Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood flow to bone was measured using the 18F clearance method described by Wootton et al. (1976) in osteomalacia (nine cases) and primary hyperparathyroidism (eight cases). Bone blood flow was elevated above normal in the osteomalacia group and was normal in the hyperparathyroid group (range 3.6%-6.8% blood volume/min). It is suggested that bone blood flow is linked with the osteoblastic response of bone, and remains normal in cases of hyperparathyroidism when no clinical signs of bone involvement are present.
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PMID:Skeletal blood flow measured with 18F in patients with osteomalacia and hyperparathyroidism. 688 80

Vitamin D appears to influence parathyroid function indirectly through its effects on calcium metabolism rather than by a direct action of its metabolites on the parathyroid glands. In states of both secondary and primary hyperparathyroidism, the quantitative production of 1,25-(OH)2D may be determined by the prevailing concentration of serum 25-(OH)D but there appears to be some constraint that limits the formation of 1,25-0(OH)2D when the provision of its precursor exceeds the physiological. From the absence of this constraint in 'type 2 vitamin D dependency' it is inferred that it may operate through 'self-inhibition' of the renal production of 1,25-(OH)2D. It is shown that the level of serum 25-(OH)D may always exert some influence on the production of 1,25-(OH)2D and that this effect is facilitated by hyperparathyroidism. In developing vitamin D deficiency the reactive secondary hyperparathyroidism may thus function as an adaptive mechanism that sustains the level of serum 1,25-(OH)2D in the face of a diminishing serum 25-(OH)D. Failure of this adaptation and the development of a critical deficiency of 1,25-(OH)2D is regarded as the direct cause of defective mineralisation of bone. This concept would explain the absence of osteomalacia in some patients with very low levels of serum 25-(OH)D and the occurrence of defective osseous mineralisation in hypoparathyroidism.
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PMID:Vitamin D and hyperparathyroidism: the Lumleian Lecture 1981. 697 36

Early reports of patients with metabolic bone diseases such as nutritional osteomalacia, Fanconi syndrome, indicated an association with aminoaciduria. This association has since been described in osteomalacia of G. I. or hepatic origin, secondary to anticonvulsant therapy, tumors, and chronic renal failure. Aminoaciduria also occurs in primary hyperparathyroidism. In nutritional osteomalacia, vitamin D deficiency was thought to be responsible for the renal tubular abnormality, since it responded to treatment with vitamin D. However, since the description of aminoaciduria in hyperparathyroidism, the literature has been divided concerning the etiology of aminoacidura in conditions associated with abnormal vitamin D metabolism because secondary hyperparathyroidism often occurs in these conditions. Recently, some cases of Fanconi syndrome and a case of tumor-associated osteomalacia have been described with low or absent plasma 1,25-dihydroxycholecalciferol levels, normal serum PTH, and aminoaciduria. In one of these cases, and more recently in patients with chronic renal failure, it has been demonstrated that treatment with 1,25(OH)2D3 can improve amino acid transport independently from changes in serum PTH levels. 1,25(OH)2D3 therefore normally opposes the aminoaciduric effect of PTH. This is an agreement with observations which demonstrate that 1,25(OH)2D3 also opposes the phosphaturic action of parathyroid hormone.
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PMID:Aminoaciduria--its relationship to vitamin D and parathyroid hormone. 699 53

A 23-year-old man with primary hyperparathyroidism which was typical except for reduced alkaline phosphatase activity is reported. Histological examination of surgical specimens revealed chief cell hyperplasia of the parathyroid glands. Systemic abnormalities of alkaline phosphatase were demonstrated, i.e., marked reduction of all isoenzymes and undetectable osseous enzyme in the serum, abnormal distribution of the enzyme in hepatocytes and diminished enzyme activities in leukocytes. In addition, diminished bone remodeling activity was revealed in a biopsy specimen of the rib. The association of hypophosphatasia is highly unlikely, because of normal urinary excretion of phosphoethanolamine, lack of osteomalacia, and no indication of an hereditary factor. The causal relationship between low remodeling activity and abnormalities in alkaline phosphatase was suggested.
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PMID:A case of primary hyperparathyroidism with low serum alkaline phosphatase levels. 723 19

Bone scans and radiographs were evaluated in 80 patients with metabolic bone disease (27 with osteoporosis, 14 with primary hyperparathyroidism, 24 with renal osteodystrophy and 15 with osteomalacia). The bone scan did not suggest a metabolic bone disorder in any of 27 patients with histologically proven osteoporosis. In 22 (81%) patients radiographs were reported as showing osteoporosis. In 10 (70%) vertebral fractures were seen on X-ray while these were noted in 11 (41%) patients on the bone scan. Vertebral fractures were usually visualised on the bone scan when these had occurred less than one year previously. In primary hyperparathyroidism the bone scan was suggestive of a metabolic bone disorder in 7 of 14 (50%) patients, while radiographs were reported as showing evidence of hyperparathyroidism in three (21%) cases. The bone scan suggested the presence of a metabolic bone disorder in all 24 patients with renal osteodystrophy and 15 patients with osteomalacia while the correct diagnosis was obtained in 14 (58%) and nine (60%) of these patients on X-ray. It is concluded that the bone scan is the more sensitive investigation in patients with osteomalacia, primary hyperparathyroidism and renal osteodystrophy. For osteoporosis radiology is the investigation of choice but the bone scan may be of value in assessing the duration of vertebral collapse.
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PMID:A comparison of bone scanning and radiology in the evaluation of patients with metabolic bone disease. 742 73

