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Biliary complications remain to pose a serious problem in patients after liver transplantation. In the past, they occurred in as many as 50% of patients, and were associated with a height mortality. This has changed and at present the incidence of this complications is lower. The authors present their own series and discuss the role of ERCP in the management of complications.

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Severe gastroduodenal bleeding after renal transplantation is effectively prevented by H2 receptor blockers. New drugs for prophylaxis include proton pump inhibitors. The aim of the present study was to compare the effects of prophylaxis with the H2 blocker ranitidine and with the proton pump inhibitor omeprazole. One hundred seventy-seven consecutive patients were included in a controlled, prospective, randomized study after cadaveric renal transplantation. In one case, ranitidine failed to prevent exsanguination due to duodenal peptic ulcer bleeding. No bleeding was noted in the omeprazole group. There were no significant differences between the groups in hospitalization time, development of renal function, amount of cyclosporin A, prednisone, azathioprine, or methylprednisoline ingested, or laboratory biochemical parameters. We conclude that prophylaxis of severe gastroduodenal bleeding after renal transplantation with omeprazole is effective. Omeprazole is certainly as good as ranitidine; its advantages are a prolonged effect and a simple dosage, independent of graft function development.

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In bioptic specimens of the gastric mucosa of 57 patients with dyspeptic complaints and/or a duodenal ulcer Helicobacter pylori was detected under the microscope in 82,4% of chronic active gastritis and in 28,6% and 61,5% resp. of chronic gastritis grade I and II. The finding of helicobacteria depended on the number of collected specimens. They were never found at sites with intestinal metaplasia and their numbers did not correspond to the intensity and character of the inflammatory changes. As compared with the antrum, in the corpus of the stomach helicobacteria were found more frequently not only in mild forms of the inflammation but also in the normal mucosa. In the duodenum the finding was negative and the inflammatory changes were only mild. In all patients with a duodenal ulcer and a scar after ulceration in the antrum chronic active or inactive gastritis grade II was found with helicobacteria in 84,6% of the observations. Cultivation was consistent with microscopic evidence in 50 patients (87,7%).

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Residual kidney function was examined in 10 patients with chronic renal insufficiency under balance conditions and in 30 outpatients on the basis of urea clearance (Curea) and potassium clearance (CK). Protein intake was 35-40 g/day (0.5 g/kg/day) and potassium intake was 30-40 mmol/day. Under these conditions the critical values of residual kidney function were as follows: 1) plasma urea concentration (Purea) did not exceed 30 mmol/l if Curea did not drop below 3.8 ml/min; 2) plasma potassium concentration (PK) did not exceed 5 mmol/l if CK did not decrease below 4.1 ml/min. Clinical examination of Curea and CK provides additional information to the examination of creatinine clearance (Ccr) or its plasma concentration (Pcr). Our results suggest that the critical value of residual kidney function cannot be defined only on the basis of examination of Ccr or Pcr. Examination of Curea and CK can help in the interpretation of very high Purea and hyperkalemia in patients with chronic renal insufficiency.

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In 14 nonobese patients after acute pancreatitis and with normal oral glucose tolerance, the response of insulin, C-peptide, and pancreatic glucagon after 100 g of oral glucose was assessed. The curves of insulin and C-peptide were significantly raised compared with those of controls, and no difference was found between the response of patients with a negative (n = 8) and a positive (n = 6) family history of type II diabetes. The curves of pancreatic glucagon did not differ from those found in controls. Our results indicate that a normal response to glucose after recovery from an attack of acute pancreatitis is maintained at the cost of increased insulin secretion.

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Very little is known about bile composition in the end stage of chronic renal sufficiency. Patients with this condition are either assigned to a dialysis-transplantation programme, or are treated temporarily with a low-protein diet. Our study was designed to determine bile composition both in a group of ten patients treated with a low-protein diet over a long period of time, and in 11 patients on regular haemodialysis. The patients on haemodialysis were found to have increased bile cholesterol and an increased saturation index in the bile, i.e. changes implying increased risk of cholecystolithiasis. These changes were further enhanced by the effect of a low-protein diet with subsequent increases in cholesterol values and the bile saturation index, as well as a decrease in primary and an increase in secondary bile acids in the bile, i.e. a change in the spectrum of bile acid characteristic for cholecystolithiasis.

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The relationships between the plasma levels of urea (P(urea)), renal clearance of urea (C(urea)) and creatinine (Ccr) at an intake of 0.5 g protein/kg body weight/day were followed in 10 patients with chronic renal failure (CRF) under balance conditions. Under these conditions, P(urea) attained a value of 30 mmol/l when C(urea) had decreased below 3.8 ml/min. By contrast, no correlation could be demonstrated between P(urea) and Ccr under these conditions. The same relationships were followed in another group of 30 outpatients with CRF. Even in patients not followed under balance conditions, C(urea) determination makes it possible to establish whether the high increase in P(urea) is due to the decrease in residual renal function below the critical level or whether extrarenal factors are involved. Likewise, no significant correlation between P(urea) and Ccr could be demonstrated under these conditions. The findings suggest that C(urea) measurement in CRF patients helps to assess residual renal function in terms of P(urea) regulation and provides information that cannot be obtained by Ccr measurement.

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The initial level of PL-beta-ED-ir was significantly lowered in a group of 14 patients with gastroduodenal ulcer disease as compared with healthy volunteers (P less than 0.05). Immediately after i.m. administration of 20 mg gastrozepin (G) the PL-beta-ED-ir level increased but not significantly. Given orally over two weeks, G (50 mg/day) led to a more than doubling of the initial level (P less than 0.05). Controls showed no significant changes. A further meaningful change represented the time relationship of PL-beta-ED-ir during 5-hour observation to i.m. administration of 20 mg G before the start and after the end of the 2-week oral therapy. The placebo character of the above findings rules out the absence of any deviations of PL-beta-ED-ir in the diseased and healthy group after i.m. injection of saline. The study deals with the findings in relation to the pathophysiology of ulcer disease, and with a potential interference of G in the interrelation of the cholinergic and endogenous opiate systems.

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