Drug-induced Pemphigus Research Articles

Case of drug-induced pemphigus: difficulties of diagnosis

Case of drug-induced pemphigus: difficulties of diagnosis

TZANCK SMEAR: A USEFUL DIAGNOSTIC TOOL IN SPECTRUM OF VESICULOBULLOUS DISEASES OF SKIN.

Introduction: The pemphigus group of autoimmune bullous disorders and mucocutaneous herpesvirus infections are generally diagnosed with the Tzanck smear. Only a few research have looked into its diagnostic value in the literature. To evaluate tzanck smear ndings in patients Objectives: with vesiculobullous skin lesions and histopathological correlation. All recei Material and Methods: ved Samples received between 01/08/2021 to 31/01/2022 were stained with May-Grunwald-Giemsa. In some patients, methylene blue staining and ZN staining were done. Tzanck Results: smear was performed on a total of 25 patients with skin lesions. The sensitivities of multinucleated giant cells and acantholytic cells in herpetic infections, dyskeratotic acantholytic cells,inammatory cells and cocci in bullous impetigo, acantholytic cells with neutrophils and lymphocytes in pemphigus foliaceous, acantholytic cells and plenty of neutrophils in drug-induced pemphigus, no acantholytic cells with neutrophils and lymphocytes in IgA pemphigus, cluster of acantholytic cells in pemphigus vulgaris, only lymphocytes with no acantholytic cells in bullous pemphigoid and dyskeratotic acantholytic cells without inammation in staphylococcal scalded skin syndrome, intracytoplasmic HendersonPatterson bodies and anucleated squamous cells in molluscum contagiosum and broblast, leucocytes with necrotic basal cells in Toxic epidermal necrolysis. The tzanck smear test is an inexpensive, useful, quick, reliable Conclusion: and an easy diagnostic tool for certain vesiculobullous skin diseases.

Experience in the diagnosis and treatment of a drug-induced pemphigus.

Drug-induced pemphigus (DIP) is a special type of pemphigus, and its pathogenesis, characteristics of treatment, and prognosis are closely related to the inducing drugs. This article reports the diagnosis and treatment of DIP (pemphigus vulgaris) caused by the administration of rifampin to a patient with tuberculosis. Combined with the literature, we discussed the types, pathogenesis, differential diagnosis, and treatment principles of DIP. We propose that in the oral clinical practice for patients with pemphigus vulgaris, the importance of investigating suspected drugs that induce DIP should be emphasized.

Pemphigus végétant

Intraepithelial autoimmune blistering dermatoses are a rare group of skin disorders characterized by the intraepithelial disruption of intercellular connections through the action of autoantibodies. The first article in this continuing medical education series explores the background, epidemiology, clinical features, and diagnostic criteria of each of the major intraepithelial autoimmune blistering dermatoses, including pemphigus foliaceus, pemphigus erythematosus, pemphigus herpetiformis, fogo selvagem, pemphigus vulgaris, pemphigus vegetans, drug-induced pemphigus, IgA pemphigus, IgG/IgA pemphigus, and paraneoplastic pemphigus/paraneoplastic autoimmune multiorgan syndrome.

A review and guide to drug-associated oral adverse effects-Oral mucosal and lichenoid reactions. Part 2.

Dental practitioners and other health professionals commonly encounter and manage adverse medicine effects that manifest in the orofacial region. Numerous medicines are associated with a variety of oral adverse effects. However, due to lack of awareness and training, these side effects are not always associated with medicine use and are underreported to pharmacovigilance agencies by dentists and other health professionals. This article aims to inform health professionals about the various oral adverse effects that can occur and the most commonly implicated drugs to improve the management, recognition and reporting of adverse drug effects. This article follows on from Part 1; however, the focus here is on lichenoid reactions and oral mucosal disorders including oral aphthous-like ulceration, mucositis and bullous disorders such as drug-induced pemphigus, pemphigoid, Stevens-Johnson syndrome and toxic epidermal necrolysis.

