S. Bank

INSULIN RESERVE IN PATIENTS WITH CHRONIC PANCREATITIS

Abstract Sixteen patients with unequivocal evidence of chronic pancreatitis were subjected to intensive β-cell stimulation by combined intravenous injection of glucagon and tolbutamide after oral glucose. The serum-immunoreactive-insulin responses of the whole group were significantly impaired when compared with normal controls. The degree of impairment seemed to be proportional to the degree of glucose intolerance. It is postulated that the diabetic syndrome of chronic pancreatitis represents an example of acquired insulinopenia and is thus a valuable clinical model for assessing the effects of this in man.

CHRONIC PANCREATITIS AND ALPHA-1-ANTITRYPSIN

110 patients with proven chronic pancreatitis have been studied to assess the prevalence of the various Pi phenotypes of alpha1-antitrypsin in this disease compared with a control group of 116 blood-donors. The phenotype PiMZ (including Mweak) was significantly more prevalent and PiMM significantly less so in the patients with pancreatitis. It is possible that a heterozygous deficiency of this protease inhibitor renders the pancreas more vulnerable to aetiological agents (e.g., alcohol).

The Cephalic Phase of Pancreatic Secretion in Man

Five cases with achlorhydria have been investigated by sham-feeding to establish the existence of a cephalic phase of pancreatic secretion in man. The results of the study showed that as far as the individual enzymes were concerned, the most consistent and greatest response to sham-feeding was found in the concentration and output of trypsin and lipase. A rise in chymotrypsin concentration and output was also found but the amylase response was more variable. Basal volume and bicarbonate concentration was maintained. Sham-feeding would appear to produce a highly concentrated pancreatic juice. The mechanism of the cephalic phase of pancreatic secretion is discussed.

Effect of Calcitonin on the Serum Amylase Levels after Endoscopic Retrograde Cholangiopancreatography

Calcitonin or placebo was infused in a double-blind study in 30 patients undergoing endoscopic retrograde cholangiopancreatography. Calcitonin was found to have no significant effect on the hyperamylasemia following this procedure.

Sweat electrolytes in chronic pancreatitis.

Sweat electrolytes were carried out in 84 adult patients with calcific pancreatitis, 51 with noncalcific pancreatitis, and the results compared to 37 adult controls. Of the patients with calcific pancreatitis, 33.5% had sweat sodium levels greater than 90 mEq/liter and 14.4% a level greater that 120 mEq/liter. Patients with noncalcific pancreatitis also had a high incidence of elevated sweat sodium levels. Sweat potassium levels were less discriminating, and there appeared to be high sweat calcium levels in a few patients so tested. The reasons for the elevated sweat sodium levels in pancreatitis is not readily apparent, and the possible relationship to heterozygous forms of cystic fibrosis is discussed.Sweat electrolytes were carried out in 84 adult patients with calcific pancreatitis, 51 with noncalcific pancreatitis, and the results compared to 37 adult controls. Of the patients with calcific pancreatitis, 33.5% had sweat sodium levels greater than 90 mEq/liter and 14.4% a level greater that 120 mEq/liter. Patients with noncalcific pancreatitis also had a high incidence of elevated sweat sodium levels. Sweat potassium levels were less discriminating, and there appeared to be high sweat calcium levels in a few patients so tested. The reasons for the elevated sweat sodium levels in pancreatitis is not readily apparent, and the possible relationship to heterozygous forms of cystic fibrosis is discussed.

The natural history of corrosive gastritis

Case reports of 5 patients with corrosive gastritis are presented. The corrosive was ingested accidentally in one, without the patients knowledge in another, and with suicidal intent in 3. Hydrochloric acid in the form of cleaning fluid was the offending substance in 4 and potassium hydroxide in 1. The natural history of the disease is outlined. The dramatic onset of dyspepsia, the liability to hemorrhage, and the relentless progression to pyloric stenosis is stressed, and the tendency of the pyloric gland area to be selectively involved is confirmed. The entire stomach was stenosed in one, and associated involvement of the esophagus was present in 2 of the patients. The radiological and clinical points of similarity between corrosive gastritis and carcinomatous infiltration of the antrum are mentioned. The danger of gastroscopy in the condition is discussed. Attention is drawn to the finding of low serum albumin values in patients with corrosive gastritis. It is tentatively suggested that the latter may constitute another cause of protein-losing gastropathy. The treatment of the condition is briefly considered.SummaryCase reports of 5 patients with corrosive gastritis are presented. The corrosive was ingested accidentally in one, without the patients knowledge in another, and with suicidal intent in 3. Hydrochloric acid in the form of cleaning fluid was the offending substance in 4 and potassium hydroxide in 1.The natural history of the disease is outlined. The dramatic onset of dyspepsia, the liability to hemorrhage, and the relentless progression to pyloric stenosis is stressed, and the tendency of the pyloric gland area to be selectively involved is confirmed. The entire stomach was stenosed in one, and associated involvement of the esophagus was present in 2 of the patients. The radiological and clinical points of similarity between corrosive gastritis and carcinomatous infiltration of the antrum are mentioned. The danger of gastroscopy in the condition is discussed.Attention is drawn to the finding of low serum albumin values in patients with corrosive gastritis. It is tentatively suggested that the latter may constitute another cause of protein-losing gastropathy.The treatment of the condition is briefly considered.

