Disease relevance of Stevens-Johnson Syndrome

• Erythema multiforme, Stevens-Johnson syndrome, and diltiazem [1].
• Allopurinol, a commonly prescribed medication for gout and hyperuricemia, is a frequent cause of severe cutaneous adverse reactions (SCAR), which include the drug hypersensitivity syndrome, Stevens-Johnson syndrome, and toxic epidermal necrolysis [2].
• Toxic epidermal necrolysis and Stevens-Johnson syndrome are induced by soluble Fas ligand [3].
• A 22-year-old man developed acute bilateral peripheral facial paralysis in association with Stevens-Johnson syndrome, probably as a result of ampicillin allergy [4].
• Thus, treatment throughout the duration of hypersensitivity is more likely to succeed for patients receiving pyrimethamine/clindamycin, whereas therapy with pyrimethamine/sulfadiazine is associated with a high risk of Lyell's syndrome and Stevens-Johnson syndrome [5].

Psychiatry related information on Stevens-Johnson Syndrome

• The incidence of serious rash with lamotrigine treatment was 0.1% in all studies of bipolar disorder and included one case of mild Stevens-Johnson syndrome [6].

High impact information on Stevens-Johnson Syndrome

• Fansidar-induced Stevens-Johnson Syndrome [7].
• A previously healthy child who developed acute, severe, rapidly progressive vanishing bile duct syndrome shortly after Stevens-Johnson syndrome is described; this was temporally associated with ibuprofen use [8].
• Didanosine as probable cause of Stevens-Johnson syndrome [9].
• Stevens-Johnson syndrome after fluconazole [10].
• Mefloquine-induced Stevens-Johnson syndrome [11].

Chemical compound and disease context of Stevens-Johnson Syndrome

• Fatal Stevens-Johnson syndrome in a patient on captopril and allopurinol [12].
• Stevens-Johnson syndrome due to pyrimethamine/sulfadoxine during presumptive self-therapy of malaria [13].
• Stevens-Johnson syndrome due to co-trimoxazole [14].
• Medicine and the law. Risk of Stevens-Johnson syndrome due to phenobarbitone too remote to be foreseeable [15].
• Stevens-Johnson syndrome during treatment with cimetidine [16].

Biological context of Stevens-Johnson Syndrome

• We speculate that in Stevens-Johnson syndrome, epithelial hyperproliferation, and transglutaminase 1 gene expression lead to the pathological keratinization of ocular surface mucosal epithelia [17].
• A slow acetylator genotype is a risk factor for sulphonamide-induced toxic epidermal necrolysis and Stevens-Johnson syndrome [18].

Anatomical context of Stevens-Johnson Syndrome

• The number of epithelial cells in Stevens-Johnson syndrome conjunctiva that were immunoreactive with a monoclonal antibody, Ki-67, to a nuclear antigen found only in proliferating cells was greater than normal (93.8+/-19.8 cells above 100 basal cells versus 12.8+/-0.5 cells above 100 basal cells; P = 0.009) [17].
• In situ hybridization documented transglutaminase 1 (keratinocyte transglutaminase) mRNA in suprabasal cells of the abnormally thickened conjunctival epithelium in all Stevens-Johnson syndrome patients [17].
• Levofloxacin was the fluoroquinolone associated with the highest rate of serious tendon disorders; phototoxic reactions were more frequent with lomefloxacin, and toxic epidermal necrolysis and Stevens-Johnson syndrome were seen only with ciprofloxacin [19].
• In all of the cases, the first signs of Stevens-Johnson syndrome (i.e., swelling of the skin and mucous membranes or slight fever) appeared about 2 weeks after the patient started taking methazolamide (75 or 100 mg/d) [20].
• We speculate that the combination of HIV and pregnancy in addition to antibiotic treatment, such as with nitrofurantoin, may induce Stevens-Johnson syndrome in patients with severely altered immune systems [21].

Gene context of Stevens-Johnson Syndrome

• CONCLUSIONS: The infiltrating cell population in the Stevens-Johnson syndrome samples includes macrophages, CD4 positive T cells, and CD8 positive T cells [22].
• The CD40/CD40 ligand system is expressed in the cutaneous lesions of erythema multiforme and Stevens-Johnson syndrome/toxic epidermal necrolysis spectrum [23].
• Expression of K3 was negative in seven patients, but was sporadically positive in a patient with Stevens-Johnson syndrome [24].
• Stevens-Johnson syndrome in association with hydroxychloroquine treatment for rheumatoid arthritis [25].
• OBJECTIVES: This study sought to identify the risk factors associated with an outbreak of Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) among Filipino laborers in Taiwan. METHODS: Forty-six SJS/TEN patients were matched to 92 controls according to month of arrival in Taiwan, sex, and age [26].

Analytical, diagnostic and therapeutic context of Stevens-Johnson Syndrome

• Erythema multiforme and Stevens-Johnson syndrome in patients receiving cranial irradiation and phenytoin [27].
• One mild case of Stevens-Johnson syndrome not requiring hospitalization occurred in a patient treated with lamotrigine [28].
• Two cases of Stevens-Johnson syndrome: toxic epidermal necrolysis possibly induced by amifostine during radiotherapy [29].
• CONCLUSIONS: Phenytoin is associated with a myriad of side effects, including, rash, eosinophilia, panhypogammaglobulinemia, pseudolymphoma, Stevens-Johnson syndrome, immunosuppression in brain tumor patients, and rarely, pulmonary complications such as Loeffler's syndrome [30].
• We treated a 53-year-old man with advanced squamous cell carcinoma of the lung who had developed Stevens-Johnson syndrome, a life-threatening cutaneous reaction, after systemic chemotherapy consisting of carboplatin and paclitaxel [31].

References