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

A 45-year-old woman reported the development of thigh pain followed within a year by proximal muscle weakness. Clinical findings included short stature, prominent kyphoscoliosis, proximal weakness, and brisk reflexes. Recognition of an increased level of serum alkaline phosphatase and hypophosphatemia led to the diagnosis of osteomalacia. Identification of iron deficiency anemia and hypocholesterolemia implicated previously unrecognized gluten-sensitive enteropathy with associated vitamin D malabsorption as the cause of the osteomalacia. Adherence to a gluten-free diet and treatment with vitamin D2 resulted in weight gain, resolution of pain, and improvement in strength within 3 months. Painful proximal weakness and hyperreflexia may be the initial and primary manifestations of osteomalacia, a readily treatable cause of muscle and bone disease.
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PMID:Osteomalacic myopathy. 787 Jan 21

X-linked hypophosphatemia, a common metabolic bone disease in humans and mice (the Hyp and Gy mutations), is characterized by decreased plasma phosphate, decreased renal tubular reabsorption of phosphate, rickets, and osteomalacia. The question of whether intestinal malabsorption of calcium contributes to the bone disease is controversial. Intestinal absorption of 45Ca was studied in three different mouse colonies: Gy on B6C3H background, Hyp on B6C3H background, and Hyp on C57BL/6J background, all at 4 weeks of age. The duodenum was isolated by sutures, and 45Ca in a 150 mM NaCl and 2 mM CaCl2 solution at pH 7.2 was injected into the lumen. Absorption was measured by the amount of 45Ca remaining in the lumen and by the plasma isotope level. The Gy and Hyp mice of both sexes significantly malabsorbed 45Ca at 4 weeks of age compared to normal littermates. Following the 4 week study, intestinal absorption was measured at 2, 7-8, and 12 weeks of age in normal and Gy mice on the B6C3H background. At 2 and 7-8 weeks of age, the Gy males significantly malabsorbed 45Ca compared to their normal littermates. Serum 1,25-dihydroxyvitamin D was not significantly altered in Gy males at 4 weeks of age. This suggests the possibility of resistance of the intestine to stimulation. Malabsorption of calcium in young Gy and Hyp mice may exacerbate the low mineralization in their rachitic bone disease.
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PMID:Intestinal malabsorption of 45calcium in young Gy mice, a second model for X-linked hypophosphatemia. 826 20

The effects of endocrine disease on bone mass continue to attract attention. Investigations include the effects on the skeleton of thyroid disease, primary hyperparathyroidism, and their treatment. The effect of growth hormone replacement in adults with panhypopituitarism has also been investigated; children with treated growth hormone deficiency appear to reach adulthood with low bone mass. The indications for surgery in asymptomatic primary hyperparathyroidism have recently been reviewed. The associations between autoimmune thyroid disease and connective tissue disease have been investigated. Although patients with Graves' disease are frequently positive for antinuclear antibodies, there appears to be no increased risk of systemic autoimmune disease. The possible pathogenesis of diabetic bone disease via calcium malabsorption, hypercalciuria, reduced bone formation, and collagen abnormalities has been reviewed. A long-term study has clarified the links among diabetic control, limited joint mobility, nephropathy, and retinopathy. The possible mechanisms by which pregnancy may induce remission in rheumatoid arthritis have been discussed.
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PMID:Endocrine disease. 843 94

Whipple's disease is a rare systemic illness, with the main clinical feature being severe malabsorption syndrome. Bone involvement in the disease has rarely been described in previous articles. The authors report a case in which an extensive skeletal evaluation was carried out. Even though osteomalacia is generally considered the most typical metabolic bone disease of malabsorption syndromes, bone biopsy demonstrated that osteoporosis was the prominent histologic feature in this patient. On the basis of serial bone mineral density measurements, antibiotic treatment was able to reverse the initial reduced bone mass.
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PMID:Case report: reversal of decreased bone mass by antibiotic treatment in a patient with Whipple's disease. 861 91

