Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an attempt to throw light on the question of age-related variations in the normal blood content of cobalamin and on the frequency of deficiencies of antimegaloblastic nutriments in the elderly, 273 geriatric patients have been investigated. Low serum vitamin B12 values were found in one third of these patients, due to latent pernicious anaemia in five and malabsorption in seven cases, and probably caused by nutritional deficiency of folate or cobalamin in 78 cases. In that part of the series with apparently normal vitamin B12 levels, the mean value (379+/-14 pg/ml) was lower than the mean (456+/-20 pg/ml) for a younger control group. However, this cannot be taken as a sign of a physiological lowering of the cobalamin values with age, as nutritional deficiencies could not be ruled out in this part of the series. It is concluded that serum vitamin B12 assays should be performed rather liberally in the aged. Patients with nutritional deficiency of cobalamin or folate should be treated, even if frank megaloblastic anaemia is not present.
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PMID:Serum vitamin B12 levels in the aged. 98 99

The existence of tropical sprue in Africa is controversial. In this paper we present 31 cases seen in Rhodesia over a 15 month period. They have the clinical features, small intestinal morphology, malabsorption pattern, and treatment response of tropical sprue. Other causes of malabsorption, and primary malnutrition, have been excluded. The severity of the clinical state and intestinal malabsorption distinguish these patients from those we have described with tropical enteropathy. The previous work on tropical sprue in Africa is reviewed and it is apparent that, when it has been adequately looked for, it has been found. It is clear that the question of tropical sprue in Africa must be re-examined and that it existence may have hitherto been concealed by the assumption that primary malnutrition is responsible for the high prevalence of deficiency states.
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PMID:Endemic tropical sprue in Rhodesia. 100 77

A 48-year-old man with previously diagnosed scleroderma with bowel involvement was admitted to hospital with severe malnutrition attributed to malabsorption. Shortly after this, he developed features of intestinal obstruction followed by paralytic ileus. Due to failure to respond to medical treatment, operation was carried out. On two occasions adhesions were divided, but the bowel failed to function. At a third operation the proximal half of the small bowel below the duodeno-jejunal flexure was excised. Following this the patient made a good recovery. Small bowel involvement in scleroderma is discussed. Malabsorption is probably related to bacterial proliferaiton in the small bowel secondary to stasis and may be helped by antibiotic drugs. Other disturbances resulting in inability of the bowel to propel its contents may comprise syndromes of obstruction and paralytic ileus. Although management of scleroderma bowel involvement is usually medical, surgical treatment may be indicated under certain circumstances. It may be life-saving.
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PMID:Scleroderma (progressive systemic sclerosis) with severe bowel involvement. Treatment by extensive resection of the small intestine. 107 79

A 46 year old man presented with selective hypogammaglobulinemia, malabsorption and long-standing secondary malnutrition. Although the patient had essentially unmeasurable levels of immunoglobulins G (IgG), M (IgA), he had normal levels of immunoglobulin E (IgE). He was found to be anergic when tested for the delayed cutaneous hypersensitivity reaction. Evaluation of his cell-mediated immunity in vivo and in vitro suggested one discrete lesion, a defective production of the lymphocyte mediator macrophage migration inhibitory factor. With improved nutrition the patient "repaired" this defect in the "efferent" limb of cellular immunity and was no longer anergic.
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PMID:Selective hypogammaglobulinemia with persistence of IgE, malabsorption and a nutritionally dependent, reversible defect in cell-mediated immunity. 109 Jan 48

Recent clinical and experimental studies suggest that zinc deficiency may play an important role in the pathogenesis of (1) acrodermatitis enteropathica, and in certain cases of (2) hypogonadal dwarfism, (3) congenital malformations, (4) hypogeusia and hyposmia, (5) nyctalopia and (6) impaired wound healing. Distrubances of zinc metabolism also occur in a broad spectrum of other clinical disorders. The pathophysiological factors which are responsible for hypozincemia include: (1) nutritional deficiency and/or intestinal malabsorption of zinc; (2) hyperzincuria secondary to aminoaciduria; (3) hormonal effects (cortisol, growth hormone, estrogens); (4) hypoalbuminemia; and (5) effects of leukocytic endogenous mediator. The clinical diagnosis of zinc deficiency in patients with specific neurological, dermatological and musculoskeletal disorders is complicated by the complex interactions of these pathophysiological factors and by the need for more dependable laboratory indices of zinc deprivation.
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PMID:Current status of zinc deficiency in the pathogenesis of neurological, dermatological and musculoskeletal disorders. 109 48

