Biomedical subjects
Publications and source records attributed to C L Morin.
Ménétrier's disease is one of the rarer causes of protein-losing enteropathies seen in childhood. At onset of symptoms, the present case and 15 others reported so far were younger than 10 yr of age. Edema was usually more conspicuous than gastrointestinal symptoms. In contrast to the usual chronicity of the disease in adults, the illness is self-limited, transient, and benign.
Three groups of rats were fed, respectively, a chemically defined diet intragastrically (IG), an equivalent diet intravenously (IV) and solid food orally (CH) for 8 days, and their small intestines and colons compared. All received equal calories. The small intestine was divided into equal proximal (A), middle (B), and distal (C) segments for measurements. Mucosal weight per cm in segments A and B of IG were, respectively, 65 and 38% higher than in IV (P less than 0.01), but 27 and 33% lower than in CH (P less than 0.01). However, in the distal segment, C, mucosal weight in IG was similar to IV and CH was 79% higher (P less than 0.01). DNA and protein followed the same pattern. Segment A sucrase activities were similar in CH and IG and were much higher than in IV (P less than 0.01). Sucrase in IG dropped very rapidly distally so that it became much lower than in CH (P less than 0.05) and similar to IV. Mucosal weight, DNA, and protein in the colon were not significantly different in IG and IV, which were both significantly lower than in CH (P less than 0.01). The results indicate that a chemically defined diet maintains intestinal mass well in the proximal small intestine, but the effect diminishes rapidly in a distal direction so that distal small intestine and colon become atrophied and similar to those in intravenous feeding.
After proximal small bowel resection the remaining small intestine undergoes adaptive hyperplasia. In the present study, the relative contributions of bile and (or) pancreatic juice to adaptive intestinal hyperplasia following proximal resection was studied. Using male Sprague-Dawley rats a 50% proximal intestinal resection was done starting 10 cm distal to the beginning of the jejunum. The animals were also subjected to diversion of bile and (or) pancreatic secretions to the distal ileum at 18 cm proximal to the ileocecal junction. After 8 days gut and mucosal weights, mucosal proteins, and DNA were measured in the duodenojejunum (gut segment proximal to the resection anastomosis) and in the ileum (first half of the small bowel segment distal to the diversion site). The results indicate that (1) in rats fed either chow (Purina rat chow) or a chemically defined diet diversion of pancreaticobiliary secretions to the ileum significantly stimulated ileal mucosa growth whereas no changes were observed in the duodenojejunum, (2) in rats fed a chemically defined diet neither bile nor pancreatic juice affected ileal mucosa when separately diverted to the ileum, and (3) pancreatic juice draining into the duodenum while bile was diverted to the ileum induced hypoplastic changes in the duodenojejunum. The present study suggests that following jejunectomy the regulation of mucosal growth by pancreatic and bile secretions is different in the proximal and distal small intestine. Pancreaticobiliary secretions are trophic for the ileum. However, in the proximal gut bile offers protection against a direct or indirect catabolic action of pancreatic juice.
To identify gastric factors likely to contribute to fat maldigestion and malabsorption in cystic fibrosis (CF), gastric emptying time, secretion rate, and preduodenal lipolytic activity were studied. Gastric emptying of a liquid test meal and gastric acid secretion were determined in five CF teenagers with pancreatic insufficiency and in five healthy controls. During the first hr, the rate of gastric emptying exhibited a linear pattern in both CF patients and controls. Neither the emptying time nor the gastric secretion rate was different. Lingual lipase activity was measured in eight other CF patients with pancreatic insufficiency and in eight controls. Lipase activity was higher (P less than 0.05) in CF patients than in controls with values (mean +/- S.E.) of 34.48 +/- 11.59 and 12.65 +/- 5.60 mumole butyric acid min-1 ml-1, respectively. No correlation with age or body surface was observed. Intragastric lipolysis of a butterfat triglyceride test meal was fast in both groups, but more extensive (P less than 0.05) in CF patients than in controls. The data show that in CF with pancreatic insufficiency, gastric factors contributing to the first step of fat digestion are preserved. In fact, lingual lipase activity was found to be increased, and a more complete intragastric lipolysis was documented.
Four children aged (11.7-13.5 yr) with protracted growth retardation related to Crohn's disease, received a 6-wk period of continuous elemental enteral alimentation with no other form of treatment. Despite drug therapy the yearly height and weight gain velocities of these children (1.7 +/- 0.3 cm and -0.8 +/- 1.4 kg, respectively) had been abnormal during the previous 2 yr. All patients experienced a complete remission of symptoms, improved nutritional status, and significant height (1.8 +/- 0.3 cm) and weight (3.8 +/- 0.5 kg) gains during the 67 wk of treatment. After cessation of elemental enteral alimentation, 3 of the 4 patients continued to grow, and over a period of 4.5 mo from the beginning of this form of nutritional therapy, they gained an average of 5.0 +/- 1.6 kg and 3.5 +/- 0.3 cm. The disease became active thereafter, and the 3 children resumed their previously abnormal growth patterns during the ensuing year. The 4th patient had surgery 2 mo after elemental enteral alimentation and experienced a subsequent second spurt of growth and pubertal changes. This study suggests that a relatively short course of elemental enteral alimentation leads to a temporary resumption of growth in children with severe growth failure and Crohn's disease. The possibility that repeated courses of elemental enteral alimentation might be beneficial needs to be explored.
