Lichenoid Rash Research Articles

Metformin Induced Lichenoïd Drug Eruption

Cutaneous lichenoid drug eruptions are rare adverse drug reactions reminiscent of lichen planus. The most frequently reported culprit drugs are Checkpoint inhibitors, tyrosine kinase inhibitors and TNF-α inhibitors, but other drugs can also be responsible. This case-report is about a 49-year-old woman with a history of type 2 diabetes. She started taking metformin 160 weeks before the onset of a pruritic lichenoid rash on the trunk and limbs, of which the histopathology was in favor of an adverse cutaneous lichenoid drug eruption caracterized by the presence of eosinophilic polynuclei in the perivascular infiltrate. The patient benefited from oral corticosteroids with discontinuation of metformin which resulted in the resumption of the lichenoid rash.

Lichenoid and psoriasiform drug induced rush during imatinib therapy: a clinical case

Tyrosine kinase inhibitor imatinib is a standard agent for treatment of gastrointestinal stromal tumors (GIST). Treatment courses are quite long and are usually well tolerated. However, skin rash can occur on treatment, with a prevalence of 7 to 88.9%. We describe a clinical case of a patient with GIST, who has been on treatment with imatinib at daily dose of 400 mg for one year. Several weeks from the treatment initiation, she had facial edema, and 4 months thereafter psoriasiform rash appeared which was initially considered to be psoriatic. After 8 months, the patient had lichenoid rash on the inguinal skin and oral, tongue and vulvar mucosae. Clinically, the lichenoid rash was similar with lichen ruber planus. To confirm the diagnosis, we performed biopsy of psoriasiform and lichenoid foci. Histological examination verified the drug-induced rash. Topical treatment of psoriasiform rash with glucocorticosteroids resulted in regression of some plaques, although a proportion of them persisted. Inguinal and vulvar lichenoid rashes completely regressed and numbers of oral and tongue foci decreased after a 6-week daily application of the 0.1% tacrolimus cream. Treatment with imatinib 400 mg daily was not interrupted. The clinical observation illustrates the possibility of skin and mucosal lichenoid and psoriasiform rash simultaneously during treatment with imatinib and demonstrates the first successful experience in the treatment of lichenoid rashes with 0.1% tacrolimus cream.

Comparison of checkpoint inhibitor treatment-related cutaneous adverse events in racial and ethnic minority and Caucasian cohorts at Memorial Sloan Kettering Cancer Center.

2632 Background: Immune-related cutaneous adverse events (irCAEs) are the most common and often the first toxicity of immune checkpoint inhibitors (CPIs). In the general population, irCAEs occur on average within 3.6 weeks of treatment initiation and most commonly manifest as maculopapular rash, lichenoid rash, and pruritus. Less is known about these irCAEs in racial and ethnic minority patients. The purpose of this study is to compare the irCAEs of cohorts of Caucasian and racial and ethnic minority patients at Memorial Sloan Kettering Cancer Center. Methods: Herein, we conducted a retrospective chart review of racial and ethnic minority patients treated with CPIs between 2012-2019 at Memorial Sloan Kettering Cancer Center. irCAEs were graded using the Common Terminology Criteria for Adverse Events (CTCAE) v5.0. These were compared to a Caucasian cohort matched by demographics and cancer therapy regimen. Results: One hundred ten racial and ethnic minority patients presented to dermatology for irCAEs. Our population consisted of 59 (53.6%) females and 51 (46.4%) males with a mean age of 59 (range 20-85). Of the patients who were seen by dermatology, 63/110 were Asian (57.3%) followed by 34/110 African American (30.9%), and 1 Native American. Twelve patients were of Hispanic ethnicity (10.9%), which included those of both African American and Caucasian race. The 110 patients that were evaluated by dermatology had 221 cutaneous adverse events. Rash (96, 43.4%), pruritus (40, 18.1%), and xerosis (23, 10.4%) were most frequently diagnosed (average time from treatment start to presentation was 125 days). Dermatology identified 87 (39.3%) grade 1, 103 (46.6%) grade 2, 30 (13.5%) grade 3, and 1 (0.4%) grade 4 events. There were 17 (15.5%) treatment interruptions, including 7 patients who required permanent discontinuation. In the Caucasian cohort, mean time to onset was 228 days (range 1-1500). Dermatology identified 48 (43.6%) grade 1, 44 (40.0%) grade 2, 18 (16.4%) grade 3, and 0 (0.0%) grade 4 events, with maculopapular rash (55, 50.0%) and pruritus (25, 22.7%) most frequently diagnosed. Conclusions: Our findings suggest that irCAEs occur frequently in cancer patients from racial and ethnic minority groups, with similar grade and morphology as Caucasian patients. When irCAEs develop in this population, the diagnosis occurred later than what has previously been reported, possibly due to these patients seeing MSK oncologists with an established dermatology consultation system and insight into how to manage these patients on their own. Prospective evaluation of underrepresented minorities receiving CPI therapy is warranted in order to identify risk factors and therapeutic strategies for these untoward events, so that optimal cancer care may be delivered.

