Comprehensive Treatment Strategies for Topical Steroid Damaged/Dependent Face (TSDF): A Case Report
Subcutaneous Phaeohyphomycosis Presenting as A Progressive Disfiguring Lesion of the Face in an Immunocompetent Individual: A Rare Occurrence
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RESIDERM: EMPOWERING THE NEXT GENERATION OF DERMATOLOGISTS
Welcome to this edition of Residerm, a journal dedicated to empowering dermatology residents with practical insights, clinical acumen, and evidence-based updates. As the future torchbearers of dermatology, it is vital to stay attuned to emerging challenges, evolving treatment paradigms, and patient-centered strategies that bridge academic knowledge with clinical application.
In this issue, we present two insightful contributions that reflect the complexity, depth, and diversity of everyday dermatological practice.
The first article, “Subcutaneous Phaeohyphomycosis Presenting as a Progressive Disfiguring Lesion of the Face in an Immunocompetent Individual: A Rare Occurrence,” highlights a highly uncommon clinical presentation and the diagnostic acumen required to manage such rare infections.
Our second feature is a compelling case report on Comprehensive Treatment Strategies for Topical Steroid Damaged/Dependent Face (TSDF). With the widespread misuse of topical corticosteroids—particularly on facial skin—this article underscores the urgent need for early recognition, structured detoxification protocols, and empathetic patient counseling to restore skin health and rebuild trust.
As always, Residerm strives to support your journey from residency to confident clinical practice by fostering critical thinking, compassionate care, and continuous learning.
Happy reading—and here’s to growing together in knowledge and purpose.
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The Editorial Team
Residerm
- Dom Daniel Executive Editor & Publisher
Subcutaneous Phaeohyphomycosis Presenting as A Progressive Disfiguring Lesion of the Face in an Immunocompetent Individual: A Rare Occurrence
Dr. Jaimin Shah
3rd Year Resident (2024)
Department of Dermatology, Venereology and Leprosy Government Medical College, Surat
Dr. Trunali Navadiya
Senior Resident
Department of Dermatology, Venereology and Leprosy Government Medical College, Surat
Dr. Yogesh Patel
Associate Professor
Department of Dermatology, Venereology and Leprosy Government Medical College, Surat
Comprehensive Treatment Strategies for Topical Steroid Damaged/Dependent Face (TSDF): A Case
Subcutaneous Phaeohyphomycosis Presenting as A Progressive Disfiguring Lesion of the Face in an Immunocompetent Individual: A Rare Occurrence
Subcutaneous Phaeohyphomycosis
Presenting as A Progressive Disfiguring Lesion of the Face in an Immunocompetent Individual:
A Rare Occurrence
Dr. Jaimin Shah
3rd Year Resident (2024)
Department of Dermatology, Venereology and Leprosy Government Medical College, Surat
Dr. Trunali Navadiya
Senior Resident
Department of Dermatology, Venereology and Leprosy Government Medical College, Surat
Dr. Yogesh Patel
Associate Professor
Department of Dermatology, Venereology and Leprosy Government Medical College, Surat
Introduction
Phaeohyphomycosis is a rare mycotic infection caused by various heterogenous groups of phaeoid (dermatiaceous) fungi. These organisms
are widespread in the environment, being found in the soil, wood and decomposing plant debris. These infections are more prevalent in tropical and subtropical climates. They
are infrequent, primarily affecting the skin and subcutaneous tissues, with rare involvement of the paranasal sinuses, ocular structures, central nervous system, lymph nodes, and bone. These infections usually result from traumatic inoculation. The clinical presentation of subcutaneous phaeohyphomycosis varies significantly depending on the host's immune status. It may manifest as solitary cutaneous nodules or progress to more extensive subcutaneous abscesses. Specific presentations can include papulonodules, verrucous or hyperkeratotic plaques, ulcerated lesions, cysts, abscesses, pyogranulomas, nonhealing ulcers, or sinuses.1
Phaeohyphomycosis ....... encompasses a diverse range of mycotic infections caused by dematiaceous fungi, leading to various clinical manifestations based on the site and severity of the infection. These infections are classified into several forms: superficial, cutaneous, subcutaneous, systemic, and disseminated. Superficial infections, the most common, affect the outer layers of the skin and mucous membranes, presenting as tinea nigra, Subcutaneous Phaeohyphomycosis Presenting as
