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Biomedical subjects

S Freier

Publications and source records attributed to S Freier.

At least 19 recordsLinked to original sources
PubMed1992

Lethal toxic encephalopathy due to childhood shigellosis in a developed country.

Shigellosis results in considerable morbidity in endemic areas, but mortality is rare in developed countries. All pediatric deaths (n = 15) in Israel following shigellosis in the past 10 years were reviewed. The patients' ages ranged from 5 months to 11 years; there were eight boys and seven girls. Three were institutionalized mentally retarded patients, 11 were healthy children. Twelve had definite clinical signs of brain death within 48 hours of onset of disease. Cause of death in all patients was consistent with toxic encephalopathy. No other systemic complication was implicated as the cause of death except for one case consistent with a "Reye-like" syndrome. Shigella species were as follows: 8 flexneri, 4 sonnei, 1 dysenteriae, and 2 were not identified. Case-control study of these patients vs surviving, hospitalized patients with shigellosis showed similar severity of fever, diarrhea, vomiting, and dehydration and similar incidence of convulsions. Headache was a prominent feature of patients who died; 5 of 7 verbal patients complained of this symptom as opposed to 2 of 20 in the control group (P less than .01). There were no significant differences in the hematological and biochemical profile (except for an increased incidence of hyponatremia in the study group), pattern of shigella species, or antibiotic sensitivity. These findings indicate that mortality from shigellosis in a developed country is due primarily to the toxic encephalopathy syndrome.

Brain Diseases↗
PubMed1991

[Familial hypobetalipoproteinemia with steatorrhea and malabsorption].

In a family in which the father was the mother's uncle, 3 of the 7 children were affected by a syndrome of malabsorption with various clinical symptoms. Diarrhea appeared in 2 of the children at birth, and in the third child at six months. The diarrhea led to failure-to-thrive, muscular wasting and abdominal swelling. However, the children improved spontaneously over the years. During childhood all 3 had manifest steatorrhea. Serum cholesterol was between 39 and 100 mg/dl, while triglycerides were normal to high. Reevaluation during the past year revealed areflexia, deficiency of vitamins A and E and of apoproteins A and B, and prolonged PT time in 2 of the children. Electron and light microscopy of small intestinal biopsies revealed vacuoles in the enterocytes. Electrophysiological tests revealed major disturbances in sensory conduction and brain-stem function. These cases differ from those described in the literature. Although in hypobetalipoproteinemia, 1 of the parents would be expected to be heterozygous and have low serum levels of APO B, in this family the parents had normal levels. Their children had low levels of serum APO A, while in patients with hypobetalipoproteinemia the levels are normal. There is a report of a case of deficiencies of both apolipoproteins, but the patient was asymptomatic, had chylomicronemia after a prolonged fast, and lower cholesterol levels than our patients. 8 other cases of apolipoprotein deficiency have been reported with biochemical characteristics similar to those of our patients, but with retention of chylomicrons in the small intestine.

Apoproteins↗
PubMed1991

Verapamil and furosemide prevent cholecystokinin-induced translocation of immunoglobulins in rat intestine.

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.

Albumins↗
PubMed1987

Familial intestinal pseudoobstruction dominated by a progressive neurologic disease at a young age.

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.

Adolescent↗
PubMed1987

Effect of cholecystokinin and of its antagonist, of atropine, and of food on the release of immunoglobulin A and immunoglobulin G specific antibodies in the rat intestine.

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.

Animals↗
PubMed1987

Rise of prostanoids in rat small intestinal mucosa following intestinal protein hypersensitivity.

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.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Prevalence of postenteritis cow's milk protein intolerance.

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.

Animals↗
PubMed1987

Use of iron supplements in infancy: a field trial.

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.

Anemia, Hypochromic↗
PubMed1986

Growth failure due to protein loss in dermatitis.

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.

Animals↗
PubMed1986

Hypovitaminosis E induced neuropathy in exocrine pancreatic failure.

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.

Ataxia↗
PubMed1986

Intestinal mast cells in different stages of celiac disease.

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.

Biopsy↗