Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005940 (bone disease)
 7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The bone histology of renal osteodystrophy is classified into osteitis fibrosa, osteomalacia, those of mixed, osteoporosis and low turnover bone. Osteitis fibrosa is the most frequent skeletal abnormality and is caused by various degrees of hyperparathyroidism. The main factors inducing hyperparathyroidism which is a well known complication in patients with renal failure include (a) phosphorus retention: 1) hypocalcemia and 2) decreased levels of 1 alpha, 25(OH)2 Vitamin D3, (b) reduced number of 1 alpha, 25(OH)2 Vitamin D3 receptors in parathyroid tissue, (c) skeletal resistance to set-point for calcium-regulated parathyroid hormone secretion. Serum or plasma levels of calcium, phosphorus, alkaline phosphatase, parathyroid hormone, calcitonin and tartrate resistant acid phosphatase are measured to evaluate hyperparathyroidism and metabolic bone disease. Dietary phosphorus restriction in chronic renal insufficiency prevents secondary hyperparathyroidism and renal osteodystrophy. Other treatment of phosphorus binders, Vitamin D metabolites or analogues, carcitonin and bisphosphonate are useful for the management of renal bone disease.
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PMID:[Secondary hyperparathyroidism and tertiary hyperparathyroidism chronic renal failure, uremia]. 775 92

No satisfactory treatment is available for metabolic bone disease associated with primary biliary cirrhosis. On the basis of the similarities to postmenopausal osteoporosis, the rationale exists for calcitonin to be tested in clinical studies in patients with primary biliary cirrhosis-associated osteoporosis. We evaluated the effect of calcitonin on bone metabolism and mineral density in 25 women with primary biliary cirrhosis and severe osteopenia. After 6 mo of observation, patients received a synthetic calcitonin or a control treatment consisting of less than one hundredth of the recommended dose of porcine calcitonin. The two treatments were administered in sequence to each patient for two 6-mo periods, with a 3-mo washout between them, according to a crossover design. After the observation period, oral calcium supplementation was started. Bone mineral density was measured by dual-photon absorptiometry of the lumbar spine at study entry and at the beginning and the end of each treatment period. During the observation period bone mineral density fell by 3.5% whereas during the following 6 mo it increased in both the patients who received calcitonin (4.3%) and those who received the control treatment (4.9%). Conversely, after the crossover, bone mineral density decreased during both calcitonin (-2.7%) and control treatment (-2.9%). A significant difference was observed between the two periods but not between the two treatments or between the two sequences of treatment administration. In conclusion, our findings indicate that parenterally administered calcitonin for 6 mo is ineffective in halting bone loss in patients with primary biliary cirrhosis-associated metabolic bone disease, whereas calcium supplementation may have a transient beneficial effect.
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PMID:Parenteral calcitonin for metabolic bone disease associated with primary biliary cirrhosis. 807 21

The physiology of the bone tissue is reviewed from the point of view of a clinical endocrinologist. The effect of the main calcium-regulating hormones and various local factors on the osteoblasts and osteoclasts is discussed. The aim of this review is to summarize the physiological and pathophysiological role of calcitonin, parathormone, vitamin D3, thyroid hormones, glucocorticoids, growth hormone and sex hormones on bone metabolism. The significance of endocrinological dysfunctions in the pathogenesis of osteoporosis, the most wide-spread metabolic bone disease, is emphasized. A theory concerning the pathogenetic role of androgen hormone deficiency in postmenopausal osteoporosis is discussed in detail.
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PMID:Osteoporosis from the point of view of the clinical endocrinologist. 807 25

