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Background: Topiramate is an anticonvulsant from sulfamate-substituted monosaccharides that is increasingly used to treat migraines. Serious topiramate intoxications have been described. Unfortunately, indications for and the effect of interventions, including hemodialysis, in severe intoxications seem expert-based and lack empirical evidence. We aim to review the literature on topiramate intoxication cases and to describe the first topiramate intoxication with toxicokinetic data following treatment with hemodialysis. Methods: A literature review was conducted using the PubMed database. Included articles were reviewed for symptoms; management, including acute hemodialysis; toxicokinetic data; and outcomes. Results: We found 61 hits in the PubMed database and checked 392 references in the snowball search; 22 were included for data extraction, reporting 29 cases. The majority of the patients were female (n = 23/29, 79%), ranging in age from 2 to 44 years (median 21). The ingested topiramate amount ranged from 175 to 40,000 mg (usual maintenance dose of 50 mg BID and a general maximum of 500 mg BID). Topiramate concentrations were reported in eight cases, ranging from 3.7 to 356.6 mg/L (for reference, the therapeutic range is 2–30 mg/L). Serious topiramate intoxications can result in seizures, coma, hemodynamic instability and severe metabolic acidosis. In no single case was hemodialysis used. Conclusion: Serious symptoms of topiramate intoxications exist, and hemodialysis is used infrequently. If symptoms are refractory to symptomatic treatment, hemodialysis can reduce topiramate concentrations and symptomatology.

Item does not contain fulltext Phenotypic characterization of T and B lymphocytes allows the discrimination of functionally different subsets. Here, we questioned whether changes in peripheral lymphocyte subset distribution reflect specific clinical and histopathological entities after renal transplantation. Sixty-five renal transplant recipients with either histologically proven (sub)clinical acute rejection or chronic allograft dysfunction, or without abnormalities were studied for their peripheral lymphocyte subset composition and compared with 15 healthy control individuals. Naive, memory and effector CD8(+) T-cell counts were measured by staining for CD27, CD28 and CD45RO/RA. In addition, we studied the CD25(+) CD4(+) T-cell population for its composition regarding regulatory Foxp3(+) CD45RO(+) CD127(-) cells and activated CD45RO(+) CD127(+) cells. Naive, non-switched and switched memory B cells were defined by staining for IgD and CD27. We found a severe decrease in circulating effector-type CD8(+) T cells in recipients with chronic allograft dysfunction at 5 years after transplantation. Percentages of circulating CD25(+) CD127(low) CD4(+) regulatory T cells after transplantation were reduced, but we could not detect any change in the percentage of CD127(+) CD45RO(+) CD4(+) activated T cells in patients at any time or condition after renal transplantation. Regardless of clinical events, all renal transplant recipients showed decreased total B-cell counts and a more differentiated circulating B-cell pool than healthy individuals. The changes in lymphocyte subset distribution probably reflect the chronic antigenic stimulation that occurs in these transplant recipients. To determine the usefulness of lymphocyte subset-typing in clinical practice, large cohort studies are necessary. 01 juni 2012 10 p.