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Biomedical subjects

J Hansky

Publications and source records attributed to J Hansky.

At least 73 records · Page 4Linked to original sources
PubMed1979

The Mallory-Weiss lesion as a cause of upper gastrointestinal bleeding.

A prospective study of patients with upper gastrointestinal bleeding admitted to a haematemesis and melaena unit has revealed an incidence of Mallory-Weiss tears of 8% (59 of 762 patients undergoing endoscopy). Prior vomiting was present in 60% and an associated upper gastrointestinal lesion in 44 percent. The majority of patients had a recent ingestion of alcohol and/or analgesics, whilst 34% had chronic heavy alcohol intake. Approximately 50% of patients required no blood transfusion, while 37% had over three units of blood. No patient in the group required surgical intervention, and one patient died because of general debility. This study suggests that the Mallory-Weiss tear accounts for a significant proportion of patients admitted with upper gastrointestinal bleeding, but that the mortality and morbidity are low.

Adolescent↗
PubMed1979

Bleeding stomal ulceration.

In a prospective study of patients with haematemesis and melaena, there were 22 admissions of patients with bleeding stomal ulceration, representing 2.5% of total admissions to the Unit. In 16 patients the bleeding was from superficial stomal lesions. These lesions, endoscopically and histologically, resembled alkaline reflux gastritis, a recently defined cause of postgastrectomy bile vomiting. Five patients presented with chronic ulceration following inadequate gastric surgery. One patient was admitted on two occasions. Nine patients received more than five units of blood and came to operation for continued bleeding. In seven of the surgical cases, the bleeding was from superficial stomal lesions. Our experience suggests that truncal vagotomy is necessary to control the bleeding in these patients. One patient presented with superficial stomal ulceration and carcinomatous change. This patient died. It is important to subject these lesions to biopsy, and biopsy with extension of a previous gastrectomy is indicated to control bleeding, and to exclude malignancy.

Adult↗
PubMed1979

The protective effect of cimetidine on stress-induced acute gastric ulceration in the rat.

The effect of intraperitoneal cimetidine, an H2 receptorantagonist, has been assessed on the development of cold-restraint induced acute gastric ulcers in rats. Cimetidine in doses ranging from 20-100 mg per kg body weight significantly reduced the incidence of acute gastric ulceration compared with saline controls in this model. The protective effect of cimetidine suggests a prophylactic role for this agent in stress-induced gastric or duodenal ulceration in man.

Animals↗
PubMed1979

The effect of cimetidine on gastrin release in ulcer disease.

The effect of a single dose of 400 mg of the H2-receptor antagonist cimetidine on protein meal stimulated immunoreactive gastrin was assessed in ten patients with gastric ulcer and ten patients with duodenal ulcer. In gastric ulcer patients, serum gastrin (mean +/- SE) rose from 34 +/- 2.2 pmol.l-1 to a peak of 80 +/- 5.0 pmol.l-1 at 45 minutes without and from 36 +/- 2.2 to 107 +/- 8.0 pmol.l-1 at 60 minutes with cimetidine; in duodenal ulcer it rose from 26 +/- 3.0 to 47 +/- 5.1 pmol.l-1 at 45 minutes without and 26 +/- 3.2 to 52 +/- 5.1 pmol.l-1 at 60 minutes with cimetidine. Integrated gastrin responses in gastric ulcer were 4900 +/- 800 pmol.l-1 120 minutes without and 7000 +/- 900 pmol.l-1 120 minutes with cimetidine and 1560 +/- 300 pmol.l-1 120 minutes without and 2620 +/- 400 pmol.l-1 120 minutes with cimetidine in duodenal ulcer patients. These gastrin increases after cimetidine are comparable to those achieved with continuous intragastric neutralisation with alkali.

Adult↗
PubMed1979

Serum gastrin after 12 months' continuous cimetidine therapy for duodenal ulcer.

Serum immunoreactive gastrin was measured in 14 patients with duodenal ulcer before and during a 12-month course of cimetidine 400 mg bd. All patients were symptomatically well during the cimetidine therapy and both basal gastrin and that in response to a protein rich meal were assessed before, at six months and at 12 months during therapy. The basal and post-prandial gastrin were significantly higher at six and 12 months on cimetidine than before cimetidine but the six and 12 month levels were similar. This study thus shows that the progressive increase in serum gastrin during six months of continuous cimetidine therapy does not occur beyond this time period.

Adult↗
PubMed1979

Evidence that the cholinergic enteropancreatic reflex may be independent of cholecystokinin release.

Studies were performed in four dogs with chronic gastric and pancreatic fistulas following intraduodenal perfusion with 10 mmole hr-1 of sodium oleate for 30 minutes. Radioimmunoassay (RIA) of plasma CCK LI was undertaken by an RIA method using labeled, desulfated CCK 8 I125 and an antiserum raised to CCK 8. The detection limit for the assay was 0.25 to 0.5 fmole and the lowest detectable plasma level was 5 to 10 fmoles ml-1. Since there was equal cross-reactivity to gastrin, a gastrin-specific assay also was employed to evaluate any changes in gastrin levels. After oleate infusion the plasma CCK increment above basal was 50 +/- 11 fmoles ml-1, with return to basal levels after 60 minutes. Administration of atropine significantly (P less than 0.01) inhibited the release of CCK in the first 20 minutes. Thereafter CCK release was not reduced. Plasma gastrin values did not change before and after oleate perfusion. Pancreatic protein output increased from 72 +/- 12 to 420 +/- 55 mg/10 min-1 after oleate administration. However, after atropinization the rise in pancreatic protein output was significantly lower (152 +/- 36 mg/10 min-1) (P less than 0.01). We have shown that, using our RIA method, there is a measurable rise in plasma CCK LI after intraduodenal oleate. After atropinization the CCK response was decreased significantly during the first 30 minutes, but was virtually unchanged during the second 30 minutes, when the fall in pancreatic protein output was most marked. We conclude that the cholinergic mechanism which plays a role in the endogenous stimulation of pancreatic protein secretion by intraduodenal oleate cannot be explained simply be decreased CCK release. This mechanism may be hormonal, distinct from secretin, or neural possibly, via activation of an enteropancreatic reflex.

