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)

The pathogenesis, clinical course and treatment of senile-postmenopausal osteoporosis are reviewed. It is likely that several factors, including genetic and racial determinants as well as nutritional calcium and/or vitamin D deficiency in the elderly play a pathogenic role. Available data are consistent with the possibility that the primary alteration of bone metabolism in senile-postmenopausal osteoporosis may be a decrease in de-novo bone formation below the level necessary to compensate for age-related bone loss. The second part of the study deals with the osteomalacia syndrome. The most common known causes of osteomalacia are vitamin D deficiency, especially secondary to malabsorption, and a defective vitamin D metabolism associated with chronic renal insufficiency or prolonged anticonvulsant therapy. The hypophosphatemic forms of osteomalacia may be induced by renal tubular dysfunction or by phosphate deficiency of other origin; in these disorders a pathogenic role of altered vitamin D metabolism has not yet been established.
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PMID:[Osteoporosis and osteomalacia]. 112 74

A permature male infant required intravenous alimentation for six weeks following extensive surgery for ileal and cecal necrosis. At 3 months he developed evidence of hepatitis. Subsequently osteoporosis and the Fanconi syndrome appeared. Urine phosphate clearance was 83 percent of creatinine clearance at a serum phosphate concentration of 1.6 mg/dl. Concentration of plasma immunoreactive parathyroid hormone was elevated at 550 pg/ml. 25-Hydroxycholecalciferol was given at 240 mug/day. Aminoaciduria disappeared and bone healing occurred. Serum phosphate rose to 6.5 mg/dl and phosphate clearance fell to 2 percent of creatinine clearance. Upon cessation of 25-OHCC therapy, the Fanconi syndrome recurred despite administration of vitamin D2. 25-OHCC was then administered at 40 mug/day, and the urine abnormalities were reversed. The patient probably developed hyperparathyroidism, secondary malabsorption, and hepatitis. The Fanconi syndrome was the consequence of the hyperparathyroidism. 25-OHCC therapy was more effective than vitamin D in reversing the disordered state, possibly because of impaired hepatic metabolism of vitamin D2.
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PMID:Fanconi syndrome following bowel surgery and hepatitis reversed by 25-hydroxycholecalciferol. 112 25

Mild rickets was present in 7, and 3 others with severe bone disease developed widespread skeletal demineralization and multiple fractures. The intake of vitamin D was apparently loosely related to the severity of the osteodystrophy. The latter however, was closely linked to both the serum inorganic phosphate and the calciumXphosphate product. The serum calcium was directly related to the infant's gestational maturity, hypocalcaemia being present in those born before 35 weeks. Pathogenetic factors have probably included reactive hyperparathyroidism and nutritional deprivation associated with preterm delivery. Five of the infants who had biliary atresia developed radiological evidence of osteoporosis from about twelve months of age. This may be related to protracted calcium malabsorption, but its true nature remains to be elucidated.
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PMID:The osteodystrophy of prolonged obstructive liver disease in childhood. 125 25

It is well known that osteoporosis is more common in chronic alcoholists than in age-matched controls. Possible aetiological factors could be: malabsorption of calcium and vitamin D, liver disease, abnormal parathyroid function. With this study, the authors investigated parathyroid hormone (PTH) behaviour in thirteen selected patients with alcohol abuse, free from any clinical or humoral sign of hepatopathy, and in ten healthy subjects as a control group. In alcohol abusers a significant reduction of plasmatic PTH, compared to normal calcium levels were found. A possible direct interaction effect between ethyl alcohol and PTH may be suggested, even if further studies are required.
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PMID:Hypoparathyroidism in chronic alcohol intoxication: a preliminary report. 130 58

