Erythematous Annular Plaques Research Articles

Drug-Induced Erythema Annulare Centrifugum after Dupilumab Therapy: A Case Report.

Introduction: Dupilumab is a fully human monoclonal antibody therapy FDA-approved to treat moderate-to-severe atopic dermatitis (AD) by interrupting the pro-inflammatory signaling pathway of interleukins 4 and 13. Common side effects of dupilumab include injection-site reactions, ophthalmic complications, and upper respiratory infections. We discuss the necessity for early recognition and management of dupilumab-induced EAC which has not been previously reported as a potential adverse effect.
 Case Report: A 48-year-old woman began treatment with dupilumab for severe AD and subsequently presented with a 3-month history of erythematous annular plaques with trailing scale on the trunk and extremities. She failed treatment with topical corticosteroids as well as topical and oral antifungals prior to being diagnosed with biopsy-confirmed erythema annulare centrifugum (EAC). The condition worsened after replacing dupilumab with tralokinumab but resolved after discontinuation of the drugs and has remained clear since.
 Conclusion: EAC is a reactive erythema that typically presents as expanding annular papules and plaques with central clearing and in some cases, trailing scale at the rim of the lesions. There are currently no reports in the literature describing the development of EAC secondary to dupilumab. Clinicians should be aware that EAC may be a potential adverse effect of dupilumab.

Coexistence of Granuloma Annulare and Castleman’s Disease: A Case Report

Granuloma annulare (GA) is a self-limited disorder that may present as localized or general. Localized GA, the most common form, presents as an erythematous annular plaque without scale. The generalized form of GA presents as widespread erythematous papules and plaques over the trunk and extremities. A cross-sectional study in the United States found a female to male prevalence ratio of 3:1 with a higher prevalence in the fifth decade of life.1 The etiology of GA is largely unknown; however, a number of potential inciting factors have been reported including viral infections, drug exposure, trauma, and insect bites.
 Castleman’s Disease is a rare heterogenous lymphoproliferative disorder that encompasses a spectrum of clinicopathologic manifestations. Unicentric disease affects one lymph node or chain of lymph nodes with primarily hyaline vascular changes. The multicentric form affects multiple chains of lymph nodes with primarily plasmacytic changes. The pathogenesis is related to hypercytokinemia due to dysregulated interleukin-6 (IL-6) activity in unicentric disease and dysregulated IL-6 and human herpes virus-8 in multicentric disease.
 We report a case of concomitant granuloma annulare and Castleman’s Disease.

Development of ANCA-Negative Eosinophilic Granulomatosis With Polyangiitis 19 years After Onset of Eosinophilic Pustular Folliculitis.