mucous membrane infections, keratomycosis, and fungal melanonychia. Cutaneous infections involve deeper layers of the skin, leading to conditions such as fungal melanonychia and other localized skin lesions without significant penetration into deeper tissues. Subcutaneous infections occur in the deeper layers of the skin and subcutaneous tissues, presenting as fungal cysts, papules, or warty plaques, typically following trauma or direct inoculation, and can result in chronic, localized lesions that may become abscessed or necrotic if untreated. Systemic infections are more severe, affecting internal organs and may present as conditions like endophthalmitis, invasive rhinosinusitis, or other serious internal infections.2
Dematiaceous fungi are characterized by their dark pigmentation from melanin in their cell walls, and are responsible for a range of mycoses collectively known as phaeohyphomycosis. These filamentous, saprophytic fungi, predominantly found in soil and decaying plant material, produce melanin, which inhibits phagocytosis and interferes with hydrolytic
enzyme action on fungal membranes, enhancing their pathogenicity even in immunocompetent hosts. The major etiological agents include genera such as Bipolaris, Exophiala, Curvularia, Exserohilum, and Wangiella species, among approximately 70 genera and 150 species identified. These fungi, which belong to orders such as Capnodiales, Dothideales, and Chaetothyriales, exhibit additional resistance mechanisms like protease enzymes and hyaluronidases. Species like Exophiala dermatitidis are linked with severe infections, including cerebral and disseminated forms, while others like Alternaria and Cladosporium are associated with cutaneous infections. Notable agents also include Neoscytalidium dimidiatum and Phialemoniopsis limonesiae. Pathologically, these fungi typically cause localized skin and subcutaneous infections but can disseminate to the central nervous system and other organs, especially in immunocompromised individuals. Risk factors include trauma, occupational exposure (e.g., agriculture), diabetes, and immunosuppression from corticosteroids or
Subcutaneous Phaeohyphomycosis Presenting as A Progressive Disfiguring Lesion of the Face in an Immunocompetent Individual: A Rare Occurrence
chemotherapy, with recent studies indicating the influence of genetic mutations in immune response and environmental reservoirs such as contaminated water sources in the spread of these fungi.2
Case report
A three years old male patient presented with swelling and disfigurement of face since 5 months. There was antecedent history of trauma over nose before 8 months. On examination, the patient has a non-tender, dull, erythematous, woody hard, non-pitting, smooth swelling over root of the nose, extending to forehead, both cheeks, both lips with right eye proptosis and corneal opacity. The patient development was age appropriate. Routine examination was normal and HIV test was nonreactive. CT and MRI findings were suggestive plexiform neurofibroma. For confirmation USG guided core needle biopsy taken from forehead. Histopathological .......... examinations showed focal dense aggregates of eosinophils, polymorphonuclear ........ cells, few lymphocytes, histiocytes, few histiocytic giant cells, occasional ill
formed granuloma and vascular proliferation. Occasional vessels showed necrotizing vasculitis with intraluminal fragment of fungal hyphae. Ocassional giant cell also showed intracellular fungal hyphae. Periodic Acid Schiff and Gomori Methamine Silver stain highlighted fungal elements, which was suggestive of tissue and vasculoinvasive fungus. KOH preparation from tissue showed broad thin walled non-septate mycelia. On the basis of diagnosis, phaeohyphomycosis has been confirmed. The treatment was commenced with itraconazole at a dose of 5 mg/kg.
Figure 1: A non-tender, dull, erythematous, woody hard, non-pitting, smooth swelling over root of the nose, extending to forehead, both cheeks, both lips with right eye proptosis and corneal opacity
Subcutaneous Phaeohyphomycosis Presenting as A Progressive Disfiguring Lesion of the Face in an Immunocompetent Individual: A Rare Occurrence
Figure 2: Histopathological examination using Hematoxylin and Eosin (H&E) Stain shows focal dense aggregates of eosinophils, polymorphonuclear cells, few lymphocytes, histiocytes, few histiocytic giant cells, occasional ill formed granuloma and vascular proliferation.
Figure 3: Histopathological examination using Gomori Methamine Silver stain highlighted fungal elements, which was suggestive of tissue and vasculo-invasive fungus.
Figure 4: Periodic Acid Schiff stain highlighted fungal elements, which was suggestive of tissue and vasculo-invasive fungus.
