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

Obviously, the relentless decrease in bone mass that accompanies aging will continue the long sought "elixir of youth" is discovered. Individuals, because of race, sex, environmental, dietary, genetic or activity differences, will be more or less predisposed to symptomatic osteoporosis with increasing age. The careful and knowledgeable physician should, however, make every attempt to rule out potentially remediable, subtle forms of demineralizing disorders, such as apathetic or T3-thyrotoxicosis, hyperparathyroidism, malabsorption and osteomalacia or multiple myeloma. Not only do these diseases result in an accelerated loss of bone mass and an increased incidence of skeletal fractures but they mimic postmenopausal or senile osteoporosis radiologically. Once the metabolic or malignant disorders of bone metabolism have been effectively considered and ruled out, the senescent or postmenopausal osteoporotic patient should be treated judiciously with short-term estrogen therapy, a diet sufficient in vitamin D and calcium content and continued attempts to insure adequate skeletal mobilization. The addition of sodium fluoride and/or calcitonin to this regimen should not be attempted without extreme caution until the potentially harmful systemic effects of prolonged therapeutic trials have been appropriately assessed.
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PMID:Senile and postmenopausal osteoporosis. 76 91

Early neonatal hypocalcemia occurs in premature infants, infants with birth asphyxia, and infants of diabetic mothers. Etiological considerations include decreased calcium (Ca) supply, increased endogenous phosphate load, hypomagnesemia, alkali therapy, functional hypoparathyroidism, defects in vitamin D metabolism, and possibly calcitonin excess. Late neonatal hypocalcemia occurs, with malabsorption of magnesium (Mg), increased exogenous phosphate loading, after alkali therapy of diarrheal acidosis, hypoparathyroidism, and vitamin D related disorders. The therapy of hypocalcemia includes oral or iv Ca salts and in the near future, possibly the newly discovered vitamin D metabolites.
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PMID:Neonatal hypocalcemia mechanism of occurrence and management. 83 1

Glucocorticoid induced osteoporosis (GC-OP) is the most important form of all secondary osteoporoses. Mainly from in vitro and animal studies a lot of information exists concerning the underlying pathogenetic mechanisms. Some findings are still controversial but it is generally accepted that the three most important mechanisms are inhibition of osteoblastic matrix formation, stimulation of osteoclastic bone resorption and deterioration of intestinal calcium resorption with consecutive mild secondary hyperparathyroidism. In the individual patients the time between the beginning of corticoid therapy and clinical manifestation of osteoporosis varies considerably. If there is really a threshold dosage of corticoids is still debated. Besides dosage and duration of steroids age, sex, other risk factors of osteoporosis and underlying disease may be important factors. In contrast to the clinical prominence of GC-OP only little experience exists in counteracting the detrimental effects of corticoids on bone tissue. For pure prevention it seems reasonable to overcome intestinal calcium malabsorption by calcium or vitamin D. Concerning treatment of manifest GC-OP we studied the effect of salmon calcitonin (sCT) in patients with chronic obstructive lung disease. 18 patients injected themselves 100 U sCT every second day subcutaneously while 18 randomized patients served as untreated controls. There was a significant pain reduction in the sCT group and after six months the mineral content of the distal radius had increased by 2.7% despite a daily mean intake of 16.2 mgs prednisone during that time. In the control group (mean daily prednisone dose 16.8 mgs) the mineral content decreased with 3.5% on the average (p less than 0.001).
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PMID:Glucocorticoid-induced osteoporosis. 266 65

Assays of serum immunoreactive parathyroid hormone are clinically useful in the differential diagnosis of hypercalcaemic states and in the assessment of the severity of parathyroid bone disease in uraemic patients. Serum immunoreactive calcitonin measurements are essential in the investigation of individuals who might be suffering from medullary carcinoma and may be used in the detection of metastases. Serum 25-hydroxyvitamin D assays should be performed in patients receiving pharmacological doses of vitamin D to monitor patient compliance and to prevent the occurrence of vitamin D intoxication. Low values in patients with renal failure and in patients with malabsorption are highly suggestive of the presence of osteomalacia. The measurement of serum levels of dihydroxylated vitamin D metabolites is currently of doubtful relevance though such measurements may become useful in monitoring patients receiving these compounds therapeutically.
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PMID:The measurement of calcium-regulating hormones in clinical medicine. 720 1

