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Query: UMLS:C0024523 (malabsorption)
7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anderson's disease is a rare autosomic recessive condition involving the transport of fat through the intestinal mucosa, which could be due to a defect in the intestinal form (B48) of apolipoprotein B. Isolated cases and one important series only have been reported. We wish here to complete the description of the disease. Seven children (age 6 months to 13 years at time of diagnosis) were followed for one month to 15 years. They presented with a malabsorption syndrome, malnutrition, fatty diarrhea (steatorrhea 4-18 g/24 h), failure to thrive (height -1 to -5.5 SD for age) and sometimes disappearance of deep tendon reflexes. Biologically they had signs of malabsorption, hypocalciuria, osteoporosis, low serum iron, decreased levels of vitamins A and E, and hypo-alpha- (50-127 mg/100 ml) and beta- (73-175 mg/100 ml) lipoproteinemia due to decreased levels of plasma cholesterol (40-70 mg/100 ml), and phospholipids (34-67 mg/100 ml); apolipoproteins A1 (26-69 mg/100 ml and B (21-44 mg/100 ml) were also low. After a fatty meal, triglycerides and apolipoproteins did not increase and chylomicrons did not appear. Jejunal biopsies showed the characteristic aspect of enterocytes loaded with lipid droplets. On electron microscopy, these fat droplets were seen in the cytoplasm but neither in the endoplasmic reticulum and the Golgi complex nor in the intercellular spaces. They did not appear to be enclosed in membranes and differed from chylomicrons by their size and density. The disease could thus be due to an abnormal apolipoprotein B48, which would prevent its binding to triglycerides and thus the formation of chylomicrons.
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PMID:[Anderson's disease. Clinical and morphologic study of 7 cases]. 259 48

The literature is briefly summarized as to how several nutrients affect immune function, susceptibility to infection, and cancer susceptibility or progression. Nutritional deficiencies can impair immunity and so influence susceptibility to infectious agents, including ones that are common and relatively virulent in acquired immune deficiency syndrome (AIDS) patients. A variety of nutrients affect several of the immune functions that are defective in human immunodeficiency virus (HIV)-infected individuals. For example, beta-carotene increased the number of CD4+ cells; vitamin E decreased the number of CD8+ cells and increased the CD4+/CD8+ ratio; vitamin D decreased the CD4+/CD8+ ratio; and iron increased the number of peripheral lymphocytes in humans receiving supplementation. Furthermore, nutritional deficiencies can influence gastrointestinal function, while infectious diseases can influence nutrient requirements by altering the efficiency of absorption and the rate of tissue metabolism. Malnutrition, depressed serum zinc levels, and intestinal nutrient malabsorption have been found in AIDS patients. The above findings suggest that dietary manipulations might diminish the immune defects in HIV infection and enhance resistance to opportunistic infections. However, dietary alterations in immune defects are generally not well quantified and may be small relative to the magnitude of the defects observed in AIDS patients. Because conflicting or adverse effects have been reported for some nutrients, recommendations for dietary supplementation in HIV-infected individuals are premature and possibly hazardous. Further studies are much needed to relate dietary nutrient intakes to clinical outcomes.
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PMID:The potential role of nutritional factors in the induction of immunologic abnormalities in HIV-positive homosexual men. 265 89

A 47-year-old nonvegan woman presented to my rural family practice with an anemia and was found to be deficient in iron, folate, and vitamin B12. Initial vitamin B12 malabsorption was documented by Schilling test and was reversed by nutritional repletion alone. This case illustrates that simple lack of intrinsic factor is not the only cause of vitamin B12 malabsorption in primary care patients and that inadequate diets may cause significant pathological consequences in ambulatory patients.
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PMID:Transient vitamin B12 malabsorption in a patient with mixed nutritional anemia. 271 80