Figure 6: Improvement seen after using itraconazole at a dose of 5 mg/kg
Diagnosis
In diagnosing phaeohyphomycosis, a detailed patient history is crucial. It should cover recent trauma, occupational exposures to fungi, and underlying conditions like immunosuppression. This information helps identify risk factors and guides diagnostic and treatment decisions.2
A skin biopsy for diagnosing phaeohyphomycosis reveals darkly pigmented hyphae with melanin, characteristic of dematiaceous fungi. It shows granulomatous inflammation, possible abscesses, yeast forms, and changes like hyperkeratosis and acanthosis, which are essential for accurate diagnosis and differentiation.2
Gomori's methenamine silver (GMS) stain and periodic acidSchiff (PAS) stain are crucial for diagnosing phaeohyphomycosis in skin biopsies. GMS stains fungal cell walls black or greenish, highlighting pigmented hyphae and tissue invasion. PAS stains those bright pink, revealing hyphae, yeast forms, and tissue damage. Both stains aid in accurate diagnosis and differentiation of the infection.2
The culture method is crucial for diagnosing phaeohyphomycosis as it allows for the growth and identification of the causative fungi. It reveals characteristic fungal colonies with pigmentation, which helps differentiate between species. Microscopic examination of cultured fungi shows essential features like pigmented hyphae, conidia, and other reproductive structures, aiding in accurate species identification. This process not only confirms the diagnosis but also guides appropriate antifungal treatment by providing detailed information on the specific fungal species involved.3
Molecular biology techniques like PCR and sequencing accurately diagnose phaeohyphomycosis by detecting fungal DNA or RNA, identifying specific genetic markers, and revealing genetic variations. These methods ensure precise species identification and differentiation, aiding effective treatment planning.3 Serum markers offer several advantages in diagnosing phaeohyphomycosis,
including non-invasive testing that avoids the need for more invasive procedures like biopsies. They can facilitate early detection of fungal infections before significant clinical symptoms appear and serve as supportive tools alongside other diagnostic methods. Additionally, serum markers may help monitor disease progression and evaluate the response to treatment, providing valuable insights into the effectiveness of therapeutic interventions.3
Treatment
Itraconazole, a triazole antifungal, is essential in treating phaeohyphomycosis by targeting a wide range of dematiaceous fungi. It works by inhibiting ergosterol synthesis, compromising fungal cell membranes and causing cell death. Effective against fungi like Exophiala, Fonsecaea, and Curvularia, itraconazole is valuable for both localized and systemic infections.4 Terbinafine treats phaeohyphomycosis by inhibiting squalene epoxidase, disrupting ergosterol synthesis and causing toxic squalene buildup, leading to fungal cell death. It's effective for superficial and cutaneous Subcutaneous Phaeohyphomycosis Presenting as
infections and useful for some subcutaneous cases.5
Amphotericin B is a key treatment option for severe or systemic cases of phaeohyphomycosis, a fungal infection caused by dematiaceous fungi. Its broad-spectrum antifungal activity makes it effective against various pathogens within this group, such as Alternaria and Curvularia.6, 7 Ketoconazole, an oral antifungal, is used for less severe or localized phaeohyphomycosis, effective against fungi like Exserohilum and Alternaria. It inhibits ergosterol synthesis and is preferred when other antifungals are less suitable or the infection is less aggressive.8
Surgical excision effectively removes localized phaeohyphomycosis ....... infections, allowing for precise diagnosis and histopathological examination. It prevents spread to healthy tissue, reduces fungal burden, and can improve outcomes when combined with antifungal therapy, potentially reducing recurrence.9 Cryotherapy treats superficial or cutaneous phaeohyphomycosis by freezing and destroying fungal lesions. It helps
eliminate localized infections and reduce fungal burden, often used alongside antifungal medications. It's suitable for skin or superficial infections but not for deep or systemic cases.9 Photodynamic therapy (PDT) uses 20% 5-ALA and red light to treat superficial phaeohyphomycosis by generating reactive oxygen species that destroy fungal cells. Effective for localized, resistant infections with minimal tissue damage, it’s used with antifungals and requires regular follow-up to monitor effectiveness and recurrence. It is not suitable for deep or systemic infections.10
Surgical debridement is crucial for severe or chronic phaeohyphomycosis, ....... removing infected tissue to lower fungal load and enhance antifungal treatment. It’s especially beneficial for resistant infections and is often combined with antifungal therapy to improve outcomes and reduce recurrence.11 Wound care and supportive care are vital for managing phaeohyphomycosis. Intensive wound care involves cleaning and dressing wounds to aid healing, while supportive care includes nutrition,
pain management, and overall health optimization to enhance recovery and immune function.11
