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Biomedical subjects

H Goebell

Publications and source records attributed to H Goebell.

At least 109 records · Page 6Linked to original sources
PubMed1990

Molecular variants of cholecystokinin after endogenous stimulation in humans: a time study.

The time-dependent release of molecular variants of cholecystokinin (CCK) into the circulation was studied before and 1, 2, and 4 h after a test meal in six healthy volunteers. At each time period, 100 ml of blood were drawn in a manner to inhibit CCK degradation. Plasma was formed and CCK concentrated by Sep-Pak C18 cartridge chromatography. Molecular variants of CCK and gastrin were well separated from each other by high-performance liquid chromatography (HPLC). Molecular forms of CCK and gastrin were measured by radioimmunoassay using an antibody that requires the presence of the carboxyl-terminal phenylalanine amide for full recognition, implying that biologically active forms were detected. HPLC elution positions of gastrin forms were determined using a gastrin-specific antibody. Chromatographic separation of CCK from gastrin forms was complete, allowing separate integration of gastrin and CCK forms. Therefore no subtraction of gastrin-like immunoreactivity from CCK-like immunoreactivity (CCK-LI) was necessary and CCK-LI could be directly determined. Peaks of CCK-LI were integrated in the column eluates and the plasma concentrations were calculated. Total plasma CCK-LI rose from a value of 2.4 +/- 0.6 pM before the test meal to 6.4 +/- 0.8, 6.6 +/- 0.9, and 5.8 +/- 1.2 pM 1, 2, and 4 h postprandially. The major molecular forms released into the circulation eluted on HPLC in the position of CCK-58 and CCK-39 (which coelutes with CCK-33). Minor amounts were detected in the position of CCK-8. There was no significant difference in the relative proportions of the molecular forms released at the different time periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Action of neurotensin on meal-stimulated gastric acid secretion in the dog.

In six to nine mongrel dogs the effect of graded doses of intravenous neurotensin (188, 375, 750, and 1500 pmol/kg h) on acid secretion basally or stimulated by distention (by isotonic glucose), peptone (0.5, 1, and 4 g%), and pentagastrin was studied. Neurotensin did not affect acid secretion basally, stimulated by distention, or the maximal peptone dose. However, when submaximal doses (0.5 and 1 g%) of peptone were instilled in the stomach, neurotensin stimulated the secretory response to intragastric peptone. This effect was observed in doses of intravenous neurotensin which mimicked circulating neurotensin concentrations after a standard test meal. Thus, neurotensin could be considered a physiologic stimulant of acid secretion when protein is present in the stomach. The mechanism for this action of neurotensin is unknown but could be partly explained by an enhanced release of gastrin. The potentiating effect of neurotensin on peptone-stimulated acid secretion could play a major role in gastric secretory function of the dog.

Animals↗
PubMed1990

[Paralytic ileus as an initial manifestation of malignant VIPoma of the pancreas--case report with review of the literature].

A 57-year old patient with a paralytic ileus of unknown origin was admitted to the intensive care unit. Because of the laboratory findings with therapy resistant hypokalemia, hypercalcemia and metabolic acidosis a VIPoma was suspected. Therapy with somatostatin resulted in correction of laboratory abnormalities and in normalization of gastrointestinal motility. Plasma concentrations of VIP and PP were elevated, ultrasonography revealed a pancreatic tumor. Postsurgical examination of the removal tumor tissue confirmed the diagnosis of a malignant VIPoma. Clinical symptoms, laboratory findings with and without somatostatin-therapy and immunhistochemical properties are described.

Biomarkers, Tumor↗
PubMed1990

[Effect of 1 week's administration of prednisone on gastric acid secretion and liberation of gastrin in healthy humans].

In a double-blind, randomized study we examined the effects of an oral administration of prednisone (60 mg/day for 6 days) or placebo on gastric acid output basally (BAO), in response to peptone meals 1%, 2%, 4% and 8%, 500 ml each) and to pentagastrin 6 micrograms/kg s.c. to determine maximal acid output, MAO) and on plasma gastrin levels in 14 healthy volunteers. Gastric acid output was measured by intragastric titration (pH 5.5). For gastrin determination we used a specific radioimmunoassay. Experiments were performed one day (day 0) before giving the drugs and one day (day 7) and one month (day 30) after finishing the treatment. Both groups were comparable in their gastric acid responses on day 0. Six days treatment with prednisone did not significantly alter BAO, MAO and the gastric acid response to peptone and pentagastrin. Also, one month after finishing the treatment there were no significant differences in gastric acid output. Both groups had similar plasma gastrin levels on each day. Prednisone did not significantly alter plasma gastrin levels. We conclude that a six-day treatment with prednisone does not alter BAO, MAO and gastric secretory responses to peptone nor release of gastrin in healthy human volunteers.

Administration, Oral↗
PubMed1990

[Risk factors in the etiology of Crohn disease].

