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

The mechanisms of vitamin D deficiency already described are triggered off by a variety of causes. Confinement indoors leads to defective photosynthesis and dietary restrictions to insufficient intake. Malabsorption results from digestive tract diseases: mainly adult coeliac disease, but also sequelae of gastrectomy, exocrine pancreatic insufficiency, chronic biliary obstruction and all other causes of steatorrhoea. Practically, osteomalacia of digestive origin usually results from multifactorial hypovitaminosis D. The same applies to primary or nutritional biliary cirrhosis, which frequently entails low vitamin D blood levels despite subnormal 25-hydroxylation. Osteomalacia is also found in renal osteodystrophy, where it is partly due to inhibition of 1,25-hydroxylase and subsequent deficiency of 1,25-dihydrocholecalciferol, though other, non vitaminic substances may also be involved. Two misleading forms of the disease must be borne in mind: one with renal tubular lsions, the other associated with functional pseudo-hypoparathyroidism. The aetiology of most cases of osteomalacia due to vitamin D deficiency can be elucidated by a few simple tests.
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PMID:[Osteomalacia due to vitamin D deficiency. Part two: Aetiology (author's transl)]. 742 86

One hundred and four children aged 0-15 years, with suspicion of malabsorption were studied. They had a proximal jejunal biopsy and, at the same time, the following measurements: 25-hydroxycholecalciferol (25-OH-CC), calcium, phosphorus and serum alkaline phosphatase, bone age on X-ray of the left hand and wrist, cortical thickness of the 2nd, 3rd, 4th metacarpal bones. For the analysis of the results, the patients were divided into two groups according to the season (winter vs. summer). None of the patients in either group had clinical or radiological signs of rickets. The following results were obtained: 1. The 25-OH-CC serum levels were significantly lower during the winter than during the summer months. This was observed more frequently in the cases with atrophy of the jejunal mucosa. 2. During the summer, the 25-OH-CC serum levels were not different in the cases with normal or pathological mucosa. This demonstrates the importance of the skin synthesis of vitamin D during the summer months. 3. The mean of the serum calcium levels was significantly lower in the group of children with atrophy of the jejunal mucosa than in children with normal intestinal biopsy. The serum calcium levels were not correlated with the serum 25-OH-CC levels. 4. The serum phosphorus levels were significantly lowered during the winter months in the children aged 0-3 years with pathological jejunal biopsy. 5. The serum alkaline phosphatase levels were lowered in cases of total atrophy of the jejunal epithelium cells. 6. Cortical thickness of the metacarpal bones becomes thinner with the progression of the alteration of the jejunal epithelium cells, independently of season or age. However, only the group of children aged 0-3 years studied during the winter months and with total atrophy of the jejunal mucosa have a significantly diminished cortical thickness of the metacarpal bones. The lowering of the calcium levels and the decrease of the cortical thickness are probably secondary to an impaired intestinal absorption of calcium. In the syndrome of malabsorption, the integrity of the jejunal epithelial cells seems to play a more important role than a vitamin D deficiency in the genesis of this calcium malabsorption.
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PMID:[Phosphorus-calcium metabolism and plasma 25-hydroxycholecalciferol in intestinal malabsorption]. 745 Dec 35

Privational vitamin D deficiency is assumed to be uncommon in the developed countries because of the routine fortification of foods with vitamin D. Malabsorption of vitamin D and calcium (especially in an environment of reduced sun exposure) therefore accounts for the majority of cases of metabolic bone disease seen in patients with various gastrointestinal disorders in the United States. Yet recognition of this often asymptomatic bone disease is unsatisfactory and frequently delayed for months or even years. This results in severe irreversible bone loss, putting patients at increased fracture risk for the remainders of their lives. As evident from the small number of published reports, it is obvious that little attention is given to understanding the pathogenesis and prevention of bone disease in patients with various gastrointestinal disorders. This review will summarize recent advances in the pathogenesis, prevention, and treatment of metabolic bone disease in patients with these disorders. We propose methods for identifying bone loss in such patients so that appropriate preventive measures can be instituted to avoid significant morbidity.
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PMID:Metabolic bone disease in gastrointestinal, hepatobiliary, and pancreatic disorders and total parenteral nutrition. 761 19