Discussion
The term “phaeohyphomycosis” ..... introduced by Ajello, encompasses cutaneous, subcutaneous, and systemic infections caused by dematiaceous (melanized) fungi. Phaeohyphomycosis encompasses a wide spectrum of primary and opportunistic mycoses. Subcutaneous infections predominantly affect the limbs, fingers, wrists, knees, or ankles. Although subcutaneous phaeohyphomycosis ....... is considered rare, its incidence appears to be rising, correlating with the increasing number of immunocompromised individuals.3 It is globally distributed infection, shows regional variations with certain genera and species exhibiting endemic patterns. It affects all ethnic groups, ages, and sexes, though it is more common in adult men in their third to fourth decades of life, particularly in tropical and subtropical climates. Species like Rhinocladiella mackenziei are endemic to the Middle East, Veronaea botryosa and Fonsecaea
monophora to southern regions, and Scytalidium hyalinum and Neoscytalidium dimidiatum to Southeast Asia and Caribbean countries. He Y. et al. documented 174 cases of phaeohyphomycosis from 1987 to 2021, with Phialophora americana reported in a 28-year-old man. Corynespora cassiicola has been underreported but is found in Colombia, Africa, and Asia. Bonifaz A. et al. reported only three cases of phaeohyphomycosis out of 160 cases of foot mycoses, all involving males with a history of trauma. Cases caused by Cladophialophora spp. are notably reported in India and the United States, with sporadic cases in other countries including Brazil, Canada, Spain, and several others. Additionally, cases of Alternaria alstromeriae, Epicoccum tritici, and Phialemonium obovatum have been noted in India. The infection typically results from traumatic inoculation of skin and subcutaneous tissue with contaminated material, with lesions frequently observed on the feet and legs of outdoor workers. Males are more commonly affected due to their outdoor occupations. Definitive diagnosis is achieved through histopathological
examination of tissue samples from affected swellings.3
Phaeohyphomycosis is caused by around 70 genera and 150 species of fungi, with Exophiala (Wangiella), Fonsecaea, Curvularia, and Lomentospora being the most common. These fungi, found in soil and plants, produce melanic pigments and enzymes that enhance pathogenicity. Notable species include Exophiala dermatitidis (disseminated infections), Cladophialophora bantiana (cerebral infections), and Neoscytalidium dimidiatum (skin invasion). In China, Exophiala spp. and other fungi like Cladosporium, Phialophora, and Alternaria are frequently identified, with rare cases involving Corynespora, Ochroconis tshawytschae, and Bipolaris oryzae.3 Phaeohyphomycosis often begins with trauma-related nodular lesions, evolving into subcutaneous abscesses, especially in farmers and those exposed to contaminated environments. Key risk factors include climate (tropical/ subtropical regions), immunosuppression (e.g., organ transplant recipients, diabetes, cancer), and genetic factors (e.g., CARD9 mutations). TH17 cell
deficiencies and handling contaminated materials also increase risk. The COVID-19 pandemic has heightened incidence due to increased immunosuppression. Fungi like E. dermatitidis, found in high-humidity environments, may spread through aerosol inhalation from bird and bat feces.3 In the differential diagnosis of subcutaneous soft swellings, it is crucial to consider fungal infections, as they can be easily mistaken for other conditions such as lipomas, fibromas, epidermal cysts, or foreign body reactions. This case highlights the importance of including fungal infections in the differential diagnosis, given that these conditions may present with similar clinical features. Accurate diagnosis is essential to ensure appropriate treatment, as misidentification could lead to inappropriate management and prolonged patient suffering. Managing phaeohyphomycosis ....... requires a tailored approach based on the fungal pathogen, infection extent, and patient health. Effective outcomes depend on thorough wound care, immune support, and regular follow-up to monitor response and prevent recurrence. A well-rounded, individualized treatment
Subcutaneous Phaeohyphomycosis Presenting as A Progressive Disfiguring Lesion of the Face in an Immunocompetent Individual: A Rare Occurrence
plan significantly improves prognosis.3
Conclusion
Phaeohyphomycosis ....... presents significant challenges due to its diverse clinical manifestations, the variety of causative fungal agents, and the frequent occurrence in immunocompromised patients. The complexity of diagnosing and treating this infection is compounded by difficulties in identifying specific pathogens and ensuring effective treatment, which often requires a combination of surgical, antifungal, and adjunctive therapies. Complications such as treatment resistance, recurrence, and the necessity for continuous monitoring further complicate management. Future research should prioritize enhancing diagnostic methods, developing novel antifungal therapies, and deepening the understanding of fungal pathogenesis. Addressing these areas is essential for overcoming current treatment challenges and improving patient outcomes in phaeohyphomycosis.