Efficacy of combined lymphoplasma exchange for the treatment of severe refractory immune-related skin diseases: a clinical observation

Objective To evaluate the clinical efficacy of lymphoplasma exchange (LPE) for the treatment of severe refractory immune-related skin diseases. Methods From May 2013 to October 2015, 8 patients with toxic epidermal necrolysis, drug-induced hypersensitivity syndrome (DIHS) , pemphigus vulgaris, pemphigoid or paraneoplastic pemphigus were enrolled from Department of Dermatology, Xiangya Hospital, Central South University, who showed no response to conventional therapy or presented with multiple organ dysfunction. After the treatment with LPE, the efficacy was evaluated, and adverse reactions were observed. Results After one session of LPE therapy, 6 patients received marked improvement, and were cured at last. In 1 patient with pemphigus vulgaris who was resistant to the treatment with high doses of glucocorticoids and immunosuppressive agents, the rashes regressed during the treatment with LPE, but recurred after the end of treatment. One patient with bullous pemphigoid presented with eruptive blisters on the next day after the treatment with LPE, which were considered as allergic reactions to allogeneic plasma. There were no obvious differences in white blood cell count, lymphocyte count, neutrophil count and blood platelet count in the peripheral blood of 8 patients before and after the treatment with LPE. During the follow-up of 3-5 years, all of the patients were recovered without recurrence, except 1 patient with bullous pemphigoid who died of disseminated tuberculosis after 1 year. Conclusion LPE is effective for the treatment of severe immune-related skin diseases, but attention should be paid to potential transfusion reaction and allergic reactions. Key words: Plasma exchange; Epidermal necrolysis, toxic; Pemphigus; Pemphigoid, bullous; Drug reaction with eosinophilia and systemic symptoms; Paraneoplastic pemphigus

Therapeutic Apheresis in Dermatological Diseases

Since the mid-1970s, membrane modules became available and plasma separation techniques have gained importance. Therapeutic apheresis (TA) has been successfully introduced in a variety of autoantibody-mediated diseases. In dermatology, TA is increasingly applied as a support treatment for severe and/or refractory autoimmune bullous diseases. All autoimmune disease are characterized by autoantibodies mediated against structural proteins of the skin and/or mucous membranes. Autoimmune blistering diseases have a high morbidity and mortality. These diseases include pemphigus vulgaris and bullous pemphigoid among others. Drug-induced pemphigus and other forms, such as dermatitis herpetiformis, herpes gestationis, scleroderma, pyoderma gangrenosum, epidermal necrolysis, Behcet disease, psoriasis vulgaris, Henoch-Schönlein purpura, and porphyria cutanea tarda, are also mentioned. Pathogenetical aspects of autoantibodies in these diseases are clearly demonstrated. TA has been shown to effectively remove the autoantibodies from blood and lead to rapid clinical improvement.

Clinical and immunological profiles in 17 Japanese patients with drug‐induced pemphigus studied at Kurume University

Drug-induced pemphigus (DIP) shows clinical, histopathological and immunological features of pemphigus. However, little is known about immunological profiles in DIP. To characterize clinical and immunological profiles in patients with DIP. We studied 17 Japanese patients with DIP who were treated at Kurume University Hospital or who consulted from other hospitals between 1997 and 2012. Complicated diseases, clinical and histopathological manifestations, responsible drugs and findings in immunofluorescence, enzyme-linked immunosorbent assays (ELISAs), immunoblotting (IB) and prognosis were analysed. Eight of the 17 patients with DIP showed pemphigus foliaceus-like appearance, three showed pemphigus herpetiformis-like appearance, and six showed atypical bullous lesions. Responsible drugs were thiol-containing drugs in 16 patients (bucillamine in nine cases, d-penicillamine in four cases, and cetapril, thiopronine and captopril in one patient each), and a nonthiol drug, sulfasalazine, in one patient. By ELISAs and/or IB analyses, nine patients reacted only with desmoglein 1 (Dsg1), four reacted with Dsg1 and Dsg3, and four showed no specific reactivity. By IB of normal human epidermal extracts, in addition to positive reactivity with Dsg1, four patients with no detectable malignancy showed paraneoplastic pemphigus-like reactivity with the 210-kDa envoplakin and the 190-kDa periplakin. Four cases showed anti-Dsg3 antibodies without mucosal lesions. While 11 cases recovered after discontinuation of the causative drugs, six patients had a very protracted or intractable disease course, and might develop true pemphigus. The present study indicated that the majority of the patients with DIP studied showed a pemphigus foliaceus-type phenotype with anti-Dsg1 autoantibodies, caused by thiol-containing drugs.

