Toxic epidermal necrolysis in patient with malignant astrocytoma.

UNLABELLED: Toxic epidermal necrolysis (TEN) is a severe, life-threatening mucocutaneus adverse reaction, most commonly triggered by medication. Treatment in some aspects is still controversial. CASE REPORT: Patient with malignant astrocytoma, treated with palliative radiotherapy, developed massive erythema with bullae. Patient suffered from tumor-related epilepsy, treated pharmacologically with carbamazepine. After dermatological consultation TEN was diagnosed. The bacterial growth tests from blood were Staphylococci positive. An antibiotic therapy was performed and carbamazepine was withdrawn. Cyclosporine was administered. After 2 weeks of treatment, skin changes vanished and patient's condition improved. TEN could not be omitted in diagnosis of extensive skin changes because the causative drug removal is crucial for survival and pharmacological treatment varies in similar conditions. TEN as a drug-related disease more likely occurs in severely ill patients.

Effects of genetic polymorphisms of glutathione S-transferase genes (GSTM1, GSTT1, GSTP1) on the risk of diabetic nephropathy: a meta-analysis.

INTRODUCTION: Glutathione S-transferases (GSTs) belong to a family of ubiquitous and multifunctional enzymes that protect the cells against oxidative stress. OBJECTIVES: The aim of the study was to evaluate the association between the polymorphisms of glutathione-S-transferase (GST) genes and diabetic nephropathy (DN). PATIENTS AND METHODS: PubMed, EMBASE, and Google Scholar databases were systematically searched to identify relevant studies. The odds ratio (OR) for the association was determined using a fixed or random effects model. Tests for heterogeneity of the results and sensitivity analyses were performed. RESULTS: A total of 9 publications (874 patients in the study group, 966 controls) were included. With the exception of 1 study, GSTT1 and GSTM1 genotypes were not assessed by methods that measure a gene copy number. A significantly increased risk of DN was found for the GSTM1(-) genotype (OR, 1.27; 95% CI, 1.02-1.58) and the combination of GSTT1(-)/GSTM1(-) (OR,2.02; 95% CI, 1.22-3.36). We did not observe a correlation between DN and the GSTT1(-) genotype or the presence of Val alleles. In a subgroup analysis, an association between DN and the GSTM1(-) genotype was significant in Asians but not in Caucasians. CONCLUSIONS: Our results indicate that the GSTM1(-) genotype and the combination of GSTT1(-)/GSTM1(-) increase the risk of DN. The combination of the GST polymorphisms rather than individual polymorphismshould be investigated. Genotyping allowing a trimodular determination of the GST copy number variations may better describe an association between the risk of disease and a given genotype.