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Terbinafine induced cutaneous lupus erythematosus. Clinical case report / Ugne Valanciute, Guste Mingailaite, Ieva Vaitkeviciute, Valentina Rimkiene, Jurgita Makstiene, Skaidra Valiukeviciene
Type of publication
Recenzuojamos išplėstinės tezės / Peer-reviewed extended theses (T1d)
Author(s)
Title
Terbinafine induced cutaneous lupus erythematosus. Clinical case report / Ugne Valanciute, Guste Mingailaite, Ieva Vaitkeviciute, Valentina Rimkiene, Jurgita Makstiene, Skaidra Valiukeviciene
Publisher (trusted)
Baltic Association of Dermatovenerologists (BADV) |
Date Issued
Date Issued |
---|
2021-09-17 |
Extent
p. 86-88.
Is part of
17th Congress of the Baltic Association of Dermatovenerologists (BADV) : 17-19 September 2021, Kaunas, Lithuania : online abstract book / Baltic Association of Dermatovenerologists ; [Editor Skaidra Valiukeviciene ; Abstracts' Reviewers: Ruta Ganceviciene, Jurate Grigaitiene, Vesta Kucinskiene]. Kaunas : BADV, 2021. ISBN 9786099616742.
Version
Originalus / Original
Description
no. PL 39–53
Plenary Sessions Abstracts
ISBN 978-609-96167-4-2
Bibliogr.: p. 88
Field of Science
Abstract
Introduction Drug-induced lupus erythematosus (LE) is characterized by clinical manifestations, immunopathological and serological findings similar to those of idiopathic LE, but is related to continuous drug exposure, typically resolving after the discontinuation of the responsible drug. Correspondingly to idiopathic lupus, drug-induced LE can be divided into systemic (SLE) and subacute cutaneous lupus erythematosus (SCLE) [3]. The cutaneous features of drug-induced SLE include purpura, erythema nodosum and photosensitivity, and the typical laboratory profile consists of positive ANA and anti-histone antibodies. Medications most frequently associated with drug-induced SLE are hydralazine, procainamide, isoniazid and minocycline. Drug-induced SCLE typically presents with annular polycyclic papulosquamous lesions, but blisters or target lesions mimicking erythema multiforme may also be associated with this condition. ANA and anti- Ro/SSA antibodies are usually present, whereas anti-histone antibodies are uncommonly found. Drugs reported to be associated with SCLE include calcium-channel blockers, angiotensin-converting enzyme inhibitors, thiazide diuretics, terbinafine, and tumour necrosis factor-α antagonists [3]. Materials and methods A 68-year-old woman presented with multiple infiltrated erythematous scaly plaques on sun-exposed areas of the chest and back. The skin lesions developed in May 2020. Before the appearance of the rash, the patient was treated for onychomycosis with oral terbinafine for 4-months (February - May 2020). During June-July of 2020, the patient was hospitalized in a regional hospital’s dermatology department. Skin biopsy and histology concluded vacuolar interface dermatitis suggestive of pityriasis lichenoides et varioliformis acuta (PLEVA), with erythema exudativum multiforme as the main differential diagnosis. Treatment with topical corticosteroids and intravenous dexamethasone 8 mg per day was begun, followed by a methylprednis
olone 32 mg/day taper to cessation. Due to disease progression and advancing lesions, in August 2020 the patient was admitted to the Department of Skin and Venereal Diseases of Kaunas Clinics. Life and medical history: Current medications included nebivolol/hydrochlorothiazide 5/12.5mg once per day (many years before the rash) for primary hypertension, betahistine 24 mg once per day for vestibular neuritis (April-May 2020), with occasional use of zopiclone 7.5 mg due to insomnia. Skin examination: annular polycyclic erythematous plaques and macules with scaling at periphery on the face, neck, chest, back and dorsal surfaces of the arms and legs, without oral mucosa involvement. Results Patient’s laboratory findings included normal levels of complement C3 and C4, positivity for anti-Ro/SSA antibodies (3+). Direct immunofluorescence of a skin biopsy displayed perivascular fibrinogen staining. On histology, hyperparakeratotic and atrofic epidermis was found, with apoptotic keratinocytes, vacuolisation at the basement membrane zone and perivascular lymphocytic infiltrate in the dermis. Based on clinical and histopathological findings the diagnosis of drug-induced SCLE was established, with terbinafine as the most likely cause. Treatment with oral prednisolone 30 mg daily (nine days) was started and tapered to cessation. Simultaneously, hydroxychloroquine (HC) 200 mg daily (after one month the dose was doubled to 400 mg), topical clobetasol 0,05% for the body, hydrocortisone 1 % for the face, and SPF50+ sunscreen were begun. After 6 months of treatment, no new lesions appeared, and skin hyperpigmentation on previous SCLE sites was seen. The treatment with HC was tapered off and stopped, with continued avoidance of direct sun exposure. Conclusions Terbinafine can induce or aggrevate SCLE [1-3] and mimic erythema exudativum multiforme or PLEVA due to similar clinical and histopathotological findings. Therefore, diagnostics of drug-induced SCLE or LE require a
Type of document
type::text::conference output::conference proceedings::conference paper
ISBN (of the container)
9786099616742
9786099616742
Other Identifier(s)
(LSMU ALMA)990001049100107106
Coverage Spatial
Lietuva / Lithuania (LT)
Language
Anglų / English (en)
Bibliographic Details
3
Affiliation(s)