Postherpetic oral ulcers misdiagnosed as pemphigus in a patient with rheumatoid arthritis under bucillamine therapy

Autoimmune bullous disease is sometimes seen in patients with rheumatoid arthritis (RA). In addition, pemphigus can be induced by certain disease modifying anti-rheumatic drugs (DMARDs) for RA, such as thiol compounds. Antibodies against desmogleins are occasionally detected in the sera of drug-induced pemphigus patients. We herein describe a case which showed ulceration following herpes zoster in the oral cavity of a patient with RA under treatment with bucillamine. The patient was misdiagnosed with pemphigus in another clinic, because of mucous membrane lesions and positive circulating levels of anti-desmoglein-1 IgG. Clinicians should know that circulating antibodies against desmogleins can be detected, although at low titers, in the sera of patients under therapies with certain drugs.

Oral bullous eruption after taking lisinopril—case report and literature review

Drug-induced lesions of oral mucosa are well-established side effect of different commonly used drugs. A female patient under treatment for hypertension with an angiotensin-converting enzyme inhibitor (ACE inhibitor), lisinopril, developed blisters and ulcerations on oral mucosa 3 weeks after lisinopril intake. Due to clinical finding drug-induced pemphigus was considered. However, direct and indirect immunofluorescence anal-ysis revealed no autoantibodies that are commonly present in pemphigus while histological study suggested allergic reaction. Lisinopril was discontinued from further therapy and after a month after her first arrival patient has experienced complete remission of the disease. This case raises the question, whether the term pemphigus in drug-induced reactions could be used when immunopathological criteria for pemphigus are not fulfilled.

Autonomisation d’un pemphigus induit par la d-pénicillamine : évolution de l’immunomarquage par l’anticorps anti-32-2B

It has been reported that D-penicillamine causes pemphigus that is typically superficial. Immunostaining with monoclonal anti-32-2B antibody targeting desmoglein 1 and 3 can help differentiate between drug-induced and classical auto-immune pemphigus. Absence of specific staining militates in favour of drug-induced pemphigus whilst positive staining suggests an auto-immune aetiology that is ongoing despite discontinuation of drug therapy. A 59-year-old male patient was referred for management of superficial pemphigus 1 year after starting D-penicillamine treatment for scleroderma. The diagnosis of pemphigus was confirmed histologically (intra-epidermal cleavage, acantholysis and perikeratinocytes, deposition of IgG and complement C3). Immunochemical staining with anti-32-2B antibody was initially normal, in keeping with drug-induced pemphigus. Despite discontinuation of D-penicillamine, pemphigus recurred in 2008. A further skin biopsy was undertaken and anti-32-2B staining was abnormal, which is consistent with auto-immune pemphigus. Numerous cases of drug-induced pemphigus have been described in the literature. In approximately half of all cases, the pemphigus recedes after cessation of the causative drug. However, there have been no previous reports that changes over time in the immunostaining with anti-32-2B antibodies can mirror a change in form of pemphigus from a drug-induced type to an idiopathic type as well as the associated clinical feature of persistence after drug withdrawal. Normal staining with anti-32-2B antibody is associated with a favourable prognosis as regards resolution of drug-induced pemphigus. When, as in this case, status changes to abnormal staining, there is a risk that the pemphigus may become chronic despite discontinuation of therapy.

