[Pathophysiology and diagnosis of malabsorption syndrome].
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Biomedical subjects
Publications and source records attributed to H Goebell.
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The effects of the intravenous administration of atropine or magnesium on pancreatic secretion which has been stimulated by secretin and induced hypercalcaemia have been studied in man. In the presence of secretin (0.5 CU/kg.h) the infusion of Ca2+ (0.3 mmol/kg.105 min) resulted in an increase in secretion of enzymes by 100-200%, and in that of Ca2+ and Mg2+ by 50-100% without affecting fluid and bicarbonate secretion. The additional injection of atropine (0.5 mg i.v. and 0.5 mg s.c.) were followed by a prompt fall in enzymes but not in Ca2+ and Mg2+ to the secretin-stimulated values. The additional infusion of Mg2+ (0.12 mmol/kg.45 min) to the Ca2+-infusion did not alter the secretion of enzymes, Ca2+ or Mg2+ compared with the calcium infusion alone. It is suggested that the hypercalcaemic stimulus depends on an intact innervation of the acinar cells. In these experiments the secretion of Ca2+ and Mg2+ seem to originate mainly from extracellular fluxes.
In Germany alcohol is responsible for 40--60 per cent of cases with chronic or chronic relapsing pancreatitis. The histologic lesions for a long time remain clinically asymptomatic. Their degree depends on the duration and the total amount of alcohol which is ingested. Promoters of alcoholic damage to the pancraes are a high intake of fat and protein and a genetic disposition. Acute application of alcohol leads to an inhibition of pancreatic secretion when the entrance of gastric acid into the duodenum is prevented. Otherwise a weak stimulation occurs with release of secretin. Chronic application of alcohol after a few months abolishes the initially seen inhibition and leads to an increase of enzyme secretion of the gland. The raised concentration of protein in the pancreatic juice is the cause of precipitation of protein plugs, and thus probably leads to the alterations which are typical for chronic pancreatitis.
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Calcitonin (CT) inhibits gastric acid and pancreatic enzyme secretion when infused intravenously. Therefore, in two patients showing excessively elevated CT-blood levels due to medullary thyroid carcinoma and in two patients with bone diseases before and under CT-treatment, gastric and pancreatic secretion were measured. Spontaneous (BAO) and pentagastrin stimulated acid as well as hormonally stimulated pancreatic enzyme secretion revealed normal in all subjects and tests. The findings are in favour of adaptation mechanisms of gastric parietal and pancreatic acinar cells against the inhibitory action of chronically elevated CT. Therefore, long term treatment with CT is no likely to induce impaired acidity or exocrine pancreatic insufficiency.
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A double-blind trial of (+)-cyanidanol-3 (2 g/day) versus placebo tablets was carried out in 100 patients with acute viral hepatitis. 51 received the drug and 49 placebo. (+)-Cyanidanol-3 accelerated the disappearance of HBsAg from the blood, lowered serum-bilirubin, and relieved symptoms such as anorexia, nausea, and pruritus. The drug was well tolerated. None of the patients had a relapse of acute hepatitis. Chronic active hepatitis developed in 1 of the placebo-treated patients. Thus, (+)-cyanidanol-3 seems to be of benefit in acute viral hepatitis.
The effect of calcitonin on human pancreatic secretion was studied under various conditions of stimulation. During administration of both secretin plus cholecystokinin-pancreozymin (CCK-PZ) or secretin plus caerulein, enzyme secretion was promptly reduced by an infusion of calcitonin of more than 50%. In contrast, vagally stimulated enzyme secretion induced by insulin-hypoglycaemia or carbamyl-choline was not altered against a background infusion of calcitonin in comparison with control experiments. Calcium-induced enzyme secretion was abolished by additional calcitonin infusion which also prevented an increase in serum calcium. On the other hand, additional high grade calcium infusion did not modify the inhibitory action of calcitonin on enzyme output stimulated by secretin and CCK-PZ. Secretion of fluids and bicarbonate remained unaffected by calcitonin in all experimental conditions, whereas the outputs of calcium and magnesium paralleled generally the changes in enzymes. It is suggested that calcitonin interferes with hormonemediated stimulation of the acinar cells without influencing cholinergic mechanisms. The inhibitory action of calcitonin on enzyme secretion does not appear to be mediated by a depletion of extracellular calcium in the pancreatic tissue by calcitonin.
