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

Malabsorption (M) is characterized by absorption defect of one or several nutriments in small bowel. Its clinical expression is rarely obvious and biological signs are: anaemia, low serum protein, albumin and lipid rates, low serum calcium, phosphorus and potassium level, and hypoprothrombinaemia. But only 4 simple and reliable tests are needed for diagnosis: i. e.: daily faecal fat amount measurement, daily faecal nitrogen excretion, the xylose test and the Schilling's test. This syndrome is related to many conditions which can be divided into 2 groups with and without intestinal abnormalities. The relationships between M and skin diseases belong to 4 types (J. Marks and S. Shuster): 1) M is responsible for the cutaneous signs, 2) M is caused by a skin disease, 3) both M and skin disease are the result of a same cause, 4) M and skin disease are associated in an indirect way. Only the two first types are dealt with in this report. Skin manifestations occur as a complication in 10 p. 100 to 20 p. 100 of cases of M. They are mostly polymorphous or non-specific, as they are related to multiple vitamin or essential amino acid deficiencies and heal with the treatment of M. The main conditions encountered are diffuse pigmentation, acquired ichthyosis, follicular keratosis, nail brittleness and hair loss. Mucous membrane lesions, purpura and eczematoid or psoriasis-like dermatitis have also been described. More uncommon are clubbing of fingers, finger print abnormalities, kwashiorkor or acrodermatitis enteropathica-like eruptions. The dermatogenic enteropathy, i. e. a M syndrome due to a skin disease, occurs as a result of widespread involvement of the body for instance in psoriasis or eczema; its clinical expression is rarely obvious, the histological record of gut biopsy usually normal and the results of biological tests often dissociated, but steatorrhoea is frequently found. The pathogenesis of the condition is still unknown but its importance is related to the extent of the skin disease and it only improves with the treatment of the latter. All these features and others are discussed in the report with a comprehensive review of the literature.
Ann Dermatol Venereol 1978 Dec
PMID:[Cutaneous manifestations of malabsorption diseases (author's transl)]. 38 Apr 45

Contamination of the small bowel with an abnormal microflora causes a variety of disturbances of intraluminal digestion and of mucosal function resulting in malabsorption of fat, protein, carbohydrate, electrolytes and vitamin B12. Indirect clinical tests for the presence of small bowel bacterial overgrowth must be supported by careful roentgenologic examination of the small intestine and intestinal aspiration studies to establish a firm pretreatment diagnosis. However, the reversal of absorptive defects by antibacterial therapy is valuable confirmatory evidence.
Am J Med 1979 Dec
PMID:The contaminated small bowel syndrome. 39 Oct 36

Intestinal parasites not only cause diarrheal illnesses but may also cause significant malabsorption in man. Separation of true malabsorption caused by a particular parasite from other factors that may coexist with and even mimic malabsorption, such as malnutrition may be very difficult. Despite these problems, it appears that giardiasis, coccidiasis, strongyloidiasis and capillariasis cause malabsorption of many important nutrients. D. latum interfere with vitamin B12 absorption.
Am J Med 1979 Dec
PMID:Parasites ana malabsorption. 39 Oct 37

The intestinal absorption of triglyceride constitutes a multistep process with active involvement of the pancreatobiliary system, the intestine and lymphatics. It is only through the integrated function of these organs that dietary triglyceride can be efficiently absorbed and delivered to the peripheral blood for subsequent metabolism. In this review we discuss each aspect of triglyceride absorption and chylomicron formation and illustrate how various diseases may interfere with the process resulting in fat malabsorption. In addition, the role of the intestine as a major synthetic source of lipoprotein constituents for circulating lipoproteins is discussed.
Am J Med 1979 Dec
PMID:Fat malabsorption--advances in our understanding. 39 Oct 40

Bone loss can be prevented by standard oestrogen replacement therapy and delayed by the administration of calcium supplements. The most suitable patients to treat are those with a raised urinary hydroxyproline or other evidence of rapid bone loss. Patients aged below 65 years with established osteoporosis, and in whom oestrogens are not contraindicated, will derive some benefit from oestrogen therapy. In those with malabsorption of calcium, vitamin D may be added to oestrogen therapy in a dose not exceeding 10,000 units daily or alternatively, small doses of one of the vitamin D metabolites, e.g. 1 alpha OHD3 (alfacalcidol) 1 microgram daily, or 1,25(OH)2D3 (calcitriol) 0.5 microgram daily. In patients aged over 65 years, supplementary calcium (not less than 1000 mg daily) is recommended.
Drugs 1979 Dec
PMID:Treatment of postmenopausal osteoporosis. 39 32

This review examines the contributions made by anorexia, loss of taste, malabsorption and disturbances of intermediary metabolism to the cachexia of cancer. Methods of nutritional assessment are outlined and mention is made of the usefulness of nutritional support as an adjunct to anti-cancer therapies.
Biomedicine 1979 Dec
PMID:The cachexia of cancer. 39 13