Lisinopril-Induced Pemphigus Foliaceus in a Patient with Diabetes Mellitus and Kaposi-Juliusberg Varicelliform Eruption

Abstract Drugs have often been implicated as the cause of pemphigus. Lisinopril is a drug of the angiotensin-converting enzyme inhibitor class primarily used in the treatment of hypertension, congestive heart failure, heart attacks, and also in preventing renal and retinal complications of diabetes mellitus. Various side-effects have been described in the English medical literature related to lisinopril, but only one case with pemphigus foliaceus as an adverse reaction to lisinopril. To the best of our knowledge, we present the second case of lisinopril-induced pemphigus foliaceus complicated with Kaposi-Juliusberg varicelliform eruption in a patient diabetes mellitus type II. A 60-year-old man presented with diffuse erythema on the face, trunk and extremities. Disseminated erosions, 2-5 mm in diameter, and umbilicated vesicles were present. Erosions with remnants of the blister roof were partially found on the trunk. Semiannular erosions were present. On the posterior part of the trunk (paravertebral and vertebral) there were inifiltrated, partially grouped, sharply delineated yellowish-reddish plaques, up to 2 cm in diameter. Direct and indirect immunofluorescence test as well as histological analysis revealed a drug-induced pemphigus foliaceus. After treatment of Kaposi-Juliusberg eruption and impetiginization, lisinopril was discontinued. Rapid involution of the skin lesions, was observed. Since, only minor skin lesions still persisted after 6 months of follow-up and treatment, the diagnosis of druginduced pemphigus foliaceus was established. It usually takes 1 - 6 months for angiotensin-converting enzyme inhibitors to induce pemphigus. All drugs taken by the patient, including homeopathic agents, over-the-counter drugs, and even medications that were discontinued should be taken into consideration. Medical history taking should be repeated in cases where there is no response to therapy.

Pyodermatitis-pyostomatitis vegetans: a differential diagnosis of pemphigus vegetans

reported a case of drug-induced pemphigus vegetans (PV). We congratulatethe authors on the thorough documentation of thepatient as well as on the detailed discussion of thetopic. However, we would like to emphasize theimportance of considering pyodermatitis–pyostomati-tis vegetans (PD-PSV) in the differential diagnosis ofPV, given that their clinical presentation and histologi-cal findings are similar.

Treatment of demodicosis in dogs: 2011 clinical practice guidelines

These guidelines were written by an international group of specialists with the aim to provide veterinarians with current recommendations for the diagnosis and treatment of canine demodicosis. Published studies of the various treatment options were reviewed and summarized. Where evidence in form of published studies was not available, expert consensus formed the base of the recommendations. Demodicosis can usually be diagnosed by deep skin scrapings or trichograms; in rare cases a skin biopsy may be needed for diagnosis. Immune suppression due to endoparasitism or malnutrition in young dogs and endocrine diseases, neoplasia and chemotherapy in older dogs are considered predisposing factors and should be diagnosed and treated to optimize the therapeutic outcome. Dogs with disease severity requiring parasiticidal therapy should not be bred. Secondary bacterial skin infections frequently complicate the disease and require topical and/or systemic antimicrobial therapy. There is good evidence for the efficacy of weekly amitraz rinses and daily oral macrocyclic lactones such as milbemycin oxime, ivermectin and moxidectin for the treatment of canine demodicosis. Weekly application of topical moxidectin can be useful in dogs with milder forms of the disease. There is some evidence for the efficacy of weekly or twice weekly subcutaneous or oral doramectin. Systemic macrocyclic lactones may cause neurological adverse effects in sensitive dogs, thus a gradual increase to the final therapeutic dose may be prudent (particularly in herding breeds). Treatment should be monitored with monthly skin scrapings and extended beyond clinical and microscopic cure to minimize recurrences.

Drug‐induced pemphigus after six years of treatment with phenytoin and carbamazepine

Drug‐induced pemphigus after six years of treatment with phenytoin and carbamazepine

Pemphigus Vulgaris Associated with Rheumatoid Arthritis in a Patient not Taking Penicillamine.

D-penicillamine is one of the disease-modifying anti-rheumatic drugs (DMARDs). Drug-induced pemphigus is not fre-quently associated with D-penicillamine, and to date, the number of reported cases is about a hundred. Most reports of D-penicillamine-induced pemphigus vulgaris are in patients with rheumatoid arthritis. It has rarely been reported in patients not taking D-penicillamine. We report a case of pemphigus vulgaris in a 48-year-old female patient with rheumatoid arthri-tis, not taking penicillamine.

