Masao Suwa

Enteric coated polymyxin B in the treatment of hyperammonemia and endotoxemia in liver cirrhosis.

SummaryEffects of enteric coated polymyxin B capsules on hyperammonemia and endotoxemia in liver cirrhosis were investigated. Six million units of polymyxin B were orally administered daily to 21 patients with liver cirrhosis and 3 patients with hepatomacum liver cirrhosis, whose plasma ammonia was higher than normal limit and/or whose plasma endotoxin was positive, for 5–32 days, and serum polymyxin B concentration (in 5 cases), changes of plasma ammonia level (in 19 cases) and plasma endotoxin (in all cases) were observed. Serum polymyxin B concentration was below the detectable limit (0.5 unit/ml) in all cases observed. In the patients with liver cirrhosis, plasma endotoxin and ammonia levels decreased rapidly after polymyxin B treatment, and the decreases in endotoxin levels were kept throughout the treatment. Twelve patients with liver cirrhosis (10 among them were treated with lactulose) were served as controls. All patients who were treated with lactulose alone showed rapid decrease in plasma ammonia, but the decrease in endotoxin in these patients was slower than that in those treated with polymyxin B. From these results, oral administration of polymyxin B is concluded to be useful in the treatment of hyperammonemia and endotoxemia in liver cirrhosis, as a poorly absorbed antibiotic and as an antiendotoxin agent.

Serum glutathione S-transferase in experimentl liver damage in rats

SummaryThe changes of serum glutathione S-transferase (GST) was observed after carbon tetrachloride (CCl4) administration to Wister rats. Serum GST activity increased rapidly and reached the peak 24 hours after CCl4 administration, and decreased rapidly thereafter. Centrilobular massive necrosis was already observed at the peak time of serum GST activity. On the other hand, serum glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) activities varied slowly, and the peak time of GOT and GPT activities was 36 hours after CCU administration.GST-containing Y fraction obtained from rat liver was injected intravenously to control and nephrectomized rats, and the plasma disappearance of GST activity was observed. The plasma disappearance of GST activity was very rapid in the control rats. When the Y fraction obtained from l/12g liver was injected, no statistically significant difference in the plasma GST half lives was observed between the control and nephrectomized rats. Half life of serum GST was significantly shorter in control rats receiving the Y fraction from 1/60g liver, comparing with that in nephrectomized rats receiving the same amount of Y fraction.From these results, serum GST is concluded to be a precise index of the early stage of hepatic necrosis in the rat, and considerable amount of GST is excreted from the kidneys, but most of the enzyme is metabolizedin vivo.

A case of Gilbert’s syndrome combined with macroamylasemia

SummaryA 30-year-old Japanese male, who had no remarkable family history, visited our hospital with a complaint of abdominal pain, and unconjugated hyperbilirubinemia and hyperamylasemia were observed. He showed negative hemolysis tests, positive nicotinic acid test, low hepatic bilirubin UDP-glucuronyltransferase activity, decreased bilirubin diglucuronide and increased bilirubin mono-glucuronide in bile, and a decrease in serum bilirubin after phenobarbital administration. He also showed high serum amylase level, low urine amylase level, and low amylase-creatinine clearance ratio. Gel filtration of serum with Sephadex G-200 revealed the existance of macroamylase. Countercurrent immunoelectrophoresis proved binding of serum amylase to lambda type IgA. From these results, the case was diagnosed as Gilbert’s syndrome combined with macroamylasemia.