Comparative studies of body weight, height, intracellular water representing cell mass, and age, and plasma concentrations of albumin, vitamins, trace elements and iron stores in Aboriginal children aged 6 to 13.5 years, from two rural Aboriginal settlements and one rural Caucasian school (Hawker) provided evidence of significant deficits in one of the Aboriginal settlements (Yalata). Yalata Aboriginal children had lower body weights and heights for age and lower intracellular water values. Plasma albumin, zinc, iron, alpha-tocopherol, beta-carotene and retinol concentrations were lower relative to the normally grown Aboriginal children at Nepabunna. The latter children did not differ from rural Caucasian children for the parameters studied. The reasons for this poorer growth at Yalata may reside in poor nutrition, or repeated bowel infection in postnatal life leading to malabsorption, or both. Limited observational evidence suggests that Giardiasis has a high prevalence at Yalata, and it has been shown elsewhere that Giardiasis is capable of inducing malabsorption with resulting nutritional deficiencies.
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PMID:Malnutrition in aboriginal children at Yalata, South Australia. 273 99

We investigated the nutritional state and pathophysiologic mechanisms involved in the malabsorption of 27 patients with total gastrectomy and esophagojejunostomy reconstruction without reservoir; they were first evaluated after a median period of 9 months after surgery and were not receiving either nutritional or pharmacologic support. Mean postoperative weight loss was -13.7 +/- 1.59%; mean daily caloric intake was 31.7 +/- 2.41 kcal/kg/day, with 70% of subjects ingesting less than 30 kcal/kg; P/kg was 1.2 +/- 0.09, with 21% of patients ingesting less than 1 g P/kg/day; mean ratio of nonprotein energy to 1 g nitrogen intake was 142 +/- 8.74:1, with only 24% of patients attaining a ratio greater than 150:1; and mean fat malabsorption was 37.4 +/- 4.6%. Hemoglobin (Hb), serum albumin, prealbumin iron, and folate were more often abnormal in the early postoperative period, whereas transferrin and vitamin B12 concentrations deteriorated later. alpha 1-Antitrypsin clearance was abnormal in almost all patients (indicating an intestinal protein loss), and the pancreolauryl test was abnormal in 60%. Neither morphological nor absorptive alterations of the small bowel nor an abnormal transit time or bacterial overgrowth was found. We conclude that inadequate caloric intake appears to be the main cause for malnutrition after total gastrectomy, but that caloric losses caused by steatorrhea and enteric protein leakage must be subtracted from intake, thus decreasing the amount of available calories.
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PMID:Malnutrition and malabsorption after total gastrectomy. A pathophysiologic approach. 279 31

In 92 children aged 3 to 24 months with suspected malabsorption syndrome the nutritional status was assessed, the results of routine diagnostic laboratory tests were analysed, and the correlation was sought between these parameters and the degree of atrophy of intestinal villi. A correlation was demonstrated between body weight deficit and the pathological result of the d-xylose test and the degree of villous atrophy only in the group of infants, and in children in the second year of life the changes of these parameters were not useful in the diagnosis of the malabsorption syndrome. The assessment of the shape of iron and glucose absorption curve shows a low usefulness nof these tests, and they should not be used in the diagnosis of the syndrome.
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PMID:[Assessment of the correlations of certain clinical and laboratory data with the morphological pattern of small intestine mucosa in the malabsorption syndrome in children]. 281 48

138 Indian patients with megaloblastic haemopoiesis were studied. All were lifelong vegetarians. The diagnosis was nutritional cobalamin deficiency in 95 and pernicious anaemia in 20; only 4 patients had folate deficiency. A third had intestinal malabsorption, 20 had features of osteomalacia, and 87 were iron deficient. Tuberculosis was diagnosed in 17. Cobalamin deficiency may have contributed to these complications via intestinal malabsorption and impaired bacterial killing of phagocytosed bacilli by cobalamin-deficient macrophages. The frequency of pernicious anaemia was the same in Indian subjects as in Caucasians.
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PMID:Megaloblastic anaemia in a vegetarian Hindu community. 286 24

