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Context: Minimal hepatic encephalopathy has been systematically investigated in cirrhotic patients. Although, there are controversies regarding the best methods as well as the role of ammonia for its diagnosis., Objective: To evaluate the frequency of minimal hepatic encephalopathy diagnosed by neuropsychological and neurophysiological methods in cirrhotic patients, as well as possible associated risk factors for this condition, including the role of arterial ammonia concentrations for its diagnosis., Methods: Cirrhotic patients were evaluated by the number connection test parts A and B (NCT-A and NCT-B), and auditory evoked-related potentials (P300). Minimal hepatic encephalopathy was diagnosed by the presence of abnormal P300 and in unless one of the performed neuropsychologic tests. Arterial ammonia concentration, scholarity and cirrhosis severity accessed by Child-Pugh classification were evaluated in all., Results: Forty-eight cirrhotic patients were evaluated, with median age 50 +/- 8 years old, 79% male. The main etiologies were alcoholic and viral. The P300 was abnormal in 75% of cases, while NCT-A and NCT-B were abnormal in 58% and 65%, respectively. The NCT-B results were influenced by scholarity. The minimal hepatic encephalopathy frequency was 50%. Arterial ammonia concentration was not significantly increased in minimal hepatic encephalopathy diagnosed patients (195 +/- 152 mmol/L versus 148 +/- 146 mmol/L; P>0,05). There was no difference between groups with or without minimal hepatic encephalopathy in the other studied variables., Conclusion: Minimal hepatic encephalopathy is a frequent condition in cirrhotic patients. The arterial ammonia concentration does not play a major role in its diagnosis.

Acute pancreatitis is one of the complications associated with severe primary and secondary hypertriglyceridemia. The frequency of hypertriglyceridemia in patients with pancreatitis ranges from 4 to 53%. The elevation in serum triglycerides probably induces the release of free fatty acids, responsible for the pancreatic damage. During a three year study, nine patients with acute pancreatitis due to hypertriglyceridemia were followed up at the University Hospital of Federal University and at the "Hospital Monte Sinai" (Juiz de Fora, MG, Brazil). Suggestive clinical manifestations, especially superior abdominal pain, nausea, vomiting and ileus, were found in all the patients; however, only three showed elevated serum amylase levels. All had triglyceride levels above 1000 mg/dl (11.3 mmol/L). The evolution after clinical treatment was good in eight patients (two needed parenteral nutrition). The only death observed was due to shock and acute respiratory distress, refractory to clinical management. The maintenance treatment aimed at withdrawing the predisposing conditions and reduction of the triglyceride levels prevented recurrence of acute pancreatitis episodes during the 23 months of follow-up.

The effect of cimetidine, a histamine H2-receptor antagonist, on basal and beta-zole-stimulated gastric acid secretion was studied in 28 patients with peptic ulcer. The results demonstrate that cimetidine (300 mg IM), is a potent inhibitor of both basal and betazole-stimulated gastric acid secretion.

A total lyophilized pig pancreas (TLP) preparation was assayed "in vitro" and "in vivo". Lipase activity of the four lots studied was 6.180 +/- 1.122 IU by gram of the commercial product. There was no free trypsin detectable in the preparation. Fifteen pancreatic exocrine insufficiency patients were studied in a period of four weeks. Adult patients received from 35.500 to 35.776 IU of lipase contained in TLP preparation by meal. All patients had their steatorrhea reduced, or normalized, stool weight reduced and body weight increased. There is not an obligatory relation between stool fat loss and stool weight. Steatorrhea decreased at least during the 14 first days of treatment before reaching a stable level. This long delay before reaching a maximum effect deserves to be known: to test the efficiency of a pancreatic extract, the treatment must be given at least two weeks before estimating its results on fecal fat excretion.