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)

In order to assess the usefulness of intestinal biopsies as indicators of end-organ responsiveness to vitamin D in uremic patients, calcium binding activity and calcium binding protein (CaBP) content were measured in intestinal biopsies from 12 uremic patients (glomerular filtration rate less than 5.0 ml/min) and 12 adult controls. Values for both were found to vary with the site of biopsy, highest values being obtained in the duodenal bulb, with lower values distally. Values for activity correlated with values for CaBP content in both normals and uremics and no difference was observed between groups. Levels of calcium binding activity and content of CaBP did not correlate with serum immunoreactive parathormone levels, but were directly related to circulating 25-hydroxycholecalciferol (25-OHD) levels. The data show that intestinal CaBP is normal in activity, quantity, and affinity for calcium in malabsorbing uremic patients, and are consistent with the hypothesis that calcium malabsorption in uremia is unrelated to deficiency of intestinal calcium binding protein.
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PMID:Intestinal calcium binding protein in uremia. 11 81

Serum 25-hydroxy-vitamin D (25-OHD) concentrations were measured in 49 patients with hepatobiliary disease in infancy. Low mean values were found in groups of patients with biliary atresia, neonatal hepatitis, choledochal cyst, and chronic intrahepatic cholestatic syndrome. In the group of patients with surgically repaired biliary atresia, the mean value did not differ from normal. Parenteral vitamin D increased 25-OHD in serum in patients with biliary atresia, but did not do so in one patient with neonatal hepatitis. In contrast, oral vitamin D did not increase serum 25-OHD concentrations in patients with biliary atresia. It is concluded that the reduction of serum 25-OHD seen in biliary atresia was largely due to the malabsorption of vitamin D, while in neonatal hepatitis it was due to impairment of 25-hydroxylation of the vitamin.
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PMID:Serum 25-hydroxy-vitamin D in hepatobiliary disease in infancy. 47 12

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

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

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

As part of a randomised controlled study to assess the effect of pasteurization of breast milk on the growth of very-low-birth-weight infants, the longitudinal changes in serum calcium, phosphorus, alkaline phosphatase, 25-hydroxyvitamin D, and bone-gla-protein concentrations were investigated. Infants fed untreated own mother's milk grew more rapidly than those fed pasteurized pooled preterm milk and had higher serum alkaline phosphatase and lower phosphorus values. Serum calcium and 25-hydroxyvitamin D (25-OHD) concentrations were similar in the two groups. Despite the provision of 750 IU vitamin D daily from the 2nd week of life, serum 25-OHD values remained low in a number of infants in both groups, suggesting that either malabsorption of vitamin D or hepatic immaturity might be responsible for the persistently low values. Bone-gla-protein rose significantly after birth and was correlated with alkaline phosphatase values, but not with 25-OHD or phosphorus values. The study supports previous work that indicates that the low phosphorus content of breast milk is probably responsible for biochemical evidence of inadequate bone mineralization and that despite vitamin D supplementation, 25-OHD values do not rise adequately. Thirty-six infants were reexamined between 4 and 11 months after birth. The 25-OHD values had risen significantly in all infants except one who had vitamin D deficiency rickets.
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PMID:Mineral homeostasis in very low birth weight infants fed either own mother's milk or pooled pasteurized preterm milk. 351 33

A 25-yr-old black man with cystic fibrosis and cirrhosis developed symptoms of osteomalacia and hypocalcemia, hypophosphatemia, secondary hyperparathyroidism, and low circulating 25-hydroxyvitamin D (25-OHD). Serum 1,25-dihydroxyvitamin D (1,25-[OH]2D) was within the normal range. Iliac crest bone biopsy confirmed the diagnosis of osteomalacia. Oral administration of 50,000 IU of vitamin D2 failed to relieve symptoms or raise serum 25-OHD levels to normal. Intramuscular vitamin D2, 10,000 IU every 8-12 week, improved symptoms, raised serum 25-OHD to normal, and increased circulating 1,25-[OH]2D to values five times normal. Over the next 10 mo circulating 1,25-[OH]2D remained elevated despite normalization of serum calcium, phosphorus, and parathyroid hormone. Repeat bone biopsy 1 yr after parenteral vitamin D showed healing of the osteomalacia. Malabsorption of vitamin D appears secondary to profound steatorrhea due to pancreatic insufficiency and secondary biliary cirrhosis. Although extensive hepatocellular disease was present, hepatic conversion of vitamin D to 25-OHD was intact. Both high and low circulating 1,25-[OH]2D levels during active osteomalacia have been reported; initially, the level was in the normal range and higher values in this patient occurred with repletion of 25-OHD substrate. This study shows that symptomatic osteomalacia may be a major manifestation of cystic fibrosis in those patients surviving into adulthood. Measurements of serum 25-OHD in cystic fibrosis patients may identify those who should receive supplemental vitamin D.
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PMID:Vitamin D metabolism and osteomalacia in cystic fibrosis. 387 14

