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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3986964PMC
http://dx.doi.org/10.5505/tjh.2012.52296DOI Listing

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Carbamazepine (CBZ) causes life-threating T-cell-mediated hypersensitivity reactions, including serious cutaneous adverse reactions (SCARs) and drug-induced liver injury (CBZ-DILI). In order to evaluate shared or phenotype-specific genetic predisposing factors for CBZ hypersensitivity reactions, we performed a meta-analysis of two genomewide association studies (GWAS) on a total of 43 well-phenotyped Northern and Southern European CBZ-SCAR cases and 10,701 population controls and a GWAS on 12 CBZ-DILI cases and 8,438 ethnically matched population controls. HLA-A*31:01 was identified as the strongest genetic predisposing factor for both CBZ-SCAR (odds ratio (OR) = 8.

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A 31-year-old man had been treated with carbamazepine (CBZ) for 6 years and warfarin with bucolome for 2 years before developing hyponatremia 7 days after an injection of interferon-alpha 2b and starting oral ribavirin for chronic hepatitis C virus infection. Despite the hyponatremia, urinary osmolality exceeded plasma osmolality, and urinary excretion volume decreased markedly after water loading. Restriction of water intake and administration of dimethylchlortetracycline improved the hyponatremia, and lithium therapy maintained the normonatremia for one year.

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Although pure red cell aplasia is a well-known side effect of carbamazepine treatment, intravascular hemolytic anemia is rare. We describe a 5-year-old boy who developed concurrent intravascular hemolytic anemia and erythroblastopenia, probably due to carbamazepine. Carbamazepine treatment was subsequently discontinued, and the patient was treated with red blood cell transfusions, haptoglobin, and methylprednisolone.

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This paper presents the first case of asymptomatic IgG1 and IgG2 deficiency induced by carbamazepine (CBZ). The patient has remained asymptomatic since CBZ was started because IgM reduced only transiently, IgA decreased but remained within the normal range, and the specific antibodies to organisms having capsular polysaccharide antigens were not defective in this case. Analysis of membrane surface immunoglobulin (sIg) on B lymphocytes indicated that the maturation of B cells was defective from sIgM+ cells to sIgG+ cells.

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