Three cases of benign pancreatic ascites have been added to 94 cases reviewed from the literature. Common characteristic of this syndrome were chronic alcoholism, intermittent abdominal pain, nausea, vomiting and considerable weight loss which occurred despite fluid accumulation. Markedly elevated protein and amylase levels in the ascitic fluid, hyperamylasemia and hypoalbuminemia were the major diagnostic clues as to the pancreatic origin of ascites. Predominant pathological findings were chronic pancreatitis with or without pseudocysts, pancreatic duct disruption, lesion which were considered to be the major pathogenic factor besides lymphatic obstruction by leaking pancreatic juice into the peritoneal cavity. Early laparotomy for diagnosis and treatment is essential. ERP might be of great value in diagnosis.
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Duodenoscopy was performed in 2 602 patients; malignant tumors were found in 5, hyperplasia of Brunner's glands in 5, hyperplasia of lymphatic follicles in 26, inflammatory pseudo-polyps in 9, and ectopic gastric mucosa in 5 cases. Only 3 of the big tumors had been detected by x-ray examinations; enlarged lymphatic follicles and the polyps had escaped x-ray detection altogether. Infiltration of the mucosa by tumor tissue can be suspected merely on the ground of endoscopic inspection with a high degree of probability. Histological diagnosis depends on forceps biopsy. Big particle biopsy of submucosal tumors with a sling carries a high risk, which however has to be taken in order to obtain a definite diagnosis. Tumors of the duodenal bulb caused by inflammatory processes do present considerable diagnostic problems. Special problems of diagnosis and therapy of the cases presenting with hyperplasia or adenoma of Brunner's glands are discussed in a special section.
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Secretion of trypsin, chymotrypsin, lipase and amylase was measured in male rats under urethane anaesthesia using a method of continuous perfusion of the duodenum. Prolonged infusion of cholecystokinin-pancreozymin (CCK-PZ) over a period lasting 200-360 min was administered either alone or together with a submaximal dose of secretin (1 unit/100 g - 10 min). Infusion of CCK-PZ was carried out using maximal doses (1--1.5 unit/100 g - 10 min) with and without secretin. Supramaximal doses of CCK-PZ (2 and 4 units/100 g - 10 min) were used only in combination with secretin. In all experiments secretion of enzymes showed a triphasic pattern including an initial peak followed by a plateau secretion after 10--20 min (phase 1), a decreasing second phase and finally base-line secretion (phase 3), thus demonstrating exhaustion of enzyme output from the gland with time. With increasing and supramaximal dose of CCK-PZ the cumulative output of enzymes from start to baseline secretion decreased progressively. Under the same conditions the levels of peak and plateau secretion were lower, the duration of plateau secretion was longer and the decreasing phase of secretion was shortened. These features indicate inhibition of secretion with increasing supramaximal doses of CCK-PZ infusion. Whereas the proteolytic enzymes and lipase reacted in a parallel way always amylase secretion was sustained on a higher level, implicating an alternative pathway for secretion.
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In 24 000 gastroscopies at 4 medical departments 705 subjects with gastric operations done more than 5 years before had been studied. 39 of 608 patients with Billroth II, 5 of 81 with Billroth I and 4 out of 15 with gastroenterostomy were found to be suffering from carcinoma of the gastric stump. The primary gastric operations were performed at a medium age of 40 years. The interval between surgery and development of carcinoma averaged 24 years and was shorter in patients operated at a higher age. Besides age and interval since operation risk factors were apparently former gastric ulcers or polyps. Indications for endoscopic follow-up studies of gastrectomized patients to improve surgical results with carcinoma of the gastric stump have been suggested.