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)

It is well recognized that patients with postmenopausal osteoporosis usually exhibit some degree of calcium malabsorption and commonly have low serum concentrations of 1,25-dihydroxyvitamin D (calcitriol). Administration of calcitriol has been shown to normalize calcium absorption in patients with osteoporosis and, over the long term may have a stimulating effect on bone formation. Clinical trials have shown a significant reduction in osteoporotic fractures among calcitriol-treated patients. Hypercalcemia and hypercalciuria are infrequent complications of calcitriol therapy with physiologic doses (0.25 microgram twice daily), and are most commonly related to excessive calcium intake (i.e., > 1000 mg daily).
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PMID:The role of vitamin D in the pathogenesis and treatment of osteoporosis. 885 46

In patients with Crohn's disease arthritis of the large joints, osteomalacia, osteoporosis and aseptic bone necrosis as a consequence of malabsorption and glucocorticoid intake may occur. The case of a patient with long-standing Crohn's disease is presented who subsequently developed abacterial osteomyelitis of the jaw ("osteomyelitis sicca"). The symptoms of the osteomyelitis improved under immuno-suppressive therapy. Because the etiopathogenetic concepts for Crohn's disease and osteomyelitis sicca are similar, the latter could be a rare extraintestinal manifestation in Crohn's disease, not described previously.
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PMID:[Osteomyelitis sicca in Crohn disease--coincidence or extraintestinal manifestation?]. 901 24

: 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

To investigate the pathogenesis of hepatic osteodystrophy (HOD) in parenchymal liver disease, we developed a laboratory model in animals using carbon tetrachloride (CCl4) and thioacetamide. Biochemical and histological parameters in the model were measured. In rats with both chronic non-cirrhotic liver injury and CCl4-induced cirrhosis, tibial bone volume was significantly lower than in controls. In CCl4-treated cirrhotic rats, the osteoid volume decreased while the urinary calcium/creatinine ratio increased. In all CCl4-treated rats, bone volume was significantly correlated with both the serum albumin concentration and the number of goblet cells reflecting intestinal villous atrophy. The serum concentration of vitamin D metabolites was not correlated with bone volume. Whole body retention of 47Ca was significantly lower in CCl4-treated cirrhotic rats than in controls. Furthermore, the bone volume in thioacetamide-treated cirrhotic rats was significantly lower than in controls. These data demonstrate that chronic parenchymal liver injury itself causes osteoporosis (i.e. HOD) due to a combination of low bone formation rates and high resorption rates, that HOD begins at the stage of chronic non-cirrhotic liver injury, that bone volume in HOD parallels liver damage and that the principal pathogenesis of HOD seems to be intestinal Ca malabsorption due to lower serum albumin and villous atrophy, while serum levels of vitamin D metabolites have little influence on the pathogenesis of HOD.
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PMID:Bone changes and mineral metabolism disorders in rats with experimental liver cirrhosis. 903 34

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

Osteoporosis and magnesium (Mg) deficiency often occur in malabsorption syndromes such as gluten-sensitive enteropathy (GSE). Mg deficiency is known to impair parathyroid hormone (PTH) secretion and action in humans and will result in osteopenia and increased skeletal fragility in animal models. We hypothesize that Mg depletion may contribute to the osteoporosis associated with malabsorption. It was our objective to determine Mg status and bone mass in GSE patients who were clinically asymptomatic and on a stable gluten-free diet, as well as their response to Mg therapy. Twenty-three patients with biopsy-proven GSE on a gluten-free diet were assessed for Mg deficiency by determination of the serum Mg, red blood cell (RBC) and lymphocyte free Mg2+, and total lymphocyte Mg. Fourteen subjects completed a 3-month treatment period in which they were given 504-576 mg MgCl2 or Mg lactate daily. Serum PTH, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and osteocalcin were measured at baseline and monthly thereafter. Eight patients who had documented Mg depletion (RBC Mg2+ < 150 microM) underwent bone density measurements of the lumbar spine and proximal femur, and 5 of these patients were followed for 2 years on Mg therapy. The mean serum Mg, calcium, phosphorus and alkaline phosphatase concentrations were in the normal range. Most serum calcium values fell below mean normal and the baseline serum PTH was high normal or slightly elevated in 7 of the 14 subjects who completed the 3-month treatment period. No correlation with the serum calcium was noted, however. Mean serum 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and osteocalcin concentrations were also normal. Despite only 1 patient having hypomagnesemia, the RBC Mg2+ (153 +/- 6.2 microM; mean +/- SEM) and lymphocyte Mg2+ (182 +/- 5.5 microM) were significantly lower than normal (202 +/- 6.0 microM, p < 0.001, and 198 +/- 6.8 microM, p < 0.05, respectively). Bone densitometry revealed that 4 of 8 patients had osteoporosis of the lumbar spine and 5 of 8 had osteoporosis of the proximal femur (T-scores < or = -2.5). Mg therapy resulted in a significant rise in the mean serum PTH concentration from 44.6 +/- 3.6 pg/ml to 55.9 +/- 5.6 pg/ml (p < 0.05). In the 5 patients given Mg supplements for 2 years, a significant increased in bone mineral density was observed in the femoral neck and total proximal femur. This increase in bone mineral density correlated positively with a rise in RBC Mg2+. This study demonstrates that GSE patients have reduction in intracellular free Mg2+, despite being clinically asymptomatic on a gluten-free diet. Bone mass also appears to be reduced. Mg therapy resulted in a rise in PTH, suggesting that the intracellular Mg deficit was impairing PTH secretion in these patients. The increase in bone density in response to Mg therapy suggests that Mg depletion may be one factor contributing to osteoporosis in GSE.
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PMID:Magnesium deficiency: possible role in osteoporosis associated with gluten-sensitive enteropathy. 911 91