To the Editor: A 47-year-old Japanese man visited our department, complaining of itchy erythema on the bilateral cheeks. Physical examination showed symmetrical infiltrative erythematous plaques with small papules and tiny pustules at the periphery, as well as papular lesions under the nostrils and around the lips (Fig. 1A). Biopsy revealed infiltration of neutrophils and eosinophils in the sebaceous glands (Fig. 1B). The patient was diagnosed as having eosinophilic pustular folliculitis (EPF), and oral intake of indomethacin (200 mg/d) resulted in a favorable effect. At the age of 56 years, he developed bronchial asthma, and a few years later, he complained of numbness of the bilateral lower legs, which was diagnosed as neuropathy. Nineteen years after the initial visit to us, he was referred to us for skin lesions. Physical examination showed brownish infiltrative plaques, papules, and vesicles on the lower extremities (Fig. 1C). Laboratory examination showed an elevated eosinophil rate in the peripheral blood (14%), and serum IgE was elevated (213 IU/mL; normal <170). Neither proteinase 3 (PR3)-anti-neutrophil cytoplasmic antibody (ANCA) nor myeloperoxidase (MPO)-ANCA was detected in the serum. HIV was negative. Histopathological examination revealed prominent infiltration of eosinophils in and around the sebaceous glands and vessels in the mid dermis (Fig. 1D). Higher magnification revealed a number of eosinophil infiltration in the vessel walls with degranulation of the infiltrated eosinophils and alteration of the affected pale-stained vessel walls, loss of endothelial cells of the affected venous vessel in the mid dermis (Fig. 1E), consistent with eosinophilic vasculitis. Neither fibrinoid degeneration of the vessel walls nor neutrophil infiltration with nuclear dust was observed. Extravascular giant cells were scattered in the dermis (Fig. 1F). Elastica van Gieson staining revealed that the affected vessels were venules. Renal disease was not observed. The patient was treated with inhaled corticosteroid for bronchial asthma, and his skin lesions were treated with topical corticosteroid ointment.FIGURE 1.: A, Facial infiltrative erythematous plaques with small papules and tiny pustules at the periphery. B, Biopsy specimen taken from the cheek showed marked infiltration of neutrophils and eosinophils in the sebaceous glands. C, Brownish infiltrative plaques, papules, and vesicles on the lower extremities. D, Histopathological features showing dermal infiltration of a number of eosinophils in and around the sebaceous glands and vessels in the mid dermis. E, Higher magnification reveals prominent infiltration of eosinophils in and around the vessel walls with eosinophilic degranulation (arrows), alteration of the affected vessel walls, and loss of endothelial cells (encircled by dotted square). F, Extravascular giant cells in the dermis. H–E, stain, original magnification: B; ×200, d; ×100, e; ×400, f; ×400).Eosinophilic pustular folliculitis is a sterile inflammatory dermatosis, frequently involving the face, presenting with annular erythematous plaques with superficial papulopustules at the periphery.1 Eosinophilic pustular folliculitis is histopathologically associated with folliculotropic infiltration of eosinophils. Our case was diagnosed as classic EPF and successfully treated with indomethacin. Thereafter, EPF did not recur, but the patient developed eosinophilic granulomatosis with polyangiitis (EGPA) 19 years later. Eosinophils play a crucial role in the pathogenesis of EGPA and release of mediators, that is, major basic protein, eosinophilic cationic protein, eosinophil peroxidase, and eosinophil-derived neurotoxin, as well as various cytokines by degranulation is important in the development of eosinophilic vasculitis.2 In EGPA, cutaneous eosinophilic vasculitis is rarely seen. The inflammatory process of eosinophilic vasculitis in EGPA begins as an angiocentric infiltrate of eosinophils in and around the small vessels.3 In the present case, angiocentric infiltrates of inflammatory cells in the affected vessels' wall were almost exclusively eosinophils without either neutrophils or histiocytes. The affected vessels were venules, and the arteries were intact. These findings suggest that the present case is the initial stage of EGPA with eosinophilic vasculitis. In addition, the present case was ANCA negative and renal involvement was absent. Previous studies have suggested that MPO-ANCA–positive patients frequently develop neutrophilic vasculitis with renal involvement, while those with eosinophil-predominant eosinophilic vasculitis frequently revealed serological ANCA negative and developed lung infiltrates, myocardiopathy, and gastrointestinal manifestations but the absence of renal involvement.4,5 Further studies are necessary to investigate the associations of cutaneous manifestations, eosinophilic vasculitis, and ANCA. Histopathological features of hypereosinophilic syndrome are eosinophilic spongiosis in the epidermis, superficial and deep dermal perivascular and interstitial infiltrate of numerous eosinophils and lymphocytes6; however, neither vasculitis nor histiocytic giant cells are observed. Therefore, hypereosinophilic syndrome was excluded in the present case. To the best of our knowledge, this is the first report of concurrent EPF and EGPA. Because EGPA occurred nearly 20 years later, the coexistence may be incidental. Nevertheless, eosinophil activation may have played a role in the induction of both disorders in our patient.

Post-traumatic ulcerated and chronic necrobiosis lipoidica of the elbow: A new entity?