DISSECTING MICROSCOPY OF RECTAL MUCOSA

Abstract Under the dissecting microscope the normal appearance of the rectal mucosa is a honeycomb pattern of units formed by a vascular network. Under oblique light, pits (presumably crypts of Lieberkuhn) can be seen in the centre of these units. This vascular pattern is clearly disturbed in biopsy specimens from patients with ulcerative colitis, and in many cases no pits can be seen.

Maximum acid output and position of peptic ulcers.

In a retrospective analysis of 2218 tests of gastric secretion 27% of patients with duodenal ulcers had an abnormal capacity to secrete acid. The abnormality was evident only in patients who had had symptoms for longer than three years, and was greatest in patients who had had symptoms for six to nine years. There was no significant difference between the capacity to secretic acid in patients who had symptoms of duodenal ulcer for less than three years and the capacity to secretic acid in normal controls. The tendency for the capacity to secrete acid to increase with duration of symptoms was also evident in patients with gastric ulcers. The positions in which ulcers were found were closely related to the maximum acid output (M.A.O.), and to the age of patients. The site of recurrent ulcers, after vagotomy and drainage, was also related to the M.A.O. after vagotomy. These influences of ageing and vagotomy on the site of ulcers can be attributed to their antecedent effect on the M.A.O. It is suggested that the capacity to secret acid alone is not responsible for the genesis of peptic ulcers but that it influences the position in which an ulcer may develop under the influence of an unknown ulcerogenic factor.

Exocrine pancreatic function in intestinal malabsorption and small bowel disease

Exocrine pancreatic function was studied by means of secretin/pancreozymin stimulation in 50 patients with small bowel disease. Forty-five patients had clinical and biochemical evidence of malabsorption. In none of the patients was there evidence of primary pancreatic disease. Impaired amylase or bicarbonate concentration was found in 62% of the patients; however, in only 6 was there gross pancreatic insufficiency and in only 2 of these was the volume output also decreased. Insufficient dietary protein intake, malabsorption and protein loss in the bowel, with subsequent amino acid and albumin deficiency, are suggested as major causes of pancreatic dysfunction in small bowel disease. In some cases a combination of factors, including folic acid deficiency and chronic malnutrition secondary to intestinal disease with weight loss, are likely causes. In this series, pancreatic function was abnormal in 78% of patients with low serum albumin and 52% of patients with normal serum albumin. The pancreatic insufficiency in intestinal disease is rarely as pronounced as that found in pancreatic steatorrhea; there is usually little difficulty in distinguishing the two, although the secretin/pancreozymin test is not completely discriminatory.Exocrine pancreatic function was studied by means of secretin/pancreozymin stimulation in 50 patients with small bowel disease. Forty-five patients had clinical and biochemical evidence of malabsorption. In none of the patients was there evidence of primary pancreatic disease. Impaired amylase or bicarbonate concentration was found in 62% of the patients; however, in only 6 was there gross pancreatic insufficiency and in only 2 of these was the volume output also decreased. Insufficient dietary protein intake, malabsorption and protein loss in the bowel, with subsequent amino acid and albumin deficiency, are suggested as major causes of pancreatic dysfunction in small bowel disease. In some cases a combination of factors, including folic acid deficiency and chronic malnutrition secondary to intestinal disease with weight loss, are likely causes. In this series, pancreatic function was abnormal in 78% of patients with low serum albumin and 52% of patients with normal serum albumin. The pancreatic insufficiency in intestinal disease is rarely as pronounced as that found in pancreatic steatorrhea; there is usually little difficulty in distinguishing the two, although the secretin/pancreozymin test is not completely discriminatory.

MAXIMUM ACID OUTPUT AND RISK OF PEPTIC ULCER

The relationship between the capacity to secrete acid and the risk of peptic ulcer has been examined prospectively in 114 healthy symptom-free students and retrospectively in 2361 patients with and without ulcers. The risk of ulcer was found to increase as te maximum acid output (M.A.O.) increased, and the risk of recurrent ulceration, after vagotomy and drainage for duodenal ulceration, was found to increase as the postvagotomy M.A.O. increased. The risk of recurrent ulcer, at any postvagotomy M.A.O., was always greater than the risk of ulceration in a healthy individual with an equivalent M.A.O.. The addition of an antrectomy to a vagotomy restored the risk of recurrent ulcer towards that of a healthy individual developing his first ulcer. The therapeutic benefit of adding an antrectomy to a vagotomy could not be attributed solely to its enhancement of the percentage reduction in M.A.O. from 65% to 95%. The major therapeutic effect of an antrectomy seems to be achieved independently of its action on M.A.O.