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LETTER TO THE EDITOR
Year : 2019  |  Volume : 10  |  Issue : 1  |  Page : 76-78  

Widespread superficial dermatophytosis in patient on secukinumab for treatment of chronic plaque psoriasis


Department of Dermatology, Command Hospital, Kolkata, West Bengal, India

Date of Web Publication14-Jan-2019

Correspondence Address:
Shekhar Neema
Department of Dermatology, Command Hospital, Kolkata - 700 027, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/idoj.IDOJ_170_18

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How to cite this article:
Neema S, Singh S, Pathak N, Khan M A. Widespread superficial dermatophytosis in patient on secukinumab for treatment of chronic plaque psoriasis. Indian Dermatol Online J 2019;10:76-8

How to cite this URL:
Neema S, Singh S, Pathak N, Khan M A. Widespread superficial dermatophytosis in patient on secukinumab for treatment of chronic plaque psoriasis. Indian Dermatol Online J [serial online] 2019 [cited 2019 Feb 17];10:76-8. Available from: http://www.idoj.in/text.asp?2019/10/1/76/250070



Sir,

Secukinumab is a recombinant, fully human IgG1 monoclonal antibody which selectively binds and neutralizes interleukin 17A (IL-17A). IL-17 is secreted by a class of helper T cells called Th17 cells, which stimulates keratinocytes to secrete proinflammatory mediator and to recruit other inflammatory cells in psoriatic skins. Secukinumab was FDA approved in January 2015 for the management of plaque psoriasis, and in January 2016 for the management of psoriatic arthritis. It is the one of the biologic approved as first-line therapy for the management of chronic plaque psoriasis. Pooled safety data from 10 Phase II/III studies have showed that secukinumab is a reasonably safe drug and serious adverse effects are uncommon. Infections like nasopharyngitis and upper respiratory tract infection were most common. Serious infections were infrequent, and reactivation of latent tuberculosis was not seen. Mucocutaneous candidiasis was more common in patients treated with secukinumab. Other adverse effects due to secukinumab are neutropenia, nonmelanoma skin cancer (NMSC), major adverse cardiac events (MACE), and inflammatory bowel disease. Neutropenia is rare and mostly Grade 1 or 2. The risk of NMSC and MACE is comparable to patients on TNF inhibitors and IL-12/23 blocker and is quite rare.[1],[2],[3] We hereby present a case of chronic plaque psoriasis whom we treated with secukinumab and the patient developed widespread tinea corporis 4 weeks after starting the therapy.

A 38-year-old male patient, with no known comorbidities but known case of chronic plaque psoriasis for 4 years, presented with acute exacerbation of his illness for the last 1 month. His previous treatments included topical steroids, narrow-band ultraviolet B therapy, and methotrexate. He was not on any treatment for the last 6 months. General and systemic examinations were within normal limits. Dermatological examination revealed the involvement of 40% body surface area in the form of erythematous scaly plaques, and the PASI score was 22.4 [Figure 1]a and [Figure 1]b. Baseline investigations including interferon-gamma release assay test to exclude latent tuberculosis infection were within normal limits. The individual was started on secukinumab 300 mg subcutaneously weekly and topical white soft paraffin. Four weeks after starting the therapy, his psoriatic plaques started clearing; however, he developed widespread annular erythematous plaques studded with pustules on the periphery of plaque [Figure 2]a. There was no fever, joint pain, or systemic symptoms. There was no family history of dermatophytosis. We performed 10% KOH mount of scale and histopathological examination of skin keeping in view differential diagnosis of generalized pustular psoriasis and tinea corporis. Histopathological examination of skin biopsy showed neutrophilic microabscess in the stratum corneum [Figure 3]a and [Figure 3]b. PAS stain showed the presence of hyphae in the stratum corneum [Figure 3]c. Ten percent KOH mount revealed the presence of septate hyphae. Diagnosis of tinea corporis was made and the patient was started on itraconazole capsule 100 mg twice a day to which the patient responded and his skin lesions improved [Figure 2]b. The patient was admitted to the dermatology inpatient ward before starting secukinumab and none of the ward patients suffered from dermatophytosis.
Figure 1: (a and b) Shows generalised involvement with chronic plaque psoriasis

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Figure 2: (a) Widespread annular erythematous plaque and pustules on the periphery of these plaques. (b) Improvement in lesion after 1 week of itraconazole 100 mg twice a day

