A prospective study of serum ghrelin levels in patients treated with clozapine.

We investigated serum ghrelin levels (SGL) in 12 patients with schizophrenia over a 10-week period after initiation of clozapine treatment. In contrast to increments of body mass indices (BMI, kg/m2) and serum leptin levels (SLL), no significant change in SGL was detected. Inverse correlations between delta SGL and delta SLL did not reach statistical significance. Linear mixed model analysis could not detect effects of age, sex, BMI, SLL and serum clozapine levels on SGL. Our results do not support a causal involvement of ghrelin in clozapine-related weight gain.

Enlarged cerebrospinal fluid spaces in opiate-dependent male patients: a stereological CT study.

Computed tomography was performed in 9 male patients with a diagnosis of opiate dependence and in 9 age-matched psychiatric controls (neurotic depression). Patients with a history or diagnosis of another substance dependence (alcohol, cocaine, cannabis) were excluded from the study. The volumes of internal and external components of cerebrospinal fluid (CSF) were measured with a point-counting stereological method. Analysis of variance with age as a covariate revealed a significant enlargement of external and external CSF spaces in male patients with opiate dependence. There was no significant correlation between the length of opiate dependence and the volumes of internal and external CSF spaces. The present results suggest that opiate dependence is associated with structural brain alterations. However, the relationship between opiate dependence and structural brain changes is complex and still not well understood.

Serum leptin levels increase rapidly after initiation of clozapine therapy.

Weight gain is a major side-effect of treatment with clozapine. In order to investigate the influence of the atypical neuroleptic clozapine on leptin secretion, serum leptin levels were measured in 12 patients at baseline and for a 10-week period after initiation of treatment. Serum clozapine levels and levels of its metabolites were simultaneously assessed. Alterations of body weight and body composition were determined. During the 10-week observation period leptin levels differed significantly from the levels determined at baseline (P < 0.0001). During the first 2 weeks of treatment serum leptin levels at least doubled in eight of the 12 patients. The maximal relative increase over baseline was 536%. Low doses of clozapine were sufficient to induce this effect. Within a 10-week period mean body weight, mean body mass index, mean fat mass and mean lean body mass all increased. Based on the results we suggest that in predisposed individuals clozapine induces an increased appetite; overeating and weight gain can ensue, which in turn underlie elevated leptin secretion.

Further support for linkage of extreme obesity to the obese gene in a study group of obese children and adolescents.

The role of the obese gene in human obesity is presently unclear. Evidence for linkage of markers flanking the gene to obesity has been found in some but not all studies. We investigated transmission disequilibrium between two highly polymorphic microsatellite markers (D7S504 and D7S1875) flanking the human obese gene (OB) and extreme obesity in a study group of German children and adolescents. Due to the early onset and severity of obesity in the ob/ob mouse we hypothesized that especially children and adolescents with extreme obesity are enriched for possible mutations in the human OB. The analysis of 88 trios (index probands and both parents) for transmission disequilibrium of a haplotype which has previously been determined to be linked to extreme obesity (Reed et al., 1996) revealed a one-sided transmission disequilibrium test (TDT) p-value of 0.039. Post hoc analyses revealed one-sided TDT p-values of 0.015 for the 214 bp allele of D7S1875 (corrected p-value = 0.03) and 0.215 for the 145 bp allele of D7S504 (corrected p-value = 0.43). These findings substantiate the evidence for linkage of extreme obesity to OB.

Thallium-201/technetium-99m pyrophosphate overlap in patients with acute myocardial infarction after thrombolysis: prediction of depressed wall motion despite thallium uptake.

Intracoronary thallium-201/technetium-99m pyrophosphate planar scintigraphy was performed in 60 patients with acute myocardial infarction undergoing intracoronary thrombolysis to predict salvage of myocardium immediately after thrombolysis. In eight patients a significant overlap of new thallium uptake and technetium pyrophosphate accumulation was found after thrombolysis. Intravenous planar thallium scintigraphy revealed thallium uptake in the region of overlap in all patients; circumferential profile analysis showed no difference in the thallium scintigrams before and after technetium injections. Both findings indicate that overlap is not the result of scattering of technetium into the thallium window. Emission computed tomography revealed thallium/technetium pyrophosphate uptake in identical slices and regions. Regional wall motion in the area of overlap remained depressed in all patients, in contrast to patients with similar thallium uptake without overlap. These data suggest that thallium/technetium pyrophosphate overlap reflects the close proximity of viable and necrotic myocardial cells and predicts depressed wall motion after thrombolysis.

[Torsion of a wandering spleen]. / Torquierte Wandermilz.

The torsion of an ectopic (= wandering) spleen is a rare entity especially in children. Clinically it presents either with signs of an "acute abdomen" or as a fairly painful abdominal "tumor" of the chronic recurrent type. Ultrasonography, arteriography, and additional scintigraphy in special cases are of greatest value in the preoperative diagnostic management. Splenopexy, sometimes after resecting parts of a very enlarged organ, is the therapy of choice. The complete exstirpation of the ectopic spleen should be reserved only for exceptional cases. By presenting a case report, the etiologic factors, the clinical signs, the diagnostic steps, the differential diagnostic considerations as well as the mode of therapy for this rare disease are described and discussed.