, the degradation was more

for up to 14 days. The conclusion was

pronounced in the samples that were not

that false negative results for faecal

dried, as when collected into a traditional

haemoglobin could occur if sampling fresh

faecal pot, versus a thin dried smeared

faeces into the tubes or delaying sampling

sample (taken directly onto the gFOBT

onto the cards of FIT collection devices.

2

With any method, sample integrity is key to the quality of result. Typically laboratories would be concerned that a layperson would be unable to provide a consistent sample. However, the collection device of the HM-JACKarc is unique, in that it has two hexagonal dimples on one side of the collection probe. This ensures that as the probe is pushed back into the collection device after sampling of the faeces, any excess faecal matter is removed and a consistent amount of sample is passed into the constant volume of buffer [Fig. 2].

This is irrespective of the consistency of the faecal sample which can vary from liquid to hard pellets.

card). The conclusion was that sampling directly onto the card should be made as

With NICE, through a Diagnostics

soon as possible following defecation. In

Assessment Committee, now focussing

addition, analysis of gFOBT should be

on the benefits of the application of FIT

delayed for a few days so that potential

as a means to triage patients with lower

interference from plant peroxidases, leading

gastrointestinal (GI) symptoms, it is

to false positive results, can be minimised.

important that any loss of f-Hb is protected.

3

Fig 2. The sampling device ensures a consistent amount of sample is collected

COMPANY NEWS Use of the HM-JACKarc specimen collection devices ensures stability of f-Hb and low variation in the ratio of faecal mass collected to volume of buffer. Such hygienic devices are simple for patients to use and encourage taking up the test in those who have concerns about handling faeces.

For more information on the HM-JACKarc quantitative FIT method please visit www.alphalabs.co.uk/FIT 1. Brown LF, Fraser CG. Effect of delay in sampling on haemoglobin determined by faecal immunochemical tests. Ann Clin Biochem.

2008;45:604-5.

2. Young GP, Sinatra MA, St John DJ. Influence of delay in stool sampling on fecal occult blood test sensitivity. Clin Chem.

1996;42:1107-8.

3. Sinatra MA, St John DJ, Young GP. Interference of plant peroxidases with guaiac-based fecal occult blood tests is avoidable.

Clin Chem. 1999;45:123-6.

4. McDonald PJ, Digby J, Innes C, et al. Low faecal haemoglobin concentration potentially rules out significant colorectal disease.

Colorectal Dis. 2013;15:e151-9.

5. Mowat C, et al. Faecal haemoglobin and faecal calprotectin as indicators of bowel disease in patients presenting to primary care with bowel symptoms. Gut. 2016;65:1463-9.

6. Godber IM, et al. Use of a faecal immunochemical test for haemoglobin can aid in the investigation of patients with lower abdominal symptoms. Clin Chem Lab Med. 2016;54:595-602.

7. Thomas CL, et al. Can immunochemical tests for faecal haemoglobin and faecal calprotectin be used to risk stratify patients for referral to colonoscopy for suspected colorectal cancer? Ann Clin Biochem. Biochemistry 2016;53 Suppl 1:38-9.

8. Carroll MR, Seaman HE, Halloran SP Tests and investigations for colorectal cancer screening. Clin Biochem. 2014;47:921-39.

NON-ALCOHILC FATTY LIVER DISEASE AND THE MICROBIOTA Introduction Non-Alcoholic Fatty Liver Disease (NAFLD) is the most common chronic

of microorganisms that reside within us’) has also been implicated in the

liver disease in developed countries affecting as much as a third of the

pathophysiology of this common disease.6

population.1 Its prevalence has increased alongside global obesity trends and it is commonly acknowledged as the hepatic manifestation of the metabolic syndrome (MetS). Non-progressive simple steatosis is seen in the majority of cases (70-90%) and, although this often follows a benign course, non-alcoholic steatohepatitis (NASH), a sinister subtype found in 25-40%2 of NAFLD patients, may progress to fibrosis and cirrhosis.

Incidental findings of deranged liver enzymes (e.g. – AST, ALT) and hepatic

The microbiota link: function and dysfunction Convincing evidence suggests that our evolution has relied on a close symbiotic relationship with bacteria.7 In fact mitochondria were ancient bacterial intruders, which, through a process of endosymbiosis, now

steatosis (fatty infiltration) on imaging, and the exclusion of possible

exist within every cell in our bodies.8 Our microbiota carries out multiple

differentials, is the common route to diagnosis, however the gold standard

functions ranging from energy harvest and bile acid metabolism, to the

investigation for confirming and staging the disease is liver biopsy.3

development of our immune system.9 Disruption in the microbiota in terms of qualitative and quantitative changes (e.g.- Clostridium difficile and anatomical location (e.g.- small intestinal bacterial overgrowth), is referred to as dysbiosis.10 Dysbiois is associated with numerous disease

