Trimethoprim/Sulfamethoxazole-Induced Higher-Level Gait Disorder Aggrenox-Induced Stevens-Johnson Syndrome Serum Sickness–Like Reaction to Efalizumab Fluoroquinolone-Associated Achilles Tendinitis Severe Hyperglycemic, Hyperosmolar, Nonketotic Coma in a Patient Without Diabetes Receiving Aripiprazole Antidepressant-Induced Nightmares

2009 ◽  
Vol 44 (5) ◽  
pp. 379-382
Author(s):  
Joel Shuster
Keyword(s):  
Adverse Drug Reactions ◽  
Serum Sickness ◽  
Stevens Johnson Syndrome ◽  
Gait Disorder ◽  
Drug Reactions ◽  
Achilles Tendinitis ◽  
Johnson Syndrome ◽  
The Us ◽  
Hyperglycemic Hyperosmolar Nonketotic Coma

The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), discuss methods of prevention, and promote reporting of ADRs to the US Food and Drug Administration's (FDA's) MedWatch program (800-FDA-1088). If you have reported an interesting, preventable ADR to MedWatch, please consider sharing the account with our readers.

scholarly journals ISMP Adverse Drug Reactions: Influenza Vaccine–Induced Stevens-Johnson Syndrome; Vilazodone-Induced Nightmares; Dabigatran-Induced Pustular Eruptions; Neurotoxic and Cardiotoxic Symptoms After Cannabis Concentrate Exposure; Rosuvastatin-Induced Skin Eruption

2017 ◽  
Vol 53 (1) ◽  
pp. 15-17 ◽  
Author(s):  
Michael A. Mancano
Keyword(s):  
Influenza Vaccine ◽  
Skin Eruption ◽  
Adverse Drug Reactions ◽  
Stevens Johnson Syndrome ◽  
Drug Reactions ◽  
Safe Medication ◽  
Temple University ◽  
Johnson Syndrome ◽  
The Us ◽  
E Mail

The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), discuss methods of prevention, and promote reporting of ADRs to the US Food and Drug Administration’s (FDA) MedWatch program (800-FDA-1088). If you have reported an interesting, preventable ADR to MedWatch, please consider sharing the account with our readers. Write to Dr. Mancano at ISMP, 200 Lakeside Drive, Suite 200, Horsham, PA 19044 (phone: 215-707-4936; e-mail: [email protected] ). Your report will be published anonymously unless otherwise requested. This feature is provided by the Institute for Safe Medication Practices (ISMP) in cooperation with the FDA’s MedWatch program and Temple University School of Pharmacy. ISMP is an FDA MedWatch partner.

scholarly journals HLA Association with Drug-Induced Adverse Reactions

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Wen-Lang Fan ◽  
Meng-Shin Shiao ◽  
Rosaline Chung-Yee Hui ◽  
Shih-Chi Su ◽  
Chuang-Wei Wang ◽  
...  
Keyword(s):  
Adverse Drug Reactions ◽  
Antithyroid Drug ◽  
Human Leukocyte ◽  
Stevens Johnson Syndrome ◽  
Drug Reactions ◽  
Drug Induced ◽  
Hla Association ◽  
Hla Genes ◽  
Johnson Syndrome ◽  
Life Threatening

Adverse drug reactions (ADRs) remain a common and major problem in healthcare. Severe cutaneous adverse drug reactions (SCARs), such as Stevens–Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) with mortality rate ranges from 10% to more than 30%, can be life threatening. A number of recent studies demonstrated that ADRs possess strong genetic predisposition. ADRs induced by several drugs have been shown to have significant associations with specific alleles of human leukocyte antigen (HLA) genes. For example, hypersensitivity to abacavir, a drug used for treating of human immunodeficiency virus (HIV) infection, has been proposed to be associated with allele 57:01 of HLA-B gene (terms HLA-B∗57:01). The incidences of abacavir hypersensitivity are much higher in Caucasians compared to other populations due to various allele frequencies in different ethnic populations. The antithyroid drug- (ATDs- ) induced agranulocytosis are strongly associated with two alleles: HLA-B∗38:02 and HLA-DRB1∗08:03. In addition, HLA-B∗15:02 allele was reported to be related to carbamazepine-induced SJS/TEN, and HLA-B∗57:01 in abacavir hypersensitivity and flucloxacillin induced drug-induced liver injury (DILI). In this review, we summarized the alleles of HLA genes which have been proposed to have association with ADRs caused by different drugs.

