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Biomedical subjects

C L Morin

Publications and source records attributed to C L Morin.

At least 73 records · Page 4Linked to original sources
PubMed1976

Small bowel mucosal dysfunction in patients with cystic fibrosis.

Jejunal biopsies were obtained from 37 children with cystic fibrosis, 16 with gluten-induced enteropathy, and 18 control subjects for the following studies: (1) disaccharidase activity, (2) L-ALA-L-Phe hydrolase activity, and (3) intestinal uptake of three 14C-labeled amino acids. Values were significantly reduced in the three determinations in patients with gluten-induced enteropathy as compared to control subjects. Lactase and L-ALA-L-Phe hydrolase activities were significantly reduced (p less than 0.01) in CF patients as compared to control subjects. Definite hypolactasia was also observed in 23% of the children with CF. Uptake of lysine was normal in CF patients whereas that of phenylalanine and cycloleucine was reduced as compared to control subjects. This study suggests an intestinal component to the malabsorption of patients with CF.

Adolescent↗
PubMed1976

Relationship between bile acid malabsorption and pancreatic insufficiency in cystic fibrosis.

Bile acid loss (mg/m2 24h) in the stools of 43 cystic fibrosis (CF) children with pancreatic insufficiency was 751-1 +/- 48-3, while that of six without clinical evidence of pancreatic disease (133-4 +/- 15-9) did not differ from values in 25 controls (109-8 +/- 9-8). There was a good correlation between the degree of bile acid (BA) and fat sequestration. Concomitant changes in bile acid and fat loss were observed in the one group of six patients studied on and off pancreatic enzymes as well as in a second group of seven children treated with pancreatic supplements and maintained on a normal diet followed by a low fat diet supplemented with medium chain triglycerides. Administration of NA bicarbonate led to a significant decrease in fat loss (15-8 +/- 2-7 leads to 10-3 +/- 1-9) without any simultaneous change in bile acid excretion (533-1 +/- 58-3 leads to 500-4 +/- 58-6). Qualitative bile acid patterns in controls, in infants after an ileal resection, and in patients with CF or with coeliac disease showed that the percentage of primary BA followed closely the total amount excreted except in situations where antibiotics were administered. The exact mechanism for the increased loss of BA in CF is unknown. It is found in all age groups and is related to the presence and degree of pancreatic insufficiency. The possibility that unhydrolysed triglycerides may interfere with the intestinal absorption of bile acid needs further confirmation.

Adolescent↗
PubMed1976

Intestinal phosphate transport in familial hypophosphatemic rickets.

The present report outlines an attempt to characterize inorganic phosphate uptake by human jejunal mucosa using biopsy material obtained from six patients affected by the X-linked form of vitamin D-resistant rickets and six control subjects. The tissue from control subjects accumulated 32P actively in a linear fashion against time. The incorporation of inorganic phosphate into organophosphate derivatives is rapid and equilibrates after 10 min at an inorganic over total phosphate ratio of 0.45. Concentrative uptake and incorporation were both suppressed by anaerobiosis or cyanide. Rates of phosphate uptake and incorporation into the organic derivatives by the tissue of hypophosphatemic patients are comparable with normal values. Saturation kinetics observed over a wide range of substrate concentrations (0.003 to 3 mM) elicits only one transport system with an apparent Michaelis constant of 0.2 mM and a maximum velocity of 0.7 mmol/liter/40 min. The kinetic data obtained from the patients do not strikingly differ from the control values. The chemical analysis of the phosphate content of intestinal mucosa from two patients and two control subjects indicates that the tissue is not specifically phosphate-depleted in the mutant individuals. These results are in accordance with the positive results obtained with the oral replacement therapy in familial hypophosphatemia.

Adolescent↗
PubMed1974

Peptic ulcer disease: a clinical study in 73 children.

Seventy-three children with peptic ulcer have been admitted to The Montreal Children's Hospital and l'Hôpital Sainte-Justine over the past 11 years. The primary ulcer group comprised 39 duodenal and nine gastric ulcers; repeat contrast studies were necessary to demonstrate a crater in 25%. Vomiting was especially prominent in the younger patients (1 month to 6 years). Pain was present in the majority of older patients (6 to 18 years) but was considered "typical" in no more than one third. Bleeding occurred more commonly in the older children but five had occult bleeding only. There was a positive family history in 11 children with primary duodenal ulcers but in none of those with gastric ulcers. Follow-up in 34 cases with primary ulcers showed that close to two thirds of the older children have had recurrent problems. Bleeding and/or perforation was the most common mode of presentation in 25 cases of secondary ulcers. Corticosteroids and increased intracranial pressure were the most frequently associated factors, the younger age group being at greater risk.

Adolescent↗
PubMed1973

[Reye's syndrome].

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Adrenal Cortex Hormones↗
PubMed1971

Biochemical and genetic studies in cystinuria: observations on double heterozygotes of genotype I-II.

10 families with cystinuria were investigated by measuring: (a) quantitative 24 hr urinary excretion of amino acids by column chromatography; (b) endogenous renal clearances of amino acids and creatinine; (c) intestinal uptake of (34)C-labeled L-cystine, L-lysine, and L-arginine using jejunal mucosal biopsies; (d) oral cystine loading tests. All four of these were studied in the probands and the first two in a large number of the family members.49 members of 8 families were found to have a regular genetic pattern as described previously by Harris, Rosenberg, and their coworkers. Clinical or biochemical differences between the homozygotes type I (recessive cystinuria) and homozygotes type II (incompletely recessive cystinuria) have not been found. Both types excreted similarly excessive amounts of cystine, lysine, arginine, and ornithine, and had high endogenous renal clearances for these four amino acids. Some homozygotes of both types had a cystine clearance higher than the glomerular filtration rate. Jejunal mucosa from both types of homozygotes exhibited near complete inability to concentrate cystine and lysine in vitro. This was also documented in vivo with oral cystine loads. The heterozygotes type I were phenotypically normal with respect to the above four measurements. The heterozygotes type II showed moderate but definite abnormalities in their urinary excretion and their renal clearances of dibasic amino acids. Of the four amino acids concerned, cystine was the most reliable marker to differentiate between the heterozygotes type II and the homozygous normals. In this study, type III cystinuria, as described by Rosenberg, was not encountered. In two additional families, double heterozygotes of genotype I/II were found. The disease affecting these is clinically and biochemically less severe than that affecting homozygotes of either type I or type II. With respect to the four parameters used in this study, the double heterozygotes type I/II have results which are intermediate between those of the homozygotes type I and II and those of the heterozygotes type II.

Adolescent↗