Growth of bacteria greater than 10-5 organisms/ml was found in 22 children, of whom 17 gave a histroy of chronic diarrhoea. The other 8 children had either no diarrhoea or where having an acute attack lasting for a few days. In those with chronic diarrhoea, Esch. coli, bacteroides, and enterococci tended to occur more frequently, whereas streptococci occurred more frequently in those with acute diarrhoea. Bacilli, staphylococci, micrococci, klebsiellas, pseudomonads, and candidas often occurred in both groups and in large numbers in those with chronic diarrhoea. This confirms previous reports in other parts of the world that some children with malnutrition have considerable bacterial contamination of the jejunum, and that this may be of aetiological significance as a cause of much of the diarrhoea seen in malnourished children. It is possible too that this may be important in the pathogenesis of malnutrition. The presence of intestinal parasites in these malnourished children is also noted. A double-blind trial in the use of antibiotics in this condition is advocated to determine whether it is possible to break the diarrhoea-malabsorption-malnutrition cycle. At the same time the effect of simply removing the child to a more sanitary environment, together with an estimate of the natural clearance of bacteria from the upper intestine, should be evaluated.
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PMID:Jejunal microflora in malnourished Gambian children. 109 72

Gastrointestinal protein loss and xylose and lactose absorption were both abnormal in underweight children with acute measles and diarrhoea. The protein loss was equivalent to a mean absolute albumin loss of 1.68 plus or minus 0.21 g/day, while the mean one-hour blood xylose level was 0.93 plus or minus 0.38 mmol/l (14.0 plus or minus 5.7 mg/100 ml) in the acute stage and 1.71 plus or minus 0.43 mmol/l (25.6 plus or minus 6.5 mg/100 ml) after recovery (P less than 0.01). Lactose intolerance was found in four children out of 17 tested. Thus faecal protein loss and malabsorption may contribute significantly to the development of malnutrition after measles.
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PMID:Protein-losing enteropathy and malabsorption in acute measles enteritis. 113 26

Xylose absorption was measured, within ten days of being admitted to hospital, in 54 alcoholics with neurological abnormalities. Small-intestine malabsorption was demonstrated in 19. Classified according to the customary clinical diagnoses, 16 of 49 with alcohol polyneuropathy had abnormal values, with no correlation to nerve conduction velocity. There was also no difference among 14 in predelirium and eight in delirium. However, all four patients with Wernicke's encephalopathy had a malabsorption syndrome. These results are similar, also quantitatively, to those reported in the literature in alcoholics without neurological signs. Alcohol may be involved in the pathogenesis of alcoholic polyneuropathy both as a toxic factor and also via nutritional deficiency.
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PMID:[Alcohol and malabsorption in the pathogenesis of peripheral and central nerve damage (author's transl)]. 113 26

Since 1964, 41 patients with strictly defined, severe primary (dietetic) protein malnutrition have been studied under metabolic ward conditions during prolonged periods, initially on a low (20 g) and later on a high (100 g) protein diet. Clinical, nutritional, hematological, intestinal absorptive and histological studies were performed in the malnourished state, during and after protein repletion. Classical signs and symptoms of malnutrition, lasting for at least 4 months, were present in most patients. Mild diarrhea was frequent. All were normoblastically anemic, hypoproteinemic, and hypocholesterolemic; serum folate values were normal or low but serum B12 values were normal or high. Liver biopsy showed fatty liver in the cases where it was performed. Mild malabsorption was detected in over one-half of the patients, with moderate intestinal radiological abnormalities. Malabsorption was independent of concomitant folate deficiency. All the clinical, absorptive and histological abnormalities reversed with treatment consisting only of a high protein diet. In addition to protein lack, another factor has to be invoked in the pathogenesis of the intestinal abnormalities present in severely malnourished adults from rural areas in the tropics.
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PMID:Enteropathy in adult protein malnutrition: a review of the Cali experience. 114 51

Light microscopy evaluation of the intestinal abnormalities seen in 35 severely malnourished adults revealed changes which are common to other well-documented enteropathies. These included shortening, widening and fusion of the villi, lost convolution of the nuclear line, and diminished epithelial cell height. With Masson's trichrome stain, dense material was seen to have accumulated in a subepthelial location in villi (as described in other enteropathies), in crypts, and perivascularly around the capillaries of the lamina propria. Two findings however appear to characterize the severely malnourished state: a consistent, significant reduction of intestinal mucosal thickness, and in many cases atrophy of the crypts. Statistical analysis of the total mucosal thickness data does not justify five but rather three histological categories. With protein repletion as the sole therapeutic modality, 17 patients in which adequate biopsy samples were available at its completion showed significant amelioration of the aforementioned histological abnormalities, as well as normalization of their previous absorptive defects. The mild enteropathy of severe protein malnutrition must be considered in the differential diagnosis of malabsorption in a tropical setting.
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PMID:Enteropathy in adult protein malnutrition: light microscopic findings. 114 52


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