Toxic epidermal necrolysis and Stevens-Johnson syndrome after COVID-19 infection and vaccination.

Stevens-Johnson Syndrome (SJS) is a rare but severe skin reaction characterized by blistering and peeling of the skin and ulcerations of mucous membranes; toxic epidermal necrolysis (TEN) is a subset of SJS characterized by the involvement of >30% of the skin. Though previously associated with drugs and infections, discussions on the association between TEN/SJS and COVID-19 have been limited. We present a review of TEN/SJS after COVID-19 infection and vaccination.

Bullous pemphigoid in a patient with a neuropsychological disorder and a possible novel drug trigger: A case report and review of the literature.

A 59-year-old woman with schizoaffective disorder presented with an itchy, blistering generalised rash. One month prior, she had started empagliflozin, a sodium glucose transporter-2 (SGLT-2) inhibitor, used in type-2-diabetes. She was already established on paliperidone, an atypical antipsychotic, for 1 year.

[Interpretation of 2021 French Guidelines for the Therapeutic Management of Bullous Pemphigoid].

Bullous pemphigoid (BP) is a common autoimmune subepidermal bullous disease.The diagnosis of BP relies on clinical manifestation,histopathology,direct and indirect immunofluorescence,and serological assay.In the past two decades,topical corticosteroids and systemic and/or topical corticosteroids were the major therapeutic options for localized/mild/moderate and extensive/severe BP,respectively.

Case of bullous pemphigoid refractory to corticosteroids by antiepileptic drug-induced CYP3A4.

The most common treatment option for patients with bullous pemphigoid is systemic corticosteroids. CYP3A4, a drug-metabolizing enzyme in the liver, metabolizes synthetic steroids to a varying degree. Although there are many CYP3A4-inducing drugs, several antiepileptic drugs, such as phenytoin and phenobarbital, strongly induce CYP3A4, thereby reducing the effects of corticosteroids.

A Case of Drug-Induced Stevens-Johnson Syndrome.

Introduction: Stevens-Johnson syndrome is a rare but consequential and often life-threatening disorder that is most often drug-induced.

Case Presentation: An 81-year-old Black man presented with 5 days of dysphagia, odynophagia, and rash. He said he had begun a course of trimethoprim-sulfamethoxazole 6 days prior for a presumed urinary tract infection.

Diagnostic and therapeutic dilemma in Stevens-Johnson syndrome-like acute graft-versus-host disease after liver transplantation: A case report.

Background: Acute graft-versus-host disease (aGVHD) is a severe and fatal complication after orthotopic liver transplantation (OLT). Clinical manifestations of severe aGVHD can resemble drug-induced Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN), and there are also various medications, such as antibiotics and immunosuppressants, used after transplantation, causing a diagnostic dilemma. Furthermore, there have been no standardized diagnostic and therapeutic strategies for OLT-aGVHD due to its rarity.

Drugs and the skin: A concise review of cutaneous adverse drug reactions.

Drug-induced skin disease or cutaneous adverse drug reactions (CADRs) are terms that encompass the clinical manifestations of the skin, mucosae and adnexa induced by a drug or its metabolites. The skin is the organ most frequently affected by drug reactions, which may affect up to 10% of hospitalized patients and occur in 1-3% of multimedicated patients. Most CADRs are mild or self-resolving conditions; however, 2-6.

Leukocytoclastic vasculitis in association with linear epidermal basement membrane zone immunoglobulin deposition: Linear vasculitis.

Cutaneous leukocytoclastic vasculitis (LCV) has a distinctive clinical and light microscopic presentation; however, the etiologic basis of LCV is varied. Most cases are attributable to immune complex deposition within a vessel wall and represent an Arthus type III immune complex reaction. The prototypic immunoreactant profile is characterized by granular deposits of components of complement activation in concert with immunoglobulin within the cutaneous vasculature.

DPP4 Inhibitor-Induced Bullous Pemphigoid in Patients with Diabetes and Chronic Kidney Disease: Clinical Case Series.

Introduction: Dipeptidyl peptidase-4 (DPP4) inhibitors (gliptins) are commonly prescribed for glucose control in patients with advanced chronic kidney disease (CKD) in whom other oral glucose-lowering agents are contraindicated. In the past few years, new reports of drug-induced bullous pemphigoid associated with DPP4 inhibitors have emerged. However, there is not enough information about the renal function of the patients with DPP4 inhibitor-induced bullous pemphigoid, and it remains unknown whether the risk of this complication is increased among patients with CKD.

Stevens-Johnson syndrome in children.

Purpose Of Review: The concept of Stevens-Johnson syndrome (SJS) in children is evolving. This manuscript reviews recent advances with the lens of new terminology namely infection-triggered reactive infectious mucocutaneous eruption and drug-induced epidermal necrolysis, with the objective of integrating this novel terminology practically.

Recent Findings: Traditionally considered to exist on a spectrum with toxic epidermal necrolysis, SJS in children is more often caused or triggered by infections instead of medications.

[A CASE OF STEVENS-JOHNSON SYNDROME SUSPECTED BY A COMMON COLD MEDICATION AS CAUSE].