BackgroundNecrobiosis lipoidica (NL) is a chronic granulomatous dermatosis usually affecting the lower limbs, although less common sites have been described. Herein we report a series of cases of NL located on the elbow, with an unusual presentation and occurring after trauma or surgery. ObservationsOur series includes three men and one woman, with a mean age of 64 years. Three had undergone surgery for elbow bursitis and one had had trauma after a fall from a horse, with exposure of subcutaneous tissue prior to healing. Within 5 years, they had all developed an atrophic erythematous annular plaque with papular and telangiectatic edges, with recurrent episodes of ulceration and scarring. Repeated tests for infectious agents were negative. Histological examinations showed granulomas and necrobiosis with palisading or early-stage palisading. Partial healing was achieved in two patients after 6 months of doxycycline. Treatment with adalimumab resulted in disappearance of the ulcers at 6 months in one patient. DiscussionUnusual sites of NL impose consideration of other types of palisading granuloma or mycobacterial infections, which we were able to rule out. Two other cases of NL of the elbow similar to ours are reported in the literature. These cases, involving multiple ulcerations over a very long period of time, probably constitute a distinct entity because of the very distinct character of these 6 cases. Tetracyclines are partially active and tumour necrosis factor alpha (TNF)-alpha inhibitors may offer an option.

Progressive annular erythematous papules and plaques in a child

Pediatric DermatologyVolume 40, Issue 2 p. 370-372 PHOTOQUIZ Progressive annular erythematous papules and plaques in a child Arti Nanda MD, DNBE, Corresponding Author Arti Nanda MD, DNBE [email protected] orcid.org/0000-0002-1223-3181 As'ad Al-Hamad Dermatology Center, Kuwait Correspondence Arti Nanda, As'ad Al-Hamad Dermatology Center, P.O. Box: 6759, 22078, Salmiya, Kuwait. Email: [email protected]Search for more papers by this authorEiman Al-Selahi MD, Eiman Al-Selahi MD Department of Pediatrics, Ameri Hospital, KuwaitSearch for more papers by this authorHamoud Al-Sabah MD, Hamoud Al-Sabah MD As'ad Al-Hamad Dermatology Center, KuwaitSearch for more papers by this authorAtlal AlLafi MD, Atlal AlLafi MD As'ad Al-Hamad Dermatology Center, KuwaitSearch for more papers by this author Arti Nanda MD, DNBE, Corresponding Author Arti Nanda MD, DNBE [email protected] orcid.org/0000-0002-1223-3181 As'ad Al-Hamad Dermatology Center, Kuwait Correspondence Arti Nanda, As'ad Al-Hamad Dermatology Center, P.O. Box: 6759, 22078, Salmiya, Kuwait. Email: [email protected]Search for more papers by this authorEiman Al-Selahi MD, Eiman Al-Selahi MD Department of Pediatrics, Ameri Hospital, KuwaitSearch for more papers by this authorHamoud Al-Sabah MD, Hamoud Al-Sabah MD As'ad Al-Hamad Dermatology Center, KuwaitSearch for more papers by this authorAtlal AlLafi MD, Atlal AlLafi MD As'ad Al-Hamad Dermatology Center, KuwaitSearch for more papers by this author First published: 29 March 2023 https://doi.org/10.1111/pde.15171Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume40, Issue2March/April 2023Pages 370-372 RelatedInformation

First Terbinafine-Resistant Trichophyton indotineae Isolates with Phe397Leu and/or Thr414His Mutations in Turkey

Fungal infections of the skin, nails, and hair caused by dermatophyte species continue to be a worldwide concern. The increase in terbinafine-resistant superficial dermatophytosis has become a major concern over the last decade. In this report, we presented two cases of infection with terbinafine-resistant Trichophyton indotineae, the first diagnosis of this species in Turkey. One patient exhibited erythematous pruritic patches and plaques in the inguinal and gluteal regions, while the other patient showed annular erythematous scaly plaques in the bilateral posterior thigh and gluteal regions. One patient harbored a CD36 mutation. Both strains harbored the same amino acid substitution in the squalene epoxidase gene, whereas one isolate had another unknown mutation. Clinical improvement was observed with resveratrol treatment in the patient with the CD36 mutation but not in the other patient.

