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)

Serum 25-hydroxyvitamin D levels were measured in 36 thalassaemic children and 27 controls aged 5-15 years. Blood specimens were collected from the beginning of April until the end of October 1976. We considered as the winter period the first 3 months and the summer period the last 4 months. We found that (a) thalassaemic children had lower levels of serum 25-hydroxyvitamin D than controls: (b) there was a seasonal variation of serum 25-hydroxyvitamin D in both groups; and (c) the thalassaemic children had malabsorption of vitamin D. We suggest that the bone lesions in thalassaemic children are related to vitamin D deficiency.
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PMID:Serum 25-hydroxyvitamin D levels in thalassaemia. 64 52

Hepatic osteodystrophy consists of three types: osteomalacia, osteoporosis, and periosteal reaction with new bone formation. Secondary hyperparathyroidism is very rare, if it occurs at all. The cause of osteomalacia appears to be vitamin D deficiency due to a lack of vitamin D substrate. In the presence of adequate substrates, 25-OHD and dihydroxy vitamin D metabolites are formed. The vitamin D deficiency results in osteomalacia and malabsorption of calcium and phosphorus. The osteomalacia can be treated successfully with vitamin D supplements. In some patients calcium, phosphorus, and magnesium supplements may be required. The aetiology and treatment of the osteoporosis and the periosteal reactions remain obscure.
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PMID:Hepatic osteodystrophy. 70 74

Vitamin D and mineral metabolism were studied in 21 adolescents and young adults with cystic fibrosis and the results were compared to those in 21 matched controls. All CF patients had been maintained on standard multivitamin supplements in combination with pancreatic enzyme replacement. Despite this supplementation, relative to control subjects the CF patients had a 36% reduction in serum 25-hydroxyvitamin D concentration, a slight but significant reduction in serum calcium concentration, evidence of calcium malabsorption with secondary hyperparathyroidism, and a 14% decrease in bone mass measured by the photon absorption technique. Currently accepted modes of pancreatic enzyme replacement and vitamin D supplementation are often inadequate to maintain normal mineral homeostasis in CF patients; additional measurements may be required to reduce the risk of clinically significant osteopenia concomitant with prolonged survival in CF.
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PMID:Reduced serum 25-hydroxyvitamin D concentration and disordered mineral metabolism in patients with cystic fibrosis. 75 19

Obviously, the relentless decrease in bone mass that accompanies aging will continue the long sought "elixir of youth" is discovered. Individuals, because of race, sex, environmental, dietary, genetic or activity differences, will be more or less predisposed to symptomatic osteoporosis with increasing age. The careful and knowledgeable physician should, however, make every attempt to rule out potentially remediable, subtle forms of demineralizing disorders, such as apathetic or T3-thyrotoxicosis, hyperparathyroidism, malabsorption and osteomalacia or multiple myeloma. Not only do these diseases result in an accelerated loss of bone mass and an increased incidence of skeletal fractures but they mimic postmenopausal or senile osteoporosis radiologically. Once the metabolic or malignant disorders of bone metabolism have been effectively considered and ruled out, the senescent or postmenopausal osteoporotic patient should be treated judiciously with short-term estrogen therapy, a diet sufficient in vitamin D and calcium content and continued attempts to insure adequate skeletal mobilization. The addition of sodium fluoride and/or calcitonin to this regimen should not be attempted without extreme caution until the potentially harmful systemic effects of prolonged therapeutic trials have been appropriately assessed.
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PMID:Senile and postmenopausal osteoporosis. 76 91

A balanced intake of alimentary lipids is necessary for calcium and phosphorus absorption, as for growth and calcification of bone. In lipid deprivation or excess, important disorders of phospho-calcic metabolism appear particularly in young growing subjects. The qualitative content of ingested fats has, too, a great influence : lipids containing short and medium-chain fatty acids, essential fatty acids and oleic acid stimulate calcium absorption. An excess of long chain and saturated lipids, or intake of erucic acid depress calcium absorption and retention. These facts are possible pathophysiological mechanisms in human disorders: The so-called humanized milks are close to human milk regarding their capacity of stimulation of phospho-calcic absorption and growth. In these milks, oleic and linoleic triglyceride level must be increased. In adult pathology, lipidic deficiency of steatorrhea is partially responsible for calcium and vitamin D malabsorption. Conversely, lipid-calcium interactions are not one-way, and an elevated dietary calcium depresses saturated lipid absorption, and has a hypolipemic action interesting in prevention of atherosclerosis of aged patients.
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PMID:[Lipid calcium interactions in experimental and human nutrition (author's transl)]. 77 52

Early neonatal hypocalcemia occurs in premature infants, infants with birth asphyxia, and infants of diabetic mothers. Etiological considerations include decreased calcium (Ca) supply, increased endogenous phosphate load, hypomagnesemia, alkali therapy, functional hypoparathyroidism, defects in vitamin D metabolism, and possibly calcitonin excess. Late neonatal hypocalcemia occurs, with malabsorption of magnesium (Mg), increased exogenous phosphate loading, after alkali therapy of diarrheal acidosis, hypoparathyroidism, and vitamin D related disorders. The therapy of hypocalcemia includes oral or iv Ca salts and in the near future, possibly the newly discovered vitamin D metabolites.
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PMID:Neonatal hypocalcemia mechanism of occurrence and management. 83 1