Analysis of 6 cases of drug-induced pemphigus

To study clinical and laboratory characteristics of drug-induced pemphigus. Using direct immunofluorescence (IF), indirect IF, ELISA and immunoblotting to characterize 6 patients with drug-induced pemphigus (DIP) and compared them with 20 cases of idiopathic pemphigus. All the 6 cases of DIP showed obvious itching (100%) and no damage to the oral mucosa. Five out of 6 DIP cases (83.33%) presented as pemphigus folicaeus (PF) since they contained circulating Dsg1-specific IgG, were sensitive to low doses of glucocorticoid, and had good prognosis. One case was showed as pemphigus vulgaris (PV). Dsg1-specific IgA was positive in peripheral blood of 4 cases (66.67%), and the antibody disappeared after treatment. In patients with idiopathic pemphigus, only 6 cases (30%) had mild itching, and 12 cases (60%) had oral mucosal lesions. Twelve cases (60%) were PV with anti-Dsg1 and -Dsg3 antibodies, and 8 cases (40%) were PF with anti-Dsg1 antibody only. One case (5%) had anti-Dsg1 IgA. Drug factors should be considered for pemphigus as some common antibiotics can cause pemphigus.

Diagnosis and Clinical Features of Pemphigus Vulgaris

Autoimmune bullous diseases are associated with autoimmunity against structural components that maintain cell-cell and cell-matrix adhesion in the skin and mucous membranes. They include those where the skin blisters at the basement membrane zone and those where the skin blisters within the epidermis (pemphigus vulgaris, pemphigus foliaceus, and other subtypes of pemphigus). The variants of pemphigus are determined according to the level of intraepidermal split formation. There are 5 main variants of pemphigus: pemphigus vulgaris, pemphigus foliaceus, pemphigus erythematosus, drug-induced pemphigus, and paraneoplastic pemphigus. This review focuses only on pemphigus vulgaris.

Drug-induced pemphigus

Pemphigus is an autoimmune bullous disease that may be influenced by genetic and exogenous factors. Drugs are a leading cause of pemphigus. There is a need for a thorough history taking so as to find the culprit medication. The diagnosis of drug-induced pemphigus is challenging. Patients have often been exposed to multiple drugs, and some drugs may have a prolonged latency period between exposure and onset of the disease. The in vitro interferon-gamma (IFN-gamma) release from lymphocytes test has been shown to be of diagnostic value in drug-induced skin reactions. Cessation of the offending drug may alleviate the clinical manifestations and reduce the need for medical treatment.

A prospective analysis of anti-desmoglein antibody profiles in patients with rheumatoid arthritis treated with thiol compounds

Drug-induced pemphigus is mainly caused by drugs containing sulfhydryl (thiol) groups in their molecules. To understand the serial alteration of anti-desmoglein (Dsg) antibody profile in patients with rheumatoid arthritis (RA) receiving thiol compounds. Anti-Dsg1 or -Dsg3 antibodies were analysed twice in a 1.6-year interval, in the same series of RA patients. Eleven of 204 serum samples (5.4%) and 6 of 139 samples (4.3%) from the same RA group showed a positive reaction against Dsg1 or Dsg3 in the first and second screening tests, respectively. The positive rates were higher than those in patients with collagen diseases including systemic lupus erythematosus, Sjögren syndrome, mixed connective tissue disease, and systemic sclerosis. In comparison with the results in the first and second screening tests, one RA patient newly gained anti-Dsg3 antibody, and at least 4 patients lost the antibodies in 1.6 years. Three patients produced antibodies to Dsg1 and/or Dsg3 in a similar fashion as did in the first screening tests. Only one RA serum sample exhibited an intercellular reactivity to human skin or monkey esophagus by immunofluorescence, and another sample bound to a 130 kDa protein suggestive of Dsg3 by immunoblotting. Most anti-Dsg antibodies in RA patients recognized EDTA-resistant epitopes of Dsg different from EDTA-sensitive epitopes recognized by pemphigus sera. RA patients receiving any of the thiol compounds may gain autoantibodies to non-conformational epitopes of either Dsg1 or Dsg3, and that such autoantibodies alone are not capable of inducing acantholysis.