Photosensitive lichenoid skin reaction to capecitabine

BackgroundCapecitabine is an oral prodrug of fluorouracil, which is a common agent used in the management of many solid tumor malignancies. Dermatologic reaction is common with various chemotherapy agents but is not commonly reported in the use of capecitabine. When adverse reactions of rashes occur, the offending agent is typically removed. We report here an unusual case of photosensitive lichenoid rash due to capecitabine which is managed conservatively without major alteration in treatment.Case presentationSeventy-three year old female with a diagnosis of stage IV breast cancer undergoing management with capecitabine presents with a rash during the summer months that is biopsy proven to be lichenoid photosensitive rash with likely offending agent being capecitabine. Her treatment was initially held despite having response to treatment, started on topical steroids after evaluation by dermatology. Given her response to treatment, drug was resumed with instructions to use sun precaution, sunscreen, and to complete course of topical steroids until rash resolution.ConclusionDrug-related rashes tend to lead to disruptions or alterations in treatments of malignancies, despite responses. Given the wide use of capecitabine in many different solid tumors, it is important to recognize this photosensitive related skin rash and to initiate appropriate precautions of sun safety and topical steroids to allow minimal disruptions in therapy and continue use of capecitabine.

Imatinib mesylate-induced severe lichenoid rash

Imatinib mesylate-induced severe lichenoid rash

Dermoscopy for Discriminating Between Lichenoid Sarcoidosis and Lichen Planus

T HE LESIONS SHOWN WERE LOCATED ON the forearm of a 47-year-old man (Figure 1A), the forearm of a 51-yearold man (Figure 1B), and the trunk of a 55-year-old woman (Figure 1C), all of them presenting with a lichenoid rash. Dermoscopy revealed 2 differential patterns in these lesions: (1) reticular, white Wickham striae (WS) (Figure 2A) in the papules shown in Figure 1A and (2) round to oval, yellowbrown, homogeneous patches (YPs) (Figure 2B and C) and absence of WS in the lesions shown in Figure 1B and C. A histopathologic diagnosis of lichen planus (LP) was made in 1 patient (Figure 1A, inset), and lichenoid sarcoidosis was diagnosed in the other 2 patients (Figure 1B and C, insets). Lichenoid sarcoidosis represents 1% to 2% of cutaneous sarcoidosis cases and mimics LP. The examples illustrated herein show that dermoscopy may be useful for discriminating between the lesions of LP and those of lichenoid sarcoidosis. The absence of WS and the presence of YPs should prompt clinicians to perform a biopsy to rule out a granulomatous skin disease in clinically lichenoid lesions. Dermoscopy and diascopy of sarcoidosis lesions reveal individual yellow nodules (“grains of sand”) or a yellow-brown discoloration (“applejelly” sign). Yellow-brown homogeneous patches are not specific for sarcoidosis, but they are indicative of a granulomatous skin disease (sarcoidosis, lupus vulgaris, leishmaniasis). Conversely, dermoscopy of active LP lesions reveals the characteristic WS but not the YPs.