Hip fractures in men account for one third of all hip fractures and have a higher mortality than in women. The public health burden will increase as the increase in the numbers of elderly men in the community increases. In addition, the age-specific incidence of hip fractures may be increasing in some, but not all, countries. Vertebral fractures may be a public health problem as recent studies suggest that the prevalence in the community is 20-30%, similar to that reported in women. Forearm fractures should probably not be regarded as a public health problem. Peak bone mass is higher in men than women because men have bigger bones. Peak bone mineral density is the same. The amount of trabecular bone lost at the spine and iliac crest during ageing is similar in men and women. Cortical bone loss is less in men because endocortical resorption is less and periosteal formation is greater. Bone loss accelerates in elderly men because endocortical resorption and increasing cortical porosity increase the surface available for resorption. Bone fragility is less in men than women because: (a) the cross-sectional surface of the bone is larger; (b) trabecular bone loss is less as a percentage of the higher peak bone mass; (c) trabecular bone loss occurs by thinning rather than perforation; and (d) periosteal appositional growth compensates for endocortical resorption by maintaining the bending strength of bone. Reduced BMD in men with fractures may be due to reduced peak bone size and mass, and bone loss. Bone loss occurs by reduced bone formation. Whether men with fractures have increased bone fragility due to reduced periosteal appositional growth during ageing is unknown. The age-related decline in testosterone, adrenal androgens, growth hormone, and insulin-like growth factor 1 may contribute to reduced bone formation and bone loss. Men with vertebral fractures often have hypogonadism or illnesses with few clinical features that should be considered with a high index of suspicion (alcoholism, myeloma, malabsorption, primary hyperparathyroidism, haemochromatosis, Cushing's disease). Secondary hyperparathyroidism may contribute to bone loss by activating bone turnover and so increasing the number of bone remodelling units with impaired bone formation in each. There is no proven treatment for osteoporosis in men because there have been no trials using anti-fracture efficacy as an end point. Testosterone replacement should be considered in men with proven hypogonadism and vitamin D deficiency should be corrected if present. Calcium supplements and bisphosphonates are reasonable options given the lack of information.
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PMID:Osteoporosis in men. 936 40

Age-related decline in intestinal calcium (Ca) absorption often occur in postmenopausal osteoporotic women. The impaired Ca absorption can be corrected by estrogen (E2) therapy. Growth hormone (GH) therapy has also been reported to increase intestinal absorption of calcium. Since 1,25-dyhydroxyvitamin D (1,25(OH)2D) is the primary regulator of calcium absorption, we explored whether the mechanisms by which E2 and GH enhance Ca absorption involves the vitamin D endocrine system. We measured serum 1,25(OH)2D concentrations and determined the binding characteristics of intestinal vitamin D receptors (VDRs) in four groups of female rats: sham operated (sham), ovariectomized (ovx), ovx + E2, and ovx + GH. Serum 1,25(OH)2D levels were 42.4 +/- 3.4 and 42.5 +/- 3.2 pg/ml in sham and ovx rats, respectively, and decreased by 63 and 34% (P < 0.001) in ovx + E2 and ovx + GH-treated rats, respectively. The numbers of total, unoccupied and occupied VDRs were 116.9 +/- 2.0, 72.1 +/- 1.1 and 44.8 +/- 1.9 fmol/mg protein, respectively, in sham operated rats, and decreased significantly following ovariectomy by 24, 27 and 19% (P < 0.01), respectively. E2 therapy not only significantly increased total, unoccupied and occupied VDRs above those of ovx rats by 55, 58 and 49% respectively, but it increased the levels above those of sham operated controls as well (P < 0.01). In contrast, GH administration prevented the decrease that occurred in ovx rats in the number of total and unoccupied VDRs (111.2 +/- 3.3; 72.6 +/- 1.4 fmol/mg protein, respectively), but it had no significant effect on the number of occupied VDRs. The dissociation constant (Kd) of intestinal VDRs was unaltered by ovariectomy, E2 and GH. We conclude that down regulation of intestinal VDRs may contribute to the Ca malabsorption that occurs in ovarian hormone deficient states such as postmenopausal osteoporosis, and that the stimulation of Ca absorption by E2 and GH may result, in part, from up regulation of intestinal VDRs.
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PMID:Modulation of intestinal vitamin D receptor by ovariectomy, estrogen and growth hormone. 948 86

Celiac disease is a genetic, immunologically mediated small bowel enteropathy that causes malabsorption. The immune inflammatory response to gluten frequently causes damage to many other tissues of the body. The condition is frequently underdiagnosed because of its protean presentations. New prevalence data indicate that symptomatic and latent celiac disease is present in one of 300 people of European descent. Age of onset ranges from infancy to old age. Symptomatic presentations include general ill-health, as well as dermatologic, hematologic, musculoskeletal, mucosal, dental, psychologic and neurologic diseases. Celiac disease has a 95 percent genetic predisposition and, thus, it is frequently associated with autoimmune conditions such as diabetes mellitus type 1 and thyroid disease. Untreated patients have an increased incidence of osteoporosis and intestinal lymphoma. Excellent diagnostic screening tests are now available, including those that detect antigliadin and antiendomysial antibodies. Therapy with a gluten-free diet is effective, resulting in complete resolution of symptoms and secondary complications in almost all patients. Local and national celiac-sprue associations facilitate care of patients with celiac disease and support dietary compliance.
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PMID:Detecting celiac disease in your patients. 951 50


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