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)

Autonomous hyperparathyroidism occurred in 15% of 152 patients maintained by long-term home dialysis during the past nine years. Twenty-two patients with elevated serum parathormone levels and progressive bone disease in the presence of normal serum phosphate and calcium levels were treated by subtotal parathyroidectomy. All had parathyroid hyperplasia. Eighteen of the 22 patients are presently alive and undergo dialysis. Symptoms of bone pain, pruritus, and muscle cramps had improved in three fourths of the patients. The serum parathormone level decreased from a preoperative average of 576 muLEq/mL to an average of 188 muLEq/mL postoperatively. All 18 patients, observed for six to 77 months, showed improvement in x-ray films of their bone disease. The autonomous hyperparathyroidism of end-stage renal disease is corrected by subtotal parathyroidectomy, and the effect is sustained.
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PMID:Results of parathyroidectomy for autonomous hyperparathyroidism. 47 37

Parathormone (PTH) excess limits renal bicarbonate reabsorption. This may aggravate the acidosis in patients with renal insufficiency and secondary hyperparathyroidism. Why parathormone, the primary action of which is thought to be stabilization of the inonized fraction of calcium, affects acid-base balance remains uncertain. Parathormone not only promotes the release of calcium from bone but also mobilizes salts, including bicarbonate and phosphate. Accumulation of these anions in the extracellular fluid would limit the ionization of calcium. Teleologically it is not unexpected to find that, coincident with evolution of a mechanism which permits rapid mobilization of calcium from bone, a system had to develop which removed the byproducts of bone dissolution. If this concept is valid, parathormone-induced depression of renal bicarbonate reabsorption in uremia represents an undesired side effect of an adaptive mechanism. This would extend Bricker's "trade-off" hypothesis which ascribes metabolic bone disease due to PTH-induced phosphate loss to include metabolic acidosis resulting from diminished renal bicarbonate regeneration. Parathyroidectomy or phosphate restriction have been proposed for correction of the side effects of secondary hyperparathyroidism. These therapeutic manipulations cannot be recommended for general use. A more rational apprach for prevention of secondary hyperparathyroidism is the combined use of phosphate restriction with a short-acting vitamin D derivative.
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PMID:Parathyroid hormone and the regulation of acid-base balance. 110 50

At least one component of the secondary hyperparathyroidism of end stage renal failure is hyperphosphatemia. Since 1968, 101 patients were treated definitively in a home dialysis program, and 78 of the patients remain active. Despite maintenance of the serum phosphate level below 5 milligrams per cent, one-fourth eventually had progressive hyperparathyroidism develop, primarily manifested by bone disease. Serum calcium levels were generally normal and, except at the extremes, were not predictive. The incidence of hyperparathyroidism was not influenced by the age of the patient, but it increased with duration of dialysis. Hyperparathyroidism developed in 13 of 15 patients with serum parathormone levels greater than 500 but in only six of 56 patients with values less than 500. The single most important manifestation was progressive bone disease. Of 16 patients treated by subtotal parathyroidectomy, all had large hyperplastic parathyroid glands. All of the patients who were observed for longer than six months had progressive improvement in the bone disease. Hyperparathyroidism is a significant problem in the dialysis patient, despite phosphate control. Progressive bone disease and elevated serum parathormone levels are the most important indicators. The incidence is directly influenced by duration of dialysis. Subtotal parathyroidectomy is effective in reversing the bone changes.
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PMID:Hyperparathyroidism in the maintenance dialysis patient. 125 11

We used quantitative assays to measure the activity of the bone, liver, and intestinal forms of alkaline phosphatase in plasma in 75 patients with endstage chronic renal failure undergoing hemodialysis. The results were correlated with radiological and other biochemical indices of bone disease and with biochemical indices of liver disease. The total activity of alkaline phosphatase in plasma increased in 28 patients. In 10 of these patients, nine of whom had increased activity of gamma-glutamyltransferase in plasma, the increase in total activity of alkaline phosphatase was from the liver isoenzyme alone (nine patients) or from the liver and bone isoenzymes together (one patient). Intestinal alkaline phosphatase in plasma, although greater than 23 U/L in eight patients, was solely responsible for the increase in total alkaline phosphatase in one patient (who had normal gamma-glutamyltransferase). Bone alkaline phosphatase in plasma was increased in 25 patients, seven of whom had normal total alkaline phosphatase, and was closely correlated (r = 0.78) with osteocalcin concentration in plasma, which was increased in a much greater proportion of patients (99%). Both total and bone alkaline phosphatase were correlated with parathyrin in plasma (r = 0.46 and 0.50, respectively) and with osteocalcin (r = 0.60 and 0.78, respectively). Osteocalcin and bone alkaline phosphatase, but not parathyrin, decreased with age, implying that the skeletal response to parathyrin may be age dependent. In patients with increased total alkaline phosphatase undergoing hemodialysis, the concurrent measurement of gamma-glutamyltransferase may help identify whether the enzyme increase originates from the liver or bone, but this approach wrongly identified the source of the increase in three of 28 patients. Therefore, we recommend a separate measurement of the bone isoenzyme of alkaline phosphatase.
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PMID:Multiple forms of alkaline phosphatase in plasma of hemodialysis patients. 204 42

