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The effectiveness of cimetidine or antacid in healing recurrent jejunal peptic ulcers after Billroth II gastric resection without vagotomy was tested in a randomized study of 18 in-patients. Mean stimulated acid secretion of the cimetidine group was 11.2 +/- 4.3 mmol/h, in the antacid group 12.6 +/- 5.6 mmol/h. Serum gastrin levels were within the normal range in all patients. Within four weeks the ulcers had healed completely in eight of the nine patients on cimetidine (1,000 mg/d), but in only three of the nine patients on antacids (magnesium-aluminiumhydroxide, neutralization capacity 564 mmol/d). The difference is statistically significant (P less than 0.025). All 11 patients with healed ulcers were given prophylactically either 800 mg cimetidine daily or magnesium-aluminiumhydroxide (neutralization capacity 564 mmol/d). During a follow-up period of one year recurrences occurred in two of the five patients on antacids, but in none of the six treated with cimetidine. The results indicate that cimetidine also accelerates the healing of recurrent jejunal peptic ulcers. But further studies are required to elucidate whether long-term treatment with histamine-H2-receptor antagonists is as good as surgery in the long-term prevention of ulcer recurrences.

Fifty-one patients, on whom a total of 64 carotid thromboendarterectomies had been performed, were followed up by duplex sonography. Five asymptomatic occlusions of the internal carotid artery (8%) and one occlusion of the common carotid artery were found. Two patients (3%) developed a restenosis of more than 50% and another two patients a restenosis of less than 50%. Changes in the vessel wall not producing significant luminal change were observed in another 18 cases (28%). Thirty-six of the operated vessels (56%) showed no change.

The postoperative blind-loop syndrome can occur after side-to-side, end-to side or by-pass anastomoses of the gut and presents clinically as malabsorption syndrome. Pathogenetically, stasis or slowing of the bowel movements will cause a rapid increase of pathogenic bacteria in the small intestine. Malabsorption is characterized by 3 symptoms: Loss of weight, anemia, steatorrhoea. The method of choice for therapy is to perform a new, end-to-end, anastomosis of the intestine in order to re-establish a physiological situation. During the last 6 years 14 patients with malabsorption syndromes of varying degrees were operated upon: 6 had pure small intestinal anastomoses, 7 anastomoses between the small and large intestine and 1 patient had a side-to-side sigmoidal anastomosis. In all patients the side-to-side or by-pass anastomoses could be reversed.

Upper gastro-intestinal bleeding or other complications after operations on this tract can lead to grave additional risk for the patient, especially in the early postoperative phase. Because of its high degree of diagnostic accuracy, emergency endoscopy is in most cases of decisive importance in planning the type (conservative or surgical) and timing of any necessary treatment. Special investigative techniques as well as the early use of endoscopy in 97 patients achieved a high rate of success at a low risk to the patients. Indications, results and risks of emergency endoscopy of the upper gastro-intestinal tract in the late postoperative phase are similar to those for the non-operated patient.

A case report is given of a 25 year old turkish patient, who had ascaridiasis and multiple stenoses of the small intestine. This syndrome was caused by extensive obliterating phlebitis of the small mesenterial veins and sclerosing lymphadenitis of the mesenterial lymph nodes. Granuloma containing epitheloid cells and giant cells could be found in the venous walls and in the lymph nodes, some of the granuloma being grouped around atrophic ascarides larvae; this demonstrates, that the intestinal stenoses represent an unusual complication of larvae migration in this worm disease. Perforation of the intestinal wall in one these stenotic areas possibly was caused by ascarides worms actively.

Seventy-three patients with vascular occlusions in the pelvis or lower limbs and three patients with upper limb lesions were treated by local low dose fibrinolysin, with strict control of any possible bleeding tendencies. Adequate recanalisation was obtained in 56 patients (73.6%). In ten patients, the occlusion recurred while the patient was still in hospital. After four to six months, 37 of the 56 (67%) of the vessels were still patent. In 18 patients, peripheral emboli resulted in some deterioration, but in 15 of these cases this could be treated successfully by operation. The methods and indications of local fibrinolysis therapy and the problems associated with it are discussed.

Fundophrenicopexy is an effective procedure for repairing important mechanical parts of the LES. Pre- and postoperative measurement of pressure in 52 patients demonstrated an increase from x = 20.1 mm Hg to x = 39.25 mm Hg. Fundophrenicopexy is the more simple surgical management compared with fundoplication and is followed less frequently by complications. If anatomical conditions allow, fundophrenicopexy is preferred in surgical treatment of reflux esophagitis.

The systemic availability of 3H-lorcainide in rats was investigated following oral doses of 1.5 to 100 mg/kg. Systemic availability increased from 14 to about 40% following the lowest and highest dose, respectively. Doses higher than 60 mg/kg produced a less marked increase of the systemic availability. In rats with portacaval shunt following an oral dose of 1.5 or 7.5 mg/kg lorcainide a systemic availability of 47% was found, indicating substantial prehepatic first-pass metabolism of lorcainide. Systemic availability of total radioactivity was 53% in control rats and 90% in rats with portacaval shunt. Since the maximal systemic availability obtained by increasing the dose was found to be identical with that obtained in rats with portacaval shunt, it is suggested that increasing doses will saturate the presystemic metabolism in the liver but will not affect the fraction of the dose which is metabolized in the gut.