Animals↗
PubMed1978

The effect of mucaine on gastrin release in man.

The effect of Mucaine and Aludrox on basal and food stimulated immunoreactive gastrin has been assessed in normal control subjects and patients with duodenal or gastric ulcer. No differences in gastrin responses were observed either in the basal period or after the protein meal with the two antacids. As previously described, release of gastrin was greatest in gastric ulcer patients but in contrast to previous results,normal subjects seemed to show a greater response than duodenal ulcer patients but this was not statistically significant. Thus the combination of a local anaesthetic oxethazaine with aluminium hydroxide gel does not lead to diminished gastrin release and is not the prime mechanism of action of this agent.

Adult↗
PubMed1977

Cimetidine in the treatment of duodenal ulcer.

In a double-blind trial performed in two centres, 67 outpatients with endoscopically confirmed duodenal (55) or pyloric canal (12) ulcers received cimetidine (34 patients) or placebo (33 patients) for six weeks. At 6 weeks complete healing of ulcers was significantly increased in patients receiving cimetidine (82%) compared with those receiving placebo (39%) (chi2=11-27; P less than 0-0008). Patients receiving cimetidine had significantly less daytime pain and required less antacid than those receiving placebo. Gastric acid secretion measured one week after cessation of treatment demonstrated that there was no rebound hypersecretion of acid in patients who had received cimetidine. The pretrial basal acid output of those patients whose ulcers failed to heal during cimetidine therapy was significantly greater than that of those whose ulcers healed during treatment with the drug (P less than 0-001). No side effects were encountered.

Adult↗
PubMed1977

Effect of atropine on food-stimulated gastrin release after truncal vagotomy in man.

Studies have been performed on man after truncal vagotomy to ascertain the effect of 1.2 mg of atropine sulfate on basal and postprandial immunoreactive gastrin. Atropine had no effect on basal gastrin, but it caused a significant increase in both the peak postprandial gastrin (135 to 240 pg per ml without the 139 to 308 pg per ml with atropine) and the integrated gastrin response (10.2 and 15.5 ng-min per ml over 2 hr respectively). This indicates that vagal integrity is not essential for the enhancement of the gastrin response by atropine and implies a direct effect on the antral gastrin cell.

Adult↗
PubMed1976

Relationship of serum gastrin response to lower oesophageal sphincter pressure.

The role of gastrin in controlling lower oesophageal sphincter pressure (LESP) has been examined by measurement of LESP and serum gastrin response to a test protein solution and a control solution in humans. Both solutions were associated with significant (P less than 0-005) rise in LESP, but serum gastrin rose significantly (P=0-05) only after the protein solution. The rise in serum gastrin after the protein solution preceded the rise in LESP by 30 minutes. These results suggest that the lower oesophageal sphincter response to feeding may be independent of protein and is unrelated to gastrin release.

Adult↗
PubMed1975

Variability of serum gastrin levels in Zollinger-Ellison syndrome. Studies with two antisera to gastrin.

A patient with recurrent peptic ulceration and presumed Zollinger-Ellison syndrome whose serum gastrin concentration varied widely is reported. Two antisera, one directed predominantly against nonsulfated gastrin and the other measuring both sulfated and nonsulfated gastrin, showed that in addition to wide variation in gastrin levels, this patient secreted his gastrin predominantly in the sulfated G34 form. The possibility of variable serum gastrin levels, which may reflect either spontaneous vaiation in gastrin output from Z-E tumors or differing specificity of the antiserum utilized in the immunoassay, may be of importance in the diagnosis and management of patients with the Zollinger-Ellison syndrome. Because of gastrin heterogeneity in the Z-E syndrome, this study reinforces the concept that a broad spectrum antibody, detecting all gastrin components should be routinely used in detection of patients suspected of having the Z-E syndrome.

Betazole↗
PubMed1975

Prolonged control of hypoglycaemia by L-asparaginase in islet cell carcinoma producing insulin and gastrin.

L-asparaginase (140,000 units) infused into the hepatic artery resulted in a remission from disabling hypoglycaemia for nine months in a man with islet cell carcinoma of the pancreas and hepatic metastases. The tumour produced insulin and gastrin with resulting hypoglycaemia and recurrent peptic ulceration which were unresponsive to other drugs. Following L-asparaginase there was a fall in both plasma and insulin and gastrin.

Adenoma, Islet Cell↗
PubMed1975

Symptomatic hypergastrinaemia with achlorhydria: reflief by antrectomy.

A women had hypergastrinaemia associated with the variety of gastritis (Type A) that is associated usually with pernicious anaemia, together with recurring bouts of severe abdominal pain. Fasting serum gastrin levels ranged between 600 and 2750 pg/ml. There was a rise in serum gastrin levels after a standard protein meal, indicative of a large G cell mass, and a fall after intragastric HCI, which led to a trial of treatment with HCI; this gave some symptomatic relief. After surgical antrectomy there was a profound fall of serum gastrin from a pre-operative level of 2500 pg/ml to constant values of 16--25 pg/ml, and complete and lasting relief from the bouts of abdominal pain.

Achlorhydria↗