Alkaline phosphatase (AlP) and tartrate-resistant acid phosphatase (TRAP) activities have been studied comparatively in needle biopsies of the iliac crest of four cases of secondary hyperparathyroidism (renal osteodystrophy). AlP activity was associated with the plasma membrane of osteoblasts and their processes, of reticular cells of bone marrow and of young osteocytes of osteoid borders and woven bone. Moreover, it was detected in the fibroblast-like cells of the endosteal "fibrosis". These cells were orderly in arrangement and were parallel to the endosteal surfaces near zones of bone formation. They were disorderly near zones of bone resorption. A strong TRAP-positive reaction was present in osteoclasts and mononuclear cells of endosteal "fibrosis" and in osteocytes located near active osteoclasts and in woven bone. These results suggest that the so-called fibrosis of hyperparathyroidism, rather than representing reparative, inert tissue, consists of osteoblast-like cells, probably precursors of osteoblasts derived by parathormone-stimulated proliferation of AlP-positive stromal cells of bone marrow, and of TRAP-positive, mononuclear cells, probably preosteoclasts. Moreover, they show that TRAP activity can be present in osteocytes, probably under stimulation by the same factors which stimulate osteoclast activity. The histochemical demonstration of AlP and TRAP facilitates the morphological diagnosis of metabolic bone disease and may improve knowledge of bone physiopathology.
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PMID:Endosteal surfaces in hyperparathyroidism: an enzyme cytochemical study on low-temperature-processed, glycol-methacrylate-embedded bone biopsies. 175 Jan 88

The incidence and severity of osteopenic bone disease in primary sclerosing cholangitis is poorly defined. Clinical, biochemical and radiographic assessment and bone mineral density measurements of the lumbar spine were carried out in two groups of patients. Group 1 consisted of 30 patients with advanced primary sclerosing cholangitis; group 2 consisted of 18 patients with newly diagnosed primary sclerosing cholangitis. Only one patient had bone pain. All patients were normocalcemic; two had elevated serum parathormone levels. Fourteen patients (47%) from group 1 but no patients from group 2 had low serum 25-hydroxyvitamin D levels. Mean bone mineral density was significantly reduced in group 1 patients (0.97 +/- 0.04 gm/cm2) compared with age-matched and sex-matched controls (1.25 +/- 0.01 gm/cm2, p less than 0.0001), and in 15 patients (50%) bone mineral density was below the fracture threshold (0.98 gm/cm2). The bone mineral density in group 2 was not significantly different from controls, and no patient was below the fracture threshold. In neither group did bone mineral density correlate with serum bilirubin, 25-hydroxyvitamin D, fecal fat excretion, previous drug therapy or the presence of chronic ulcerative colitis. Histomorphometrical examination of bone from four group 1 patients showed increased bone resorption, reduced bone formation, moderate-to-severe osteopenia and no osteomalacia. In conclusion, severe osteopenic bone disease is common in advanced primary sclerosing cholangitis and, like that seen in other cholestatis diseases, is consistent with osteoporosis.
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PMID:The metabolic bone disease of primary sclerosing cholangitis. 186 Jun 83

Proximal femur fractures in elderly people are more and more frequent. Falls and senile bone disorders are the risk factors of this fracture. In order to understand the mechanisms of these bone disorders, we studied 21 consecutive patients with this fracture using bone histomorphometry. Measurements of serum intact parathormone (PTH), 25-(OH)-vitamin D, 1,25-(OH) 2-vitamin D and osteocalcin have been performed in these 21 patients, included in a larger series. We excluded patients with renal failure (serum creatinine greater than 140 mumols/l), cancer, or previous metabolic bone disease. There were 19 female and 2 male patients, ranging from 75 to 96 years, (mean 84.9). We found a low frequency of cortical (2/21) and trabecular (3/21) osteoporosis. There was no case of clearcut osteomalacia. Following histomorphometric bone study, two patients showed a typical pattern of hyperparathyroidism, and in a third one, this condition seemed very likely. In these three patients who were among the oldest, and who had high levels of serum PTH, chronic renal failure and primary hyperparathyroidism could be excluded. High bone remodeling was frequent in our patients, as reflected by the enhancement of eroded surfaces (13 cases) and of osteoid thickness (7 cases). Intact PTH level was elevated in our series compared to normal values in adults (in accordance to the PTH elevation in the case control study in a larger series). These findings suggest a major role of a secondary hyperparathyroidism in senile bone disorders favoring proximal femur fractures. This hyperparathyroidism is probably secondary to mild calcium and vitamin D deficiency. It may lead to architectural bone changes favoring this fracture.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperparathyroidism in proximal femur fractures biological and histomorphometric study in 21 patients over 75 years old. 191 14

