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

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

Vitamin A and zinc metabolism are affected both by ethanol and by hepatic cirrhosis. Ethanol causes abnormal dark adaptation by acting as a competitive inhibitor with retinol for alcohol dehydrogenase in the eye. In animals oral ethanol intake results in increased losses of zinc by the urinary and fecal routes. Vitamin A malnutrition in cirrhotics may be caused by poor diet, malabsorption, decreased hepatic vitamin A uptake, and decreased hepatic storage capacity for vitamin A. In some cirrhotic patients zinc deficiency and or protein deficiency may limit the ability to respond to vitamin A. Combined vitamin A and zinc deficiencies are common in cirrhotics and either may result in abnormal dark adaptation or impaired taste and smell. The interaction of these two micro-nutrients must be kept in mind by the clinician caring for alcoholic or alcoholic cirrhotic patients.
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PMID:Vitamin A and zinc metabolism in alcoholism. 700 92

Night blindness from vitamin A deficiency was observed in a patient with intestinal malabsorption, which in turn was attributable to duodenal diverticulosis and bacterial growth. Monthly supplementation with vitamin A and correction of bacterial overgrowth with tetracycline resulted in a normalisation of plasma retinol levels and resolution of the night blindness.
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PMID:Intestinal malabsorption presenting with night blindness. 829 82

The effect of Ascaris lumbricoides infection on retinol absorption was investigated in young children from a slum area of Dhaka City, Bangladesh. Twenty-four children aged 4-10 years were screened and in every case eggs of either Ascaris, Trichuris or hookworm were isolated from the stool. The average serum retinol was 0.91 (SD 0.35) mumol/l and sixteen children had levels below 1.05 mumol/l. This compared with a serum retinol concentration of 1.70 (SD 0.52) mumol/l in five reference children from a more privileged social background. An oral dose of retinol (41.8 mumol) was given to ten children in whom the concentration of Ascaris eggs in the stool varied. Less than 1% of the supplement could be recovered in the stools collected over the following 48 h. Ascaris worms were isolated from the stool and assayed for retinol content. In no case was retinol detected in the worms. These findings do not support the contention that infection with Ascaris predisposes to malabsorption of vitamin A.
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PMID:Vitamin A absorption in children with ascariasis. 832 56

1. Vitamin A: There are very few reports on vitamin A deficiency in Japan because of the rising national status of nutrition, while vitamin A deficiency is still an important nutritional problem in developing and poorly developed countries. In the pediatric field, relationship between vitamin A nutrition and the mechanism for development of bronchopulmonary dysplasia have been discussed, since vitamin A acts as a protector from the keratinization of epithelial cells in the mucosal layer and the skin. The changes in the lung tissues with inadequately supplied vitamin A, probably cause the chronic lung disease resulting from mechanical ventilation in neonates, in whom the plasma vitamin A and retinol binding protein levels are usually low. 2. Vitamin E: In keeping with the view that newborn infants and especially premature infants suffer from vitamin E deficiency. On the basis of recent findings of the vitamin E content in the neonatal cells, the previous concept would agree, as an existing marginal deficiency in neonates. The neurologic deficits manifested in a beta-lipoproteinemia is confirmed to be vitamin deficiency in humans. It has also become clear that similar neurologic impairment occurs in other chronic fat malabsorptive states, such as cholestatic liver diseases, extensive resection of the gut. More recently several patients with spinocerebellar degeneration from vitamin E deficiency without other evidence of malabsorption in whom progression of the diseases is terminated by the vitamin E therapy (isolated vitamin E deficiency) have been reported. The above items are discussed.
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PMID:[Vitamin A and E deficiency in children, including the marginal deficiency]. 848 80