Inflammatory bowel disease (Crohn's disease and ulcerative colitis) is associated with decreased bone mineral density and increased risk of osteoporosis. However, the pathogenesis of this bone loss is not yet fully understood. In the present study we measured lumbar bone mineral density (by dual photon absorptiometry), serum levels of parathyroid hormone (PTH) and vitamin D metabolites, and serum markers of bone turnover (alkaline phosphatase and osteocalcin) in 15 patients with Crohn's disease and in 4 patients with ulcerative colitis. The median duration of the disease was 4 years and the median lifetime steroid dose was 10g of prednisone. We compared our results to a control group of 19 normal persons, who were matched for age and sex to the patients. We found that lumbar bone density was reduced by 11% in patients compared with control persons (Z-score -0.6 +/- 0.6 versus -0.1 +/- 0.8; p < 0.05). In patients, the serum levels of PTH, 25-hydroxyvitamin D3, and calcitriol (1,25(OH)2D3) were significantly reduced compared with control persons. Serum alkaline phosphatase activity (AP) was significantly higher in the patients and was inversely related to lumbar bone density. Osteocalcin values were not different between patients and control persons. There was also no difference in serum levels of calcium between the two groups, whereas phosphorus levels were higher in patients. We conclude that malabsorption of calcium was not a primary cause of bone loss in our patients, because we did not find secondary hyperparathyroidism. Accordingly, we did not find a severe vitamin D deficiency, since 25-hydroxyvitamin D3 levels were within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bone mineral density and calcium regulating hormones in patients with inflammatory bowel disease (Crohn's disease and ulcerative colitis). 800 8

Brown bowel syndrome is the name applied to a brown discoloration of the intestine. This is due to lipofuscin deposition in intestinal smooth muscle and occurs in association with malabsorption. Three cases occurring in a coeliac registry of 559 patients are described. One patient presented with acute massive bleeding per rectum, and two were diagnosed at autopsy. The syndrome may be accompanied by vitamin E deficiency and neurologic dysfunction. Two patients had evidence of peripheral neuropathy, and one had low vitamin E levels. Concomitant vitamin D deficiency was present. Fat-soluble vitamin malabsorption, especially if there is a poor response to a gluten-free diet or neuropathy, might alert the clinician to the possibility of brown-bowel syndrome and suggests careful search for lipofuscin in biopsy material, using special histologic techniques.
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PMID:Brown bowel syndrome occurring in coeliac disease in the west of Ireland. 812 83

Hypophosphatemia due to parenteral nutrition has been described frequently. It was attributed to the lack of phosphorus content in parenteral nutrition solutions. With modern parenteral nutrition regimens containing phosphorus, this problem has been virtually eliminated. Enteral nutrition solutions contain adequate phosphate for patients with normal phosphate stores. Hypophosphatemia has therefore rarely been reported in enteral nutrition. We describe two patients with protein-energy malnutrition who developed severe hypophosphatemia during tube feeding with phosphorus-containing formula diets. Chronic alcoholism and vitamin D deficiency due to malabsorption because of Crohn's disease were additional risk factors in these two patients. Patients with depleted phosphate stores and high metabolic demand have a higher daily requirement for phosphorus than is available in routine isotonic enteral formulas. This case report emphasizes the importance of monitoring serum phosphate concentration daily during the first week of refeeding.
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PMID:Enteral supplementation of phosphate does not prevent hypophosphatemia during refeeding of cachectic patients. 820 56

: There is a decline in serum 25 hydroxyvitamin D (25OHD), 1,25 dihydroxyvitamin D (1,25(OH)2D), and calcium absorption with advancing age, which may lead to secondary hyperparathyroidism and bone loss. Studies show a relationship between serum 25OHD and bone density in older men and women, with an inverse correlation between bone density and parathyroid hormone (PTH). Vitamin D supplementation in this age group improves calcium absorption, suppresses PTH, and decreases bone loss. Vitamin D many also reduce the incidence of hip and other nonvertebral fractures, particularly in the frail elderly who are likely to have vitamin D deficiency. Patients with established vertebral osteoporosis have lower calcium absorption than age-matched control subjects, possibly due to reduced serum 1,25(OH)2D or to relative resistance to the action of vitamin D on the bowel. Malabsorption of calcium in women with vertebral crush fractures does not usually respond to treatment with physiological doses of vitamin D, but can be corrected by pharmacological doses of vitamin D or by low doses of calcitriol or alfacalcidol. In a recent randomized, controlled study in 46 elderly women with radiological evidence of vertebral osteoporosis, alfacalcidol 0.25 micro;g twice daily improved calcium absorption, decreased serum PTH, and reduced alkaline phosphatase, whereas vitamin D2 500-1000 IU daily had no effect over the 6-month study period. Studies of the effect of the vitamin D metabolites in the management of elderly women with established vertebral osteoporosis have yielded conflicting results, but suggest that alfacalcidol and calcitriol may decrease spinal bone loss and reduce the incidence of vertebral fractures. Although vitamin D supplementation decreases bone loss and fracture risk in the frail elderly, vitamin D metabolites may prove more useful in the treatment of elderly women with vertebral osteoporosis.
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PMID:Is there a differential response to alfacalcidol and vitamin D in the treatment of osteoporosis? 903 Apr 91