Patch testing in severe cutaneous adverse drug reactions, including Stevens-Johnson syndrome and toxic epidermal necrolysis

1996 ◽  
Vol 35 (4) ◽  
pp. 234-236 ◽  
Author(s):  
Pierre Wolkenstein ◽  
Oliver Chosidow ◽  
Marie-Laure Fléchet ◽  
Odile Robbiola ◽  
Muriel Paul ◽  
...  
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Adverse Drug Reactions ◽  
Patch Testing ◽  
Stevens Johnson Syndrome ◽  
Drug Reactions ◽  
Johnson Syndrome

scholarly journals Severe Cutaneous Adverse Drug Reactions in Bangladesh: A Review in a Tertiary Level Hospital

2016 ◽  
Vol 12 (2) ◽  
pp. 71-75
Author(s):  
Md Niamul Gani Chowdhury ◽  
Mohammad Enamul Hoque ◽  
Md Abdul Latif Khan ◽  
Md Shirajul Islam Khan
Keyword(s):  
Adverse Drug Reactions ◽  
Armed Forces ◽  
Stevens Johnson Syndrome ◽  
Military Hospital ◽  
Case Report Form ◽  
Drug Reactions ◽  
Female Ratio ◽  
Medical College ◽  
Johnson Syndrome ◽  
Systemic Symptoms

Introduction: The Severe Cutaneous Adverse Drug Reactions (SCADRs) are rare but life-threatening as these encompass drug reaction with eosinophilia and systemic symptoms (DRESS), Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN) and acute generalized exanthematous pustulosis (AGEP). Objective: To estimate the incidence of SCADRs and to find out the cause in Bangladesh. Materials and Methods: 50 patients with SCADRs were studied over a period of 1 year from January 2015 to December 2015 in the Department of Dermatology, Combined Military Hospital, Dhaka. Data were collected from the informant and recorded in structured Case Report Form. Quantitative data were expressed as mean and standard deviation and qualitative data as frequency and percentage. Results: Clinical diagnosis of the study subjects recognized 46.0% cases as SJS, 28(19.0%) as TEN, 16.0% as DRESS and 10.0% as AGEP. The maximum incidence (46%) was seen in the age group of 31-50 years; mean age of the patient was 37.42+5.3 years. Male and female ratio was 2.84:1. Anticonvulsant group of drugs could give rise to maximum incidence of SCADRs. Carbamazepine was responsible in 22.0% cases of SCADRs, followed by Phenytoin in 16.0% patients and Phenobarbital in 14.0% cases. Conclusion: SCADRs were seen mostly with the anticonvulsant drugs belonging to Carbamazepine and Phenytoin group. SCADRs deserve continuous monitoring to plan preventive strategies. Journal of Armed Forces Medical College Bangladesh Vol.12(2) 2016: 71-75

scholarly journals Dermoscopic Aspects of Cutaneous Adverse Drug Reactions

2021 ◽  
pp. e2021136
Author(s):  
Gabriela Rossi ◽  
André Da Silva Cartell ◽  
Renato Marchiori Bakos
Keyword(s):  
Adverse Drug Reactions ◽  
Adverse Reactions ◽  
Stevens Johnson Syndrome ◽  
Drug Reactions ◽  
Acute Generalized Exanthematous Pustulosis ◽  
Johnson Syndrome ◽  
Vascular Structures ◽  
Systemic Symptoms ◽  
Exanthematous Pustulosis ◽  
Cutaneous Adverse Reactions

Background: Little is known about the dermoscopic evaluation of cutaneous adverse drug reactions (CADRs). Objectives: To evaluate the dermoscopic patterns of CADRs and identify those associated with severe cutaneous adverse reactions to drugs (SCARDs). Patients and Methods: Patients included in this study from May 2015 to April 2016 had presented with CADRs. CADR presentation and classification were based on standard criteria. SCARDs included Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), overlap SJS/TEN, drug reaction with eosinophilia and systemic symptoms (DRESS), and acute generalized exanthematous pustulosis (AGEP). The dermoscopic features of CADRs were described and compared according to the severity of the reactions. Results: Sixty-nine patients were included. Sixteen patients (23.2%) presented SCARDs. The main dermoscopic findings in SJS, overlap SJS/TEN and TEN were black dots or necrotic areas (100%). Erosion [respectively, 4/6 (66.7%), 3/3 (100%) and 1/1 (100%)], necrotic borders [respectively, 4/6 (66.7%), 3/3 (100%) and 1/1, (100%)] and epidermal detachment [respectively, 5/6 (83.3%); 2/3 (66.7%) and 1/1 (100%)] were also common among these reactions. Erythema and purpuric dots were the main dermoscopic findings [respectively, 5/6 (83.3%) and 4/6 (66.7%)] in DRESS. In non-severe reactions, the most prevalent structures were erythema and purpura in exanthema [respectively, 31/33 (93.9%) and 24/33 (72.7%)] and erythema and vascular structures in urticarial reactions [respectively, 6/6 (100%) and 3/6 (50%)]. Black dots or necrotic areas, epidermal detachment, necrotic borders and erosion were highly associated with SCARDs (P < 0.001). Conclusions: Dermoscopy improves clinical recognition of SCARDs.