In this prospective study, 18 consecutive children suspected of cow's milk protein intolerance (C.M.P.I.) on clinical grounds were investigated before and after challenge with cow's milk. One-hour blood-xylose, serum-IgE, eosinophil count, serum-complement (C3) and a jejunal biopsy specimen for histology and disaccharidase activity were obtained from all patients before challenge. Serum-complement was measured again 24 h after the beginning of the challenge and the first three tests were repeated on the fifth day. A second jejunal biopsy was obtained in 9 of the first 10 children. 15 of the 18 children were considered to have C.M.P.I. The one-hour blood-xylose test emerged as a simple and valuable test in the diagnosis of C.M.P.I. A significant drop (51--81%) in the one-hour blood-xylose level was observed in all 15 patients. In all patients but one it dropped below 25 mg/dl. Mean value (+/- S.D.) for the group was 47.5 +/- 11.1 mg/dl before and 17.2 +/- 4.2 mg/dl after cow's milk ingestion.
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A retrospective analysis of oral D-xylose tolerance tests in 435 pediatric patients was performed. A significant difference was found between 126 normal subjects and 47 untreated children with celiac disease one hour after load. The one-hour value was found to be more reliable than was fecal fat analysis in screening children for celiac disease. Sex, age, weight, and body surface did not influence the results of the one-hour value in the control subjects. Forty-eight children with cystic fibrosis had one-hour xylose levels within the normal range, but the means at 90, 120, and 180 minutes after load exceeded significantly (P less than 0.01) those of the controls. In a nonceliac group of 63 children with abnormally low xylose levels, almost all were found to have clinical conditions compatible with upper small bowel mucosal impairment. This study shows that a single estimation of xylose in blood one hour after load is a reliable index of small bowel mucosal function. It is a good screening test for celiac disease and small bowel disorders producing malabsorption in children.
After 48 h of bile duct ligation, enterokinase activity in rat mucosa was significantly lowered in comparison with controls or rats with bile fistula. Rats with bile fistula were similar to controls. Sucrase levels were similar in all groups. Without endogenous trypsinogen, duodenal perfusion with a trypsinogen-containing solution led to more conversion to trypsin by controls. When their own pancreatic secretion was the source of trypsinogen, trypsin was much higher in perfusate from bile-ligated rats. Solubilized enterokinase was also higher in this group. These results indicate that bile stasis leads to decreased mucosal enterokinase activity and increased pancreatic function. The latter may have caused accelerated loss of enterokinase into the lumen, leading to lower mucosal levels.
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Because of the increased incidence of gallstones in cystic fibrosis we compared biliary lipid composition in 26 patients with cystic fibrosis, seven children with cholelithiasis but no cystic-fibrosis and 13 controls. Eighteen of the cystic fibrosis group had cholecystograms, and only one had gallstones. In 14 patients with cystic fibrosis who had stopped taking pancreatic enzymes for one week molar percentage of lipid composition accounted for by cholesterol (mean +/- S.E., 16.3 +/- 2.9) and saturation index (2.0 +/- 0.3) were comparable to values of the cholelithiasis group and higher (P less than 0.01) than those of controls. In 12 patients with cystic fibrosis taking pancreatic enzymes, molar percentage of cholesterol (8.6 +/- 1.7) and saturation index (1.0 +/- 0.1) did not differ from those of controls; in cystic fibrosis there was a preponderance of cholic over chenodeoxycholic acid both off (1.7 +/- 0.2) and on (1.9 +/- 0.3) therapy as compared to the cholelithiasis (0.7 +/- 0.1) and control (0.8 +/- 0.0) groups. The glycine/taurine ratio of conjugated bile acids were lower in enzyme-treated patients with cystic fibrosis (3.7 +/- 0.6) than in patients off treatment (6.4 +/- 1.0), but was higher (P less than 0.01) than in controls (1.8 +/- 0.2). Bile is lithogenic in untreated cystic fibrosis and responds to pancreatic enzymes.
Pseudomembranous enterocolitis is reported in five children. The clinical syndrome, characterized by the acute onset of profuse diarrhea, occurred postoperatively in 2 patients. All the patients had received or were taking antibiotics (penicillin, ampicillin, clindamycin). The disease was severe in 4 persons who presented with hypoproteinemia. Related complications were edema, ascites, pleural effusion, septicemia and/or shock. The diagnosis was made on the basis of typical rectosigmoidoscopic findings. Despite intensive therapy 2 children died. The use of parenteral nutrition is advocated in severe cases with exudative enteropathy. When profuse diarrhea occurs postoperatively or does not rapidly subside with discontinuation of antibiotic therapy, a high index of suspicion should be maintained, even in children, for the possibility of pseudomembranous enterocolitis. An emergency rectosigmoidoscopy should be done in order to make an early diagnosis.
Twenty-two children aged 2 months to 11 years were seen at our institution from January 1970 to March 1975 with clinical, laboratory, and/or histological features consistent with the diagnosis of Reye's syndrome. There were three pairs of siblings. Severity of the illness ranged from relatively benign to rapidly fatal forms. Five received live attenuated vaccines within the three weeks prior to admission. Four relapsed 1 to 21 months after the initial episode, and in one there were multiple recurrences. Six developed major neurological sequelae. All patients graded levels IV and V by EEGs on admission subsequently died in contrast to none from grades 1 and 2. Peritoneal dialysis was carried out in the more severely affected patients. The procedure did not influence final outcome as predicted by the first EEG and is thought to be of limited value.
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