A 68 year old man with prostatic carcinoma and extensive painful osteoblastic metastases was discovered to have hypocalcemia (serum calcium 7.1 mg/dl) without evidence of hypoalbuminemia, renal failure or malabsorption. Baseline studies revealed hypocalciuria (24 hour urine calcium less than 5 mg/day), normal serum phosphate (3.4 mg/dl), low tubular reabsorption of phosphate (68 percent), undetectable serum calcitonin, normal serum 25-hydroxyvitamin D, slightly elevated serum parathyroid hormone level and increased urinary cyclic AMP (8.87 mumol/g creatinine). These studies were compatible with secondary hyperparathyroidism. The intravenous administration of parathyroid extract produced no further change in urinary phosphate but a 25-fold increase in nephrogenous cyclic AMP. Three days administration of intramuscular parathyroid extract slowly and temporarily restored serum calcium to normal levels while increasing urinary cyclic AMP and phosphate. Chemotherapy with cyclophosphamide and 5-fluorouracil rendered the patient free of pain while reducing serum acid and alkaline phosphatase levels and restoring serum total and ionized calcium and urinary cyclic AMP excretion to normal.
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PMID:Hypocalcemia with osteoblastic metastases in patient with prostate carcinoma. A cause of secondary hyperparathyroidism. 724 80

Assays of serum immunoreactive parathyroid hormone are clinically useful in the differential diagnosis of hypercalcaemic states and in the assessment of the severity of parathyroid bone disease in uraemic patients. Serum immunoreactive calcitonin measurements are essential in the investigation of individuals who might be suffering from medullary carcinoma, and such measurements may be used in the detection of metastases. Serum 25-hydroxyvitamin D assays are useful in patients receiving pharmacological doses of vitamin D, to monitor patient compliance and to prevent the occurrence of vitamin D intoxication. Low values in patients with renal failure and in patients with malabsorption and highly suggestive of the presence of osteomalacia. The measurement of serum levels of dihydroxylated vitamin D metabolites is currently of doubtful clinical relevance, though such measurements may become useful in monitoring patients receiving these compounds therapeutically.
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PMID:Testing for disorders of calcium metabolism. 746 49

In humans, gastric surgery results in in osteopenia via mechanisms that are insufficiently understood; surgery-induced changes in the hormonal axes involving the stomach, thyroid, and the parathyroids may play a role. To study this in more detail, we evaluated calcium (Ca), magnesium (Mg), and phosphorus (P) metabolism as well as physical, chemical, and histomorphometric bone parameters in rats rendered hypergastrinemic by fundectomy (FX). In independent experiments, the response to an oral Ca challenge was investigated in intact rats versus FX, and in thyroidectomized versus thyroid-intact FX rats. Sixteen weeks following FX, body weight was approximately 80% that of sham-operated controls. In urine, P excretion was elevated fivefold, the pH was significantly decreased, and cAMP excretion was elevated as compared with controls; serum parathyroid hormone (PTH), calcitonin, 25OHD, Ca, Mg, and P were normal; gastrin and 1,25(OH)2D were elevated. On the basis of bone ash mineral content, FX rats developed significant osteopenia, and histomorphometry indicated only slightly elevated bone turnover and mineralization. Following oral Ca, thyroid-intact FX rats developed hypercalcemia, serum gastrin decreased, and calcitonin increased significantly; in thyroidectomized FX rats, calcitonin remained at baseline levels although there was a similar degree of hypercalcemia; PTH decreased during the hypercalcemic period in both groups. Serum gastrin did not correlate with calcitonin or PTH, and in multivariate regression analysis the only predictor of serum 1, 25(OH)2D was urinary phosphorus. It was concluded that in the FX rat (1) osteopenia is not caused by intestinal Ca malabsorption, vitamin D, Ca deficiency, or secondary hyperparathyroidism; (2) osteopenia may be related to PTH-independent urinary hyperexcretion of P, followed by a rise of serum 1,25(OH)2D; (3) the existence of endocrine axes among gastrin, calcitonin, and PTH cannot be substantiated. FX osteopenia appears to be related to gastric acid abolition, and the reactive hypergastrinemia probably stabilizes the mass and turnover of bone.
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PMID:Gastric fundectomy in the rat: effects on mineral and bone metabolism, with emphasis on the gastrin-calcitonin-parathyroid hormone-vitamin D axis. 979 30