Ciprofloxacin-Induced Bullae of the Lower Extremity: A Case of a Fixed Drug Reaction

2019 ◽  
Vol 109 (2) ◽  
pp. 155-158 ◽  
Author(s):  
Anthony J. Mollica ◽  
Albert J. Mollica ◽  
Elaine Grant ◽  
Ali Malik ◽  
Marc Claydon
Keyword(s):  
Drug Reaction ◽  
Adverse Drug Reactions ◽  
Hypersensitivity Syndrome ◽  
Stevens Johnson Syndrome ◽  
Adverse Side Effect ◽  
Drug Reactions ◽  
Johnson Syndrome ◽  
Fixed Drug ◽  
Cutaneous Drug Reactions ◽  
Exanthematous Pustulosis

Cutaneous adverse drug reactions make up 1% to 2% of all adverse drug reactions. From these adverse cutaneous drug reactions, 16% to 21% can be categorized as fixed drug reactions (FDR). Fixed drug reactions may show diverse morphology including but not limited to the following: dermatitis, Stevens-Johnson syndrome, urticaria, morbilliform exanthema, hypersensitivity syndrome, pigmentary changes, acute generalized exanthematous pustulosis, photosensitivity, and vasculitis. An FDR will occur at the same site because of repeated exposure to the offending agent, causing a corresponding immune reaction. There are many drugs that can cause an FDR, such as analgesics, antibiotics, muscle relaxants, and anticonvulsants. The antibiotic ciprofloxacin has been shown to be a cause of cutaneous adverse drug reactions; however, the fixed drug reaction bullous variant is rare. This case study was published to demonstrate a rare adverse side effect to a commonly used antibiotic in podiatric medicine.

Neutrophils initiate and exacerbate Stevens-Johnson syndrome and toxic epidermal necrolysis

2021 ◽  
Vol 13 (600) ◽  
pp. eaax2398
Author(s):  
Manao Kinoshita ◽  
Youichi Ogawa ◽  
Natsumi Hama ◽  
Inkin Ujiie ◽  
Akito Hasegawa ◽  
...  
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Toxic Epidermal Necrolysis ◽  
Adverse Drug Reactions ◽  
Cytotoxic T Cells ◽  
Formyl Peptide Receptor ◽  
Stevens Johnson Syndrome ◽  
Lipocalin 2 ◽  
Drug Reactions ◽  
Johnson Syndrome

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening mucocutaneous adverse drug reactions characterized by massive epidermal detachment. Cytotoxic T cells and associated effector molecules are known to drive SJS/TEN pathophysiology, but the contribution of innate immune responses is not well understood. We describe a mechanism by which neutrophils triggered inflammation during early phases of SJS/TEN. Skin-infiltrating CD8+ T cells produced lipocalin-2 in a drug-specific manner, which triggered the formation of neutrophil extracellular traps (NETs) in early lesional skin. Neutrophils undergoing NETosis released LL-37, an antimicrobial peptide, which induced formyl peptide receptor 1 (FPR1) expression by keratinocytes. FPR1 expression caused keratinocytes to be vulnerable to necroptosis that caused further release of LL-37 by necroptotic keratinocytes and induced FPR1 expression on surrounding keratinocytes, which likely amplified the necroptotic response. The NETs-necroptosis axis was not observed in less severe cutaneous adverse drug reactions, autoimmune diseases, or neutrophil-associated disorders, suggesting that this was a process specific to SJS/TEN. Initiation and progression of SJS/TEN keratinocyte necroptosis appear to involve a cascade of events mediated by innate and adaptive immune responses, and understanding these responses may contribute to the identification of diagnostic markers or therapeutic targets for these adverse drug reactions.

