[Clinical evaluation of one-year controlled studies of duodenal ulcer recurrence rate in patients treated with the preparation Ulfamid]. / Ocena kliniczna rocznych, kontrolowanych badan nawrotowosci choroby wrzodowej dwunastnicy u pacjentów leczonych preparatem Ulfamid.

The purpose of the work was an evaluation of duodenal ulcer recurrence rate in patients with a history of at least two years of ulcer treated during one year with the preparation Ulfamid (famotidine) Krka in a maintenance dose of 20 mg before sleep. The study involved 30 patients of either sex in whom complete healing of the ulcer niche was obtained in the first phase. Control endoscopy was carried out after 3, 6, 9, and 12 months. In the first phase of the study, complete healing of the ulcer niche after the treatment with Ulfamid in a therapeutic dose of 40 mg for six weeks was obtained in 94.9%. In the second phase of the study, after three months on Ulfamid in a maintenance dose, the recurrence rate was 13.3%, after six months 26.6%, after nine months another 6.1%. After 12 months the recurrence rate of duodenal ulcer reached jointly 46.7%. Of interest is the observation of a large number of the so called asymptomatic ulcers which accounted for 50% of the observed recurrencies.

The effect of a cholecystokinin receptor antagonist lorglumid on the proteinase-antiproteinase balance in taurocholate acute experimental pancreatitis (AEP) in rats.

The effect of new CCK receptor antagonist, lorglumid on taurocholate AEP in rats was studied. Lorglumid was applied intraperitoneally at a dose of 5.6 mg/kg BW immediately after taurocholate injection into choledochopancreatic duct. Activity of amylase, antithrombin III (AT III), alpha 1 protease inhibitor (alpha 1 PI), alpha 2 antiplasmin (alpha 2 AP) and alpha 2 M) in plasma, trypsin and chymotrypsin in pancreata were measured after 1, 3, 6 h of AEP. In AEP treated by lorglumid serum amylase activity and pancreatic wet weight was significantly reduced. The use of lorglumid prevented the increase of alpha 1 PI and alpha 2 AP compared to not treated animals. AT III and alpha 2 M in plasma and trypsin and chymotrypsin activity in pancreata did not change significantly in all groups. The mortality of the lorglumid treated rats was significantly lower in comparison with control group. It is concluded that lorglumid in taurocholate AEP moderates the changed plasma proteinase-antiproteinase balance. Our results indicate a protective effect of lorglumid in this model of acute experimental pancreatitis.

Tissue plasminogen activator, plasminogen activator inhibitor, and other parameters of fibrinolysis in the early stages of taurocholate acute pancreatitis in rats.

It is well known that fibrinolytic activity in the early stages of acute experimental pancreatitis (AEP) as assessed by euglobulin lysis time (ELT) is depressed. The aim of this study was to evaluate changes in the fibrinolytic system in the early stages of taurocholate AEP in rats. Tissue plasminogen activator (t-PA) activity, plasminogen activator inhibitor 1 (PAI-1) activity, plasminogen, alpha 1 proteinase inhibitor (alpha 1 PI), alpha 2 antiplasmin (alpha 2 AP), antithrombin III (AT III), fibrinogen, and ELT were measured 0.5, 1, 3, and 6 h after the induction of taurocholate AEP in rats, as well as in sham-operated animals and the control group, which was not submitted to any operation. T-PA activity decreased significantly after 3 and 6 h of AEP; PAI activity had a time course reverse to t-PA and was parallel to alpha 1 PI activity. ELT was slightly prolonged after 0.5, 1, and 3 h, whereas alpha 2 AP activity and plasminogen levels increased significantly; AT III activity was increased after 1 h in comparison to control group. Sham operation caused nonsignificant changes in fibrinolysis. Increase of PAI activity and decrease of t-PA could be a reasonable explanation for inhibited plasma euglobulin fibrinolytic activity noted in the early period of AEP.

Seasonal prevention of duodenal ulcer recurrences with pirenzepine.

Seasonal accumulation of duodenal ulcer recurrences suggests that maintenance therapy could be limited to the more risky periods. We carried out a 2-year, multi-centre, randomized, double blind study in 250 patients in whom the last ulcer proved to be healed at the endoscopy on entry. One-hundred-and-twenty-six patients in group A were given pirenzepine 2 X 25 mg while 124 in group B had 2 X 50 mg daily from the beginning of January to the end of March, and from the beginning of September to the end of November for two consecutive years. Test endoscopies were performed each year at the end of February, May and November. Both groups proved to be well comparable. Thirty-five patients dropped out from group A in the first and 10 in the second year; in group B 27 and 29, respectively. As the effect did not show any dose relation, the four yearly cycles were summarized. Recurrence rate checked in May was 22.1% while in both pirenzepine protected months it was 11.3% (p less than 0.0005) and 13.4% (p less than 0.001), respectively. We conclude that pirenzepine administered in the risky seasons prevents the peak ulcer incidence and reduces the recurrence rate to a level lower than in the non-risky season. Thus pirenzepine is effective in ulcer prevention even if administered in an interrupted manner.

Does heparin modify protease-antiprotease balance in acute experimental pancreatitis in rats.

A rat model of taurocholate-induced acute pancreatitis has been employed to investigate the effect of heparin on the protease-antiprotease balance. Heparin was applied intraperitoneally at a dose of 6 mg/kg body weight during 24 hrs. At 24 and 48 hours of acute pancreatitis, heparin evidently diminished the consumption of trypsinogen in pancreatic tissue and decreased trypsin generation. The use of heparin prevented the consumption of alpha 1 anti-chymotrypsin, alpha 1-anti-trypsin and AT-III in pancreatic tissue, whereas in plasma the concentration of the mentioned inhibitors was restored or even increased. Heparin does not affect evidently lowered alpha 2-macroglobulin concentration, either in pancreatic tissue or in plasma. We conclude that heparin applied in acute pancreatitis markedly moderates the dysfunction of protease-antiprotease balance both in plasma and in pancreatic tissue.