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Year : 2022  |  Volume : 67  |  Issue : 6  |  Page : 821-822
Development of secondary prurigo nodularis in steroid modified tinea corporis- Documenting a curious phenomenon

1 From the Nirvan Skin Clinic, Makarpura Road, Vadodara, Gujarat, India
2 Bhojani Clinic, Earth Classic, Babasaheb Ambedkar Road, Matunga, Mumbai, Maharashtra, India

Date of Web Publication23-Feb-2023

Correspondence Address:
Shyam Bhanushankar Verma
Nirvan Skin Clinic, Makarpura Road, Vadodara, Gujarat
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijd.ijd_115_22

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How to cite this article:
Verma SB, Vasani R. Development of secondary prurigo nodularis in steroid modified tinea corporis- Documenting a curious phenomenon. Indian J Dermatol 2022;67:821-2

How to cite this URL:
Verma SB, Vasani R. Development of secondary prurigo nodularis in steroid modified tinea corporis- Documenting a curious phenomenon. Indian J Dermatol [serial online] 2022 [cited 2023 Mar 29];67:821-2. Available from:


We describe three Indian women in their 7th decade presenting with itchy plaques of tinea corporis (TC) of lower extremities of seven-to-thirteen-month duration. The plaques were well defined with inflamed active borders, scaling and central clearing. Multiple intensely pruritic, hyperpigmented, hyperkeratotic papules and nodules were seen within the plaques [Figure 1]a, [Figure 1]b, [Figure 1]c, [Figure 1]d which had developed after four to eight months of the disease in all patients. They were predominantly using fixed dose combination (FDC) creams containing clobetasol propionate + miconazole + gentamicin with erratic use of assorted topical and oral antifungal drugs for the entire duration. Overt signs of topical steroid abuse were absent. Two patients had diabetes of more than eight-year duration and had atopic diathesis. All had varying degrees of xerosis but no other dermatological history. Ten per cent potassium hydroxide mount showed multiple septate hyphae, and culture grew Trichophyton mentagrophytes in two patients, while one patient was diagnosed only clinically due to financial constraints. Routine haematology profile, thyroid, liver and kidney function tests were normal. Dermoscopy showed white starburst pattern surrounding brown yellowish crust [Figure 2]a. Histopathological findings in the two biopsied patients were consistent with the diagnosis of prurigo nodularis [Figure 2]b and [Figure 2]c. A final diagnosis of active steroid-modified tinea with secondary prurigo nodularis was made. Treatment with itraconazole 200mg daily, 1% luliconazole cream, emollients and levocetirizine for six weeks led to complete resolution of both TC and PN [Figure 2]d. No recurrence of TC or PN was reported at three-month follow-up.
Figure 1: (a) Well-defined plaques of TC with erythematous scaly margin, central clearing. Hyperpigmented and hyperkeratotic papules and nodules of PN within the plaques. (b) Close up of active margin of tinea corporis with lesions of PN. (c) Patient 2 of tinea corporis and PN. (d) Patient 3 of tinea corporis and PN

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Figure 2: (a) Dermoscopy polarised mode – White starburst pattern surrounding yellow brown crust (Dermlite DL3N, 10×). (b) Compact hyperkeratosis with focal parakeratosis, moderate epidermal hyperplasia and papillomatosis (H and E 100×). (c) Thickened collagen bundles arranged in a vertical array. Increased dermal capillaries with moderate perivascular lymphocytic infiltrate (H and E 400×). (d) Post-treatment clearance of TC and resolution of PN with residual pigmentation after six weeks of antifungal therapy

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A variety of clinical phenomena have been described in the epidemic of dermatophytosis in India attributed to the recently described dermatophyte called trichophyton (T.) indotineae, formerly T. mentagrophytes ITS genotype VIII of T.mentagrophytes/T.interdigitale complex.[1] However, antecedent dermatophytosis under treatment with FDCs containing clobetasol propionate leading to secondary prurigo nodularis confined to the affected area has never been reported in dermatology literature.

This curious phenomenon merits an explanation of its pathomechanism. Inflammatory dermatophytosis leads to impairment of skin barrier and increased transepidermal water loss that contributes to the itch. FDC creams containing potent steroids lead to incomplete clearance of the dermatophytes due to local immunosuppression and their erratic application prolongs inflammation and the accompanying itch.[1] In addition, they cause drying, thinning, atrophy and delayed barrier recovery which perpetuates the itch.[2] Both the dermatophyte and the application of a superpotent steroid in patients of chronic dermatophytosis induce a Th2 predominant immunological response.[3] The same response is also accentuated in atopic individuals. The Th2 cytokines mediate neuronal priming and promote protective behavioural responses like scratching. Among these, IL4 and IL13 are known to directly activate sensory neurons and are therefore thought to be responsible for the chronic debilitating itch in recalcitrant dermatophytosis.

The itching and inflammatory cells in turn release neurotrophins and neuropeptides, leading to neural proliferation as well as keratinocyte proliferation and differentiation.[4] These events in tandem result in epidermal proliferation, clinically manifesting as secondary prurigo nodularis, as exemplified in these cases.

Additionally, the long-standing diabetes in all three patients could also cause autonomic neuropathy and sudomotor dysfunction, which in turn aggravates the xerosis compounded by the environmental factors, age and topical steroid abuse. The associated decreased nociception is thought to be the triggering factor for the itch–scratch–itch response.[5]

The development of PN secondary to steroid-modified TC, failure of clobetasol propionate to resolve PN and successful treatment of both conditions with appropriate antifungal therapy all point to the deleterious role of such FDCs in dermatophytosis. Appropriate treatment leading to clearance of secondary PN is an encouraging observation in contrast to the otherwise refractory nature of primary PN. Patients of chronic dermatophytosis, especially the elderly, with associated conditions like atopy, diabetes, and age-related xerosis may be particularly vulnerable to this phenomenon.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Tang C, Kong X, Ahmed SA, Thakur R, Chowdhary A, Nenoff P, et al. Taxonomy of the trichophyton mentagrophytes/T. interdigitale species complex harboring the highly virulent, multiresistant genotype T. indotineae. Mycopathologia 2021;186:315-26.  Back to cited text no. 1
Kao JS, Fluhr JW, Man MQ, Fowler AJ, Hachem JP, Crumrine D, et al. Short-term glucocorticoid treatment compromises both permeability barrier homeostasis and stratum corneum integrity: Inhibition of epidermal lipid synthesis accounts for functional abnormalities. J Invest Dermatol 2003;1203:456-64.  Back to cited text no. 2
Sardana K, Gupta A, Mathachan SR. Immunopathogenesis of dermatophytoses and factors leading to recalcitrant infections. Indian Dermatol Online J 2021;12:389-99.  Back to cited text no. 3
  [Full text]  
Agrawal D, Sardana K, Mathachan SR, Bhardwaj M, Ahuja A, Jain S. A prospective study examining the expression of STAT 1, 3, 6 in prurigo nodularis lesions with its immunopathogenic and therapeutic implications. J Cosmet Dermatol 2021;21:4009-15.  Back to cited text no. 4
Murao S, Murao K. Multiple skin ulceration and itch–scratch cycle in a diabetic patient. J Diabetes Investig 2021;1211:2102-3.  Back to cited text no. 5


  [Figure 1], [Figure 2]


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