We describe here the case of a 7-year-old male patient with Stevens-Johnson syndrome (SJS), which was suspected to be caused by treatment with tipepidine hibenzate (Asverin). The day after taking tipepidine hibenzate and L-carbocysteine (Carbocysteine DS) for relief of a cold, he began presenting with the following symptoms: fever above 38°C, wheezing, and decreased oxygen saturation. Two days later, mucous membrane rashes, such as erosions on the lips, eye mucosa, vulva, and blisters on the trunk appeared, and SJS was thus diagnosed.

Management of Drug-Induced Epidermal Necrolysis (DEN) in Pediatric Patients: Moving from Drug-Induced Stevens-Johnson Syndrome, Overlap and Toxic Epidermal Necrolysis to a Single Unifying Diagnosis of DEN.

Pediatric Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but life-threating blistering diseases triggered by medications that affect the skin and mucosae. Drug-induced epidermal necrolysis is a better term for medication-triggered cases because there is a spectrum of disease severity that otherwise is divided into the separate entities of SJS, overlap SJS/TEN, and TEN. This manuscript reviews the management of drug-induced epidermal necrolysis (DEN), including diagnosis, investigations to exclude differential diagnoses, and treatment.

Carbamazepine-modified HLA-A*24:02-bound peptidome: Implication of CORO1A in skin rash.

Background: Previous studies have demonstrated that human leukocyte antigen (HLA)-A*24:02 is a common genetic risk factor for antiepileptic drug-induced skin rash, while HLA-B*15:02 is a specific risk factor for carbamazepine (CBZ)-induced Stevens Johnson syndrome and toxin epidermal necrolysis. The HLA-B*15:02 allele can alter the repertoire of endogenous peptides to trigger CBZ-induced hypersensitivity. However, it is uncertain whether HLA-A*24:02 could produce alterations in the peptide repertoire during treatment with antiepileptic drugs.

Stevens-Johnson syndrome precipitated by Moderna Inc. COVID-19 vaccine: a case-based review of literature comparing vaccine and drug-induced Stevens-Johnson syndrome/toxic epidermal necrolysis.

The Moderna COVID-19 vaccination was approved for use in the United States in December of 2020 and since that time massive public health efforts have been made to vaccinate patients against the COVID-19 infection. Adverse reactions from the vaccination are well-reported and include both local skin reactions, such as pain, swelling, and erythema at the injection site, as well as systemic reactions including fever, malaise, headache, muscle aches, drowsiness, nausea, and vomiting. While severe serious cutaneous adverse reactions, such as Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN), remain rare; two cases of SJS/TEN related to COVID-19 vaccination have been reported.

Undiagnosed and Rare Diseases in Critical Care: Severe Mucocutaneous Medication Reactions.

There have been major advances in the understanding of severe cutaneous adverse reactions (SCARs). Early recognition and withdrawal of culprit medications can decrease morbidity and mortality significantly. SCARs encompass a variety of entities that present with extensive mucocutaneous involvement and systemic symptoms, often requiring management in an intensive care setting.

Pearls for the diagnosis and possible pathophysiological mechanisms of valproic acid-induced lupus erythematosus: A literature review.

Drug-induced lupus erythematosus (DILE) accounts for 10-15% of systemic lupus erythematosus (SLE) cases, with more than 100 pharmaceutical agents implicated in its development. Depending on the offending drug, clinical and serological manifestations present great variability and, thus, DILE may be overlooked in clinical practice. Valproic acid (VPA) - induced lupus erythematosus has not been analytically reported in the literature, rendering the recognition of such cases even more difficult.

Drug induced cicatrizing conjunctivitis: A case series with review of etiopathogenesis, diagnosis and management.

Drug induced cicatrizing conjunctivitis (DICC) is defined as a disease in which conjunctival cicatrization develops as a response to the chronic use of inciting topical and, rarely, systemic medications. DICC accounts for up to one third of cases of pseudopemphigoid, a large group of cicatrizing conjunctival diseases sharing similar clinical features to those of mucous membrane pemphigoid (MMP) but generally without the morbidity of progressive scarring or the need for systemic immunosuppression. The preservatives in topical anti-glaucoma medications (AGM) are the most frequently implicated inciting causes of DICC although topical antivirals, vasoconstrictors and mydriatics and some systemic drugs have been implicated.

Gliptin-associated bullous pemphigoid shows peculiar features of anti-BP180 and -BP230 humoral response: Results of a multicenter study.

Background: Recently, several case-control studies demonstrated an association between gliptins and bullous pemphigoid (BP) occurrence. However, data on the clinical and immunologic features of gliptin-associated bullous pemphigoid (GABP) are controversial.

Objective: This study aimed to clinically and immunologically characterize a large cohort of GABP patients to get an insight into the pathophysiology of this emerging drug-induced variant of BP.

Drug allergy and non-HIV immune reconstitution inflammatory syndrome.

Non-HIV immune reconstitution inflammatory syndrome (non-HIV IRIS) is associated with the recovery from an immunocompromised condition. It is defined as inflammatory disorders caused by antigens, including drugs or pathogenic microorganisms present prior to immune recovery, or by the exacerbation of an inflammatory disorder that was already present. Drug-induced hypersensitivity syndrome is a prototype of IRIS, and the pathophysiology of non-HIV IRIS can be recognized in several disorders treated with corticosteroids, immunosuppressants, molecular-targeted drugs, TNF-α antibody drugs, immune checkpoint inhibitors, and dipeptidyl peptidase-4 inhibitors.