So far the aetiology of Crohn's disease remains unclear. Besides a genetic predisposition a causal role of environmental factors has been taken into consideration within the last time period. A number of case-control studies have consistently reported about an increased consumption of dietary sugar in patients with Crohn's disease as compared with controls. Furthermore cigarette smoking and the use of oral contraceptive drugs have been shown to increase disease risk. While the role of the former can be regarded as established the role of the latter still remains controversial.

Cohort Studies↗
PubMed1990

Feedback regulation of human pancreatic secretion. Effects of protease inhibition on duodenal delivery and small intestinal transit of pancreatic enzymes.

To determine the effects of luminal protease inhibition on duodenal delivery and the intraluminal fate of pancreatic enzymes, six healthy subjects were intubated with an oro-ileal multilumen tube assembly. By using nonabsorbable markers, cumulative trypsin, chymotrypsin, lipase, and amylase activities were measured as delivered to duodenum, midjejunum, and distal ileum, with or without simultaneous duodenal perfusion of the protease inhibitor camostat at graded doses. Compared with saline, camostat (a) inhibited trypsin activity in the entire small intestinal lumen by up to 99%, and significantly reduced chymotrypsin activity by up to 89%; (b) significantly increased duodenal deliveries of lipase activity, amylase activity and volume; (c) did not influence plasma cholecystokinin concentrations; and (d) significantly increased jejunal and ileal deliveries of lipase but not amylase activity. Small intestinal transit and motility were not affected by camostat. In additional in vitro studies, camostat significantly reduced the spontaneous decline in lipase activity in fresh human duodenal juice incubated at 37 degrees C. These findings demonstrate that duodenal deliveries of lipase and amylase activities increase when intraluminal protease activity is decreased; they suggest that this increase is not caused by slower proteolytic destruction of enzyme protein but by stimulation of pancreatic secretion. Thus, luminal protease-mediated feedback regulation of pancreatic secretion may be operative in humans. Because plasma cholecystokinin concentrations were not affected, these effects may in part be independent of cholecystokinin. The data further suggest that proteolytic digestion plays a major role in the rapid loss of luminal lipase activity on small intestinal transit.

Adult↗
PubMed1989

[Calcium homeostasis and exocrine pancreas: physiological ans pathological interrelations].

Calcium homeostasis and exocrine pancreas interact on several levels under both physiologic and pathophysiologic conditions. (1) Calcium ions are important intracellular mediators of cholinergic and hormonal stimulation of the pancreatic acinar cell, and thus play a central role in the stimulus-secretion coupling of ecbolic pancreatic function. (2) The calcium concentration in pancreatic juice is lower than in the interstitial fluid: pancreatic juice calcium is composed of two fractions, one of which is secreted together with enzyme proteins and the other diffuses along paracellular pathways dependent on serum calcium. Disturbed calcium secretion in pancreatic juice can be observed even following slight pancreatic alteration; conversely, disturbed calcium secretion may be of importance in the pathogenesis of chronic calcifying pancreatitis. (3) Hypocalcemia is an important symptom of acute pancreatitis whose pathogenesis has not been fully elucidated. (4) On the other hand, pancreatitis complicates chronic and acute hypercalcemic syndromes though the pathogenic mechanisms is uncertain. Experimental chronic hypercalcemia in animal models causes characteristic pancreatic secretory changes and disturbs the diffusion barrier for calcium. Experimental acute hypercalcemia causes stimulation of pancreatic enzyme secretion and cholecystokinin release. In addition, extracellular calcium has a direct stimulatory effect on pancreatic acinar cells in vitro.

Acute Disease↗
PubMed1989

Prostaglandin analogue protects pancreatic B-cells against cyclosporin A toxicity.

Cyclosporin A toxicity on pancreatic B-cells and its prevention by rioprostil, a prostaglandin E1 analogue, were studied in the model of the isolated perfused pancreas of rats treated with both compounds for 8 days. At toxic doses of cyclosporin (10 and 20 mg/kg b.wt), the B-cells showed severe hydropic degeneration of the endoplasmatic reticulum and slight degranulation of the B-cells. Accordingly, the insulin secretion was markedly impaired. Administration of rioprostil ameliorated the insulin secretion significantly, but not the ultrastructural changes. At therapeutic levels of cyclosporin (5 mg/kg b.wt), the hydropic degeneration and the drop in insulin secretion were completely prevented by rioprostil. This observation might have therapeutic implications in the treatment of patients, in particular those undergoing pancreatic transplantation.

Animals↗
PubMed1989

[Acute pancreatitis. 2: Treatment of the complicated course].

Owing to its tendency to produce severe local and systemic complications, the hemorrhagic necrotic form of acute pancreatitis is still associated with a high mortality rate. Major local complications are pseudocystic space-consuming masses, arterial bleeding and abscess formation. The major systemic complications include circulatory shock, metabolic disorders, renal failure, respiratory insufficiency and sepsis. Of decisive importance for the prognosis is prophylaxis, early detection, and suitable treatment of these threatening complications, which is achieved on the basis of a combination of standardized basic treatment with problem- and symptom-oriented supplementary treatment. In the present paper, the current prophylactic, diagnostic and therapeutic concepts are described. In addition, a number of invasive measures and the indications for surgery are discussed.