Vitamin D deficiency, which causes osteomalacia, may also be important in the pathogenesis of age-related osteoporosis. We studied serum vitamin D metabolites in 52 young women (mean age: 30 +/- 3 y; range: 25-35 y), 64 elderly free-living women (mean age: 71 +/- 4 y; range: 65-82 y), and 60 elderly women living in nursing homes (mean age: 84 +/- 9 y; range: 61-102 y). Mean serum 25-hydroxyvitamin D (calcidiol) was 10.8 +/- 4.4 nmol/L (27 +/- 11 ng/mL) in women living in nursing homes and was similar to that of free-living young (11.3 +/- 4.2 nmol/L, or 28 +/- 10 ng/mL) and elderly (11.5 +/- 3.2 nmol/L, or 29 +/- 8 ng/mL) women. Vitamin D deficiency (defined as serum calcidiol < 4.8 nmol/L, or 12 ng/mL) occurred in 8% of women living in nursing homes, in 6% of the young women, and in 1.6% of the free-living elderly women. Serum calcidiol was significantly correlated with vitamin D intake (r = 0.25, P < 0.05) and inversely correlated with serum intact parathyroid hormone (iPTH) (r = -0.16, P < 0.03). Serum iPTH increased with age and secondary hyperparathyroidism was observed in 17% of the women living in nursing homes. Calcium absorption declined with age, but calcium absorption and serum 1 alpha,25-dihydroxyvitamin D (calcitriol) were significantly lower in women living in nursing homes, which probably contributed to the secondary hyperparathyroidism. In conclusion, normal serum calcidiol may avoid the problem of osteomalacia, but it does not correct malabsorption of calcium. Although calcitriol corrects the malabsorption of calcium, it remains to be seen whether higher amounts of vitamin D can normalize the calcium malabsorption of aging.
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PMID:Serum vitamin D metabolites and calcium absorption in normal young and elderly free-living women and in women living in nursing homes. 906 31

Osteoporosis, a silently progressing metabolic bone disease that leads to loss of bone mass, is widely prevalent in India and osteoporotic fractures are a common cause of morbidity and mortality in adult Indian men and women. This review of the international patterns of osteoporosis reveals two distinctive clinical features of this disease in Indians. Firstly, hip fractures occur at a relatively earlier age in Indian males and females, compared to their western counterparts; and secondly, a higher male-to-female ratio suggests that Indian males are at a higher risk for hip fractures. The reasons for these differences are not known. It is possible that a dietary deficiency of calcium, beginning early in life, leads to a lower peak bone mass, and consequently osteoporosis at an earlier age. Furthermore, malabsorption of calcium due to a subclinical deficiency of vitamin D may lead to osteoporosis, without causing osteomalacia. With the increase in life expectancy, osteoporosis has become a formidable public health problem in India and a multidisciplinary approach is needed to identify its aetiological factors and devise strategies for mass prevention of calcium and vitamin D deficiency (possibly by fortification of food with these nutrients). Another issue that needs to be addressed is the social dogma against hormone replacement therapy in postmenopausal women. These measures, coupled with health education of the masses, should help promote bone health and control osteoporosis in India.
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PMID:Osteoporosis in India--the nutritional hypothesis. 911 86

Osteomalacia is a generalized bone disorder characterized by impairment of mineralization, leading to accumulation of unmineralized matrix or osteoid in the skeleton. The classical clinical features of osteomalacia include musculoskeletal pain, skeletal deformity, muscle weakness and symptomatic hypocalcaemia. In childhood the features of osteomalacia are accompanied by rickets, with widening of the epiphyses and impaired skeletal growth. The major cause of osteomalacia is vitamin D deficiency, which is most often due to reduced cutaneous production of vitamin D in housebound elderly people, immigrants to Northern countries and women who adopt strict dress codes which prohibit exposure of uncovered skin. Vitamin D deficiency osteomalacia may also occur with malabsorption, liver disease and anticonvulsant therapy. Less commonly, osteomalacia may result from abnormal vitamin D metabolism, resistance to the action of vitamin D, hypophosphataemia or toxic effects on osteoblast function.
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PMID:Osteomalacia. 922 90


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