[Neuroleptic malignant syndrome: case report with recurrence associated with the use of olanzapine]. / Síndrome neuroléptica maligna. Relato de caso com recorrência associada ao uso de olanzapina.

The neuroleptic malignant syndrome (NMS) consists in an idiosyncratic reaction to neuroleptic drugs, probably related to a blockage of dopamine receptors in basal ganglia. Research criteria for diagnosing NMS from DSM-IV require severe rigidity and fever accompanied by 2 of 10 minor features including diaphoresis, dysphagia, tremor, incontinence, altered mentation, mutism, tachycardia, elevated or labile blood pressure, leukocytosis and elevation of creatine phosphokinase. From a clinical point of view, the NMS may range a large spectrum of presentations. Haloperidol is the most frequent drug associated with this syndrome. We report the case of a 30 year-old man who developed NMS at two different occasions, the first related to haloperidol and chlorpromazine and the second related to olanzapine, to our knowledge without previous mention in the indexed literature.

Can the fast bone loss in osteoporotic and osteopenic patients be stopped with active vitamin D metabolites?

The aim of this study was to evaluate whether fast trabecular bone loss in osteoporotic and osteopenic patients can effectively be treated with active vitamin D metabolites. Thirty-one osteoporotic and osteopenic patients were monitored between 4 and 22 months before and between 8 and 18 months during the treatment. Fast bone losers were designated as osteoporotic or osteopenic patients with a loss of trabecular bone density in the radius of 3% or more calculated for 1 year. For this differentiation, the high precise peripheral quantitative computed tomography system (DENSISCAN 1000) was used (reproducibility 0.3% in mixed collectives). The pretreatment loss and the "gain" under treatment with active vitamin D metabolites was calculated for 1 year. The treatment consisted of either 0.5 micro;g calcitriol daily or 1 micro;g of alfacalcidol daily. Before treatment, the trabecular bone loss in the radius/year was -6.6 +/- 0.5% (mean +/- SEM). After treatment with vitamin D metabolites, the trabecular bone gain in the radius/year was 0.01 +/- 0.6% (mean +/- SEM). The difference was highly significant (P < 0.001). In contrast to this, the loss of cortical bone density before treatment was -1.8 +/- 0.3% (mean +/- SEM) and the reduced loss after treatment -0.2 +/- 0.4% (mean +/- SEM), both values calculated for 1 year. This difference was less significant (P < 0. 05). This study shows that the treatment with active vitamin D metabolites is very effective in slowing fast trabecular bone loss in osteoporotic and osteopenic patients.