The influence of insulin on plasma and bone mineral homeostasis was studied in the BB rat model, which develops an autoimmune form of diabetes at the age of about 100 days. Untreated diabetes of short duration resulted in hypercalciuria and intestinal calcium malabsorption despite increased free concentrations of serum 1,25-dihydroxyvitamin D. The concentrations of two vitamin D-dependent calcium-binding proteins were also decreased: a low duodenal calbindin-D 9K concentration corresponding to the low intestinal active calcium absorption and a low serum osteocalcin concentration, corresponding to a low bone formation and highly correlated with serum IGF-I concentration. Indeed, on bone histology a very low number of osteoblasts and low osteoblast activity (osteoid formation and mineral apposition rate) were observed. Similar abnormalities persisted in rats with long-standing diabetes resulting in markedly decreased bone mass and increased brittleness of bone. Diabetes therefore resulted in low-turnover osteoporosis. Several hormones (testosterone, growth hormone and 1,25-dihydroxyvitamin D) and growth factors (IGF-I and its binding proteins) with known effects on bone were markedly decreased in diabetic rats. A continuous infusion of testosterone, GH or 1,25-(OH)2D3 for 14 d by miniosmotic pumps could not improve the biochemical or histomorphometric abnormalities. Insulin infusion for 2 weeks, however, rapidly increased and overcorrected the number of osteoblasts, normalized serum osteocalcin and IGF-I concentrations but could not yet normalize bone mineralization. Continuous infusion of IGF-I alone did not improve the osteoblast number of osteocalcin but markedly stimulated bone mineralization. From these data we can conclude that both insulin and IGF-I are potent bone growth factors but with different mode of action. In human type 1 diabetes, a similar decrease in serum osteocalcin and IGF-I was observed. A reduction of regional bone mass, both in long and trabecular bones, is frequently observed in human diabetes. Cumulative data from case control studies indicate that the life-time fracture risk is increased in diabetes.
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PMID:Diabetic bone disease. Low turnover osteoporosis related to decreased IGF-I production. 146 60

Serum 25-hydroxyvitamin D declines in elderly subjects. This decrease reflects, in part, a lower vitamin D intake. But changes in serum 25-hydroxyvitamin D are more marked in the northern latitudes of the world because less vitamin D synthesis occurs n the skin as a result of a reduced amount of ultraviolet light. Consequently, vitamin D deficiency leading to osteomalacia is more common in thr northern latitudes, particularly among the elderly. The Recommended Daily Allowance of 200 IU of vitamin D in the elderly may be insufficient, since higher doses of 800 IU/day have been shown to reduce the incidence of osteoporotic fractures. The use of more potent analogues of vitamin D, such as calcitriol (Rocaltrol), should be reserved only for those patients who have established vertebral osteoporosis and who generally have more pronounced malabsorption of calcium.
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PMID:Vitamin D metabolism and therapy in elderly subjects. 150 13

The synthesis of osteocalcin or bone gla protein by osteoblasts is markedly stimulated by 1,25-(OH)2D, a key hormone in the regulation of bone mineralization. The circulating levels of osteocalcin have been shown to reflect both the osteoid matrix production and the formation rate of mineralized bone in several metabolic bone diseases (osteoporosis, thyrotoxicosis, primary hyperparathyroidism) in which both mechanisms are tightly coupled because of the absence of mineralization defect. In this study, we measured in 12 patients (7 women, 5 men, 56 +/- 15 yr old) with untreated osteomalacia serum osteocalcin and vitamin D metabolites (25OHD and 1,25-(OH)2D). The results were correlated with biochemical and histomorphometric assessment of bone remodeling. Osteomalacia was due to vitamin D deficiency (5 cases), to vitamin D malabsorption (6 cases), and to hypophosphataemia in 1 case. When compared to control values, serum osteocalcin was increased in patients with osteomalacia (7.4 +/- 4 vs. 3.7 +/- 1.3 ng/mL; P less than 0.001) and was positively correlated with serum alkaline phosphatase (r = 0.65; P = 0.03) and negatively with 25 OHD (r = -0.61; P = 0.04). Serum osteocalcin was not correlated with 1,25-(OH)2D [r = -0.45; not significant (NS)] even after exclusion of the patient with hypophosphataemia. Serum osteocalcin was positively correlated with the osteoid volume and osteoid perimeter (r = 0.71 and 0.69 respectively; P less than 0.01) but not with any of the tetracycline-based parameter of bone mineralization at the tissue level (r ranging from -0.41 to +0.42, NS). Serum 25 OHD, but not 1,25-(OH)2D, was positively correlated with the mineralization rate (r = 0.59; P less than 0.05 and r = 0.54; NS). We conclude that in patients with osteomalacia, a condition which is characterized by an increased osteoid accumulation due to a decreased mineralization rate, the increased level of serum osteocalcin reflects the increased osteoid synthesis but not the mineralization defect. In this disease, serum osteocalcin is inversely correlated to the severity of vitamin D deficiency reflected by serum 25 OHD, but not to the serum levels of 1,25-(OH)2D.
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PMID:Serum osteocalcin is increased in patients with osteomalacia: correlations with biochemical and histomorphometric findings. 156 62

