We studied the relationship between changes in platelet aggregability and platelet membrane lipid in alcoholic liver disease. The maximal rate of ADP‐induced platelet aggregation was significantly increased in the alcoholic liver disease group than in the control group. No significant difference was observed in the maximal rate of collagen‐induced platelet aggregation. However, a lag time required for the start of platelet aggregation was significantly shortened in the alcoholic liver disease group, indicating increased platelet aggregability. Results of the platelet aggregation test suggested that alcoholic liver disease patients have their platelet aggregation affected by the abnormality of prostaglandin metabolism. The alcoholic liver disease group was further divided into two subgroups: the hyperaggregation group and the unchanged aggregation group. Both free cholesterol and phospholipid in the platelet membrane were significantly increased in the alcoholic liver disease group. In phospholipid compositions, phosphatidylserine plus phosphatidylinositol were significantly decreased in the alcoholic liver disease group, whereas a significant decrease in phosphatidylserine plus phosphatidylinositol was observed in the hyperaggregation group of alcoholic liver disease. Analysis of fatty acid compositions of platelet membrane showed significantly decreased palmitic acid in the alcoholic group. There was no significant change of arachidonic acid, which directly affects platelet aggregation. Eicosapentaenoic acid significantly decreased in the alcoholic liver disease group, but there was no difference in docosahexaenoic acid. Meanwhile, the thrombogenic index, calculated from the fatty acids of platelet membrane, showed no difference between the alcoholic liver disease group and the control group. However, the thrombogenic index was significantly increased in the hyperaggregation group than in the unchanged aggregation group. These data suggested that platelet aggregation is affected by not only a change in arachidonic acid, but also changes in fatty acid compositions of the platelet membrane.
The anaerobic threshold, which is the limit of the aerobic glycolytic system (i.e., the so-called aerobic exercise limit) was not influenced by exercise under an acute alcoholic load. However, after the production of lactate started, the respiratory compensation point, which is the limit of the metabolic compensatory action, appeared earlier. This suggested that the intake of alcohol would influence the energy metabolism of skeletal muscles by a mechanism in which the disturbed metabolism of lactate in skeletal muscles was mainly involved.
The results of expired gas analysis during exercise indicate that the aerobic energy metabolism of skeletal muscle had been disturbed in alcoholic liver disease. The reduced RCP suggests that the lactate metabolism in skeletal muscle is also disturbed in alcoholic liver disease. Expired gas analysis during exercise allows determination of the amount of exercise required to treat liver diseases through analysis of AT.
Many esophageal granular cell tumors (GCT) diagnosed incidentally during endoscopic examinations are less than 10 mm in diameter and can be treated endoscopically for histological examination of the entire lesion. However, it is difficult to remove them with sufficient surgical margins by conventional endoscopic methods because GCT, even if small in diameter, lie in the submucosal layer and lesions in the esophagus make it difficult to manipulate cutting devices. To overcome these drawbacks we tried using a ligating device that has recently been employed for endoscopic resection of early gastrointestinal carcinoma. Two patients diagnosed with GCT by biopsy, and with lesions confirmed to be in the submucosal layer by endoscopic ultrasonography, were treated easily and completely by this method without any complications. The tumors measured 5 × 5 mm and 8 × 6 mm. Endoscopic resection with the ligating device is thought to be the simplest and most effective endoscopic treatment for GCT.
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