Drug Induced Steven- Johnson Syndrome (SJS)

Miya, Riyaz; Malpani, Ashok Kumar; Keri, Sangamesh; Panagaon, Rohit

doi:10.5530/ijopp.12.2.28

Cited by 7 publications

(11 citation statements)

References 1 publication

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“…Adverse drug reactions (ADRs) are estimated as the fourth to sixth leading cause of death (Dormann et al, 2000;Pouyanne et al, 2000;Miya et al, 2019). While the majority are classified as type A, predictable based on drug pharmacology, the remainder are off-target type B ADRs and inclusive of T-cell-mediated delayed drug hypersensitivity reactions (DHRs).…”

Section: Introductionmentioning

confidence: 99%

“…SJS and TEN are the same disease across a spectrum of severity with the higher end of mortality (TEN) associated with up to 50% death (Patel et al, 2013;Langley et al, 2018). SJS/TEN is characterized by blistering and involvement of at least two mucous membranes (Paulmann and Mockenhaupt, 2015;Miya et al, 2019;Zimmerman and Dang, 2020). Despite clinical distinction, lack of mechanistic delineation has precluded development of disease-specific treatment and prevention strategies (Pavlos et al, 2015;Redwood et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

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Genomic Risk Factors Driving Immune-Mediated Delayed Drug Hypersensitivity Reactions

Deshpande

Hertzman

et al. 2021

Front. Genet.

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Adverse drug reactions (ADRs) remain associated with significant mortality. Delayed hypersensitivity reactions (DHRs) that occur greater than 6 h following drug administration are T-cell mediated with many severe DHRs now associated with human leukocyte antigen (HLA) risk alleles, opening pathways for clinical prediction and prevention. However, incomplete negative predictive value (NPV), low positive predictive value (PPV), and a large number needed to test (NNT) to prevent one case have practically prevented large-scale and cost-effective screening implementation. Additional factors outside of HLA contributing to risk of severe T-cell-mediated DHRs include variation in drug metabolism, T-cell receptor (TCR) specificity, and, most recently, HLA-presented immunopeptidome-processing efficiencies via endoplasmic reticulum aminopeptidase (ERAP). Active research continues toward identification of other highly polymorphic factors likely to impose risk. These include those previously associated with T-cell-mediated HLA-associated infectious or auto-immune disease such as Killer cell immunoglobulin-like receptors (KIR), epistatically linked with HLA class I to regulate NK- and T-cell-mediated cytotoxic degranulation, and co-inhibitory signaling pathways for which therapeutic blockade in cancer immunotherapy is now associated with an increased incidence of DHRs. As such, the field now recognizes that susceptibility is not simply a static product of genetics but that individuals may experience dynamic risk, skewed toward immune activation through therapeutic interventions and epigenetic modifications driven by ecological exposures. This review provides an updated overview of current and proposed genetic factors thought to predispose risk for severe T-cell-mediated DHRs.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Genomic Risk Factors Driving Immune-Mediated Delayed Drug Hypersensitivity Reactions

Deshpande

Hertzman

et al. 2021

Front. Genet.

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“…Chloroquine is also a commonly prescribed drug for malaria, rheumatoid arthritis, and amoebic liver abscess. Both the drugs are considered as comparatively safer, but undesirable, untoward adverse effects mainly cutaneous hypersensitivity reactions have been reported in only few instances due to these drugs [3,4].…”

Section: Introductionmentioning

confidence: 99%

Stevens-Johnson Syndrome Due to Adverse Drug Reactions: A Case Series

Ansari

Srivastava

Rohatgi

2021

Asian J Pharm Clin Res

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Stevens-Johnson syndrome (SJS) is a rare, serious disorder affecting skin and mucous membranes. It is one of the few serious dermatological adverse effects of drugs encountered in clinical practice which is characterized by blisters and rash on skin, mucous membranes, swelling over face and lips, and hyperpigmentation. After that, the outer layer of affected skin becomes dead, sheds, and starts to heal after several days of inflicting injury. Here, we present a case series of ofloxacin and chloroquine induced SJS after the consent given by patients. First case is a 62 years old male received Ofloxacin and second patient is a 40 years old male received chloroquine. Both patients experienced a severe skin reaction which was diagnosed as SJS. The above-mentioned medications will be implicated in cases of SJS. We should prescribe these medications with extreme caution.

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“…It accounts 6% of the total hospital admission and it leads to the economic burden to patient and health care system. 1 Among the various ADR cutaneous drug reactions mainly Stevens Johnson syndrome (SJS) is a rare immune-mediated adverse reaction it is the result of extensive death of keratinocytes, which leads to the separation of areas of skin in the dermal-epidermal junction. The incidence rate of SJS is 0.05 to 2 persons per million populations per year.…”

Section: Introductionmentioning

confidence: 99%

“…2 The most common drugs which cause SJS are sulphonamides, non-steroidal anti-inflammatory drugs, imidazole antifungal, cephalosporins, anticonvulsants, allopurinol, broad-spectrum bactericidal agents and highly active antiretroviral therapy highly active antiretroviral therapy (HAART) regimen. 3 Sulfadiazine is the antibiotic it is mainly used in combination with pyrimethamine to treat the toxoplasmosis it inhibits the tetrahydrofolic acid formation from para-amino benzoic acid, preventing the formation of folic acid in bacterial cell. It mainly acts on the gram-positive bacteria.…”

Section: Introductionmentioning

confidence: 99%

Sulfadiazine induced Stevens Johnson syndrome in toxoplasmosis patient: a case report

Raju

Shashidharan

Kurian

et al. 2020

Int J Basic Clin Pharmacol

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Stevens johnson syndrome is an acute, self-limited disease, presenting as severe mucosal erosions with widespread erythematous, cutaneous macules or atypical targets. Even though sulfadiazine has been mainly associated with haematological-related adverse effects, sulfadiazine induced skin necrosis has received less attention or went unrecognized. Here is a 29-year- old Indian male received T. Sulfadiazine 500mg 1-1-1-1 and experienced a severe skin reaction which was diagnosed as stevens johnson syndrome (SJS). The above drug will be implicated in cases of stevens johnson syndrome (SJS)/toxic epidermal necrosis (TEN). There are few case reports of that have been associated with stevens johnson syndrome (SJS)/toxic epidermal necrosis (TEN). We hope that this case report creates awareness to the health care professionals. Clinicians must be aware of these adverse reactions and advise their patients to contact them as soon as they observe any unexpected clinical response. Early diagnosis helps the clinician to elude secondary infection and subsequent complications. The offending drug should be discontinued and never be rechallenged.

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Drug Induced Steven- Johnson Syndrome (SJS)

Cited by 7 publications

References 1 publication

Genomic Risk Factors Driving Immune-Mediated Delayed Drug Hypersensitivity Reactions

Genomic Risk Factors Driving Immune-Mediated Delayed Drug Hypersensitivity Reactions

Stevens-Johnson Syndrome Due to Adverse Drug Reactions: A Case Series

Sulfadiazine induced Stevens Johnson syndrome in toxoplasmosis patient: a case report

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