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

Home total parenteral nutrition (HTPN) is in its infancy but has proved to be lifesaving for patients unable to manage on enteral nutrition alone. However, this mode of nutrition therapy is not without problems. Aside from mechanical and other metabolic complications, a peculiar metabolic bone disease has been reported to occur in some HTPN recipients. The disease, characterized by abnormalities in calcium and phosphorus homeostasis, often results in osteomalacia, bone pain, and fractures. Reports of approximately 50 cases of metabolic bone disease have been published by centers in the United States and Canada. Factors that have been implicated as possible causes include infusion of excess vitamin D, aluminum, calcium, protein, or glucose; cyclic vs. continuous TPN administration; and the patient's previous nutritional state. Although removal of vitamin D or aluminum from the TPN solution and discontinuation of TPN altogether have been associated with improvement in symptoms, histology, and laboratory values, no single factor has been identified as the cause of this troubling phenomenon.
 ...
PMID:Metabolic bone disease in home total parenteral nutrition. 311 Feb 49

Inadequate dietary phosphorus intake is a contributing factor to the occurrence of metabolic bone disease in very low birth weight infants. This article reviews the clinical presentation and the pathophysiology of the phosphorus deficiency syndrome in premature infants. Recommendations for therapy and prevention of phosphorus deficiency are presented.
 ...
PMID:Phosphorus deficiency syndrome in very low birth weight infants. 311 18

Rats were subjected to a two-stage subtotal nephrectomy or sham operation, and treated with aluminum (Al) or both aluminum and vitamin D3 metabolites for 5 weeks with a cumulative dose of 13.6 mg aluminum. Animals were injected with 3H-thymidine and 3H-proline. The following analyses were performed: quantitative histology of tibial metaphyses and cytomorphometric electron microscopy of osteoclasts, quantitative (ICP-spectroscopy) and qualitative determination (histochemical staining) of aluminum within organs, and serum biochemistry (Ca, P, Mg, vitamin D3 metabolites, alkaline phosphatase, urea). The following new facts of the aluminum-related bone disease became evident: (a) Application of aluminum to growing uremic rats induced rickets, whose major epiphyseal growth plate changes were 1 alpha,25(OH)2D3-dependent. Addition of 1 alpha,25(OH)2D3 prevented the formation of rachitic metaphysis, but failed to prevent osteoid accumulation on epiphyseal and metaphyseal trabecular surfaces. Moreover, calcitriol produced hyperosteoidosis and osteosclerosis in the same rats. Aluminum did not alter the function of osteoblasts, while osteoclasts seemed inactivated. (b) The development of rickets was associated with suppressed serum levels of 1,25(OH)2D3, reduced phosphorus level and the high content of aluminum in the bone, kidney, and liver. The addition of 24R,25(OH)2D3 markedly exaggerated the reduction of serum levels of calcitriol. We suggested that aluminum induces rickets in growing uremic rats, which consists of two components: vitamin D refractory osteomalacia and 1 alpha,25(OH)2D3-dependent epiphyseal growth plate changes.
 ...
PMID:Effects of 1 alpha,25- and 24R,25-dihydroxyvitamin D3 on aluminum-induced rickets in growing uremic rats. 350 83

Histologic bone changes of osteitis fibrosa and osteomalacia are commonly present in patients with end-stage renal disease. Although many patients are not symptomatic from these bone changes, some patients are severely disabled. Altered metabolism of vitamin D, calcium, phosphorus, and parathyroid hormone occurs in renal failure and contributes to the development of uremic bone disease. This article reviews the current theories of pathogenesis and treatment of renal osteodystrophy. In addition, the clinical presentation, pathogenesis, and treatment of the various aluminum-associated osteomalacic syndromes in uremia are discussed.
 ...
PMID:Review: Renal osteodystrophy--pathogenesis and treatment. 351 48

Geminal bisphosphonates are a new class of drugs recently developed. They are characterized by a phosphorus-carbon-phosphorus (PCP) bond and are thus analogs of pyrophosphate. The bind strongly to hydroxyapatite crystals and inhibit in vitro both their formation and dissolution. In vivo they inhibit soft tissue calcification and in some instances normal calcification. Bone resorption is also inhibited. The mechanism of action for the inhibition of calcification is probably the inhibition of calcium phosphate crystal growth. However, the mode of action on bone resorption is not yet known but is more likely to be cellular. These properties have been used in man to prevent heterotopic calcification, to retard dental calculus, and to slow down bone resorption in conditions such as Paget's disease, tumoral bone disease, and osteoporotic immobilization.
 ...
PMID:Experimental basis for the use of bisphosphonates in Paget's disease of bone. 354 97

Hypophosphatemic osteomalacia may present as severe disability from bone disease. This report describes a patient with long-standing disease and multiple fractures. Medical management of the phosphate loss may be successful in promoting bone healing when it is not possible to establish the cause of the phosphaturia. Judicious increases in calcium, 1,25-dihydroxyvitamin D, and phosphorus supplements were carefully monitored to avoid failure of therapy or hypercalcemic complications from pharmacologic amounts of these supplements.
 ...
PMID:Medical reversal of acquired hypophosphatemic osteomalacia. 357 46