Aluminium-related osteodystrophy results in osteomalacia or in the so-called aplastic bone. In this particular bone disease bone cells activities are distinctly reduced but there is no disorder of bone mineralization. Aluminium exerts a direct toxic effect on bone tissue, notably on osteoblasts which are always strongly depressed in case of major aluminium overload. Aluminium-related osteopathy is regularly accompanied by low levels of parathormone due to accumulation of aluminium in the parathyroid glands. Parathormone modulates the bone aluminium overload: hyperparathyroidism "protects" bones against the deleterious effect of aluminium, whereas aluminium deposit in bone increase after parathyroidectomy. The respective roles played by low parathormone levels and by aluminium deposits in aplastic bone lesions is difficult to determine since hypoparathyroidism itself can probably cause the aplastic osteopathy. The role of parathormone stands out more clearly now that in patients under dialysis the bone aluminium overload has markedly decreased. Many patients with aplastic bone (initially described in aluminium poisoning) show no aluminium deposits in bones but have, for some unknown reason, a normal or even low parathormone level. The clinical course of this type of osteopathy remains to be determined, but there seems to be no reason to worry since numerous patient are asymptomatic. Preventing secondary hyperparathyroidism while refraining from prescribing aluminium hydroxide is the principal therapeutic objective in osteodystrophy of haemodialysis patients.
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PMID:[Renal osteodystrophy: aluminium and secondary hyperparathyroidism]. 232 87

99mTc-HEDP bone scan was carried out on 12 long-time haemodialysed patients, suffering from bone pains. X-ray examinations of the bone and laboratory tests (serum calcium, -phosphor, -alkaline phosphatase, -parathormone, -aluminium, -ferritin) were also performed. The scintigrams were evaluated by two semiquantitative scores. Based on diffuse, increased radiopharmacon uptake of the bones and more than five points in the Fogelman score 5 patients most likely had serious and 3 had moderate hyperparathyroidism. In two patients osteomalacy was presumed based on decreased radiopharmacon uptake of the bones, increased uptake of the soft tissues and zero Fogelman score. Mixed or other bone disease was suggested in two other patients. Good correlation was found between the results of bone scans, the parathormone values and the results of histology obtained after parathyreoidectomy of 4 patients and autopsy of two others. This non-invasive examination (ie. bone scan) is helpful in differential diagnosis of uraemic osteodystrophy and its wide use is proposed in domestic nephrological practice.
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PMID:[Bone scintigraphy in uremic osteodystrophy]. 260 56

We studied the effects of acute modifications in plasma calcium on parathormone (PTH) secretion in 23 patients with primary hyperparathyroidism (PHPT). In 12 patients, PTH hypersecretion was autonomous, and basal plasma calcium concentration was positively correlated with maximal serum PTH(1-84) reached during Na2EDTA infusions. In 11 patients, PTH hypersecretion remained suppressible, but with elevated set point value, and basal plasma calcium concentration was positively correlated with set point. Thus, the degree of hypercalcemia seems mainly determined by the magnitude of maximal PTH secretion and set point error in autonomous and suppressible PHPT, respectively. We have previously suggested that high serum calcitriol levels might chronically inhibit PTH hypersecretion in PHPT. We showed that hyperparathyroid patients with renal stone presentation exhibited an abnormally high value of circulating calcitriol and a moderately elevated PTH activity, while patients with severe bone disease presentation displayed a low to normal calcitriol value and a dramatically increased PTH activity. The hypothesis was supported by a recent study from our Unit in one hyperparathyroid patient with severe bone disease and normal serum calcitriol level. Increment of serum calcitriol after daily intravenous Rocaltrol for 5 days directly suppressed PTH hypersecretion without change in plasma ionized calcium.
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PMID:Determinants of parathormone secretion in primary hyperparathyroidism. 269 19


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