Multiple Annular Erythematous Plaques

A 59-year-old man was admitted to the medical ward with multiple annular erythematous plaques and polyarthralgia of several months’ duration. His medical history included low-grade stage IIA follicular lymphoma diagnosed 6 months prior to presentation, substance abuse with opiates and cocaine, coronary artery disease, ascending aortic aneurysm, and chronic lower back pain.

Erythematous annular plaques in a patient with systemic lupus erythematosus.

International Journal of DermatologyEarly View Clinicopathologic challenge Erythematous annular plaques in a patient with systemic lupus erythematosus Elena Lucía Pinto-Pulido MD, Corresponding Author Elena Lucía Pinto-Pulido MD [email protected] orcid.org/0000-0002-1075-5103 Department of Dermatology, Hospital Universitario Príncipe de Asturias, Universidad de Alcalá, Madrid, Spain Correspondence Elena Lucia Pinto-Pulido, MD Department of Dermatology, Hospital Universitario Príncipe de Asturias Carretera de Meco S/N 28805 Madrid Spain E-mail: [email protected]Search for more papers by this authorMarta González-Cañete MD, Marta González-Cañete MD Department of Dermatology, Hospital Universitario Príncipe de Asturias, Universidad de Alcalá, Madrid, SpainSearch for more papers by this authorMaría Dolores Vélez-Velázquez MD, María Dolores Vélez-Velázquez MD Department of Pathology, Hospital Universitario Príncipe de Asturias, Universidad de Alcalá, Madrid, SpainSearch for more papers by this authorAna Rodríguez-Villa Lario MD, Ana Rodríguez-Villa Lario MD orcid.org/0000-0001-6156-4115 Department of Dermatology, Hospital Universitario Príncipe de Asturias, Universidad de Alcalá, Madrid, SpainSearch for more papers by this author Elena Lucía Pinto-Pulido MD, Corresponding Author Elena Lucía Pinto-Pulido MD [email protected] orcid.org/0000-0002-1075-5103 Department of Dermatology, Hospital Universitario Príncipe de Asturias, Universidad de Alcalá, Madrid, Spain Correspondence Elena Lucia Pinto-Pulido, MD Department of Dermatology, Hospital Universitario Príncipe de Asturias Carretera de Meco S/N 28805 Madrid Spain E-mail: [email protected]Search for more papers by this authorMarta González-Cañete MD, Marta González-Cañete MD Department of Dermatology, Hospital Universitario Príncipe de Asturias, Universidad de Alcalá, Madrid, SpainSearch for more papers by this authorMaría Dolores Vélez-Velázquez MD, María Dolores Vélez-Velázquez MD Department of Pathology, Hospital Universitario Príncipe de Asturias, Universidad de Alcalá, Madrid, SpainSearch for more papers by this authorAna Rodríguez-Villa Lario MD, Ana Rodríguez-Villa Lario MD orcid.org/0000-0001-6156-4115 Department of Dermatology, Hospital Universitario Príncipe de Asturias, Universidad de Alcalá, Madrid, SpainSearch for more papers by this author First published: 02 November 2022 https://doi.org/10.1111/ijd.16489 Conflict of interest: None. Funding source: None. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. Early ViewOnline Version of Record before inclusion in an issue RelatedInformation

The Expansion of Lyme Disease: A Case of Infection in the Absence of Known Exposure

Lyme disease is a systemic infection caused by the spirochete Borrelia burgdorferi often carried the Ixodes tick. It is associated with dermatologic manifestations, most notably the “bullseye rash” of erythema migrans. The disease can progress in stages to involve other organs such as joints, heart, and the nervous system. Lyme disease is continuing to spread, with West Virginia cases increasing dramatically in the last 2 decades. As a result, physicians are likely to encounter this disease more often, making recognition and early treatment a top priority in order to prevent potentially dangerous sequelae. We present a case of a 60-year-old man who presented with multiple erythematous annular plaques and was subsequently diagnosed with Lyme disease. He had no known exposure to ticks, was treated for Lyme Disease, and subsequently developed a Jarisch- Herxheimer reaction (JHR).

