Obstructive sleep apnea syndrome induced by clonazepam in a narcoleptic patient with REM-sleep-behavior disorder.
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Biomedical subjects
Publications and source records attributed to M Haack.
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OBJECTIVE: Leptin is produced by fat cells and is presumed to signal the size of the adipose tissue to the brain. The authors investigated whether antipsychotic drugs that often induce weight gain affect circulating levels of leptin. METHOD: Weight, body mass index, and leptin plasma level were measured weekly over 4 weeks in psychiatric inpatients who received clozapine (N = 11), olanzapine (N = 8), haloperidol (N = 13), or no psychopharmacological treatment (N = 12). RESULTS: In patients receiving clozapine or olanzapine, significant increases in weight, body mass index, and leptin level were found, whereas these measures remained stable in patients who received haloperidol or no pharmacological treatment. CONCLUSIONS: Weight gain induced by clozapine or olanzapine appears to be associated with an increase in leptin level that cannot be attributed to dietary changes upon hospitalization.
A multidisciplinary group examined the patient placement practices for two large pediatric units in an academic medical center. Hospital medical bylaws were revised and nurses now assign patient charges and transfers.
The objective of this study was to determine the feasibility and clinical impact of hepatic venous oxygenation monitoring in patients undergoing positive end-expiratory pressure (PEEP) ventilation after OLT. The design comprised a prospective study using repeated-measures design, within an intensive-care unit for liver-transplanted patients in a university hospital. Sixteen consecutive adult patients undergoing orthotopic liver transplantation were enrolled. Postoperatively, a fiber-optic pulmonary artery catheter was inserted into the right hepatic vein. Patients were submitted to controlled ventilation with three different levels of end-expiratory pressure (PEEP): 0, 5 and 10 mbar. Hemodynamics, hepatic venous pressure, mixed venous (SvO2) and hepatic venous oxygenation (SvhO2) were measured. The average time required for hepatic venous catheterization was 2.9 +/- 1.2 min; serious complications were not observed. PEEP 5 mbar did not alter hemodynamics and SvhO2; PEEP 10 mbar significantly reduced cardiac index, SvO2 and widened arteriovenous content difference (p < 0.05). The mean difference between SvO2 and SvhO2 was 6.3 +/- 6.0% and did not change during PEEP ventilation. A significantly positive relationship was observed between SvO2 and SvhO2 (r = 0.91, p < 0.05). Hepatic venous catheterization appeared to be practical and could be utilized to evaluate the effects of therapeutic interventions on the transplanted liver. However, the small number of patients studied will not allow the assessment of any risk-benefit ratio of the technique investigated. Low levels of PEEP provided hemodynamic stability and did not alter hepatic oxygen supply-demand ratio.(ABSTRACT TRUNCATED AT 250 WORDS)
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Cellular and intercellular metabolism of the developing otic capsule of the newborn hamster is investigated by means of autoradiography. The labelling patterns of periostal and endostal osteoblasts are compared with the finding on long bones. The low metabolic turnover within the cartilage before ossification and histological changes in an ossification center are discussed. The number of interglobular spaces decreases in the early phase of life and do not show activity. The globuli ossei appear to be a bony new formation. No indication for metaplastic development from the original cartilage was found. Labelling patterns appeared identical as in other developing ossicular bone. Intralacunar apposition of osteocytes was seen.
It has been known since the 1950s that phenothiazines have immunomodulatory effects. This review summarizes recent evidence suggesting that antipsychotic drugs, in particular chlorpromazine and the atypical compound clozapine, influence the production of cytokines. Cytokines, organized in networks of related peptides with pleiotropic functions, are pivotal humoral mediators of infection and inflammation, and they play an important role in hematopoiesis and autoimmunity. Therefore, the effects of antipsychotic drugs on cytokine networks are important for the understanding of immune-mediated side effects of these drugs, e.g. agranulocytosis. In addition, modulation of cytokine production by antipsychotic agents suggests that these drugs might be useful for the treatment of diseases which primarily involve the immune system. Moreover, because cytokines are known to have numerous effects on the CNS, they may mediate effects of antipsychotic drugs on brain functions. Finally, the influence of antipsychotic drugs on cytokine networks is an important confounding factor in studies investigating disease-related immunopathology in psychiatric disorders. This review provides a synopsis of the data published on these topics and outlines future research perspectives.
It has been hypothesized that the immune system plays a pathogenetic role in psychiatric disorders, in particular in major depression and schizophrenia. This hypothesis is supported by a number of reports on altered circulating levels and in vitro production of cytokines in these disorders. However, the respective evidence is not consistent. This may be in part due to an incomplete control for numerous confounding influences in earlier studies. We investigated the plasma levels of cytokines and soluble cytokine receptors in psychiatric patients (N = 361) upon hospital admission and compared the results to those obtained in healthy controls (N = 64). By multiple regression analysis we found that circulating levels of interleukin-1 receptor antagonist (IL-1Ra), soluble IL-2 receptor (sIL-2R), tumor necrosis factor-alpha (TNF-alpha), soluble TNF receptors (sTNF-R p55, sTNF-R p75) and IL-6 were significantly affected by age, the body mass index (BMI), gender, smoking habits, ongoing or recent infectious diseases, or prior medication. Cytokine or cytokine receptor levels were significantly increased in patients treated with clozapine (sIL-2R, sTNF-R p75), lithium (TNF-alpha, sTNF-R p75, IL-6) or benzodiazepines (TNF-alpha, sTNF-R p75). Taking all these confounding factors into account, we found no evidence for disease-related alterations in the levels of IL-1Ra, sIL-2R, sTNF-R p75 and IL-6, whereas levels of TNF-alpha and sTNF-R p55 in major depression and sTNF-R p55 in schizophrenia were slightly decreased compared to healthy controls. We conclude that, if confounding factors are carefully taken into account, plasma levels of the above mentioned cytokines and cytokine receptors yield little, if any, evidence for immunopathology in schizophrenia or major depression.
OBJECTIVE: To examine whether increased sleep during viral or bacterial infections supports host defense mechanisms. METHODS: To test this assumption in humans, healthy male subjects were assigned either to sleep from 2300 to 0700 hours (n = 10) or to stay awake through the night (n = 10). In the sleeping subjects Salmonella abortus equi endotoxin (0.4 ng/kg) or placebo were intravenously injected in balanced order during the first SWS episode. The age-matched, sleep-deprived subjects were injected at the same time point. RESULTS: As expected, endotoxin significantly increased rectal temperature, the plasma levels of cortisol, tumor necrosis factor-alpha (TNF-alpha), the soluble TNF receptors p55 and p75, Interleukin (IL)-6, the IL-1 receptor antagonist (RA), leukocyte, and granulocyte counts in both sleeping and sleep-deprived subjects, whereas lymphocyte and monocyte counts were transiently reduced. Time courses of endotoxin-induced host responses did not differ between the sleep and sleep deprivation groups. Endotoxin did not affect the amount of nocturnal wakefulness, nonrapid-eye-movement (NREM) sleep, or rapid-eye-movement (REM) sleep across the total night compared with placebo, but significantly increased electroencephalogram-arousals (EEG-arousals) in stage 2 and decreased arousals in SWS. In addition, the amount of SWS, spectral EEG-delta and -theta power was increased at the beginning and at the end of the sleep period, respectively, when the degree of immune activation was relatively low. CONCLUSION: The present results support the notion that short-term sleep deprivation is unlikely to harm the immune system as far as unspecific acute responses are concerned. The effects of endotoxin on sleep in this case support prior observations that in humans, enhanced SWS and intensified NREM sleep occur when host defense activation is subtle.