References
1. Chintagunta S, Arakkal G, Damarla SV, Vodapalli AK. Subcutaneous phaeohyphomycosis in an
immunocompetent Individual: A case report. Indian Dermatol Online J. 2017; 8(1):29-31. doi:10.4103/2229-5178.198770.
2. Mishra D, Singal M, Rodha MS, Subramanian A. Subcutaneous phaeohyphomycosis of foot in an immunocompetent host. J Lab Physicians. 2011; 3(2):122-124. doi:10.4103/0974-2727.86848.
3. Sánchez-Cárdenas CD, Isa-Pimentel M, Arenas R. Phaeohyphomycosis: A Review. Microbiology Research. 2023; 14(4):17511763. https://doi.org/10.3390/ microbiolres14040120.
4. Sharkey PK, Graybill JR, Rinaldi MG, et al. Itraconazole treatment of phaeohyphomycosis. J Am Acad Dermatol. 1990; 23(3 Pt 2):577-586. Doi: 10.1016/01909622(90)70259-k.
5. Pérez A. Terbinafine: broad new spectrum of indications in several subcutaneous and systemic and parasitic diseases. Mycoses. 1999; 42 Suppl 2:111114.
6. Petraitis V, Petraitiene R, Katragkou A, et al. Antifungal efficacy of isavuconazole and liposomal amphotericin B in a rabbit model of Exserohilum rostratum meningoencephalitis: A preclinical paradigm for management of CNS phaeohyphomycosis. Med Mycol. 2021; 59(2):189-196. doi:10.1093/mmy/myaa102.
7. Coldiron BM, Wiley EL, Rinaldi MG. Cutaneous
phaeohyphomycosis caused by a rare fungal pathogen, Hormonema dematioides: successful treatment with ketoconazole. J Am Acad Dermatol. 1990; 23(2 Pt 2):363-367. Doi: 10.1016/01909622(90)70223-5.
8. Koo S, Klompas M, Marty FM. Fonsecaea monophora cerebral phaeohyphomycosis: case report of successful surgical excision and voriconazole treatment and review. Med Mycol. 2010; 48(5):769-774. Doi: 10.3109/13693780903471081.
10. Wu X, Hu Y. Photodynamic Therapy for the Treatment of Fungal Infections. Infect Drug Resist. 2022; 15:32513266. Published 2022 Jun 21. doi:10.2147/IDR.S369605.
11. Singla AA, Garg P, and Chui JN, et al. Phaeohyphomycosis in Kidney Transplant Recipients: Highlighting the Importance of Early Recognition and Surgical Debridement. Transplant Direct. 2022; 9(1):e1430. Published 2022 Dec 12. doi:10.1097/ TXD.0000000000001430
Addiction to topical corticosteroids can occur not only with shortterm use of more potent topical corticosteroids but also with prolonged use of milder topical corticosteroids. Withdrawal of topical corticosteroids leads to the cessation of their vasoconstrictive effects, causing persistent vasodilation, which contributes to the rebound flare observed after discontinuation of the drug. Chronic application of topical corticosteroids inhibits the action of nitric oxide (NO), leading to sustained vasoconstriction. Upon withdrawal of topical corticosteroids, endothelial Comprehensive
Comprehensive Treatment Strategies for Topical Steroid Damaged/ Dependent Face (TSDF): A Case Report
Dr. Keerthana Bhaskar Pappuri
MD, DVL
Consultant Dermatologist & Cosmedic Triology
Bangalore
Introduction
Topical steroid damaged/ dependent face (TSDF) is a condition increasingly recognized for its complex manifestations and challenges in dermatological practice. This syndrome primarily affects the facial skin, which is uniquely vulnerable due to its thinness, increased drug absorption, and exposure to environmental factors like sunlight and pollution. Often triggered by the irrational, unsupervised, or prolonged use of topical corticosteroids (TCs), topical steroid damaged/ dependent face leads to a spectrum of cutaneous signs and symptoms, alongside psychological dependence
on the medication.1
Comprehensive Treatment Strategies for Topical Steroid Damaged/Dependent Face (TSDF): A Case Report