A Rare Case Presentation of Erythema Annulare Centrifugum-Like Acute Psoriasis

We report a case of erythema annulare centrifugum-like psoriasis occurring in a 44-year-old female. The patient presented with annular erythematous plaques with trailing collarette scales affecting the elbows and antecubital fossae, which are consistent with a clinical diagnosis of erythema annulare centrifugum (EAC). Given the presence of classical clinical features of EAC, this case was notable due to biopsy findings, which revealed classic histologic changes of psoriasis. This finding supports the diagnosis of erythema annulare centrifugum-like psoriasis and represents a rare presentation of acute psoriasis. Treatment with topical mometasone led to rapid and sustained long-term remission.

Misdiagnosis of neutrophilic erythema of infancy as leukocytoclastic vasculitis: A potential diagnostic pitfall in an infantile inflammatory dermatosis.

The authors declare no conflict of interest. The data that support the findings of this study are openly available in NFEI at https://pubmed.ncbi.nlm.nih.gov/. F IGURE 1 Annular erythematous plaques in an infant. Erythematous annular plaque on the right thigh (A) and progression after 3 weeks (B) F IGURE 2 Histopathology of annular erythematous plaque. Punch biopsy specimen from the right leg shows perivascular and interstitial dermal inflammatory infiltrate (A, ×100) primarily composed of neutrophils (B, ×400). Perivascular and interstitial inflammatory infiltrate with primarily neutrophilic inflammation with occasional admixed eosinophils (C, ×400). Leukocytoclasis is present (D, ×400) and definitive vessel wall damage is not observed (A–D)

Annual health care utilization and cost of granuloma annulare in the United States, 2016 to 2019: A cross-sectional study

To the Editor: Granuloma annulare (GA) is a granulomatous skin condition characterized by annular erythematous papules and plaques and/or subcutaneous nodules, which may be localized or generalized. The annual incidence in the United States is approximately 0.04%.1 GA is a heterogeneous disease, with some patients having minimal disease and some having more widespread disease; in case series, generalized GA has been reported in approximately 20% to 25% of all patients.2 Numerous treatment modalities are used; however, there is little consensus on appropriate treatment and even fewer well-controlled studies on treatment efficacy.

Reactive granulomatous dermatitis: A useful and encompassing term

Reactive granulomatous dermatitis: A useful and encompassing term

Annular elastolytic giant cell granuloma mimicking cutaneous sarcoidosis.

Annular elastolytic giant cell granuloma (AEGCG) is a benign skin disorder, with, unknown cause. It appears as erythematous papules or annular plaques. Few challenging cases of AEGCG have been reported in the literature. We describe a rare clinical presentation of AEGCG mimicking cutaneous sarcoidosis.

Erythema annulare centrifugum associated with insulin therapy: a case report

Abstract A 52‐year‐old man with type 2 diabetes presented with peripherally spreading erythematous annular eruptions around the insulin injection sites on the anterior thighs. These lesions appeared shortly after initiation of subcutaneous premix human insulin injection. On examination, two well‐defined annular erythematous plaques of size around 10cm x 5cm with a rim of trailing scale over the margin were seen over the anterior aspect of bilateral thighs. He underwent assessment for diabetic complications screening and other relevant investigations. Histopathological examination of the lesion revealed uninvolved epidermis along with classical coat sleeve appearance of perivascular lymphocytic infiltration and dermal oedema in the upper dermis, which was suggestive of a diagnosis of erythema annulare centrifugum (EAC). The lesions resolved completely in two weeks after stoppage of insulin.Insulin administration is associated with many cutaneous adverse reactions such as lipohypertrophy, lipoatrophy, oedema and allergic reactions. Allergic reactions to insulin may be localised cutaneous ones or systemic ones necessitating stoppage or change of insulin preparation. EAC is an uncommon inflammatory dermatologic condition whose exact aetiology is unknown and most probably represents delayed type hypersensitivity to various allergens. To the best of our knowledge, the association of insulin therapy induced EAC has not been previously reported in the literature. Copyright © 2022 John Wiley &amp; Sons.