The ‘multi-hit’ hypothesis of NAFLD pathogenesis describes a number

states including inflammatory bowel disease, colorectal cancer, and

of stresses to hepatic physiology.2 Insulin resistance, the first hit,

functional gastrointestinal disorders.11 The underlying cause of dysbiosis

leads to adipocyte lipolysis and the generation of free fatty acids (FFAs). Hepatocytes ingest excess serum FFAs in an unregulated

is likely multifactorial involving both genetic influences and the shock of industrialisation (e.g. – antibiotics and western diets).12

fashion, which, in combination with increased hepatic lipogenesis, may exceed the capacity of lipid export leading to hepatic steatosis.4 The subsequent ‘second hits’, which advance simple steatosis

Evidence of dysbiosis in NAFLD

to steatohepatitis, have not been conclusively defined. FFAs themselves may activate a range of intracellular pathways that result

Evidence for the influence of dysbiosis in NAFLD and NASH comes

in hepatocyte apoptosis,4 a key hallmark of progressive NAFLD, and

from numerous animal and human studies. Intriguingly transferring

various adipokines, such as adiponectin, may also contribute to the

the microbiota from mice that develop characteristics of MetS, via

pathogenesis of NASH.5 The gut microbiota (‘the collective community

exposure to a high fat diet, to germ free mice leads to the development

GASTROENTEROLOGY TODAY - AUTUMN 2016

NAFLD pathophysiology

infection), metabolic function (e.g.- obesity microbiota phenotype),

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COMPANY NEWS of insulin resistance and NAFLD.13 Human studies have identified significant differences in the microbiota profile of patients with NAFLD/ NASH compared to controls.6 Michail et al.14, using advanced analytical technology, found a clear distinction between the microbiome of NAFLD and healthy subjects, with the former possessing more energy metabolism pathways and a higher alcohol production, which would contribute to metabolic diseases.

Mechanistic evidence for microbiota impact on NAFLD Innate immune system function (e.g.- inflammasome signalling), microbial metabolite profile (e.g. – type and quantity of short chain fatty acids produced and ethanol production etc.) and bile acid metabolism (e.g. – composition and abundance) and mucosal barrier integrity are all influenced by the microbiota, and are all implicated in the pathogenesis of NAFLD/NASH.6 Perhaps the most crucial of these elements is the intestinal mucosal barrier. This vital interface, which exists between our external and internal environment, has the onerous task of differentiating between friend and foe whilst simultaneously absorbing essential nutrients and blocking the passage of microorganisms and toxins.

This process relies upon the integrity of mechanical protein structures (tight junctions) and a host of fundamental immunological components.

Physiologic disruption, and resultant ‘leaky gut’, may be caused by dysbiosis, such as in MetS and NAFLD, permitting the passage of microbially derived toxic compounds (e.g.- lipopolysaccharide (LPS)) into the blood stream, a phenomenon known as ‘metabolic endotoxaemia’.15 These toxins travel through the hepatic portal circulation and stimulate toll-like receptors (e.g.- TLR4) precipitating the release of pro-inflammatory cytokines that ultimately result in hepatocyte

2. Lam B, Younossi ZM. Treatment options for nonalcoholic fatty liver disease. Therap Adv Gastroenterol 2010; 3: 121–37.

3. LaBrecque DR, Abbas Z, Anania F, Ferenci P, Khan AG, Goh KL, Hamid SS, Isakov V, Lizarzabal M, Penaranda MM, Ramos JF, Sarin S, Stimac D, Thomson AB, UmarM, Krabshuis J LA. World Gastroenterology Organisation Global Guidelines: Nonalcoholic Fatty Liver Disease and Nonalcoholic Steatohepatitis. J Clin Gastroenterol 2014; 48: 467–73.

4. Malhi H, Gores GJ. Molecular Mechanisms of Lipotoxicity in Nonalcoholic Fatty Liver Disease. Semin Liver Dis 2008; 28: 360–9.

5. Kaser S, Moschen A, Cayon A, et al. Adiponectin and its receptors in non-alcoholic steatohepatitis. Gut 2005; 54: 117–21.

6. Bashiardes S, Shapiro H, Rozin S, Shibolet O, Elinav E. Non-alcoholic fatty liver and the gut microbiota. Mol Metab 2016; 5: 782–94.

7. Ley RE, Peterson DA, Gordon JI. Ecological and evolutionary forces shaping microbial diversity in the human intestine. Cell 2006; 124: 837–48.

8. Andersson SG, Kurland CG. Origins of mitochondria and hydrogenosomes. Curr Opin Microbiol 1999; 2: 535–41.

9. Aureli P, Capurso L, Castellazzi AM, et al. Probiotics and health: An evidence-based review. Pharmacol Res 2011; 63: 366–76.