To assess the effect of different dialysis modalities on renal osteodystrophy, a controlled study was performed in six patients undergoing continuous ambulatory peritoneal dialysis and six hemodialysis-treated patients. All patients were enrolled at the initiation of dialysis, and age, sex, cause of renal failure, prior treatment of renal osteodystrophy, and baseline serum and bone histologic variables were similar in the two groups. After initial blood samples and bone biopsy specimens (with double-tetracycline labels) were obtained, renal osteodystrophy in both groups received comparable treatment with aluminum hydroxide to maintain serum phosphorus levels between 3.5 and 5.5 mg/dl, and with calcium carbonate and calcitriol to maintain total serum calcium levels between 10 and 11 mg/dl. Blood and bone samples were obtained again after nine months. All patients were asymptomatic at the beginning and end of the study. Phosphorus values were well controlled, and total calcium increased similarly in both groups. Although ionized calcium levels increased in both groups, the final level was higher in hemodialysis-treated patients than in patients undergoing continuous ambulatory peritoneal dialysis (2.82 +/- 0.07 meq/liter and 2.5 +/- 0.05 meq/liter, respectively; p = 0.005). Amino-terminal parathyroid hormone levels normalized in both groups, and histologic improvement of osteitis fibrosa occurred in a similar proportion of patients in both groups; however, quantitative improvement was greater in the hemodialysis-treated patients. Osteomalacia, assessed qualitatively and by dynamic histomorphometric measurements, was ameliorated to a much greater degree in patients undergoing continuous ambulatory peritoneal dialysis compared with hemodialysis-treated patients. Bone aluminum staining was absent in all biopsy specimens. Overall, bone histologic findings improved to a greater degree in patients undergoing continuous ambulatory peritoneal dialysis. When patients undergoing continuous ambulatory peritoneal dialysis or hemodialysis and receiving similar treatment for renal osteodystrophy were compared, patients treated with continuous ambulatory peritoneal dialysis appeared to have a greater improvement in their metabolic bone disease.
 ...
PMID:Controlled study of renal osteodystrophy in patients undergoing dialysis. Improved response to continuous ambulatory peritoneal dialysis compared with hemodialysis. 360 32

Of the 90 cases of primary hyperparathyroidism surgically treated in our department over the last decade (1975-1985), ten cases had a mediastinal parathyroidal adenoma. In only two of these patients was a median sternotomy required for excision of the mediastinal adenoma. Three of the ten patients underwent the initial operation in other institutions, having undergone a previous neck exploration. There were seven males and three females, ages ranging from 41-68 years. Six patients had nephrolithiasis, four had both renal stones and bone disease and two had peptic ulcer disease. One of them was operated on as an emergency because of hyperparathyroidism crisis with calcium levels of 15/16 mg%. Four patients were asymptomatic and had hypercalcemia detected by SMA screening. The calcium level ranged from 11.5-16.2 mg%. The phosphorus ranged from 1.6-2.8 mg% with a mean of 2.0 mg%. All ten patients had plasma PTH determination by radioimmunoassay, the values ranged from 1.5-3 times normal. In seven of the ten cases, the mediastinal parathyroid adenoma was localized within the thymus, the other three were adjacent to the great vessels, two to the aortic arch and one to the pulmonary artery-size ranging from 1.2-5.4 cm. Preoperative localization techniques: venous sampling in four cases; technetium scanning in three cases. No preoperative localization techniques were used in the other three cases. There was no mortality nor other significant postoperative complications.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Primary hyperparathyroidism due to mediastinal parathyroid adenoma. 361 May 35

Assessment of osteomalacia using rigorous histologic definition was carried out in 36 unselected patients with chronic cholestatic liver disease, 33 with primary biliary cirrhosis, and 3 with primary sclerosing cholangitis. Disease duration varied from 1 to 11 years. The mean values for total trabecular bone volume, osteoid volume, osteoid surface, and mineralization appositional rate were all decreased when compared to age-matched and sex-matched controls. There was a highly significant decrease in the mean osteoid seam width in both females (P = 0.001) and males (P = 0.02), and a significant prolongation of the mineralization lag time was found in females (P = 0.05), but failed to reach significance in males. These results excluded osteomalacia but were more indicative of osteoporosis. Biochemical evidence of osteomalacia was also absent, with serum calcium, serum phosphorus, and mean 25-hydroxyvitamin D levels not significantly different from control values, although there was a nonsignificant decrease in the mean value of 25-hydroxyvitamin D in patients with elevated serum bilirubin levels, and all patients with levels below 20 nmol/L had avoided sunlight exposure. The present results suggest that osteoporosis is the major type of metabolic bone disease in patients with chronic cholestatic liver disease.
 ...
PMID:Lack of osteomalacia in chronic cholestatic liver disease. 376 95

To investigate the mechanism for bone disease caused by exposure to cadmium serum samples were collected from 5 itai-itai disease patients, 36 Cd-exposed residents with renal tubular damage and 17 non-exposed individuals and analyzed for 1 alpha,25-dihydroxyvitamin D[1 alpha,25(OH)2D], parathyroid hormone, beta 2-microglobulin, calcium and inorganic phosphorus. Measurement of percentage tubular reabsorption of phosphate (%TRP) were performed only on the Cd-exposed subjects. Serum 1 alpha,25(OH)2D levels were lower in itai-itai disease patients and cadmium-exposed subjects with renal damage than in non-exposed subjects. Parathyroid hormone and beta 2-microglobulin concentrations in serum were higher in the Cd-exposed subjects. Decrease in serum 1 alpha,25(OH)2D levels were closely related to serum concentrations of parathyroid hormone, beta 2-microglobulin and %TRP. This study suggests that cadmium-induced bone effects were mainly due to a disturbance in vitamin D and parathyroid hormone metabolism, which was caused by the cadmium-induced kidney damage.
 ...
PMID:Mechanism for bone disease found in inhabitants environmentally exposed to cadmium: decreased serum 1 alpha, 25-dihydroxyvitamin D level. 379 41


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>