Patients with the acquired immunodeficiency syndrome (AIDS) are characterized by a decrease in the number of T helper cells, a defect that is linked to the impaired immunologic competence. Vitamin A and its dietary precursor, beta-carotene, increase absolute T helper cell counts as well as indices of T cell function in both human and animal models. To determine if short-term beta-carotene treatment affects T lymphocyte subsets in patients with AIDS, a single-blind, non-randomized clinical trial of beta-carotene was performed in seven patients with AIDS. Enrollment criteria included no evidence of: a) active opportunistic infection: b) greater than 1 kilogram change in weight in the month preceding enrollment; c) chronic diarrhea or malabsorption; and d) hepatic disease or significant anemia. Beta-carotene was given with meals in two divided doses of 60 mg/day for four weeks; this was followed by no therapy for six weeks. Samples for total white blood cell, lymphocyte and T lymphocyte subset counts were measured at baseline, at the end of four weeks of treatment and another six weeks after treatment had stopped. P24 antigen, beta-2 microglobulin and liver function tests were also measured. All subjects tolerated the treatment well without evidence of toxicity. In response to beta-carotene, total lymphocyte counts rose by 66 percent (.05 < p < .10), and CD4+ cells rose slightly, but insignificantly, in the entire group. In all three of the patients who had baseline CD4+ cells greater than 10/microliters, however, the mean absolute increase in CD4+ cells in response to beta-carotene was 53 +/- 10 cells/microliters (p < .01). Six weeks off beta-carotene treatment, the absolute CD4+ cell count returned to pretreatment levels (p < .01). No change was observed in CD8+ cells. P24 antigen and beta-2 microglobulin did not change during treatment. These preliminary observations suggest that short-term treatment with beta-carotene may increase CD4+ cell counts in patients with AIDS who have greater than 10 cells/microliters.
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PMID:The effect of supplemental beta-carotene on immunologic indices in patients with AIDS: a pilot study. 874 63

Systemic mastocytosis is characterized by an increased number of mast cells in multiple organs particularly skin. A 55-year-old man with mastocytosis presented with nyctalopia caused by malabsorption of vitamin A. Diagnosis was made by documenting a low vitamin A level and an ERG that showed rod-cone deficiency with rods affected more than cones. Vitamin A therapy led to return of good visual function. To our knowledge, this is the first reported case of mastocytosis induced nyctalopia. Vitamin A deficiency should be considered as a potential cause of visual loss in patients with sudden onset of night blindness.
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PMID:Mastocytosis-induced nyctalopia. 879 68

Vitamin A is an essential nutrient for epithelial cell maintenance and repair, and it is known that infectious stresses may depress plasma vitamin A concentrations. Patients with cystic fibrosis are at risk for vitamin A deficiency because of fat malabsorption as well as for the inflammatory stresses of pulmonary exacerbations of their underlying disease. We therefore hypothesized that acute pulmonary exacerbations of CF would depress plasma retinol concentrations, and that these concentrations would return to baseline values when clinical symptoms improved. We prospectively studied 35 CF patients (mean age: 24.2 y) consecutively admitted with pulmonary exacerbations. Plasma retinol, vitamin E, retinol binding protein (RBP), and C-reactive protein (CRP) concentrations were measured on hospital admission and discharge. Dietary intake was measured by using a semiquantitative food-frequency questionnaire. Regression analysis was used to identify significant clinical and laboratory correlates of retinol concentrations. On admission, mean (+/- SD) concentrations of plasma retinol were 1.14 +/- 0.5 mumol/L compared with 1.70 +/- 0.6 mumol/L on discharge (P = 0.0001). Of 35 subjects, 8 (22.9%) had plasma retinol concentrations considered to be in the deficient range (< 0.70 mumol/L). Concurrently, mean concentrations of plasma RBP increased during hospital admission (from 1.46 to 2.24 mumol/L, P = 0.003), and the mean CRP concentration declined (from 25.7 to 9.8 mg/L, P = 0.002). Significant positive correlations were found between plasma retinol concentrations at admission and age, weight, body mass index, triceps-skinfold-thickness percentile, midupper arm circumference percentile, plasma vitamin E, and RBP concentration, thus suggesting that better-nourished patients had more optimal vitamin A status. At admission, plasma retinol concentrations were negatively correlated with maximum body temperature and CRP concentrations, which indicated that the body's acute-phase response was associated with the depression in retinol concentrations. We conclude that plasma retinol concentrations are depressed in acute pulmonary exacerbations of cystic fibrosis, and that concentrations considered to be in the deficient range are common. Vitamin A metabolism during acute inflammatory stress deserves further study.
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PMID:Vitamin A status in acute exacerbations of cystic fibrosis. 883 11

