Gastroenterology
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Because of observations that patients with acute episodes of alcoholic pancreatitis had high serum lipase levels whereas patients with gall stone pancreatitis had high serum amylase levels, a prospective study was undertaken to determine whether the ratio of serum lipase to serum amylase, a newly computed ratio, would discriminate between acute episodes of alcoholic and nonalcoholic pancreatitis. In phase one, 30 consecutive patients with acute pancreatitis were entered into the study and divided into groups A and B. Patients with renal failure were excluded from the study. ⋯ Thirteen patients had a lipase/amylase ratio of greater than 2; in 11 of them, the etiology of the pancreatitis was alcohol. Eight patients had a lipase/amylase ratio of less than 2; of them, only 1 patient had an alcoholic etiology for the pancreatitis. These differences were statistically significant (P less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
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The aim of this study was to assess the cause of enhanced fibrinolysis in cirrhosis by studying the balance between profibrinolytic and antifibrinolytic proteins in 24 patients with mild or severe cirrhosis. Antigen levels of both tissue-type plasminogen activator and plasminogen-activator inhibitor 1 were increased in mild and severe cirrhosis. Activity levels showed a very wide variability, but median activity levels of both proteins were normal. ⋯ Clot lysis experiments were performed to see if equal decreases in plasminogen and alpha 2-antiplasmin levels, as found in cirrhosis, result in a change in the rate of fibrinolysis. It was found that the proportionate decreases led to enhancement of fibrinolysis, indicating that the inhibitor depletion is more important than the proenzyme depletion. The authors conclude that enhanced fibrinolysis frequently found in cirrhosis may be attributed to an increased tissue-type plasminogen-activator activity relative to plasminogen-activator-inhibitor activity and decreased levels of alpha 2-antiplasmin, resulting in a reduced binding of alpha 2-antiplasmin to fibrin.