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)

Experimental evidence is presented which suggests that age-induced changes in the collagenous matrix, the main constituent of the organic portion of bones, are at least partially responsible for age-induced physiological osteoporotic changes in the skeleton. In particular, there seems to be a labile fraction of recently synthesized collagen in bones, which loses its metabolic activity rapidly with advancing age. Experimental and clinical hormonal disorders and disturbances in calcium metabolism also cause changes in skeletal metabolism; these changes seem to be largely mediated through changes in the collagenous matrix. In experimental hyperthyroidism and hyperparathyroidism, the rate of degradation of the collagenous matrix appears to act as a moderator or "final messenger" in hormone-induced bone resorption. In conditions with altered calcium metabolism, such as malabsorption associated with hypocalcemia, altered bone metabolism may be due to osteomalacia or hypocalcemia-induced hyperparathyroidism. An increase in the rate of bone destruction in relation to the rate of bone formation is probably also the cause of postmenopausal osteoporosis. At present there is no optimal form of hormonal treatment for age-induced or post menopausal osteoporosis. Estrogen replacement therapy may be the best available treatment for postmenopausal osteoporosis, but slowing down the already low rate of bone catabolism in elderly subjects by estrogen or other therapeutic means requires long periods of treatment before pronounced increases in the total mass of bones take place and prophylactic administration of estrogen may produce better results.
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PMID:Relation to osteoporosis of age- and hormone-induced changes in the metabolism of collagen and bone. 97 17

A permature male infant required intravenous alimentation for six weeks following extensive surgery for ileal and cecal necrosis. At 3 months he developed evidence of hepatitis. Subsequently osteoporosis and the Fanconi syndrome appeared. Urine phosphate clearance was 83 percent of creatinine clearance at a serum phosphate concentration of 1.6 mg/dl. Concentration of plasma immunoreactive parathyroid hormone was elevated at 550 pg/ml. 25-Hydroxycholecalciferol was given at 240 mug/day. Aminoaciduria disappeared and bone healing occurred. Serum phosphate rose to 6.5 mg/dl and phosphate clearance fell to 2 percent of creatinine clearance. Upon cessation of 25-OHCC therapy, the Fanconi syndrome recurred despite administration of vitamin D2. 25-OHCC was then administered at 40 mug/day, and the urine abnormalities were reversed. The patient probably developed hyperparathyroidism, secondary malabsorption, and hepatitis. The Fanconi syndrome was the consequence of the hyperparathyroidism. 25-OHCC therapy was more effective than vitamin D in reversing the disordered state, possibly because of impaired hepatic metabolism of vitamin D2.
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PMID:Fanconi syndrome following bowel surgery and hepatitis reversed by 25-hydroxycholecalciferol. 112 25

Mild rickets was present in 7, and 3 others with severe bone disease developed widespread skeletal demineralization and multiple fractures. The intake of vitamin D was apparently loosely related to the severity of the osteodystrophy. The latter however, was closely linked to both the serum inorganic phosphate and the calciumXphosphate product. The serum calcium was directly related to the infant's gestational maturity, hypocalcaemia being present in those born before 35 weeks. Pathogenetic factors have probably included reactive hyperparathyroidism and nutritional deprivation associated with preterm delivery. Five of the infants who had biliary atresia developed radiological evidence of osteoporosis from about twelve months of age. This may be related to protracted calcium malabsorption, but its true nature remains to be elucidated.
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PMID:The osteodystrophy of prolonged obstructive liver disease in childhood. 125 25

Osteomalacia is characterized by large osteoid seams and a preserved volume of bone trabeculae. The mineralization of newly formed bone requires adequate concentrations of calcium and phosphate: the Ca.P product has been regarded as a useful, empirical diagnostic test of osteomalacia. It decreases in patients with osteomalacia mainly because they have very low plasma phosphate levels. At present total body bone mineral and total body bone density can be directly measured by whole body absorptiometry, which indicates the lowest total mineral content of the skeleton which can increase quickly after adequate treatment. The main symptoms of osteomalacia are: bone pain; muscular weakness (commonly as pelvic girdle myopathy); Looser-Milkman pseudofractures or more often a pattern of generalized demineralization at X-ray. The main biochemical parameters in osteomalacia include: defective calcium absorption with hypocalcemia and hypocalciuria; defective intestinal phosphate absorption with hypophosphatemia; there is often increased renal phosphate clearance due to hypocalcemia and secondary hyperparathyroidism; elevated alkaline phosphatase and osteocalcin levels; high bone turnover confirmed by kinetic studies carried out with radiocalcium or 99mTc-MDP. An etiological classification of the osteomalacias includes: 1) nutritional osteomalacia: a) inadequate exposure to sunlight and/or insufficient vitamin D intake; b) defective intestinal absorption of vitamin D because of malabsorption syndromes (e.g. jejuno-ileal bypass for obesity).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The osteomalacias. 166 41

The action of 1 alpha-hydroxycholecalciferol (oxydevit) was estimated in 204 patients with renal osteodystrophy, osteoporosis of varying etiology, osteomalacia because of malabsorption, congenital rickets-like diseases. The drug was shown to be highly effective in the treatment of secondary hyperparathyroidism in uremia, steroidal and senile osteoporosis. The treatment involved replacement therapy.
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PMID:[Experience in treating metabolic osteopathies with 1 alpha-hydroxyvitamin D3 (oksidevit)]. 181 42

