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

The pathogenesis of primary hyperparathyroidism (I degrees -HPT) and secondary hyperparathyroidism (II degrees -HPT) remains to be elucidated. To characterize their pathophysiology, we investigated the effects of calcium and phosphate on cell proliferation and PTH release in an organ culture of parathyroid tissues. Dissected parathyroid tissues obtained from patients with I degrees -HPT (adenoma) or II degrees -HPT (nodular hyperplasia) were precultured on a collagen-coated membrane for 1-4 week. After changing the medium for one containing various concentrations of phosphate, PTH release and [(3)H]thymidine incorporation were studied. In contrast to dispersed parathyroid cells cultured in a monolayer, calcium decreased PTH release in a concentration-dependent manner in parathyroid tissues. Furthermore, when parathyroid tissues obtained from II degrees -HPT were precultured for 1-4 weeks, PTH release and parathyroid cell proliferation were significantly increased in high-phosphate medium. These phosphate effects were also observed to a lesser extent in parathyroid tissues obtained from I degrees -HPT, but there was no significant difference between I degrees -HPT and II degrees -HPT. Microarray analyses revealed that mRNA levels of PTH, CaSR, and VDR were well preserved, and several growth factors (e.g. TGF-beta1-induced protein) were abundantly expressed in II degrees -HPT. Using organ cultures of hyperparathyroid tissues, in which PTH release and CaSR are well preserved for a prolonged period, we have demonstrated that phosphate stimulates parathyroid cell proliferation not only in II degrees -HPT but also in I degrees -HPT. Although the mechanism responsible for phosphate-induced cell proliferation remains to be elucidated, our in vitro findings suggest that both parathyroid tissues preserve to some extent a physiological response system to hyperphosphatemia as observed in normal parathyroid cells.
 ...
PMID:Stimulating parathyroid cell proliferation and PTH release with phosphate in organ cultures obtained from patients with primary and secondary hyperparathyroidism for a prolonged period. 1919 73

Primary hyperparathyroidism (HPT) is the main cause of hypercalcemia and the most common parathyroid glands disease. The diagnosis is easy in patients with hypercalcemia and elevated PTH serum level. Minimally invasive parathyroidectomy (PTx) represents the treatment of choice for symptomatic patients, leading to several advantages, including immediate normalization of hypercalcemia and significant improvement of bone mineral density, cardiovascular dysfunctions, neuropsychological symptoms and quality of life. Secondary and tertiary HPT are relatively common complications in patients with chronic kidney disease (CKD) or advanced kidney failure, and in kidney transplant recipients who did not achieve complete calcium/phosphate metabolism normalization, respectively. The drugs available for patients with secondary HPT, and to treat hyperphosphatemia include non-calcium-containing phosphate binder, calcitriol analogues, calcimimetic agents, or a combination of two or more drugs. Although recent studies report that PTx significantly improves survival also in patients with CKD and severe secondary HPT, the indications for surgery are not yet well established. Subtotal or total PTx with or without autotransplantation are the surgical options for treating all patients with secondary HPT. Total PTx leads to a faster reduction in serum calcium level and normalization of PTH, but the risk of hypoparathyroidism is higher than after subtotal PTx. Further studies are needed to confirm the usefulness of the drugs currently recommended, and others will have to be tested in the near future.
...
PMID:Pathophysiology and treatment of nonfamilial hyperparathyroidism. 2564 26


<< Previous 1 2