Alkaline phosphatase (ALP) is present in human serum in the form of several isoenzymes. The two major circulating ALP isoenzymes, bone and liver, are difficult to distinguish because they are the products of a single gene and differ only by posttranslational glycosylation. Quantitative measurement of bone ALP (BAP) activity in serum can provide an index for the rate of bone formation. Furthermore, increased BAP activity in serum is indicative of bone disorders. We describe a method in which serum samples are added to a microtiter plate coated with monoclonal anti-BAP antibody and incubated 3 h at room temperature. After the unbound materials are washed off, the bound BAP activity is measured by adding p-nitrophenyl phosphate substrate. The assay demonstrated no cross-reactivity to intestinal or placental ALP and only 3-8% cross-reactivity to liver ALP. The intraassay (n = 21) CVs were 3.9-5.9%, and interassay (n = 8) CVs were 4.4-7.0%. Comparisons of the assay (y) with an IRMA (x) and a wheat germ agglutinin precipitation method (x') gave regression equations of y = 1.32x-6.4, r = 0.99, and y = 1.41x' + 4.8, r = 0.99. The assay detected increased BAP in sera from patients with osteoporosis, Paget disease, osteomalacia, or primary hyperparathyroidism.
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PMID:Monoclonal antibody assay for measuring bone-specific alkaline phosphatase activity in serum. 758 41

Metabolic bone diseases often present in old age and some are more easily treatable than others. Osteoporosis is best managed by prevention, with maximisation of peak bone density and reduction of subsequent bone loss. Although hormone replacement therapy is most useful in prevention, it also has a role in established osteoporosis. Other treating agents include calcium, calcitriol, calcitonin and bisphosphonates. Osteomalacia in the elderly mainly results from vitamin D deficiency and supplementation should be considered in those at risk. The newer bisphosphonates show great promise in the treatment of Paget's disease, while surgery remains the only treatment option in primary hyperparathyroidism.
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PMID:Metabolic bone diseases. 760 87

By histomorphometry bone biopsy specimens were evaluated from 10 patients with severe primary hyperparathyroidism (PHPT). The data suggest that the mean trabecular width and trabecular bone volume were slightly, but not significantly increased. As indices of bone remodeling activity, both trabecular osteoid surface and trabecular resorption surface were significantly increased indeed, indicating high bone turn-over occurred in PHPT. The dynamic study showed that much more trabecular bone surface was covered either with single or double tetracycline labels in PHPT than in control. The overproduction of osteoid in the patients leads to the accumulation of osteoid on the trabecular surface. Moreover, the mean osteoid width seemed to be thicker in PHPT than in control, suggesting the co-existence of osteomalacia, which might be a possible explanation for eucalcemia usually seen in the majority. Part of chinese PHPT patients.
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PMID:[The morphological changes in trabecular architecture of bone in severe primary hyperparathyroidism]. 775 Apr 25

Careful examination as well as biochemical and hormonal investigations should be performed in men suffering from vertebral crush fractures, in order to detect a destructive skeletal process (multiple myeloma, bone metastatic lesions, lympho and myeloproliferative disorders), a mineralization defect (osteomalacia) or a secondary osteoporosis: primary hyperparathyroidism, hypogonadism, hyperthyroidism, renal hypercalciuria, alcoholism and tobacco smoking. The diagnosis of idiopathic osteoporosis should be made only after these causes have been excluded; the pathogenesis of the disease is unclear but risk factors have been identified: family history of osteoporosis, low dietary calcium intake, delayed puberty, ethanol use, tobacco smoking, inactive lifestyle and lean body build. Correction of risk factors, calcium supplementation, regular program of weight bearing physical activity, in some instances correction of testosterone deficiency may be of benefit to reduce bone loss. Severe osteopenia or osteoporosis may require sodium fluoride therapy.
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PMID:[Male osteoporosis]. 793 30

Full-thickness biopsy specimens of iliac bones were submitted to morphometric analysis of intratrabecular osteons to study whether and how much the number and density of osteons increase in some metabolic bone diseases such as osteomalacia (OM), primary hyperparathyroidism (PHPT) and renal osteodystrophy (ROD). The biopsies were taken from 16 patients with OM of various causes, 18 with PHPT, 12 with ROD, and from 41 control cases. All the specimens were methacrylate-embedded, sectioned undecalcified and stained with solochrome cyanine or HE. Morphometry included measurements of the density of osteons and the volume of bone and osteoid, partially assisted with a semiautomatic digital image analyzer. Intratrabecular osteons were found to be more numerous in patients with metabolic disorder than in control. It was shown by discriminant analysis that the elevated number of osteons/cm2 tissue area contributes to the differentiation of abnormal from normal bones. The presence of blood vessels in the osteons indicated the biological significance of osteon formation which extends the metabolic surface of trabeculae, providing a basis for trabecular hypertrophy.
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PMID:Histomorphometric study of intratrabecular osteons in the iliac bone in three metabolic bone diseases. 794 May 22


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