Mucosal lesions of the stomach in liver cirrhosis with a special reference to phospholipid metabolism

Gastric mucosal lesions are an inevitable complication in patients with liver cirrhosis. Their etiology, however, is as yet unknown. The present study investigated phospholipid metabolism in the gastric mucosa of rats with cirrhosis induced by carbon tetrachloride. Gastric mucosal lesions were induced by taurocholic acid (TCA) which was given through a gastric tube. Levels of phospholipids, phosphatidylcholine, and disaturated-phosphatidylcholine were found to be markedly reduced at the mucosal surface in the cirrhotic rats, and they were increased in the gastric juice. Metabolism of phospholipids in the gastric mucosa was visualized by³H-choline autoradiography and the rate of phospholipid metabolism was found to be reduced. These results strongly suggest that mucosal lesions induced by bile regurgitation into the stomach are due to disturbance of phospholipid metabolism in the gastric mucosa.     

Evaluation of neuropsychological function in patients with liver cirrhosis with special reference to their driving ability

Ability to drive an automobile was evaluated in 16 patients with well compensated liver cirrhosis. Four tests were performed, namely the emergency reaction test, the continuous emergency reaction test, the signal confirmation test and the accelerator reaction test. Test scores were compared to those of a group of age-matched healthy volunteers. 31% of patients were found to be unfit to drive. Alcoholic cirrhotics fared as poorly as non-alcoholic cirrhotics. In patients with subclinical hepatic encephalopathy (defined by neuropsychologic testing), 44% were unfit to drive. Routine testing of cirrhotic patients for ability to drive could have a major impact on motor vehicle accident rates.     

Muscle biopsy studies in patients with moderate liver cirrhosis with special reference to energy-rich phosphagens and electrolytes

Energy-rich phosphagens, water, and electrolytes were determined in skeletal muscle biopsy specimens from five elderly women and five elderly men with moderate liver cirrhosis. At the time of the study the patients were in their usual condition without evidence of deterioration of the disease. When compared with findings in apparently healthy subjects of similar age, the distribution and level of electrolytes and water were within normal limits in the female patients. The male patients showed increased contents of muscle water, and Mg2+ was reduced. The values calculated for the intracellular concentration of K+ and Mg2+ were also below normal. The pattern and levels of energy-rich phosphagens were abnormal in all but one female patient. As a general finding, ATP and the total level of adenine nucleotides were markedly reduced, as were phosphocreatine, the ATP/ADP ratio, and the energy charge potential.     

Endoscopic measurement of gastric mucosal blood flow with special reference to the effect of sclerotherapy in patients with liver cirrhosis

Gastric mucosal blood flow plays an important role as a background factor in the pathogenesis of acute gastric mucosal lesion. In this study, endoscopic measurement of regional gastric mucosal blood flow was performed on 41 patients with esophageal varices due to liver cirrhosis to ascertain the possible relations of this parameter to liver function, portal pressure, and acute gastric mucosal lesion. The effect of sclerotherapy and of esophageal transection on gastric mucosal blood flow were also investigated. Regional gastric mucosal blood flow in either the antrum or the corpus was significantly decreased in these patients, compared with normal controls. There was also a significant difference in gastric mucosal blood flow between two subgroups of patients, one with gastric mucosal lesions and the other without these lesions. Sclerosing therapy for esophageal varices tended to affect this parameter. Gastric mucosal blood flow had no significant correlation with portal pressure.     

肝硬化患者凝血、抗凝及纤溶指标的变化与Child-Pugh分级的关系

目的 探讨肝硬化患者凝血、抗凝及纤溶指标的变化及其与Child-Pugh分级的关系。 方法肝硬化患者43例,Child-Pugh分级A级13例,B级15例,C级15例。正常对照组16例,男11例,女5例。均检测凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、纤维蛋白原(Fib)、凝血因子Ⅱ、Ⅴ、Ⅶ、Ⅷ、Ⅸ、Ⅹ、血管性假性血友病因子(vWF)、抗凝血酶-Ⅲ(AT-Ⅲ)、蛋白-C(PC)、D-二聚体(D-d)、组织纤溶酶原激活物(t-PA)抗原和组织纤溶酶原激活物抑制剂(PAI)。 结果 PT、APTT随病情加重而显著延长,F值分别为32.828和18.743,P值均<0.01;Fib随病情加重逐渐降低,F=4.747,P<0.01。凝血因子Ⅱ、Ⅴ、Ⅶ、Ⅸ、Ⅹ随病情加重活性逐渐降低,F值分别为43.129、12.677、36.405、9.380和21.988,P值均<0.01。Ⅷ、vWF因子随病情加重活性逐渐增高,F值分别为16.672和14.657,P值均<0.01。AT-Ⅲ、PC随病情加重活性逐渐降低,F值分别为22.602和15.430,P值均<0.01。D-d、t-PA抗原随病情加重逐渐增高,F=5.957,P<0.05。PAI活性正常对照组和3组患者检测结果近似,差异无统计学意义。 结论 肝硬化患者存在明显的凝血、抗凝血以及纤溶机制的异常,且与肝硬化程度密切相关。在防治肝硬化患者出血时,不仅要纠正患者的凝血因子异常,还要给予一定的抗纤溶治疗。