NO is released, resulting in vasodilation and subsequent erythema. Additionally, topical corticosteroidinduced dermal atrophy reduces vascular support, exacerbating erythema. Chronic topical corticosteroids use also suppresses the immune system, leading to microbial overgrowth. These microorganisms act as superantigens. Upon topical corticosteroid withdrawal, the removal of immunosuppression results in an inflammatory reaction characterized by inflammatory papules and pustules. Diagnosis of topical steroid damaged/ dependent face involves careful evaluation of clinical history, skin examination revealing characteristic signs such as skin thinning, telangiectasia, and rebound erythema. Psychological assessment may also be necessary to address dependence issues.1,2 Clinical presentation of topical steroid damaged/ dependent. face is characterized by a spectrum of dermatological manifestations primarily affecting the facial region. Misuse of topical corticosteroids, whether on diseased skin or for cosmetic purposes like
fairness creams, results in a range of adverse cutaneous effects on the face. These include erythematous papules, pustules, acneiform eruptions, dryness, perioral dermatitis, telangiectasia, rosacea-like features, hypoor hyperpigmentation, and allergic contact dermatitis. Patients may also experience photosensitivity reactions. Withdrawal of topical corticosteroids typically results in a transient phase of erythema (redness of the face) lasting approximately two weeks, followed by desquamation (skin peeling). If topical corticosteroid use is not resumed, the flareup resolves temporarily but recurs within two weeks. This cycle of flare-ups and remissions continues for a period, with diminishing intensity of flares and longer durations of remission until complete resolution is achieved. The rebound phenomenon may extend beyond the initial application site to larger areas of the face or even to distant sites. Some patients may also exhibit symptoms resembling status cosmeticus or chronic actinic dermatitis. A distinctive clinical feature of topical steroid damaged/dependence .....
syndrome, observed both as a consequence of topical corticosteroid misuse and during withdrawal, is diffuse erythema. Erythema can thus be considered the hallmark manifestation of topical steroid damaged/ dependence syndrome, initially recognized as red face syndrome.3
Topical steroid damaged/ dependence syndrome presents complex challenges that necessitate a comprehensive and tailored approach to treatment. Early recognition, accurate diagnosis, and the implementation of a structured management plan are critical in alleviating symptoms, reducing dependence on topical corticosteroids, and restoring skin health. Continued research efforts and heightened awareness are essential to refine treatment strategies further and enhance outcomes for individuals affected by topical steroid damaged/ dependent face.
Case Report
A 35-year-old female patient presented with topical steroid damaged/ dependent face following a history of abusing topical steroids for 4 years. The severity of topical steroid damaged/dependent....
Comprehensive Treatment Strategies for Topical Steroid
face manifestations was observed to be more profound than initially assessed, posing challenges in accurately documenting with conventional imaging methods. On physical examination, red acneiform lesions appeared on the chin, cheeks, and glabella, based on this topical steroid damaged/dependent face has been diagnosed. Treatment was initiated with metronidazole to address secondary infections and inflammation, complemented by monthly sessions of black peel and Low-Level Laser Therapy (LLLT) to manage hyperpigmentation and improve skin texture. After 5 months, significant clinical improvement was noted, marked by reduced erythema and enhanced skin texture, highlighting the efficacy of this multidimensional approach in managing topical steroid damaged/dependent face.