Twenty-eight Sioux and 29 Saluteaux Indians from a southern and an isolated northern Manitoban community were screened for lactose malabsorption; 55 were also screened for sucrose tolerance. Sixty percent of the subjects were lactose malabsorbers; the incidence increased with age. Lactase deficiency appeared, on the average, between 8 and 15 years of age. About 45% of the subjects were lactose intolerant. Malabsorbers who did not regularly drink milk had the highest symptom scores. The northern subjects consumed significantly more lactose and sucrose than the southern subjects. Two Sioux children were sucrose malabsorbers. It was hypothesized that the significantly greater sucrose consumption by the Saulteaux subjects were responsible for their markedly higher blood glucose curve following the sucrose tolerance tests. Dietary sucrose increases jejunal sucrase activity and the intestinal transport of glucose and fructose. Three of eight children less than 4 years were lactose malabsorbers; hence, medical personnel treating noninjective diarrhea in Indian children should examine for lactase deficiency. It was recommended that vitamin D fortified milk supplements to Indian school children be continued and that the milk be treated so as to reduce abdominal symptoms in the intolerant individuals.
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PMID:Disaccharide consumption and malabsorption in Canadian Indians. 85 12

Plasma levels of 25-hydroxyvitamin D (25-OHD) were found to be significantly reduced in a group of patients with small bowel resection when compared with normal controls. Plasma levels of 25-OHD after an oral dose of 25-hydroxyvitamin D3 (25-ohd3) were also reduced in the patient group. Dietary intake of vitamin D tended to be low in many patients, but seasonal variation of plasma 25-OHD levels indicated normal exposure to sunlight in most of the patients studied. It is suggested that these studies provide some evidence for malabsorption of 25-OHD after small bowel resection, which, it is postulated, may be due to interruption of the enterohepatic circulation of bile acids and of 25-OHD. These factors may contribute towards the low plasma levels of 25-OHD found in the patient group.
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PMID:Plasma levels and intestinal absorption of 25-hydroxyvitamin D in patients with small bowel resection. 85 74

Calcium metabolism was studied prospectively in 12 patients with amyotrophic lateral sclerosis. Two patients showed mild hypocalcemia, malabsorption of calcium, and elevated plasma parathyroid hormone concentrations. Serum 25-hydroxyvitamin D was decreased in one and low-normal in the second. These two patients and a third showed aminoaciduria on thin layer chromatography. Calcium metabolism was apparently restored to normal by dihydrotachysterol, a vitamin D analog, but no improvement in neurologic function resulted. Bone radiographs taken in search of metabolic bone disease showed a significant increase in the incidence of congenital vertebral anomalies in the ALS patients (50% versus 8%). The relationship of the abnormalities in calcium metabolism and in vertebral structure to the etiology of motor neuron disease is not known.
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PMID:Calcium metabolism in amyotrophic lateral sclerosis. 86 4

Pharmacologic doses of corticosteroids impair intestinal calcium absorption and contribute to negative calcium balance. However, the relationship between the impaired calcium absorption and a possible defect in the conversion of vitamin D to its physiologically active form, 1,25-dihydroxyvitamin D, is unknown. We compared fractional calcium absorption (double-isotope method, 100-mg carrier) and serum 25-hydroxyvitamin D (25-OH-D) (Haddad method) in 27 patients receiving pharmacologic doses of prednisone with 27 age-, sex-, and season-matched normal subjects. In patients receiving high daily doses of prednisone (15-100 mg/day), calcium absorption (P < 0.02) and serum 25-OH-D (P < 0.001) were decreased. However, in patients receiving low doses (8-10 mg/day) or high doses (30-100 mg) of prednisone on an alternate-day schedule, both of these parameters were normal. Calcium absorption in the patients treated with daily prednisone correlated inversely with the dose of corticosteroids (r = -0.52, P < 0.025) and, in all steroid-treated patients, correlated directly with serum 25-OH-D (r = 0.58, P < 0.01). In four patients who received high-dose corticosteroid therapy for an average of 4 wk, serum 25-OH-D decreased by 35.5% from pretreatment values. Administration of a physiologic or near-physiologic dose of synthetic 1,25-dihydroxyvitamin D(3) (0.4 mug daily for 7 days) to patients receiving high-dose corticosteroids led to an increase in calcium absorption in all patients. These results suggest that calcium malabsorption in the corticosteroid-treated patients is due to a dose-related abnormality of vitamin D metabolism and not to a direct effect of corticosteroids on depressing transmucosal intestinal absorption of calcium.
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PMID:Intestinal calcium absorption in exogenous hypercortisonism. Role of 25-hydroxyvitamin D and corticosteroid dose. 87 87


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