A case of a delayed granulomatous reaction on the face following microneedling: A case report

Background:Microneedling is a common non-invasive procedure used for a variety of dermatologic conditions. It is associated with a low rate of adverse events which are typically temporary. Hypersensitivity reactions, including granuloma formation, are a rare adverse event, with only 10 cases previously reported.Case Summary:We report a case of a 49-year-old female who presented with asymptomatic edematous erythematous annular plaques on her left cheek following a microneedling procedure in which a Vitamin C cosmeceutical was applied to the skin beforehand. Skin biopsy confirmed non-necrotizing granulomatous dermatitis with negative tissue cultures. Systemic workup for sarcoidosis was negative.Conclusion:Delayed facial granulomatous reaction is an uncommon adverse event following microneedling. Increased risk may be related to peri-procedure use of cosmeceuticals such as Vitamin C. Given the popularity of microneedling, and that it is an unregulated procedure, it is important for dermatologists to be aware of this possible sequela in order to counsel patients appropriately and understand management options.

Exploring the association between granuloma annulare and severity of type 2 diabetes in a large administrative database

To the Editor: Granuloma annulare (GA) is a granulomatous skin condition characterized by annular erythematous plaques, diffuse papules, and subcutaneous nodules, with an annual incidence of approximately 0.04%.1 Previous studies have associated GA with type 2 diabetes mellitus (T2DM); however, little is known about whether GA is associated with more severe T2DM and whether GA presages worsening diabetic severity or complications, which could guide recommendations for ancillary testing and follow-up.

Treatment of Eosinophilic Annular Erythema: Retrospective multicenter study and literature review

BackgroundEosinophilic annular erythema (EAE) is a rare eosinophil-related skin disease which typically manifests with annular erythematous plaques and severe pruritus. Besides the diagnosis, the treatment of EAE is challenging since relevant published data are sparse. MethodsThe aim of this study was to assess the underlying diseases, treatments and outcomes of patients with EAE. To this end, we conducted a retrospective multicenter study and a systematic review of the MEDLINE database. ResultsWe included 18 patients with EAE followed in 8 centers. The MEDLINE database search yielded 37 relevant publications reporting 55 cases of EAE with 106 treatment sequences. The most common and efficient treatments included topical or systemic corticosteroids, hydroxychloroquine and dapsone. In refractory patients, a combination of systemic corticosteroids with hydroxychloroquine was associated with 88% of complete clinical response. DiscussionTo improve the management of EAE patients, we discuss the following treatment strategy: in topical steroid-resistant patients, hydroxychloroquine can be given as first-line systemic treatment. Dapsone, hydroxychloroquine or systemic corticosteroids are second-line options to consider. Last, monoclonal antibodies or JAK inhibitors targeting type 2 inflammation could represent promising last-resort options in refractory patients.

Ring within a ring appearance: A confounding manifestation of erythema annulare centrifugum

Erythema annulare centrifugum is one of the figurate erythemas which clinically presents by annular, polycylic, erythematous plaques which is characterized by scaling behind the progressing edge. It is considered to be a hypersensitivity reaction to an antigen. Various etiological factors like cutaneous or systemic infections, drugs, malignancy, pregnancy are considered. Hereby we report a case of erythema annulare centrifugum which was treated for long period of time considering to be a dermatophytosis. This report highlights the need to be vigilant for diagnosing this condition in patients presenting with erythematous annular plaques.

A Curious Case of Drug-induced Subacute Cutaneous Lupus Erythematosus.