1. The best way to prevent early growth failure in children with renal disease is by the use of specified nutrition and appropriate buffer, activated vitamin D, and calcium-containing phosphate binders as needed. With prenatal diagnosis of anatomically abnormal kidneys available, this type of early intervention may be much more feasible in the 1990s. 2. Supplemental sodium and water in children with polyuria and intravascular volume depletion may prevent growth failure. Cow milk is detrimental in this group of individuals because of high solute and protein load, often causing intravascular volume depletion, hyperphosphatemia, and acidosis. 3. Children with acquired glomerular disease may need sodium restriction and, if treated with steroids, a diet low in saturated fat. 4. Children with nephrotic syndrome and severe edema should be evaluated for malabsorption and subsequent malnutrition. Protein intake should be supplemented only at the RDA and to replace ongoing losses. Long-term sodium restriction is appropriate. Hyperlipidemia should be monitored: if nephrosis is chronic, a low saturated fat diet should be instituted. Angiotensin-converting enzyme inhibitors can decrease urinary protein loss and may ameliorate hyperlipidemia. Children resistant to therapy can have very high morbidity. 5. Children with <50 % of normal creatinine clearance should have PTH measured and activated vitamin D therapy should be started if PTH is elevated more than two to three times normal. Thereafter careful monitoring of calcium, phosphorus, and PTH is crucial to prevent renal osteodystrophy, low turnover bone disease, and hypercalcemia with hypercalciuria and nephrocalcinosis. 6. Children with tubular defects with severe polyuria also may benefit from low-solute, high-volume feedings. 7. All physicians caring for children with renal disease should have pediatric nephrology consultation available. Prevention of growth failure is much more cost effective than pharmacologic therapy. Before initiating growth hormone treatment for growth retardation, assiduous treatment of co-existing renal osteodystrophy and provision of optimal nutritional intake should be accomplished.
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PMID:Nutritional management of the child with mild to moderate chronic renal failure. 876 44

A 41-year old female patient with metabolic bone disease is presented. The disease was caused by malabsorption which developed as a result of gluten induced enteropathy. The diagnosis was confirmed by histological finding of the small intestine mucosa and bones. Following gluten-free diet, calcitriol and calcium tablets, the patient started to move independently and the bone mineralisation improved.
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PMID:[Metabolic bone disease in a female patient with gluten enteropathy]. 896 20

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

Parenteral nutrition-associated metabolic bone disease in children is manifested primarily as osteopenia and, on occasion, fractures. The etiology is likely multifactorial, with calcium and phosphate deficiency playing a major role in the preterm infant and with the role of aluminum toxicity yet to be clearly defined in this population. Lack of normal values of bone histomorphometry in the premature infant as well as lack of normal data for biochemical markers of bone turnover in these patients contribute to the uncertainty. Other factors that may play a role in the pathogenesis include lack of periodic enteral feeding; underlying intestinal disease, including malabsorption and inflammation; the presence of neoplasms; and drug-induced alterations in calcium and bone metabolism. The true incidence and prevalence of parenteral nutrition-associated bone abnormalities in pediatric patients remain unknown.
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PMID:Metabolic bone disease of total parenteral nutrition. 943 1

Osteoporosis is increasingly recognised in men. Low bone mass, risk factors for falling and factors causing fractures in women are likely to cause fractures in men. Bone mass is largely genetically determined, but environmental factors also contribute. Greater muscle strength and physical activity are associated with higher bone mass, while radial bone loss is greater in cigarette smokers or those with a moderate alcohol intake. Sex hormones have important effects on bone physiology. In men, there is no abrupt cessation of testicular function or 'andropause' comparable with the menopause in women; however, both total and free testosterone levels decline with age. A common secondary cause of osteoporosis in men is hypogonadism. There is increasing evidence that estrogens are important in skeletal maintenance in men as well as women. Peripheral aromatisation of androgens to estrogens occurs and osteoblast-like cells can aromatise androgens into estrogens. Human models exist for the effects of estrogens on the male skeleton. In men aged > 65 years, there is a positive association between bone mineral density (BMD) and greater serum estradiol levels at all skeletal sites and a negative association between BMD and testosterone at some sites. It is crucial to exclude pathological causes of osteoporosis, because 30 to 60% of men with vertebral fractures have another illness contributing to bone disease. Glucocorticoid excess (predominantly exogenous) is common. Gastrointestinal disease predisposes patients to bone disease as a result of intestinal malabsorption of calcium and colecalciferol (vitamin D). Hypercalciuria and nephrolithiasis, anticonvulsant drug use, thyrotoxicosis, immobilisation, liver and renal disease, multiple myeloma and systemic mastocytosis have all been associated with osteoporosis in men. It is possible that low-dose estrogen therapy or specific estrogen receptor-modulating drugs might increase BMD in men as well as in women. In the future, parathyroid hormone peptides may be an effective treatment for osteoporosis, particularly in patients in whom other treatments, such as bisphosphonates, have failed. Men with idiopathic osteoporosis have low circulating insulin-like growth factor-1 (IGF-1; somatomedin-1) concentrations, and IGF-1 administration to these men increases bone formation markers more than resorption markers. Studies of changes in BMD with IGF-1 treatment in osteoporotic men and women are underway. Osteoporosis in men will become an increasing worldwide public health problem over the next 20 years, so it is vital that safe and effective therapies for this disabling condition become available. Effective public health measures also need to be established and targeted to men at risk of developing the disease.
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PMID:Osteoporosis in men. New insights into aetiology, pathogenesis, prevention and management. 988 98


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