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Figure 3: (a) Microphotograph shows the presence of neutrophilic microabscess in the epidermis (H and E, ×10). (b) Neutrophilic collection and mild spongiosis (H and E, ×40). (c) Microphotograph shows PAS-positive hyphae in the stratum corneum (PAS, ×40)

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IL-17 plays an important role in mucocutaneous microbial defense. Congenital impairment of IL-17 pathway results in increased susceptibility to candida and mucocutaneous candidiasis.[4] In patients with adult T-cell leukemia/lymphoma (ATLL), peripheral Th17 cell and serum IL-17 levels are decreased. Th17 induces keratinocyte to produce antimicrobial peptide-like human B defensin-2 and LL-37, which plays a role in innate immunity. Fifty percent of the patients with ATLL develop cutaneous mycotic infection.[5] Burstein et al. provided an animal model for the role of IL-17 in immunity against superficial dermatophytosis. The study suggested that the absence of functional IL-17 pathway results in widespread colonization of epidermis by Microsporum canis and shifts to T-helper type 1 response which is nonprotective. They also observed that mice with wild-type IL-17 develop epidermal thickening on exposure to M. canis, while IL-17-deficient mice do not develop this protective barrier function. However, deficiency of IL-17 does not affect neutrophil accumulation in the epidermis and appears to be independent of this pathway.[6] IL-17 blockade with secukinumab also increases the risk of infection, especially mucocutaneous candidiasis. Oral and vulvo-vaginal candidiasis was seen during clinical trials and is also seen in clinical practice. A total of four cases of tinea pedis were also reported in four clinical trials.[1],[2],[3] There has been a report of perianal dermatophytosis in patients on secukinumab; however, there are no reports of widespread superficial dermatophytosis after secukinumab use.[7] The exact reason why widespread dermatophytosis is not reported in patients with psoriasis while it is common in patients with ATLL may be because of increased production of antimicrobial peptide by psoriatic skin, which results in fewer infections of psoriatic lesional skin.[8]

In view of increasing usage of IL-17 blockers and dermatophyte epidemic especially in tropical humid climate, it is important to keep in mind that widespread dermatophytosis may occur after IL-17 blockade and it should be suspected and treated at the earliest.

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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
van de Kerkhof PC, Griffiths CE, Reich K, Leonardi CL, Blauvelt A, Tsai TF, et al. Secukinumab long-term safety experience: A pooled analysis of 10 phase II and III clinical studies in patients with moderate to severe plaque psoriasis. J Am Acad Dermatol 2016;75:83-98.  Back to cited text no. 1
    
2.
Langley RG, Elewski BE, Lebwohl M, Reich K, Griffiths CE, Papp K, et al. Secukinumab in plaque psoriasis – Results of two phase 3 trials. N Engl J Med 2014;371:326-38.  Back to cited text no. 2
    
3.
Blauvelt A, Prinz JC, Gottlieb AB, Kingo K, Sofen H, Ruer-Mulard M, et al. Secukinumab administration by pre-filled syringe: Efficacy, safety and usability results from a randomized controlled trial in psoriasis (FEATURE). Br J Dermatol 2015;172:484-93.  Back to cited text no. 3
    
4.
Marinoni B, Ceribelli A, Massarotti MS, Selmi C. The Th17 axis in psoriatic disease: Pathogenetic and therapeutic implications. Auto Immun Highlights 2014;5:9-19.  Back to cited text no. 4
    
5.
Sawada Y, Nakamura M, Kabashima-Kubo R, Shimauchi T, Kobayashi M, Tokura Y, et al. Defective epidermal innate immunity and resultant superficial dermatophytosis in adult T-cell leukemia/lymphoma. Clin Cancer Res 2012;18:3772-9.  Back to cited text no. 5
    
6.
Burstein VL, Guasconi L, Beccacece I, Theumer MG, Mena C, Prinz I, et al. IL-17-mediated immunity controls skin infection and T helper 1 response during experimental microsporum canis dermatophytosis. J Invest Dermatol 2018;138:1744-53.  Back to cited text no. 6
    
7.
Quach OL, Hsu S. Perianal dermatophytosis during secukinumab therapy for plaque psoriasis. JAMA Dermatol 2016;152:486-7.  Back to cited text no. 7
    
8.
Harder J, Bartels J, Christophers E, Schröder JM. A peptide antibiotic from human skin. Nature 1997;387:861.  Back to cited text no. 8
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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