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)

Side effects are common in individuals who have undergone small-bowel bypass surgery for morbid obesity. Most of these side effects subside after a few months. More serious complications may require reestablishment of the bypassed loop. Rarely have vitamin deficiencies been observed. Development of vitamin A deficiency in a patient was characterized by phrynoderma and night blindness. This was promptly reversed by oral treatment with vitamin A. There was no improvement in low to subnormal serum levels of fat-soluble vitamins after a course of tetracycline hydrochloride. Studies suggested presence of a malabsorption state probably due to rapid transit time through the small bowel and reduced absorptive surface.
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PMID:Vitamin A deficiency following small-bowel bypass surgery for obesity. 36 88

Quantitative analyses of plasma concentrations of retinol binding protein (RBP), prealbumin and total proteins were performed in normal subjects and in forty-two patients suffering from diseases of the intestine and liver. The visual dark adaptation ability (DAA) was also assessed. Reduction of DAA and of RBP and prealbumin levels was noted in patients with chronic liver disease and fat malabsorption. In sixty-eight patients with intestinal diseases the RBP concentration seemed to be reduced in relation to the degree and duration of steatorrhoea. Furthermore, inflammatory activity, as revealed by laborabory tests, markedly reduced the RBP level. Treatment with vitamin A increased the RBP and prealbumin concentrations and restored the DAA to normal in patients with malabsorption but normal liver function. In patients with liver disease reduced DAA and serum RBP values were not affected by vitamin A therapy. Only at RBP concentrations below half the normal was impairment of the dark adaptation observed, suggesting that serum RBP is a more sensitive indicator of vitamin A deficiency than measurement of dark adaptation.
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PMID:Plasma vitamin A transport and visual dark adaptation in diseases of the intestine and liver. 56 71

Vitamin A absorption was studied in a group of 28 adult patients with ascariasis and 12 healthy adult controls, using a simplified vitamin A absorption test. In over 70% of the patients with ascariasis malabsorption of vitamin A was demonstrated. Stool egg counts for ascaris were not related to the degree of vitamin A malabsorption. Of the 23 patients in whom a D-xylose absorption test was performed, seven showed excretion less than 20% in 5 hr. Immediately after expulsion of the worms, vitamin A absorption improved in 13 out of 14 patients tested (in nine to normal level). The results of this study suggest that ascariasis in populations on marginal intakes of vitamin A and its precursors is an important contributing factor in producing clinical vitamin A deficiency.
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PMID:Vitamin A absorption in ascariasis. 99 48

A 51/2-month-old infant had the single problem of a bulging fontanelle. A diagnosis of cystic fibrosis with secondary hypovitaminosis A was made by the findings of high sweat chloride values and a low serum carotene level. A greatly accelerated rate of weight gain following the addition of pancreatic enzyme supplements confirmed the presence of malabsorption. The infant developed characteristic fibrosis pulmonary disease at 20 months of age. Animal studies have shown vitamin A deficiency to be associated with increased cerebrospinal fluid (CSF) pressure, diminished absorption of CSF, and pathological findings of thickening and infiltration with mucopolysaccharides of the dura mater around the arachnoid villi.
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PMID:Bulging fontanelle as presenting sign in cystic fibrosis. Vitamin A metabolism and effect on cerebrospinal fluid pressure. 99 79

Hypovitaminosis A caused by a malabsorption syndrome had led to nearly selective disturbance of rod function in a 30 years old female. No rod dark-adaptation could be recorded. The b-wave in the ERG was lacking and the EOG was flat. The cone function appeared to be unimpaired. This could be documented by normal cone-ERG, colour vision, visual acuity and central visual fields. Following treatment with vitamin A the subjective dark-adaptation, the b-wave in ERG and the EOG recovered. The results show that cones contribute barely to the oscillations of EOG.
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PMID:[The influence of vitamin A deficiency on the electrooculogram (author's transl)]. 108 97

We treated two infants with failure to thrive who presented with clinical evidence of conjunctival and corneal xerosis. One patient was referred with possible infectious corneal ulcer thought to exist because there were deep peripheral ulcerations of the cornea and associated hypopyon. The other patient was initially thought to have a nasolacrimal duct obstruction because of excessive tearing. Xerophthalmia secondary to vitamin A deficiency was suspected and led to the diagnosis and treatment of cystic fibrosis in each case. Therapy with vitamin A promptly resolved the xerosis, but it also caused a transient rise in intracerebral pressure. Xerophthalmia can still be a problem in developed countries when underlying disorders, such as cystic fibrosis, lead to vitamin A malabsorption.
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PMID:Xerophthalmia and cystic fibrosis. 231 Mar 33

Xerophthalmia is a common complication of vitamin A deficiency in communities where malnutrition is found. We report on a 16-month-old infant with severe photophobia and failure to thrive. On examination, her major presenting sign was corneal xerosis, with corneal and conjunctival keratinization, and corneal stromal edema with opacification. Based on these findings, vitamin A deficiency secondary to fat malabsorption was suspected, and a workup confirmed the diagnosis of cystic fibrosis. With parenteral vitamin A supplementation, she had complete resolution of her ocular signs and symptoms. This case illustrates the value of a complete ophthalmic examination in the diagnosis of fat malabsorption syndromes.
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PMID:Advanced xerophthalmia as a presenting sign in cystic fibrosis. 274 92

A 22 year old Caucasian girl living in Glasgow presented with eye disease due to Vitamin A deficiency. There was no evidence of liver disease or malabsorption and the vitamin deficiency was found to be due to her bizarre dietary habit.
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PMID:A case of eye disease due to dietary vitamin A deficiency in Glasgow. 360 90

Night vision was tested electroretinographically and psychophysically in a vitamin A deficient patient before and after therapy. Vitamin A deficiency resulted from malabsorption due to a jeujunoileal bypass operation. Before therapy the patient had severely reduced cone and rod function. After the reversal operation, accompanied by 5 injections of a total of 500,000 units of vitamin A, complete recovery of cone and rod functions was observed within 7 months. Shortly after therapy rod sensitivity reached the normal level, while the time course of rod adaptation remained slower than normal and the dark-adapted electroretinographic (ERG) responses were subnormal. At later stages the ERG responses reached normal amplitudes but rod adaptation stayed slow. Only after 7 months did night vision reach the normal level with regard to the time course of rod adaptation, rod sensitivity, and ERG responses.
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PMID:Night vision in a case of vitamin A deficiency due to malabsorption. 660 Feb 10

Vitamin A deficiency remains an important cause of ocular morbidity among patients with chronic liver disease and lipid malabsorption, and is a major cause of blindness in developing countries. Early ocular surface changes include keratinization of the conjunctiva and development of superficial punctate keratopathy. More severe deficiency results in corneal keratinization, ulceration, and necrosis. Vitamin A is necessary for normal differentiation of nonsquamous epithelium; keratinization is a direct consequence of its deficiency. Exposure exacerbates the process and surface phenomena, especially localized drying from loss of mucus-secreting goblet cells, reduced aqueous tear production, and irregularities of the keratinized surface may all contribute to stromal melting, which can occur in the absence of inflammatory infiltration or bacterial invasion. Surface abnormalities respond rapidly to systemic vitamin A. Significantly, corneal changes disappear long before the reappearance of goblet cells. Inflammation sometimes masks or reverses the xerotic process.
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PMID:Effects of vitamin A deficiency on the ocular surface. 660 47


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