scholarly journals Immunohistopathological Findings of Severe Cutaneous Adverse Drug Reactions

2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
Mari Orime
Keyword(s):  
Adverse Drug Reactions ◽  
Clinical Manifestations ◽  
Hypersensitivity Syndrome ◽  
Conclusive Evidence ◽  
Stevens Johnson Syndrome ◽  
Drug Reactions ◽  
Drug Induced ◽  
Cutaneous Manifestations ◽  
Johnson Syndrome ◽  
Systemic Symptoms

Diagnosis of severe cutaneous adverse drug reactions should involve immunohistopathological examination, which gives insight into the pathomechanisms of these disorders. The characteristic histological findings of erythema multiforme (EM), Stevens–Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN) provide conclusive evidence demonstrating that SJS/TEN can be distinguished from EM. Established SJS/TEN shows full-thickness, extensive keratinocyte necrosis that develops into subepidermal bullae. Drug-induced hypersensitivity syndrome (DIHS) and exanthema in drug reaction with eosinophilia and systemic symptoms (DRESS) each display a variety of histopathological findings, which may partly correlate with the clinical manifestations. Although the histopathology of DRESS is nonspecific, the association of two or more of the four patterns—eczematous changes, interface dermatitis, acute generalized exanthematous pustulosis- (AGEP-) like patterns, and EM-like patterns—might appear in a single biopsy specimen, suggesting the diagnosis and severe cutaneous manifestations of DRESS. Cutaneous dendritic cells may be involved in the clinical course. AGEP typically shows spongiform superficial epidermal pustules accompanied with edema of the papillary dermis and abundant mixed perivascular infiltrates. Mutations in IL36RN may have a definite effect on pathological similarities between AGEP and generalized pustular psoriasis.

scholarly journals Association Between HLA genotypes and Oxcarbazepine-induced Cutaneous Adverse Drug Reactions: A Systematic Review and Meta-Analysis

2018 ◽  
Vol 21 (1) ◽  
pp. 1 ◽  
Author(s):  
Wimonchat Tangamornsuksan ◽  
Norman Scholfield ◽  
Manupat Lohinavy
Keyword(s):  
General Population ◽  
Adverse Drug Reactions ◽  
Meta Analysis ◽  
Maculopapular Rash ◽  
Cochrane Library ◽  
Stevens Johnson Syndrome ◽  
Drug Reactions ◽  
Johnson Syndrome ◽  
Hla Genotypes ◽  
General Populations

PURPOSE: To systematically review and quantitatively synthesize associations between HLA genotypes and oxcarbazepine-induced cutaneous adverse drug reactions (OXC-cADRs), including Stevens–Johnson syndrome (SJS) and maculopapular rash. METHODS: Studies investigating associations between HLA genotypes and OXC-cADRs were systematically searched irrespective of language, in PubMed, HuGENet (Human Genome Epidemiology Network), and the Cochrane Library from their inception until January, 2017. Inclusion criteria were studies investigating associations between HLA genotypes and OXC-cADRs that reported sufficient data for calculating the frequency of HLA genotype carriers among cases and controls. Overall odds ratios (ORs) with corresponding 95%CIs were calculated using a random-effects model to determine the association between HLA genotypes and OXC-cADRs.  RESULTS: The initial searches identified 91 articles, of which 6 studies met the selection criteria. The studies included 229 patients with OXC-cADRs, 251 OXC-tolerant patients, and 2,358 participants from general populations of Han Chinese, Korean, and Thai ethnicities.  Associations between HLA-B*1502 and OXC-induced SJS were found in both the general population [OR=30.2 (95%CI=3.45-264)] and in OXC-tolerant individuals [OR=26.4 (95%CI=7.98-87.6)]. An association between the HLA-B*1502 and OXC-induced maculopapular rash was found in the general population [OR=5.67 (95%CI=2.03-15.9)] while HLA-A*3101 also associated with OXC-induced maculopapular rash [overall OR=29.2 (95%CI=6.70-128)].  CONCLUSIONS: Strong associations between the HLA-B*1502 and OXC-cADRs (SJS and maculopapular rash) were found in both controls from general population and OXC-tolerant groups. There was also an association between HLA-B*3101 and OXC-induced maculopapular rash. For patient safety, genetic screening especially for HLA-B*1502 prior to OXC therapy at least in these closely related ethnicities is warranted. Further studies need to better define other ethnicities at risk and a wider range of MHC gene subtypes. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

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