Effect of renal failure or portacaval shunt on release of neurotensin in man.

Neurotensin-like immunoreactivity (NTLI) is released into the circulation following a meal. However, the factors influencing its degradation and metabolism are uncertain, but it is presumed that the kidneys and liver are involved. This study has determined the release of NTLI after a liquid fat meal (200 ml 20% Intralipid) in 10 healthy control subjects, five patients with stable chronic renal failure (CRF), and five patients after a portacaval shunt (PCS), to assess the possible role of the liver and kidney in NTLI metabolism. NTLI was measured by radioimmunoassay using both specific C and N terminally directed antisera. The results showed: Basal NTLI levels are similar in controls, after PCS, and in CRF. A liquid fat meal produces a single early peak of NTLI and levels are greater after PCS than in controls or CRF. Levels return much more slowly to basal in CRF and after PCS. Thus it is likely that both the liver and kidney are involved in the metabolism and clearance of NTLI.

The effect of atropine and vagal stimulation on the release of neurotensin-like immunoreactivity in man.

This study investigated the food stimulated release of neurotensin-like immunoreactivity (NTLI) in man with and without the administration of atropine, and the influence of vagal stimulation by modified sham feeding and insulin hypoglycaemia. NTLI was measured, after ethanol extraction, by specific C- and N-terminally directed antisera. With both a liquid fat meal and a mixed meal an early peak of NTLI occurred. The mixed meal also produced a second sustained rise in plasma NTLI. An intramuscular injection of 0.6 mg atropine sulphate abolished the early peak, but had no effect on the late peak. Modified sham feeding and insulin hypoglycaemia did not release NTLI. We conclude that it is possible that a cholinergic non-vagal mechanism is responsible for the early phase of food stimulated release of NTLI in man, and that the second sustained rise may be cholinergically independent.

Chronic idiopathic megaduodenum in a family.

This paper reports a family in which idiopathic megaduodenum occurred. The index case was a 17 year old male with lifelong steatorrhea, episodic vomiting of food consumed days before, offensive belching, and recurrent abdominal pain and distention. The diagnosis was made by a barium meal examination, but only after a failed small bowel biopsy suggested some anatomical abnormality. Direct questioning about family members then revealed that his father, aged 43 years, had similar symptoms and a subsequent barium meal confirmed the diagnosis. Screening of the family revealed megaduodenum in the 20 year old sister who was totally asymptomatic and had normal fecal fat levels but an abnormal breath test. The remainder of the family members were asymptomatic and had normal radiology. This family, in which idiopathic megaduodenum occurred in three of six members, is reported because it illustrates some of the features of idiopathic megaduodenum and chronic idiopathic intestinal pseudo-obstruction. It also demonstrates the need to investigate the families of apparent sporadic cases. Such investigation may uncover additional symptomatic and asymptomatic individuals who may be presenting diagnostic difficulty, and who, by virtue of an early diagnosis, may be spared unnecessary surgery.

Cholestyramine induced hyperchloremic metabolic acidosis.

The first reported case, in an adult, of cholestyramine induced hyperchloremic metabolic acidosis is a 70 year old female with a two year history of primary biliary cirrhosis confirmed by histologic and immunologic criteria. After taking cholestyramine II sachets twice daily for two months she presented with lethargy, confusion and drowsiness. Examination revealed confusion, jaundice, signs of chronic liver disease, portal hypertension and hepatic encephalopathy. Laboratory investigations confirmed a metabolic acidosis (pH 7.15) and hyperchloremia. Multiple cultures failed to reveal sepsis and a urinary pH of 4.85 together with tests of renal acidification, excluded renal tubular acidosis. She received 600 mEq of sodium bicarbonate intravenously over 36 hours by which time her mentation, electrolytes and pH were normal. It is presumed that her hyperchloremic metabolic acidosis was secondary to cholestyramine because of the similarity to pediatric reports; the rapid and lasting response to intravenous sodium bicarbonate; the absence of another etiology; normal serum potassium, chloride and bicarbonate despite continued spironolactone therapy after recovery.

Training in sigmoidoscopy. An assessment in three teaching hospitals.

To assess the standard of training in postgraduate sigmoidoscopy in Melbourne, a questionnaire was prepared and distributed to resident medical officers (RMOs) in three teaching hospitals. The survey showed that practical instruction in technique is inadequate, and that most individuals perform too few sigmoidoscopies to become competent at either examining or recognizing lesions. A substantial number of RMOs had never seen common and important lesions such as polyps or colorectal cancer. Most RMOs considered their training to be poor and stated that they lacked confidence in their ability to perform sigmoidoscopy. The current training programme needs detailed reassessment and improvement.

Collagenous colitis: a recently recognised reversible clinicopathological entity.

A case of collagenous colitis is reported in an 86 year old man who presented with watery diarrhea. This case differs from previous reports in that five of the six reported cases involved women, mostly in their mid-forties, and that previously the collagenous band has been demonstrated in the mucosa of the left side of the colon only. This case is the first report to demonstrate the collagenous band in the right side of the colon as well as the left, and is the thickest band reported to date. In keeping with the two reported cases with follow-up, the subepithelial collagenous band was shown to have disappeared three months after the initial biopsy with a corresponding clinical improvement after symptomatic treatment only. The diagnosis needs to be considered in all patients presenting with watery diarrhea, and can only be confirmed after rectal or colonic biopsy.

The influence of smoking on the healing of duodenal ulcer treated with oxmetidine or cimetidine.

The influence of smoking on duodenal ulcer healing was examined during a double blind study of 83 patients randomly allocated to oxmetidine or cimetidine treatment. Smoking habits were recorded but patients were not advised to change these. Smokers and nonsmokers were similar clinically and did not differ in compliance with medication. Both H2-receptor antagonists were equally effective and after four weeks of treatment ulcers were healed in 76% of patients. Ulcer healing occurred significantly less frequently in smokers (69%) than nonsmokers (89%). Smokers with healed ulcers consumed fewer cigarettes per day (mean +/- SE: 15.8 +/- 1.4) than those whose ulcers did not heal (22.2 +/- 2.7). When smokers were grouped according to daily cigarette consumption, a direct relationship was found between increasing cigarette consumption and decreasing frequency of ulcer healing. No reduction in ulcer healing was apparent in patients who smoked nine cigarettes a day, or less.

Influence of cigarette smoking on healing and relapse in duodenal ulcer disease.

There are conflicting reports on the influence of cigarette smoking on healing in patients with duodenal ulcer; some studies show an adverse effect on healing rate and others no effect. This study reports the influence of smoking on short-term healing and relapse rate in 135 patients with duodenal ulcer who were treated with cimetidine (90), ranitidine (25), and oxmetidine (20), all powerful H2-receptor antagonists. Ulcer healing and relapse were documented endoscopically and all studies were performed in a double-blind manner. In the short term, 95% of nonsmokers healed compared with 63% smokers (p less than 0.01) and there was a positive correlation between failure to heal and number of cigarettes smoked. During a 12-mo follow-up examination after healing and on no treatment, 53% of nonsmokers and 84% of smokers relapsed (p less than 0.01). These results show that smoking adversely affects healing of duodenal ulcer with H2-receptor antagonists and that continued smoking leads to a higher relapse rate.