Transgenic mice lacking a functional c-src gene have osteopetrosis, a bone disorder characterized by defective osteoclast function. We have investigated the effects of selective protein tyrosine kinase inhibitors that are known to inhibit c-src, on osteoclast activity in the bone slice assay. Geldanamycin, herbimycin A and monorden (0.001-10 microM) all dose-dependently inhibited bone resorption with IC50 values of 8, 70 and 86 nM, respectively. At concentrations of 0.001-1 microM, the compounds were not cytotoxic as judged by osteoclast morphology and survival on bone slices. In order to determine whether c-src plays a role in signal transduction associated with osteoclast activation prior to bone resorption commencing, or in the resorptive process itself, we performed kinetic experiments using human calcitonin as a positive control. Calcitonin inhibited all bone resorption subsequent to its addition at t = 0, 3 or 6 hr (100%, approximately 90% and approximately 50% inhibition, respectively), after the start of the 24 hr bone slice assay. Similar results were obtained with herbimycin A and geldanamycin (1 microM) added at t = 0, 3 or 6 hr, and with monorden (1 microM) added at t = 0 and 6 hr. These results indicate that c-src plays a crucial and continuous role in the process of osteoclastic bone resorption, most likely related to the translocation and/or fusion of exocytic vesicles to the ruffled border membrane.
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PMID:Evidence that c-src is involved in the process of osteoclastic bone resorption. 814 65

Highly selective vagotomy (HSV) or sham operation was performed in male rats. Fifteen weeks later bone mineralization, fractional intestinal absorption and balance, urinary excretion, and serum levels of calcium, magnesium and phosphorus, together with serum gastrin, parathyroid hormone, calcitonin, vitamin D metabolites, osteocalcin, isoenzymes of alkaline phosphatase, and the urinary excretion of cyclic AMP and hydroxyproline were assessed. HSV induced chronic hypergastrinemia and enhanced the weight of the fundus, antrum, and pancreas. Body weight, food intake, intestinal absorption, mineral balance, and bone mineralization were unaffected by HSV, whereas serum parathyroid hormone levels and urinary hydroxyproline excretion were increased. It is concluded that in the rat 1) HSV has a trophic effect on gastric and extragastric tissues; 2) gastric acid production is not a major determinant of intestinal calcium absorption; and 3) normal bone mass in the presence of signs of hyperparathyroidism indicates an intrinsic capacity of HSV to interfere with calcium metabolism, probably via hypergastrinemia, gastrin being an element of the gastro-parathyroid axis. Our present findings underscore the fact that osteopenia after HSV in man may be a rare finding, but it cannot be ruled out that bone disease found after partial or total gastrectomy may be due in part to concomitant vagotomy.
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PMID:Highly selective vagotomy in the rat: effects on bone and mineral metabolism. 820 82

Primary hyperparathyroidism is usually associated with normal or elevated serum 1,25-dihydroxyvitamin D [1,25(OH)2D] levels. We report a 63-year-old patient with extreme hypercalcemia (ionized serum calcium, 2.51 mmol/l; normal range, 1.19-1.36), very high serum concentrations of intact immunoreactive parathyroid hormone (iPTH) (145 pmol/l; normal range, 1-6.8), radiological lesions of osteitis fibrosa cystica, only mildly impaired renal function (creatinine clearance, 69 ml/min/m2) and very low serum levels of 1,25(OH)2D (28.8 pmol/l; normal range, 72-120). Presurgery normalization of the calcemia with normal saline, salmon calcitonin and pamidronate caused an increase in 1,25(OH)2D serum concentration to 228.3 pmol/l. A negative correlation could be established between ionized calcium and 1,25(OH)2D levels during that period (r2 = 0.80, P < 0.04). While serum calcium decreased with treatment, serum iPTH also decreased to 48.6 pmol/l, suggesting some 1,25(OH)2D inhibition of parathyroid adenoma function. Serum alkaline phosphatase also rose from 309 to 390 units/l (normal range, 25-97), suggesting the beginning of resolution of her osteitis fibrosa cystica prior to surgery. Surgical removal of a parathyroid adenoma was associated with a decrease in serum calcium and iPTH levels. To our surprise, the hypocalcemia could be managed easily with 1500 mg of oral calcium carbonate daily, even if the hungry bone disease became more active with an increase in alkaline phosphatase to 486 units/l. This was explained by the very high levels of serum 1,25(OH)2D (> 200 pmol/l) which prevailed in the postsurgery period and were probably related to decreased bone resorption and increased bone formation. This case illustrates that normalizing serum calcium prior to surgery in patients with primary hyperparathyroidism and osteitis fibrosa cystica can be highly beneficial.
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PMID:Inhibition of 1,25(OH)2D production by hypercalcemia in osteitis fibrosa cystica: influence on parathyroid hormone secretion and hungry bone disease. 827 76

