ISSN:1062-4821    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

The parathyroid hormone/parathyroid hormone-related peptide receptor belongs to a distinct family of G proteincoupled receptors, the members of which usually signal through at least two second messenger systems, adenylate cyclase and phospholipase C. The parathyroid hormone/ parathyroid hormone-related peptide receptor is most abundantly expressed in patients with Jansen's metaphyseal chondrodysplasia was screened for mutations in all coding exons of the receptor gene. Inactivating parathyroid hormone/parathyroid hormone-related peptide receptor mutations were excluded in patients with pseudohypoparathyroidism type lb. However, a receptor mutation that causes agonist-independent, constitutive cAMP accumulation was identified in a patient with Jansen's metaphyseal chondrodysplasia, a rare form of short-limbed dwarfism associated with hypercalcemia despite normal or low concentrations of parathyroid hormone and parathyroid hormone-related peptide. These findings allow the conclusion to be drawn that parathyroid hormone/parathyroid hormone-related peptide receptors mediate the endocrine actions of parathyroid hormone, which are required for the control of calcium homeostasis and the autocrine-paracrine actions of parathyroid hormone- related peptide, which are required for normal growth-plate development.

ISSN:1062-4821    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Parathyroid hormone-related peptide was originally identified as a tumor-produced factor that mediated malignancy-associated hypercalcemia by binding to the common parathyroid hormone/parathyroid hormone-related peptide receptor to stimulate osteoclastic bone resorption and renal tubular resorption of calcium. Its role as a humoral factor in hypercalcemia of malignancy is well established, and recent work has demonstrated its importance as a tumor-produced factor in the pathogenesis of bone metastasis. Besides these cancer-related functions, work in the past decade has clearly established that parathyroid hormone-related peptide has many important functions in normal physiology related to growth and development, reproductive function and smooth muscle relaxation. Many other physiological functions are also being attributed to this versatile peptide. An understanding of these functions in malignancy and normal physiology should lead to innovative therapy for malignancy as well as other disorders not previously related to calcium homeostasis.

ISSN:1062-4821    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Our knowledge of renal phosphate handling and its regulation has expanded in the past 2 years because of the molecular identification of sodium-phosphate cotransport systems. New tools (molecular probes and antibodies) have allowed dissection out of some of the molecular and cellular mechanisms underlying the adaptation of phosphate transport to dietary content, the phosphaturic effect of parathyroid hormone or glucocorticoids and the renal phosphate leak in hypophosphataemic rickets.

ISSN:1062-4821    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Hyperparathyroidism is a common finding in patients with renal failure. Phosphorus retention is known to be an important factor in the development of secondary hyperparathyroidism. Exciting new work has demonstrated that a high extracellular phosphorus concentration directly stimulates parathyroid hormone secretion and synthesis. Dietary phosphorus also modulates parathyroid function indirectly by decreasing calcitriol production, and it interferes with the calcaemic response to parathyroid hormone. The information available suggests that the control exerted by phosphorus is critical, via indirect and direct actions, in preventing the development of secondary hyperparathyroidism.

ISSN:1062-4821    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

It is well known that hyperparathyroidism begins early in renal failure and progresses, probably not linearly, throughout the natural course of renal diseases and dialysis therapy. Recent progress in basic medical science has improved our understanding of the mechanisms by which the classically known stimuli for parathyroid hormone synthesis and secretion may act, including hypocalcaemia, hyperphosphataemia and vitamin D3metabolism disturbances. In the treatment of hyperparathyroidism, although some authors stress the benefit of treating one of these stimuli, it is probably more effective to combine the treatment of them all. There is conclusive recent work showing the efficacy of using both CaCO3and vitamin D3, either in chronic renal failure or in dialysis patients at every stage of hyperparathyroidism. Therefore, the treatment of hyperparathyroidism should start early, long before dialysis, and it should aim to correct any of the causal factors. Both CaCO3and vitamin D3derivatives may be used in the prevention and treatment of renal bone disease. The limits of this association are the increasingly often reported adynamic bone disease, which in our experience has not yet given major clinical problems, and hyperphosphataemia. Uncontrolled serum phosphate levels would counterbalance the beneficial effect of vitamin D3derivatives on hyperparathyroidism.

ISSN:1062-4821    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Information on genetic abnormalities in primary hyperparathyroidism has accumulated gradually. Genetic alterations responsible for tumorigenesis have been identified in multiple endocrine neoplasia types 1 and 2. Point mutations in a calcium-sensing receptor gene were recently found to be responsible for familial hypocalciuric hypercalcaemia and neonatal severe hyperparathyroidism. Evidence has been provided that abnormalities of cell cycle regulation participate at tumorigenesis in parathyroid adenoma and carcinoma. Clonal analysis has shown that in renal hyperparathyroidism the parathyroid glands initially grow diffusely and polyclonally, after which foci of nodular hyperplasia are transformed to monoclonal neoplasia. Somatic changes of specific genes have been suspected of being responsible for parathyroid tumorigenesis in renal hyperparathyroidism. However, the genetic loci responsible for the frequent monoclonality largely remain to be identified, and heterogeneous genetic abnormalities may contribute to the progression of secondary parathyroid hyperplasia.

ISSN:1062-4821    

出版商:OVID    

年代:1996

数据来源: OVID