In the past decade, we have studied four unrelated children with what we believe is a previously unreported disorder affecting the bone marrow and exocrine pancreas. During infancy these patients had the onset of severe, transfusion-dependent, macrocytic anemia plus a variable degree of neutropenia and thrombocytopenia. Their bone marrows had normal cellularity but were characterized by remarkable vacuolization of erythroid and myeloid precursors, hemosiderosis, and ringed sideroblasts. The vacuoles probably represented manifestations of cellular degeneration and death. In two patients, in vitro bone marrow cultures showed abnormal erythroid and myeloid progenitor cell growth and, in one child, abnormal vacuolated erythroid colonies. Family histories were unrevealing, parents were hematologically normal, and both sexes were involved. There was no evidence of specific nutritional deficiencies or exposure to agents associated with marrow vacuolization. A number of therapeutic interventions produced no effect. One child had clinical malabsorption. This child and one other had extensive pancreatic fibrosis at autopsy. The other two patients had findings indicating exocrine pancreatic dysfunction. Two children had splenic atrophy. This new syndrome, with associated bone marrow and exocrine pancreatic dysfunctions, differs in several respects from the syndrome of pancreatic liposis and neutropenia described by Shwachman et all and Bodian et al, and from other conditions with vacuolization of the marrow or sideroblastosis.
J Pediatr 1979 Dec
PMID:A new syndrome of refractory sideroblastic anemia with vacuolization of marrow precursors and exocrine pancreatic dysfunction. 50 2

Protein digestion and absorption was studied in rats with 6-week-old surgically constructed self-filling intestinal blind loops and steatorrhea, ie, blind-loop animals and controls were fed a 14C-labeled protein meal containing a nonabsorbable marker, 51CrCl3, and sacrificed 1 or 2 hr later. Intestinal contents were analyzed for 14C, 51Cr, protein, trypsin, and the products of digestion. At 1 hr, 14C absorption was greater in controls, but at 2 hr there was no difference in absorption between the two groups. Marker studies showed that blind-loop filling resulted in a delay of the progression of intestinal contents distally. Intraluminal trypsin and porteolysis were similar in the two groups. Endogenous protein was greater in the blind-loop animals. The early stages of the blind-loop syndrome may be characterized by delayed protein absorption secondary to blind-loop filling, which is compensated for by the distal gut resulting in an absence of overall protein malabsorption.
Dig Dis Sci 1979 Dec
PMID:Protein digestion and absorption in the blind loop syndrome. 51 93

Bile acid studies were performed in patients with Crohn's disease, radiologically confined to the colon. The bile acid pool size of 10 patients with isolated Crohn's colitis was significantly lower than that of 10 normal control subjects (P less than 0.001) and of 10 ulcerative colitis patients (P less than 0.005). Measurements of 14C-excretion in breath and in 24 hours stool collections after the administration of 5 muCi 14C-glycocholate showed a normal 14C-excretion in breath and usually a markedly increased loss of 14C in the stool (greater than 7% of the dose). The simultaneous administration of 5 muCi 3H-polyethylene glycol MW 4000 (3H-PEG) as a marker indicated that the 14C/3H ratio in the patients with Crohn's colitis was significantly greater than in a control series of patients with diarrhoea not due to bile acid malabsorption. Studies on the composition of duodenal bile showed a significantly decreased concentration of deoxycholic acid in duodenal bile. These observations suggest bile acid malabsorption in patients with Crohn's disease apparently confined to the colon.
Gut 1979 Dec
PMID:Bile acid studies in patients with Crohn's colitis. 52 81

To investigate the possibility of measuring urinary oxalate output instead of faecal fat excretion as an outpatient screening test for steatorrhoea, we determined 24 hour urinary oxalate and five day faecal fat excretion before and during an oral load of sodium oxalate 600 mg daily (oxalate 4.44 mmol), in 32 patients with suspected malabsorption on a diet containing oxalate 30 mg (0.33 mmol), fat 50 g (180 mmol), and calcium 1 g (25 mmol). Nineteen patients proved to have steatorrhoea (mean faecal fat 62 mmol/24 h, range 19--186 mmol) of varying aetiologies. On the diet alone, urinary oxalate was raised in only nine of these patients (mean 0.25 mmol/24 h, range 0.08--0.59 mmol) (normal less than 0.20). By contrast, when the diet was supplemented with oral sodium oxalate, all 19 patients with steatorrhoea had hyperoxaluria (mean 0.91 mmol/24 h, range 0.46--1.44 mmol) (normal less than 0.44). There was a significant positive linear relationship between urinary oxalate and faecal fat when the 32 patients were on the high oxalate intake (r = 0.73, P less than 0.001), but not when they were on the low oxalate intake. Mean percentage absorption of orally administered oxalate was 5.8 +/- 0.99% (+/- 1 SD) in normal subjects and 14.7 +/- 6.0% (P less than 0.002) in patients with steatorrhoea. Measurement of urinary oxalate output during oral sodium oxalate loading appears to be a reliable and convenient screening test for steatorrhoea.
Gut 1979 Dec
PMID:Oxalate loading test: a screening test for steatorrhoea. 52 84


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