Serum testosterone and estradiol decline with advancing age in men, but the contribution of these changes to age-related bone loss remains unclear. Most studies show a closer relationship between bone density and serum estradiol than with serum testosterone. Nevertheless, hypogonadism is widely considered to be an important cause of male osteoporosis, occurring in up to 20% of men with vertebral fractures and 50% with hip fractures. Bone loss in hypogonadal men has been attributed to androgen and estrogen deficiency, low 1,25 dihydroxyvitamin D concentrations, malabsorption of calcium, and reduced circulating calcitonin. These abnormalities are corrected by testosterone replacement, which also decreases bone resorption and stimulates bone mineralization. Long-term testosterone replacement increases spine bone density by over 25%, although much of the improvement occurs in the first few years of treatment. There appears to be an inverse relationship between the basal serum testosterone and the increase in bone density observed with testosterone treatment, such that little change is seen in men with normal basal concentration. In contrast, an observational study in eugonadal men with vertebral fractures showed an increase in spine bone density of 5% after 6 months' treatment with testosterone, probably mediated by an increase in serum estradiol and a reduction in bone resorption. Although testosterone has beneficial effects on the skeleton, there may be adverse effects on the prostate and cardiovascular risk factors. Further studies are required to confirm the safety and efficacy of testosterone replacement in hypogonadal and eugonadal men with osteoporosis.
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PMID:Androgen replacement in aging men. 1173 Feb 58

Inflammatory bowel diseases, most frequently Crohn's disease, are frequently accompanied by decreased bone mineral content (30-70%). The osteopenia is not explained by the side effects of treatment or the secondary malabsorption. There must be a common pathological pathway in the background. The mineral content of bones is most easily measured by dual-ray absorptiometry. The measurement should be performed at the time of the diagnosis of bowel disease. It is useful to perform some routine laboratory examinations (serum calcium and phosphate, urinary calcium excretion level, etc.) and some special tests (serum osteocalcin and crosslaps) to exclude some other pathological pathways as well as to plan the anti-osteoporotic therapy. Appropriate calcium and vitamin-D supplementation is essential in prevention and therapy as well. Several drug-classes have proven useful in the therapy of severe osteoporosis associated with inflammatory bowel diseases such as bisphosphonates, hormone replacement therapy, selective estrogen receptor modulators and calcitonin. The authors provide an algorithm for the therapy of metabolic bone disease in inflammatory bowel disease.
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PMID:[Osteoporosis associated with inflammatory bowel diseases]. 1520 26

Osteoporosis in children is rare and mostly secondary to such conditions as prolonged immobilization, malabsorption syndromes, corticosteroid excess, osteogenesis imperfecta, celiac disease, Turner syndrome, and malignancy. Idiopathic juvenile osteoporosis (IJO) is a very rare condition of primary bone demineralization that presents in childhood. IJO, a disease of unknown etiology, manifests typically by pain, bone deformities, and fractures. Diagnosis of IJO was made by excluding other common causes of osteoporosis in this age. Bisphosphonates, calcitriol, fluoride, and calcitonin have been administered therapeutically, but the results were equivocal. Usually the disease remits by itself. Patient that has serious osteoporosis and high thyroid stimulating hormone level was diagnosed as IJO by eliminating secondary reasons. We report this case, whose symptoms were disappeared after parenteral pamidronat treatment, and he was reexamined owing to anemia and trombositopenia, and diagnosed as B-cell acute lymphoblastic leukemia, just to emphasis the importance of close follow-ups of IJO patients.
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PMID:Severe osteoporosis and high level TSH in a child before the diagnosis of acute lymphoblastic leukemia. 1963 64


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