Before treatment
After 5 months of treatment
Figure 1: Red acneiform lesions on face, significant clinical improvement within 5 months of treatment
Diagnosis
Diagnosing topical corticosteroid damage involves a thorough approach that includes patient history, clinical evaluation, and sometimes supportive tests to rule out other conditions. Key aspects include understanding the duration, frequency, and potency of steroid use, as prolonged use of potent steroids increases the risk of withdrawal symptoms. Diagnosis often requires identifying underlying conditions like eczema or psoriasis that may have led to dependency. Symptom exacerbation after discontinuation, with flareups followed by gradual improvement, is a critical diagnostic clue. A key diagnostic step is observing how symptoms worsen after stopping steroids, typically presenting as flare-ups with increased erythema, itching, dryness, and possible oozing. Over weeks to months, symptoms gradually improve as the skin recovers. Clinical assessment focuses on the pattern and severity of symptoms, including skin texture changes, scaling, thinning, and the distribution of affected areas, particularly where steroids were frequently
Comprehensive Treatment Strategies for Topical Steroid Damaged/Dependent Face (TSDF): A Case Report
applied. Dermoscopy can reveal various features in skin affected by topical corticosteroid damage, including erythema, scales, crusts, and skin thinning, all indicative of inflammation and atrophy from prolonged steroid use. Telangiectasia and pigmentary changes like hypo- or hyperpigmentation may also be observed, reflecting vascular and inflammatory effects. Additionally, signs of secondary infections, excoriations, and lichenification may complicate the condition. However, since specific dermoscopic signs are generally lacking, diagnosis relies heavily on clinical presentation, steroid use history, and the skin's response to discontinuation.4 A skin biopsy is essential for diagnosing suspected topical corticosteroid damage, particularly on the face. It provides histopathological evidence of epidermal atrophy, collagen alterations, and other changes indicative of prolonged steroid use. Biopsies also evaluate the severity and extent of the damage, including potential secondary infections, guiding targeted treatment decisions. By confirming the diagnosis and ruling out
other conditions, biopsy results enable precise and effective therapeutic strategies, optimizing patient care and outcomes.5
Treatment
Treatment of topical steroid damaged/dependence ..... syndrome requires a comprehensive approach that addresses both the physical and psychological aspects of the condition. Central to this strategy is the gradual withdrawal and tapering of topical corticosteroids under medical supervision to effectively manage withdrawal symptoms and prevent rebound flares of skin inflammation. Alongside tapering, alternative therapies such as emollients, calcineurin inhibitors, and phototherapy play a crucial role in controlling symptoms, promoting skin healing, and reducing reliance on corticosteroids, tailored to individual patient needs.5
Metronidazole, known for its antimicrobial properties, also exhibits antiinflammatory effects that may be beneficial in treating topical steroid damage factor. Its mechanism involves interfering with neutrophil release of reactive oxygen species, which are
compounds involved in inflammatory processes. By reducing these inflammatory mediators, metronidazole can potentially alleviate symptoms such as redness, swelling, and irritation associated with topical steroid damaged/dependent face.6
Tranexamic acid, used in dermatology for its antiinflammatory properties and ability to lighten skin pigmentation, shows potential in managing conditions associated with topical steroid damage by inhibiting inflammation and reducing erythema. Tacrolimus and pimecrolimus, which inhibit calcineurin to reduce inflammation, spare steroid use, and preserve skin barrier integrity, are pivotal in treating topical steroid damage. Ivermectin shows potential in treating topical corticosteroid damage factor by inhibiting the innate inflammatory cascade through targeting Demodex mites, whose proliferation can be exacerbated by the immunosuppressive effects of topical corticosteroids, thus modulating inflammatory responses. Brimonidine, an alphaadrenoceptor agonist used for facial redness in rosacea, may manage topical steroid
Comprehensive Treatment Strategies for Topical Steroid
damaged/dependent face symptoms by causing vasoconstriction of cutaneous microcirculation, reducing facial redness and erythema, and providing symptomatic relief poststeroid discontinuation, though its efficacy and safety in topical steroid damaged/dependent ..... face need further study. Similarly, xylometazoline offers theoretical benefits for topical steroid damaged/ dependent face by causing vasoconstriction to reduce facial redness and erythema, but requires careful consideration of formulation and concentration for safe use on facial skin and further clinical research to confirm its efficacy and safety. Azelaic acid is a versatile topical treatment for acne and rosacea, known for its anti-inflammatory and antimicrobial properties that reduce redness, swelling, and irritation while normalizing skin cell turnover and improving skin texture, aiding in the restoration of the skin barrier and managing post-inflammatory hyperpigmentation ...... associated with topical steroid damaged/dependent face. Clindamycin, with its dual action of reducing bacterial superantigens and possessing antiinflammatory properties,
effectively manages topical steroid damaged/ dependent face symptoms. Sunscreen is essential for photoprotection against UV light, mitigating transepidermal water loss, and restoring compromised skin barrier function.