Acute Disease↗
PubMed1989

[Acute pancreatitis. 1: Principles of conservative therapy].

Any patient with suspected acute pancreatitis should be hospitalized in an intensive care unit. Since the course even of an apparently initially uncomplicated attack of pancreatitis can rapidly become severe and life-threatening, close clinical monitoring in accordance with the rules of critical care medicine is necessary. The major therapeutic measures comprise fasting, parenteral replacement of fluid, electrolytes and calories, and pain treatment. The care of patients with acute pancreatitis should be a joint effort on the part of the internist and the surgeon right from the start. At the present time, there is no specific treatment regimen for pancreatitis. Therapeutic concepts of hormonal inhibition of pancreatic secretion, or the inactivation of autodigestive enzymes, have not proved successful, or have not yet been adequately demonstrated to be effective. On resolution of the pancreatitis, an attempt must always be made to identify the cause of cause of the condition, since this forms the basis for further prophylactic and therapeutic consequences.

Acute Disease↗
PubMed1989

[Amyloidosis in Crohn disease. Case reports and review of the literature].

A review of the literature on Crohn's disease with secondary amyloidosis and four own case reports are presented. At least 1% of patients with Crohn's disease develop amyloidosis. The extent of the inflammatory bowel disease seems to have an influence on the occurrence of amyloidosis. The survival time of 40 out of 72 patients was 2.1 years after the onset of diagnosis. The complications induced by the amyloidosis determine the fate of the patients. Therefore the periodical protein determination in urine and the Congo-red-colouring of rectal mucosa after rectoscopy are justified. After the diagnosis of amyloidosis in patients with Crohn's disease the inflammation should be treated consequently, according to the principles of the treatment of the underlying disease. But the resection of the inflammatory bowel should be avoided if the renal function is still sufficient, because frequently there occurs a postoperative renal failure. In the case of renal amyloidosis with a creatinin-clearance of more than 10 ml/min, a therapeutic attempt should be made with 1.0 to 1.5 mg/day of colchicin or 10 g/day dimethylsulphoxid (DMSO) for at least six months. During existing renal failure the proceeding of amyloidosis in other organs is to be expected. The secondary amyloidosis disposes the fate of the patients.

Adult↗
PubMed1989

Clinical relapse of Crohn's disease under standardized conservative treatment and after excisional surgery.

The course of 205 patients with Crohn's disease at one gastroenterological center was studied in patients with conservative drug treatment or with operative management of their disease. The decision for one or the other treatment regimen was made by an interdisciplinary team of gastroenterologists and surgeons. Using life-table analysis the 205 patients showed a clinical relapse rate of 27% after two years and 38% after four years. Clinical relapse was defined by a Crohn's disease activity index (CDAI) over 150. We used a standardized drug regimen of salazosulfapyridin and prednisone; the indication for excisional surgery was limited strictly to life-threatening situations, absolute nonresponse to drug treatment, and severe intervisceral fistulae. The operated patients (N = 93) had a lower relapse rate than the patients treated conservatively (N = 112), 20% and 51%, respectively, after four years. There were considerably fewer relapses in Crohn's colitis patients who were operated upon than in conservatively treated patients (18% versus 67% after four years); the same was found for ileocolitis (20% vs 49% after four years), but there was no difference between the treatment groups in ileitis (25-30% relapses for both after four years). In addition the patients with Crohn's disease of the colon had a more favorable course after resection with respect to symptoms, clinical and laboratory findings, and CDAI in remission. This paper gives data only for surgery in severe clinical situations and does not give a rationale for earlier surgery. This problem should now be studied in a randomized trial.

Adult↗
PubMed1989

Differential effects of acute mental stress on interdigestive secretion of gastric acid, pancreatic enzymes, and gastroduodenal motility.

To study the effects of acute mental stress on gastric and pancreatic secretion, 12 healthy fasting volunteers swallowed two multilumen tubes, which allowed continuous aspiration of gastric and duodenal juices and measurement of motility of the stomach and the duodenum. In each study at least three duodenal phase III complexes of the migrating motor complex were recorded. In randomized order after the first or second duodenal phase III, mental stress was induced for 60 min by means of solving anagrams and doing mental arithmetic. Mental stress significantly increased the duration of the migrating motor complex by 60% (137.9 +/- 16.3 vs 86.1 +/- 13.0). Gastric flow rate and gastric acid output were not significantly altered. Duodenal flow rate was not changed during the stress period but significantly decreased by more than 52% in the following 30-min resting period. Duodenal concentration and output of chymotrypsin were significantly increased during the second 30-min period of acute mental stress; chymotrypsin output was significantly reduced in the poststress period. We conclude that acute mental stress has different effects on the stomach, the pancreas, and the upper gastrointestinal motility. The mechanisms by which the central nervous activity induced by mental stress affects the motility and secretion of the upper gastrointestinal tract remain to be elucidated.

Adult↗