[Soy-based formula in infant nutrition].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S Freier.
Explore the source record for details and available documents.
Our previous studies have shown that cholecystokinin and pilocarpine are known to be extracellular messengers promoting the release of immunoglobulins A and G antibody activity in the lumen of the rat intestine. In the present study, which was also performed in rats, we show that CCK also promotes the translocation of albumin, electrolytes, and water into the lumen of the intestine. The effect of CCK on the translocation of immunoglobulins, albumin, and electrolytes is reduced by the prior injection of the calcium-channel blocker verapamil and the chloride-channel blocker furosemide. Taken together, the above observations suggest that the translocation of immunoglobulins, albumin, and electrolytes in the intestine appears to be stimulated by identical mechanisms and to proceed simultaneously.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Chronic neuropathic intestinal pseudoobstruction is a rare entity, characterized by recurrent episodes of bowel obstruction without a mechanical obstructive cause. We report five members of two Jewish-Iranian families in whom chronic neuropathic intestinal pseudoobstruction was associated with an identical and unique progressive severe neuronal disease. It appeared within the first two decades of life. The disease consisted of external ophthalmoplegia, ptosis, and severe sensory and motor peripheral neuropathy. Three patients also had neuronal hearing loss. There was no evidence of central nervous system involvement and all patients were mentally intact. The combined disease was confirmed by radiologic, electrophysiologic, and histologic studies. Specific nutritional deficiencies, toxic elements, and systemic diseases affecting both the gastrointestinal tract and the nervous system were ruled out. It seems that these patients suffer from an autosomal recessive, presently unrecognized variant, of chronic neuropathic intestinal pseudoobstruction. In a patient with severe peripheral neuropathy of unknown etiology associated with symptoms suggestive of intestinal obstruction, the possibility of chronic neuropathic intestinal pseudoobstruction has to be considered.
Cholecystokinin has previously been shown to produce a rise in immunoglobulin A (IgA) antibodies in the intestinal fluid of human volunteers. Whether the source of these antibodies was pancreatic, biliary, or mucosal had not been defined. The object of the present investigation was to study factors involved in regulating the release of IgA and IgG antibodies from the intestinal mucosa. Hooded-Lister rats were sensitized to ovalbumin. After the sensitization protocol, which lasted 21 days, the rats were anesthetized and a segment of intestine 10 cm long was isolated and perfused in vivo. This segment was flushed with normal saline for 30 min to remove all pancreatic, biliary, and other secretions. It was found in this model that after the intravenous injection of cholecystokinin-octapeptide there was a rise of IgA and IgG antibodies within 2.5 min. Significantly increased secretion of IgA lasted for 10 min, and increased secretion of IgG lasted for 20 min. The cholecystokinin antagonist proglumide reduced the secretions of both immunoglobulins. Atropine reduced baseline IgA secretion by one-half. Intragastric protein hydrolysate, which left the body through the severed end of the duodenum, also raised IgA and IgG levels significantly in the perfused intestine. Control animals receiving intragastric normal saline did not have an elevation of IgA or IgG levels. The phenomena described here demonstrate that the rate of IgA release from the mucosa is influenced by endocrine and nervous stimuli. The rate of IgG release is, as far as could be ascertained, only under endocrine control and not significantly influenced by the cholinergic antagonist atropine.
The purpose of the present study was to establish whether there is an elevated prostaglandin concentration in the intestinal mucosa in rats suffering from an immediate type hypersensitivity reaction. Rats of the Hooded-Lister strain were sensitized and challenged with ovalbumin. Control rats were given adjuvant only. Prostanoid content of scraped mucosa was determined by radioimmunoassay. It was found that the prostaglandin E2 content in the sensitized intestine was significantly elevated as compared to the controls. There was no significant rise of 6-keto prostaglandin F alpha or thromboxane E2 in the sensitized rats. These results show that prostaglandin B2 participates in intestinal immediate type responses and may explain some of the clinical manifestations of food protein allergy.