Histamine H2-receptor antagonists are widely used in the treatment of gastrointestinal diseases related to gastric acid hypersecretion. Cimetidine was introduced into medical practice in 1976 and ranitidine, famotidine and nizatidine in 1981, 1985 and 1987, respectively. Haematological adverse effects are relatively uncommon and most have been reported in cases of cimetidine administration. These adverse effects are reviewed under 4 main headings: (a) blood cytopenias and leucocytosis; (b) coagulation disorders related to drug interactions with oral anticoagulants; (c) reduction of dietary iron absorption; and (d) reduction of dietary cobalamin absorption. 85 reported cases of blood cytopenias attributed to these drugs are reviewed, of which 75 (88%) were associated with cimetidine therapy. In postmarketing surveillance studies, the incidence of cimetidine-associated blood cytopenia has been evaluated at about 2.3 per 100,000 patients. Neutropenia and agranulocytosis are by far the most frequently encountered. Whatever the drug or the type of cytopenia, this adverse effect is almost always rapidly reversible when treatment is stopped. Moreover, in several cases other factors such as underlying diseases or additional drugs could have been responsible, at least partly, for the cytopenia. The pathophysiological basis of these adverse effects remains poorly explained. Various mechanisms have been proposed, which in some cases are probably associated: (a) direct toxicity for haemopoietic stem cells; (b) drug-induced immune reactions leading to blood or bone marrow cell damage, and (c) drug interactions, with increased and prolonged action of potentially haematotoxic drugs. Mechanisms (a) and (c) appear to be of particular clinical importance in cases of impaired renal elimination of H2-receptor antagonists. Cimetidine and probably to a lesser extent ranitidine potentiate the action of oral anticoagulants of both coumarin and indanedione structure. This may result in haemorrhagic complications. Such action is a consequence of the reduced hepatic metabolism of oral anticoagulants through a dose-dependent, reversible inhibition of cytochrome P450. Malabsorption of dietary iron and cobalamin appears to result from inhibition of gastric secretion by the H2-receptor antagonists. This is of no clinical importance in short term treatment, but long term use of H2-receptor antagonists may theoretically contribute to the occurrence of iron or cobalamin deficiency anaemia.
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PMID:Haematological adverse effects of histamine H2-receptor antagonists. 290 59

Plasma or erythrocyte levels of ten nutrients (vitamins A, C, B12 and B6; folate; thiamine; riboflavin; zinc; copper; iron) were assayed in 73 patients with various forms of inherited epidermolysis bullosa (EB). Whereas the mean level for each nutrient was within its normal range, deficient levels were noted in individual EB subsets for selected nutrients. Notable abnormalities included low levels of plasma iron and zinc (in junctional EB and recessive dystrophic EB), vitamin C (primarily in EB simplex), vitamin A (in junctional and recessive dystrophic EB), vitamin B12 (primarily in EB simplex), and vitamin B6 (especially in recessive dystrophic EB). With the exception of low plasma iron and zinc levels in junctional and recessive dystrophic EB, however, only a minority of patients in any of the EB subsets had low levels of most of the other nutrients, and an apparent correlation with malabsorption was possible with only selected nutrients.
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PMID:Blood vitamin and trace metal levels in epidermolysis bullosa. 292 44

Dietary intakes of energy and nutrients were calculated from diet history interviews in 30 patients with dermatitis herpetiformis, before and after 18 months on a gluten-free diet. In spite of great changes in the intake of different foods, the mean intake of dietary fibre did not decrease. There was only a small decrease in the intake of iron in women, while the intake in men did not change. Patients with a previous high intake of gluten had indirect evidence of malabsorption.
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PMID:Changes in food consumption and its nutritional quality when on a gluten-free diet for dermatitis herpetiformis. 299 Nov 72


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