“Stevens-Johnson syndrome (SJS) and toxic epidermal necros

“Stevens-Johnson syndrome (SJS) and toxic epidermal necrosis (TEN) are rare but life-threatening severe cutaneous adverse

reactions (SCARs), which are majorly (65-75%) induced by a variety of drugs. SJS/TEN could be CH5183284 recognized as SCARs or drug immune reactions, if the reactions are elicited by drugs. The recent studies suggested that SJS/TEN is a specific immune reaction initiated by the cytotoxic T lymphocytes (CTLs) via human leukocyte antigens (HLAs)-restricted pathway. The patho-mechanism involving HLA-restricted presentation of a drug or its metabolites for T-cell activation is supported by the findings of strong genetic associations with HLA alleles (e.g. HLA-B*15:02 and carbamazepine-SJS/TEN, and HLA-B*58:01 and allopurinol-SJS/TEN). However, the genetic associations of SJS/TEN or drug induced cutaneous immune reactions are complex, which are drug specific and ethnicity specific. The genetic polymorphisms and diversity of HLA alleles may provide different

binding affinities for drug antigens to launch the activation of specific find more CTLs responses, further leading to the unique clinical manifestations in SJS/TEN. Fas-FasL and perforin/granzyme B have been advocated mediating the epidermal necrosis in SJS/TEN. Our recent study showed that granulysin, a cytotoxic protein produced by CTLs or natural killer (NK) cells, is the key mediator for disseminated keratinocyte death in SJS/TEN. From the point of view of a physician, the profounder understanding of the genetic predisposition and patho-mechanism we discover, the better strategies for prevention, clinical management, and therapeutic methods of SJS/TEN we can develop in the near

Selleck AL3818 future. (C) 2012 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.”
“Purpose: We investigated the effects of clinical and laboratory properties at the time of the initial application of patients recently diagnosed and presenting metabolic indicators of diabetic ketoacidosis who were given disease prognoses in years 1 and 2 after discharge.

Materials and methods: A total of 94 patients admitted to Bakirkoy Maternity and Children’s Diseases Training and Research Hospital with diabetic ketoacidosis and recently diagnosed with type 1 diabetes mellitus were investigated. Patient files were examined within 2 years following discharge.

Findings: All 94 study patients (53.2% male and 46.8% female) presented acidosis, ketonuria and hyperglycemia. While a moderate correlation was detected between the prodromal period and HbA(1c) values in year 1, only a slight correlation was seen in HbA(1c) values in year 2. In addition, a slight correlation was observed between the prodromal period and the number of hospitalizations due to diabetic ketoacidosis in the first year. Again, while a moderate correlation was observed between HbA(1c) values and the number of hospitalizations due to diabetic ketoacidosis in year 1, only a slight correlation was seen in year 2.

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