Chemical peels, although requiring cautious use due to heightened sensitivity and compromised barriers in topical steroid damaged/ dependent face, can promote exfoliation, reduce hyperpigmentation, and improve skin texture, with certain peels stimulating collagen production to support skin healing and regeneration. Together, these treatments play critical roles in the comprehensive management and recovery of topical steroid damaged/ dependent face -affected skin.6,7
The treatment of topical steroid damaged/dependent face requires a multifaceted approach aimed at addressing both the visible symptoms and underlying causes of steroid misuse. Long-term management includes regular monitoring, patient education on proper skincare practices, and adherence to prescribed therapies to sustain and enhance treatment outcomes. A collaborative
effort between healthcare providers and patients is pivotal in effectively managing topical steroid damaged/dependent face, ensuring optimal skin health restoration and quality of life.
Discussion
In society today, there is a concerning rise in the misuse of topical corticosteroids on facial skin, driven largely by the desire for fairer skin tones and the easy availability of these products as over-thecounter (OTC) remedies. This trend poses significant risks to individuals, leading to a condition known as topical steroiddamaged/dependent face, characterized by a complex syndrome of adverse effects resulting from prolonged and unsupervised topical corticosteroid use without medical guidance.1 The rebound phenomenon, characterized by severe flare-ups, is a consequence of prolonged and repeated use of topical corticosteroids. This misuse leads to skin atrophy and vasoconstriction.2, 4
Topical corticosteroids are prone to developing tachyphylaxis, which is characterized by a rapid decrease in response to successive doses of the drug, reducing its
effectiveness over time.3
Clinical trials investigating tachyphylaxis in topical corticosteroid therapy are sparse. It is now suggested that in treating psoriasis, the mechanism of action of topical corticosteroids is primarily through immunosuppression rather than processes that lead to tolerance development.5
Prior to the diagnosis of topical steroid addiction (TSA) or topical steroid withdrawal (TSW), patients often received alternative diagnoses such as worsening underlying dermatitis, allergic contact dermatitis, rosacea, or systemic lupus erythematosus due to facial redness.5
During the withdrawal phase of TSA/TSW, general measures recommended include lifestyle modifications such as dietary changes and stress management, psychological support, and adjunctive therapies such as cold water and ice, systemic antibiotics, astringents to prevent and treat bacterial infections, analgesics, sedatives, antihistamines, anxiolytics, and oatmealcontaining bath products.8 Other treatment modalities attempted include topical calcineurin inhibitors like crisaborole,
phototherapy, systemic immunosuppressants like cyclosporin, and biologics such as dupilumab. Acneiform eruptions such as steroid rosacea and perioral dermatitis may be managed with oral antibiotics such as doxycycline. However, responses to these therapies have been inconsistent, with studies often limited to case reports or small series, thus precluding definitive treatment recommendations.6
Psychological support through counseling helps patients cope with anxiety and dependence issues associated with topical corticosteroid withdrawal, empowering them to navigate the emotional challenges of treatment. Education is fundamental in topical steroid damaged/ dependence syndrome management, ensuring patients and caregivers understand proper topical corticosteroid use, potential side effects, and the importance of medical oversight, thereby enhancing treatment adherence and long-term outcomes. This integrated approach aims to alleviate symptoms, minimize dependence, and restore skin health, underscoring the need for continued research and
awareness to optimize care for those affected by topical steroid damaged/ dependent face.4
Conclusion
Topical steroid damaged/ dependent face has emerged as a prevalent condition affecting facial skin health due to widespread and unregulated use of steroids ranging from mild to superpotent strengths. This misuse occurs without authorization or supervision, often for prolonged periods and for inappropriate indications such as skin lightening. Consequently, a rash epidemic resembling corticosteroid side effects and addiction has ensued, particularly on the face. Discontinuing the offending agent presents both psychological and physical challenges. There is a notable increase in global literature reporting this phenomenon. Addressing this epidemic requires urgent and coordinated efforts involving government entities, health authorities, medical professionals, pharmaceutical companies, and chemists. A comprehensive approach is imperative to manage and mitigate the widespread implications of topical steroid damaged/ dependent face effectively. Comprehensive Treatment Strategies for Topical Steroid Damaged/Dependent Face (TSDF): A Case Report
Comprehensive Treatment Strategies for Topical Steroid
Damaged/Dependent Face (TSDF): A Case Report
References
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WebiQuiz 2025
A Webinar + Real Time Quiz for Residents in Dermatology
Topic: Comprehensive Acne Management:
From
Basics to Breakthroughs
Speaker
Dr. Kiran Godse
MD, PhD, FRCP
Professor, Department of Dermatology
D. Y. Patil University School of Medicine Navi Mumbai