The object of this study was to ascertain the frequency of postinfectious cow's milk protein hypersensitivity (CMPH). Twenty-four infants less than 3 months old were included in the study. Following hospitalization for acute gastroenteritis, the infants were given a protein hydrolysate formula for a period of 6 weeks, after which an intestinal biopsy was performed. Thereafter, a milk challenge was given. The existence of CMPH was defined as a postchallenge reduction of one or more of the mucosal disaccharidases below the normal levels for our laboratory. A bacterial etiology of the gastroenteritis was found in 10. Nineteen infants had no adverse reaction to cow's milk after 6 weeks on a hypoallergenic formula. Only two could be confidently diagnosed as having developed secondary CMPH; both had been infected by Escherichia coli 0 111. One infant had primary CMPH and one extra-intestinal CMPH. The incidence of secondary CMPH with gastrointestinal manifestations in this series was considerably less than described elsewhere.
Iron-deficiency anaemia in infancy, which is an important public health problem even in countries where gross malnutrition is not prevalent, can be prevented by iron supplementation or by fortification of infant foods with iron. A programme of iron supplementation was carried out in two places in Israel through the Maternal and Child Health services in the course of their routine duties. Though 89% of the mothers complied and gave iron supplements to their infants for a period of 1-9 months, only 26% continued for the full 9 months. A stastically significant difference was found in the haemoglobin and mean erythrocyte volume levels between the iron-supplemented group and the controls. The results indicate that the use of a higher daily dose of iron for a shorter period might lead to better compliance and greater benefits.
Explore the source record for details and available documents.
A 10-month-old infant is described who suffered from extensive atopic dermatitis, failure to thrive, hypoalbuminaemia and oedema. Large amounts of sticky exudate were lost through the skin and were shown to be rich in albumin. As renal and intestinal loss of protein was excluded, the patient's condition was ascribed to the loss of albumin through the skin at a rate that out-stripped the synthesis of this protein. Treatment with steroids resulted in dramatic clearing of his dermatitis, and subsequent rapid correction of his hypoalbuminaemia, oedema and anaemia.
A 4 year old girl with congenital nerve deafness and pancreatic insufficiency had incapacitating ataxia. Electrophysiological studies of the median nerve and the brain stem evoked response were abnormal. Serum vitamin E concentration was low. After intramuscular injections of vitamin E the ataxia disappeared and electrophysiological variables reverted to normal.
A study of mast cell content of the small intestinal mucosa in children with celiac disease is presented. Twenty patients with true celiac disease were studied and compared with 7 patients with transient gluten intolerance and 20 normal control patients. In healthy children we found (mean +/- SE) 142.5 +/- 16.4 mast cells/mm2. In children with active celiac disease, only 40.1 +/- 19.5 cells were found. This difference was highly significant (P less than 0.001). On a gluten-free diet for 1.5 years, the number of mast cells was 82.2 +/- 27.2/mm2 and still remained significantly depressed (P less than 0.001). Upon gluten challenge in celiac disease, the numbers fell to 58.3 +/- 32.6/mm2, while in transient gluten intolerance the numbers of mast cells attained were 102.5 +/- 22.5/mm2, near normal values. These findings indicate that during the untreated phase of celiac disease the number of mast cells is depressed. On a gluten-free diet, the number rises but does not reach normal control levels even after prolonged remission. It is suggested that even during remission of celiac disease the mast cells continue to be damaged by unidentified toxic agents.
Explore the source record for details and available documents.
The aim of the present study was to create clearly documented immediate-type allergy to food protein in the intestine of rats and to study some pathophysiological phenomena induced by challenge with the allergen. To achieve this, rats were sensitized with ovalbumin. A passive cutaneous anaphylaxis reaction to ovalbumin was negative in all controls and positive in all test animals when Bordetella pertussis was used as adjuvant. Sixty minutes after an intravenous injection of 125I-human serum albumin and 45 min after an ovalbumin challenge, given by gavage, the rats were sacrificed. The intestine was removed and sections taken for morphologic studies. The remainder was rinsed, opened, cut into measured segments, weighed, and the radioactivity was measured. Disaccharidases, alkaline phosphatase, and protein were estimated in homogenates of epithelium. Results in both control and test animals showed that radioactivity decreased as one moved distally along the intestine. However, radioactivity was significantly higher (p less than 0.01) in the intestine of test animals than in controls. Radioactivity in liver, kidney, spleen, and lungs was identical in test and control animals. There was significant reduction in levels of alkaline phosphatase (p varied from less than 0.05 to less than 0.001), maltase (p less than 0.05), and sucrase (p less than 0.05 to less than 0.01). Lactase activity in contrast was significantly raised (p less than 0.05). There was no change in intestinal morphology or in the intestinal mast cell count.