A secondary hyperparathyroidism resulting from decreased intestinal calcium (Ca) absorption has been proposed as a contributory factor to glucocorticoid-induced osteoporosis. Inhaled steroids do not usually suppress adrenal gland function unless daily doses above 1,500 microgram are used. A recent study, however, has shown a reduced total body calcium in patients on regular beclomethasone treatment. In theory, osteopenia in these patients could be due to a direct effect of inhaled steroids on bone or due to an impaired intestinal calcium absorption. In this study, Ca absorption and parathyroid hormone (PTH) secretion were evaluated in three groups: 1) asthmatics on continuous oral and inhaled steroid treatment (11.3 +/- 4.4, range 5-33.5 mg.day-1 prednisone and 660 +/- 265, range 400-1,600 microgram.day-1 beclomethasone, respectively); 2) asthmatics on regular beclomethasone therapy (585 +/- 210, range 400-1,200 microgram.day-1); and 3) healthy subjects. The prevalence of vertebral fractures was evaluated by a spinal X-ray. No differences were found in either Ca absorption or PTH serum levels between asthmatics and healthy subjects (analysis of variance-ANOVA). Vertebral fractures were significantly more frequent in patients from group 1 (14 of 25) than in those from group 2 (2 or 25). We conclude that both prolonged oral steroid treatment and inhaled steroids, at doses lower than 1,600 microgram.day-1 do not cause Ca malabsorption, and that hyperparathyroidism does not contribute to osteoporosis in these patients.
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PMID:Intestinal calcium absorption and parathyroid hormone secretion in asthmatic patients on prolonged oral or inhaled steroid treatment. 185 73

Changes in the calciotropic hormones with age contribute significantly to the pathogenesis of osteoporosis. In both postmenopausal (Type I) and senile osteoporosis (Type II) it is common to find reduced levels of serum 1,25-dihydroxyvitamin D and malabsorption of calcium. In Type I patients a reduced level of serum parathyroid hormone causes a real decrease in serum 1,25-dihydroxyvitamin D production and malabsorption of calcium, whereas in Type II patients the decline in 1 alpha-hydroxylase activity in the kidney causes a decline in serum 1,25-dihydroxyvitamin D which leads to malabsorption of calcium and secondary hyperparathyroidism. In the final analysis both pathways lead to bone loss. In some Type II patients there may be a decline also in the function or number of the vitamin D-binding receptors in the gut. Treatment of patients with vitamin D analogues, however, normalizes calcium absorption and improves calcium balance. The improvement in calcium balance reduces bone resorption and prevents further bone loss; in addition recent studies have shown that therapy with vitamin D analogues leads to a reduction in fracture incidence.
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PMID:The pathogenesis of osteoporosis. 219 2

We report results for adjusted ionized calcium (at pH 7.4) and actual ionized calcium (at actual pH) in capillary blood from 183 patients with disorders of calcium metabolism (primary hyperparathyroidism, secondary hyperparathyroidism of malabsorption, primary hypoparathyroidism, Paget's disease, acromegaly, hypercalcemia of malignancy, osteoporosis, sarcoidosis, idiopathic hypercalciuria, and familial hypocalciuric hypercalcemia). The correlation and the equation for the linear regression between adjusted ionized calcium (y) and actual ionized calcium (x) were y = 1.011x + 0.005 mmol/L, r = 0.992, Sy,x = 0.021 mmol/L. Results were similar within each diagnostic group. Consistent agreement between adjusted and ionized calcium was observed in 96.7% of patients representing a variety of the most frequently encountered disorders of calcium metabolism. Thus we find adjusted ionized calcium to be as useful as actual ionized calcium for evaluation of patients with such disorders. Adjusted ionized calcium may therefore also be a logical choice for establishing agreement between laboratories for reference intervals in healthy adults.
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PMID:Adjusted ionized calcium (at pH 7.4) and actual ionized calcium (at actual pH) in capillary blood compared for clinical evaluation of patients with disorders of calcium metabolism. 231 Dec 30

Calcium deficiency causes osteoporosis in experimental animals because the skeleton is sacrificed for the preservation of the plasma (ionic) calcium and to meet obligatory calcium losses in the feces and urine. (Vitamin D deficiency, on the other hand, causes rickets and osteomalacia largely because of the loss of the calcemic action of vitamin D, which leads to hypocalcemia, secondary hyperparathyroidism, and hypophosphatemia.) The concept that human osteoporosis, particularly in postmenopausal women, results from negative calcium balance represents a working hypothesis that fits many, but not all of the available data. In normal women, the crucial event is a rise in obligatory urinary calcium loss, which may result from an increase in the complexed fraction of the plasma calcium, due in turn to an increase in plasma bicarbonate. Prospective trials with calcium supplements have, however, yielded conflicting results. In osteoporotic women, a further increase in urinary calcium combined with calcium malabsorption produces a further increase in bone resorption, but some impairment of bone formation due to declining androgens may constitute an additional risk factor with advancing age. The suppressibility of urinary hydroxyproline by calcium supplementation in those patients who can absorb calcium, and by calcitriol in those who cannot, supports the calcium deficiency model, but more trials are needed to establish its validity.
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PMID:The calcium deficiency model for osteoporosis. 264 3

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


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