A case with severe malabsorption of fat soluble vitamins is described. The malabsorption developed after an intestinal bypass operation due to morbid obesity. Night blindness occurred as the first symptom of vitamin A deficiency. The cone visual sensory threshold was elevated about one log unit and the rod threshold abot two and a half log units. No changes of the a- and b-waves of the electroretinogram (ERG) was observed. However, during the initial phase of very low serum reninol level (0.21 mumol/l) the summed amplitudes of the oscillatory potentials (OPs) were lower. After parenteral therapy with vitamin A the night blindness disappeared and the dark-adapted rod and cone threshold sensitivity recovered to normal. However, the time-course of rod adaptation first reached normal levels after 5 months. The amplitudes of the OPs of the ERG response returned to normal when the serum retinol level had increased close to normal. Serum retinol levels of 0.7 mumol/l or higher were always associated with normal or close to normal dark-adapted rod sensitivity. However, a normal serum retinol level (> 0.95 mumol/l) and a normal dark-adapted rod threshold sensitivity were not always associated with a normal time-course of the rod adaptation. It is concluded, that the maintenance dosage of vitamin A must be individualized and that patients who have undergone jejuno-ilea bypass surgery must be carefully monitored for vitamin A deficiency by both serum levels and dark adaptation measurements.
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PMID:Attempts to define the minimal serum level of vitamin A required for normal visual function in a patient with severe fat malabsorption. 1099 58

Previously we demonstrated that the digestion, absorption and lymphatic transport of lipid and key essential fatty acids (EFA) from randomly interesterified fish oil/medium-chain structured triglycerides (STG) were significantly higher than an equivalent physical mixture (PM) in a normal lymph fistula rat model and in a rat model of lipid malabsorption caused by ischemia/reperfusion (I/R) injury. The goals of this study were to further explore the potential absorptive benefits of STG by comparing the intestinal absorption and lymphatic transport of tocopherol and retinol when delivered gastrically with either STG or PM under normal conditions and after I/R injury to the small bowel. Food-deprived male Sprague-Dawley rats were randomly assigned to two treatments (sham controls or I/R). Under halothane anesthesia, the superior mesenteric artery (SMA) was occluded for 20 min and then reperfused in I/R rats. The SMA was isolated but not occluded in control rats. In both groups, the mesenteric lymph duct was cannulated and a gastric tube was inserted. Each treatment group received 1 mL of the fish oil/MCT STG or PM (7 rats/group) along with (14)C-alpha-tocopherol and (3)H-retinol through the gastric tube followed by an infusion of PBS at 3 mL/h for 8 h. Lymph was collected hourly for 8 h. Under steady-state conditions, the amount of (14)C-alpha-tocopherol and (3)H-retinol transported into lymph was significantly higher in the STG-fed rats compared with those fed PM in both control and I/R groups. In addition, control and I/R rats given STG had earlier steady-state outputs of (14)C-alpha-tocopherol and (3)H-retinol and maintained approximately 30% higher outputs in lymph throughout the 8-h lymph collection period compared with rats given the PM. We conclude that STG provides the opportunity to potentiate improved absorption of fat-soluble vitamins under normal and malabsorptive states.
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PMID:Randomized structured triglycerides increase lymphatic absorption of tocopherol and retinol compared with the equivalent physical mixture in a rat model of fat malabsorption. 1148 11


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