A patient who had been supported with total parenteral nutrition (TPN) for over 8 years is herein presented, with emphasis on the changes observed in calcium metabolism. The patient was a 31-year-old female, who had undergone a subtotal jejunal and ileal resection for superior mesenteric artery occlusion. TPN was started soon after the surgery. She had been on TPN support for 105 months. Back pain developed at 97 months after the initiation of TPN. During her course, the serum calcium levels were judged to be within the normal ranges, while the 1 alpha, 25(OH)2Vit.D declined. Intermittent hypercalciuria was occasionally observed. Both the serum level of calcium and urinary calcium loss correlated closely to the amount of calcium infused, but they were not influenced by the amount of vitamin D (ergocalciferol) received. The serum level of parathormone and calcitonin were also within the normal ranges. The patient's vertebral bone, which was obtained at autopsy, revealed histopathological changes characteristic of osteoporosis. Based on the above, we conclude that a careful monitoring of the amount of calcium infused is called for to prevent bone disease in patients on long-term parenteral nutrition.
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PMID:Long-term total parenteral nutrition and osteoporosis: report of a case. 829 58

Bone disease occurring in the setting of chronic liver disease is being recognized increasingly often. The osteopenia may be an important cause of morbidity in these patients, particularly as effective treatments become available for the liver diseases and especially if these treatments actually worsen the coexistent bone disease. Although no specific treatments are of proven benefit for the bone disease in most instances, adequate exercise and calcium intake as well as vitamin D supplementation when deficiencies are present are recommended for all patients. Information is lacking about specific treatment for patients with PSC, hemochromatosis, and alcoholic liver disease. For patients with PBC, other than the above general measures, preliminary information suggests that supplemental estrogens in postmenopausal women and the use of calcitonin may offer promise; both measures are deserving of further study in this group of patients.
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PMID:Management of osteopenia of liver disease with special emphasis on primary biliary cirrhosis. 830 18

After a near total small bowel resection for an acute thrombosis of the mesenterial artery, a 61 year-old man was treated with total parenteral nutrition at home for five years. The treatment was complicated by episodes of sepsis, anaemia and uremia. After four years he developed pain in long bones and the back and grave hypercalcuria. Roentgenogram showed demineralisation. There was no hyperparathyroidism and serum phosphate and serum calcium were normal. His chronic metabolic acidosis was treated continuously with enteral acetate. He received basal amounts of vitamin D and amino acids. By administering calcitonin we were able to cure his progressive bone pains and normalize his calcium urinary output. No side effects were observed. Therefore, calcitonin may contribute to the treatment of bone disease associated with total parenteral nutrition.
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PMID:[Calcitonin treatment of metabolic bone disease induced by parenteral nutrition]. 832 48

The authors treated 18 patients with Paget's disease of bone (12 men and 6 women, age 65 +/- 5 years) with pamidronate (bisphosphonate of the second generation). Three patients from this group were treated previously without success with calcitonin or bisphosphonate of the first generation (etidronate) 50% of the patients suffered from the polyostotic form of the disease. In one patient a rare combination of primary hyperparathyroidism with Paget's bone disease was found and in another patient later an osteosarcoma developed in the affected bone. To all patients sodium pamidronate was administered (Aredia, Ciba-Geigy) 30 mg per day by i.v. infusion for 2 hours during three days. Four patients developed fever, two patients phlebitis at the site of injection. These side-effects are described by the manufacturer. Two patients developed transient regional alopecia, not described so far. Subjective pain relief of the affected skeleton occurred in one patient after one month of treatment, after three months in 78%. Laboratory manifestations of activity of the disease (serum activity of alkaline phosphatase, tartrate resistant acid phosphatase and hydroxyprolinuria) declined gradually from the 1st to the 6th month after onset of treatment. There was a less marked decline of the osteocalcin serum concentration. The concentration of calcium, phosphorus and vitamin D metabolites did not change markedly. Twelve months after treatment 14.7% of the patients were inactive according to laboratory tests, 73% however experienced another rise of parameters of osteoresorption and osteoformation. Pamidronate treatment in patients with Paget's disease of bone is effective and safe.
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PMID:[Paget's disease of bone and treatment with pamidronate]. 837 65


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