Drug‐induced dermatomyositis after zoledronic acid

A 57-year-old woman with prior exposure to bisphosphonates developed myalgia, proximal muscle weakness and lichenoid rash over the upper extremities and face 3 days after infusion of zoledronic acid for the management of osteoporosis. The diagnosis of dermatomyositis was made on the basis of clinical, laboratory and histological findings. This is the first report of drug-induced dermatomyositis secondary to zoledronic acid.

Constrictive Pericarditis Due to Graft-vs-Host Disease

A 29-year-old man experienced a diffuse lichenoid rash that extended to his palms (panel A) and soles, peripheral blood eosinophilia, blurry vision, and recalcitrant generalized edema 2 weeks after donor lymphocyte infusion (DLI) for relapsed T-cell acute lymphoblastic leukemia. Skin biopsy revealed vacuolar interface inflammation consistent with graft-vs-host disease (GVHD). The rash improved with topical corticosteroids; however, the edema gradually worsened during the ensuing weeks, and the patient gained 23 kg. A thorough endocrine/metabolic evaluation for causes of anasarca was unremarkable. Transthoracic echocardiography, which had been completely normal 2 weeks before DLI, revealed a thickened pericardium, paroxysmal ventricular septal motion (supplemental video online linked to this article), high medial mitral annular velocity (panel B), and phasic respiratory changes of mitral valve inflow (E wave velocity; panel C). Cardiac magnetic resonance imaging demonstrated abnormal concentric delayed pericardial enhancement (arrow, panel D). The patient's condition was unresponsive to oral colchicine of 1 month's duration. Because his symptoms attributable to constrictive pericarditis occurred in the setting of GVHD development in other organs after DLI, the patient was treated with a moderate dose of corticosteroids (prednisone, 0.5 mg/kg/d). The anasarca rapidly improved. Six weeks after initiation of prednisone and 6 months after DLI, the patient remained in remission from T-cell acute lymphoblastic leukemia. His symptoms due to chronic GVHD were manageable; however, he died of infectious complications of profound immunosuppression. Pericarditis is an uncommon manifestation of chronic GVHD,1 and, to our knowledge, has been reported after DLI only once previously.2

Fatal paraneoplastic pemphigus associated with a mediastinal tumor

Paraneoplastic pemphigus (PNP) is a rare life-threatening autoimmune bullous skin disease which is an obligate paraneoplasma. A 34-year-old woman presented with recalcitrant stomatitis and a generalized lichenoid rash. A diagnosis of PNP was established based on clinical findings, immunofluorescence, histopathology and biochemistry. A localized mediastinal mass was found with CT imaging and excised. The histologic diagnosis was dendritic cell sarcoma. Despite removal of tumor and immunosuppressive therapy, the PNP progressed rapidly and the patient died of septic multiorgan failure.

Manifestations cutanées observées au cours d’un traitement par anti-TNF alpha : 11 observations

TNFalpha blockers have recently extended the therapeutic arsenal available in dermatology. However, dermatologists must be informed of their potential adverse dermatological effects. While the chief adverse effect of TNFalpha blockers is risk of infection, cutaneous adverse effects have not yet been clearly elucidated and publications on this topic are few and far between. The aim of our study is to report various dermatological problems noted during treatment with TNFalpha blockers. This was a retrospective study of patient files. The study population comprised patients receiving TNFalpha blockers and presenting cutaneous reaction, and seen in the dermatology department between August 2001 and December 2004. Eleven patients were included. The following cutaneous reactions were seen: delayed skin rash (1 case), lupus syndrome (1 case), cutaneous vasculitis (2 cases), palmoplantar pustulosis (2 cases), psoriasis vulgaris (1 case), atopic dermatitis (1 case), lichenoid rash (1 case), purpuric capillaritis (1 case) and melanoma (1 case). The cutaneous manifestations seen represented a wide range of different clinical pictures. Dermatologists must be aware of these potential adverse effects. Future improvement of knowledge of the physiopathological mechanisms as well as the institution of prospective cohort studies should provide clearer guidance on the management of such symptoms.