10. Paolella G. Gut-liver axis and probiotics: Their role in non-alcoholic fatty liver disease. World J Gastroenterol 2014; 20: 15518.

11. Tojo R, Suárez A, Clemente MG, et al. Intestinal microbiota in health and disease: Role of bifidobacteria in gut homeostasis. World J Gastroenterol 2014; 20: 15163–76.

12. Sonnenburg JL, Bäckhed F. Diet–microbiota interactions as moderators of human metabolism. Nature 2016; 535: 56–64.

13. Le Roy T, Llopis M, Lepage P, et al. Intestinal microbiota determines development of non-alcoholic fatty liver disease in mice. Gut 2013; 62: 1787–94.

injury and progression from NAFLD to NASH.15

14. Michail S, Lin M, Frey MR, et al. Altered gut microbial energy and metabolism in children with non-alcoholic fatty liver disease. FEMS Microbiol Ecol 2015; 91: 1–9.

Evidence for probiotics in NAFLD treatment

15. Cani PD, Amar J, Iglesias MA, et al. Metabolic Endotoxemia Initiates Obesity and Insulin Resistance. Diabetes 2007; 56: 1761–72.

Compelling evidence from the use of faecal microbial transplantation

16. Guarner F, Khan AG, Garisch J, et al. Probiotics and prebiotics. Probiotics prebiotics-World Gastroenterol Organ Glob Guidel 2011; : 1–28.

and probiotics11,16 has shown that the deleterious impact of dysbiosis may be ameliorated by microbial modification. Probiotics are defined as ‘live microorganisms which when administered in adequate amounts confer a health benefit to the host’.17 In a recent animal study multi-strain probiotics were shown to significantly reduce steatosis scores and lobular GASTROENTEROLOGY TODAY - AUTUMN 2016

inflammation compared to single strain preparations.18 This finding is supported by a number of human clinical trials in which multi-strain probiotics significantly reduced liver aminotransferases,19,20 indicating improvement in inflammation at this site, improved the degree of steatosis and fibrosis,21 and even improve insulin resistance in NAFLD/NASH20.

A meta-analysis of nine randomised controlled trials published this year concluded that probiotics provided improvements in total cholesterol, high density lipoprotein, and TNF-α in all NAFLD patients.22

Conclusion The routine use of multi-strain probiotics presents a beneficial, and comparatively safe, adjunct to lifestyle modification in the management of NAFLD/NASH.

30

1. Dyson J, Day C. Treatment of non-alcoholic fatty liver disease. Dig Dis 2014; 32: 597–604.

17. Food and Agricultural Organization of the United Nations and World Health Organization. Health and Nutritional Properties of Probiotics in Food including Powder Milk with Live Lactic Acid Bacteria. 2001 ftp://ftp.fao.org/es/esn/food/probio_report_en.pdf.

18. Kobyliak N, Falalyeyeva T, Virchenko O, Mykhalchyshyn G, Bodnar P. Comparative experimental investigation on the efficacy of mono- and multiprobiotic strains in non-alcoholic fatty liver disease prevention. BMC Gastroenterol 2016; 16: 1–9.

19. Wong VW, Wong GL, Chim AM, et al. Treatment of nonalcoholic steatohepatitis with probiotics . A proof-of-concept study. Ann Hepatol 2013; 12: 256–62.

20. Eslamparast T, Poustchi H, Zamani F, Sharafkhah M, Malekzadeh R, Hekmatdoost A. Synbiotic supplementation in nonalcoholic fatty liver disease : a randomized, double-blind, placebo-controlled pilot study. Am J Clin Nutr 2014; 99: 535–42.

21. Ahmad Shavakhi, Mohammad Minakari, Hassan Firouzian RA, Hekmatdoost2 A, Ferns3 G. Effect of a Probiotic and Metformin on Liver Aminotransferases in Non-alcoholic Steatohepatitis: A Double Blind Randomized Clinical Trial. Int J Prev Med 2013; 15: 1090–5.

22. Gao X, Zhu Y, Wen Y, Liu G, Wan C. Efficacy of probiotics in nonalcoholic fatty liver disease in adult and children: A meta-analysis of randomized controlled trials. Hepatol Res 2016; Feb 11: 1–8.

Following the huge success of Endolive 2015, the British Society of Gastroenterology invites you to the 2nd National Endolive meeting, to be held at the International Conference Centre (ICC) Birmingham on 2nd and 3rd March 2017. This interactive meeting will aim to showcase UK endoscopy and to challenge, debate and inform all areas of endoscopic practice.

The very best of diagnostic and therapeutic endoscopy will be demonstrated via live links to two of the UKâ&#x20AC;&#x2122;s premier endoscopic centres, St Markâ&#x20AC;&#x2122;s Hospital in London, and Glasgow Royal Infirmary.

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