Intestinal disease might contribute to osteopenia. Measurements of IgA antibodies to gliadin have been established as an accepted screening procedure for detection of coeliac disease. When we applied these measurements to 92 patients with verified osteoporosis, 11 subjects (12%) were found to have elevated levels. This is markedly higher than the incidence in healthy subjects (3%). However, the patients with raised levels of IgA antibodies displayed no clinical symptoms and no laboratory evidence of calcium malabsorption. Thus their values for serum calcium, phosphate, parathyroid hormone (PTH), alkaline phosphatase and osteocalcin, as well as the fasting urinary excretion of hydroxyproline and calcium, were similar to those found in other patients with osteoporosis. Intestinal biopsy verified coeliac disease in three patients and was normal in another three. This gives an incidence of verified coeliac disease in this patient group that is approximately tenfold higher than that in the healthy population. Subclinical coeliac disease appears to be unusually over-represented among patients with idiopathic osteoporosis, and screening for gliadin antibodies might therefore be a valuable addition to the routine assessment of the osteopenic patient. The mechanisms underlying the relationship are not clear, but calcium malabsorption is not evident.
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PMID:Screening for antibodies against gliadin in patients with osteoporosis. 158 66

The action of 1 alpha-hydroxycholecalciferol (oxydevit) was estimated in 204 patients with renal osteodystrophy, osteoporosis of varying etiology, osteomalacia because of malabsorption, congenital rickets-like diseases. The drug was shown to be highly effective in the treatment of secondary hyperparathyroidism in uremia, steroidal and senile osteoporosis. The treatment involved replacement therapy.
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PMID:[Experience in treating metabolic osteopathies with 1 alpha-hydroxyvitamin D3 (oksidevit)]. 181 42

A secondary hyperparathyroidism resulting from decreased intestinal calcium (Ca) absorption has been proposed as a contributory factor to glucocorticoid-induced osteoporosis. Inhaled steroids do not usually suppress adrenal gland function unless daily doses above 1,500 microgram are used. A recent study, however, has shown a reduced total body calcium in patients on regular beclomethasone treatment. In theory, osteopenia in these patients could be due to a direct effect of inhaled steroids on bone or due to an impaired intestinal calcium absorption. In this study, Ca absorption and parathyroid hormone (PTH) secretion were evaluated in three groups: 1) asthmatics on continuous oral and inhaled steroid treatment (11.3 +/- 4.4, range 5-33.5 mg.day-1 prednisone and 660 +/- 265, range 400-1,600 microgram.day-1 beclomethasone, respectively); 2) asthmatics on regular beclomethasone therapy (585 +/- 210, range 400-1,200 microgram.day-1); and 3) healthy subjects. The prevalence of vertebral fractures was evaluated by a spinal X-ray. No differences were found in either Ca absorption or PTH serum levels between asthmatics and healthy subjects (analysis of variance-ANOVA). Vertebral fractures were significantly more frequent in patients from group 1 (14 of 25) than in those from group 2 (2 or 25). We conclude that both prolonged oral steroid treatment and inhaled steroids, at doses lower than 1,600 microgram.day-1 do not cause Ca malabsorption, and that hyperparathyroidism does not contribute to osteoporosis in these patients.
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PMID:Intestinal calcium absorption and parathyroid hormone secretion in asthmatic patients on prolonged oral or inhaled steroid treatment. 185 73


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