Mitochondria of patients with alcoholic liver disease are morphologically abnormal, and mitochondria isolated from animals exposed to ethanol exhibit functional deficiencies in vitro. Because the functional consequences of the morphological alterations and the relevance of in vitro observations to mitochondrial function in alcoholic subjects are not clear, we assessed mitochondrial function noninvasively with a breath test. Mitochondrial function was assessed by measuring the exhalation of 14CO2 after administration of 1 microCi 2-keto[1-14C]isocaproic acid, the decarboxylation of which occurs in mitochondria. The results of the 2-keto[1-14C]isocaproic acid breath test in 17 alcoholic subjects were compared with the results in healthy controls and patients with nonalcoholic liver disease. The peak exhalation of 14CO2 and the fraction of the administered dose decarboxylated in 60 min were significantly lower in alcoholic patients than in healthy controls or patients with nonalcoholic liver disease. In alcoholic patients 2-keto[1-14C]isocaproic acid decarboxylation was impaired in the presence of normal conventional and quantitative liver function as assessed by aminopyrine breath test and galactose elimination capacity, indicating that 2-keto[1-14C]isocaproic acid decarboxylation does not simply reflect decreased functional liver mass. We conclude that mitochondrial function as reflected by 2-keto[1-14C]isocaproic acid decarboxylation is impaired in chronic alcoholic patients. The functional impairment is specific for excessive ethanol consumption and not a reflection of decreased global liver function or the presence of cirrhosis. 2-Keto[1-14C]isocaproic acid decarboxylation could thus be useful as a marker of excessive ethanol consumption.
We investigated 64 former psychiatric inpatients who had committed suicide within 1 year after their discharge and compared them with a carefully matched control group of patients who did not commit suicide. One third of the patients in both groups were no longer in treatment at the time of the suicide or, for controls, at the corresponding point in time. At that time, a significantly higher proportion of controls had been receiving psychopharmacotherapy and a significantly higher proportion of them were on lithium.
We studied therapeutic factors influencing suicide during out-patient treatment in severely ill discharged psychiatric in-patients. A subsample of 25 suicide and 27 control patients were all treated by psychiatrists at the time of their suicide or at a corresponding point of time. We were not able to identify any significant psychosocial or clinical pre-discharge differences between the two groups. After discharge, the patients of the control group were treated by psychiatrists with substantially longer professional training-plus-experience, the therapist's experience being the most important therapy factor contributing to the different outcome. On the whole, the contribution of the therapy factors was modest, however, explaining only 26 per cent of the group variance.
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