Twenty-five consecutive in-patients who had suffered from rheumatoid arthritis for at least five years were investigated radiologically, histologically and biochemically for evidence of metabolic bone disease. Dietary intake of vitamin D was universally well below recommended levels. Serum 25-hydroxycholecalciferol (25-OHD) concentrations did not correlate with dietary intake of vitamin D but correlated significantly with a sunlight exposure score (p less than 0.01). Despite seven patients having 25-OHD levels below the normal reference range, no cases of osteomalacia were found. Pathological fractures, often initially unrecognized, had occurred in the lower limb bones of seven patients in the previous five years. Those with fractures of the leg bones had evidence of more pronounced osteoporosis of the axial skeleton radiologically and histologically and five of the seven had been taking oral corticosteroids. There was close agreement between qualitative histological assessment of osteoporosis and radiographic evidence of vertebral collapse and those with the severest osteoporosis had lower serum levels of 25-OHD than the rest (p less than 0.02). Ten subjects had reduced xylose absorption tests, although frank malabsorption was not found, and in five patients studied the jejunal mucosa was normal.
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PMID:Metabolic bone disease among in-patients with rheumatoid arthritis. 648 30

A survey of vitamin D status in 152 patients with chronic gastrointestinal conditions and 104 patients with chronic liver diseases is presented. Mild deficiency was common and severe deficiency, as judged by plasma 25-OHD levels less than 8 nmol/l, was encountered in every disease category tested. In the gastrointestinal disease patients, deficiency was significantly more common in patients following gastroenterostomy than other gastric surgery, in patients with active Crohn's disease than in those with inactive disease and in patients with chronic pancreatitis or pancreatic carcinoma with cholestatic features than in those without cholestatic features. Deficiency was as common in patients with Crohn's disease who had not been treated surgically as in those who had. There was no significant correlation between plasma 25-OHD levels and any laboratory index of malabsorption or malnutrition except for serum albumin in the gastric surgery patients, haemoglobin and ESR in the Crohn's disease patients and albumin and vitamin E in the group of patients with gastrointestinal disorders taken as a whole. In the chronic liver disease patients, those with late primary biliary cirrhosis had lower plasma 25-OHD levels than those with histological Stage I and II disease who all had normal levels, and those with pruritus and jaundice were more commonly severely deficient. Whatever the underlying disease process, patients with other coincidental medical conditions were much more likely to be deficient as were patients with cholestasis. Evidence of secondary hyperparathyroidism and osteomalacia on bone histology indicated the clinical relevance of the vitamin D deficiency. This study showed no relationship between abnormal plasma vitamin D binding protein levels and vitamin deficiency.
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PMID:A survey of vitamin D deficiency in gastrointestinal and liver disorders. 654

Four infants with less than 35 cm of jejunum and ileum remaining following neonatal operations and after being weaned from long-term total parenteral nutrition onto an "elemental" formula, developed the syndrome of vitamin D deficiency rickets at 9-15 mo of age. The diagnosis of rickets was confirmed by biochemical and radiographic findings. Serum 25 hydroxy vitamin D (25 OHD) values were significantly lower than normal and oral 25 OHD absorption studies indicated severe vitamin D malabsorption. This report emphasizes the importance of prospective assessment of all neonates having distal ileal resection to detect the early stages of vitamin D deficiency rickets.
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PMID:Vitamin D deficiency rickets as a late complication of the short gut syndrome during infancy. 697 20


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