Sir, Drugs causing drug-induced systemic lupus erythematosus (DI-SLE) are different from drugs causing drug-induced subacute cutaneous lupus erythematosus (DI-SCLE) except for tumor necrosis factor antagonists.[1] Isoniazid is known to cause DI-SLE. However, isoniazid causing DI-SCLE has been infrequently described in the literature. A 60-year-old female, a known case of tubercular osteomyelitis, presented with multiple erythematous scaly lesions over the body for the last 2 months. The patient was on antitubercular drugs HRZE (isoniazid, rifampicin, pyrazinamide, and ethambutol (HRZE) for 2 months and isoniazid, rifampicin, and ethambutol (HRE) for 2 months. The lesions developed after nearly 8 weeks of intake of HRZE. The cutaneous examination showed multiple annular erythematous scaly plaques over the face, trunk, and limbs with accentuation in the photo-exposed sites along with multiple targetoid lesions [Figure 1a and b]. The complete hemogram showed eosinophilia of 11%. The liver function test, renal function test, chest X-ray, 24-hour urine protein, and electrocardiogram (ECG) were within normal limits. Antinuclear antibody (ANA) was positive (1:90, homogenous pattern). The anti Ro/La, antihistone, anti dsDNA, antismith antibodies, and rheumatoid factor were negative.Skin biopsy revealed basal cell vacuolization, colloid bodies, pigment incontinence, infiltration of the vessel wall by inflammatory cells, and karyorrhectic debris [Figure 2a]. The patient was diagnosed as a case of SCLE and started on hydroxychloroquine 300 mg daily along with oral prednisolone 30 mg daily for 2 weeks, topical mometasone, and sunscreen; however, the lesions persisted. Because of the refractory nature of lesions, the drug was suspected as a possible trigger. As isoniazid is more commonly incriminated in systemic lupus erythematosus, isoniazid was stopped and replaced by oral levofloxacin. Rifampicin, ethambutol, and levofloxacin were continued along with levocetrizine and topical mometasone, and oral steroids were stopped. After 2 weeks of stopping isoniazid, there was a significant improvement in cutaneous lesions with complete subsidence of lesions at 4 weeks [Figure 2b]. The patient is on follow-up and has not reported any new lesions or systemic symptoms since then.Figure 1: Multiple erythematous annular scaly plaques over the gluteal area (a). Close-up photograph of the thigh showing annular scaly plaques and targetoid lesions (b)Figure 2: (a) Skin biopsy showing hyperkeratosis, parakeratoses, basal layer vacuolization, colloid bodies, and infiltration of the vessel wall by inflammatory cells. (H & E 10×). (b) Subsiding lesions over the thigh after 2 weeks of stopping isoniazidDI-LE has predominantly systemic symptoms such as fever, arthritis, and serositis, whereas LE-specific skin changes are relatively uncommon.[234] However, in DI-SCLE, there are specific cutaneous lesions and systemic features are minimal or absent. Anti-histone antibodies are frequently present in DI-LE,[3] whereas anti Ro/SSA antibodies are more frequently positive in DI-SCLE.[2] It is also important to identify and differentiate this subset of patients from idiopathic SCLE (I-SCLE) as removal of the culprit drug is the mainstay of management in DI-SCLE. DI-SCLE usually has an older age of onset than I-SCLE.[34] Latent period between exposure to the drug and the onset of symptoms is 4 to 8 weeks.[2] The disease is more widespread, and involves areas that are usually spared by I-SCLE. Bullous, erythema multiforme–like lesions, purpura, necrotic-ulcerative lesions, malar rash, and the involvement of lower legs are more common in DI-SCLE.[34] Recently, one case of isoniazid-induced SCLE was described in a HIV-positive female.[5] In our patient, temporal correlation with the intake of drugs, widespread involvement including legs, erythema multiforme–like lesions, and eosinophilia suggested drug as a possible etiology. The patient did not meet the criteria for Rowell syndrome,[6] and SLE was ruled out because of lack of systemic involvement. The mainstay of treatment is the discontinuation of the culprit drug which leads to the resolution of lesions in a period of nearly 6 to 12 weeks.[4] Other treatment modalities are topical steroids, topical tacrolimus, hydroxychloroquine, and oral steroids.[2] Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name 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.