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Hypertension and nephrology

DECEMBER 08, 2012

[Terciary hyperparathyreosis or not? ? You cannot solve it alone: combined treatment in severe osteitis fibrosa cystica]

HERSZÉNYI Eszter, PATÓ Éva, SZALAY László, BÍRÓ Zsolt, György Andrea, DEÁK György

[Phosphate retention, consequential rise of the phosphaturic fibroblast growth factor-23 that decreases the level of calcitriol resulting in hypocalcemia facilitates the development of secondary hyperparathyroidism (sHPT) in chronic kidney disease (CKD). Hyperphosphatemia, hypocalcemia and low calcitriol level result in increasing secretion of parathormone (PTH). While sHPT occures frequently in CKD, the development of therapy-resistant and hypercalcemic tertiary hyperparathyroidism is rare due to current therapeutic approaches. We present the case of a 41 year old, treated schizophrenic, hemodialized male patient with severe osteitis fibrosa cystica, severe hyperparathyroidism (PTH 2500 pg/ml) - considered to be tertiary - and with repeated pathologic fractures. While hospitalized, the patient was under supervised, combined therapy with the vitamin D receptor activator paricalcitol and the calcimimetic cinacalcet that resulted in marked decrease of PTH level to 1589 pg/ml. However, after discharge from the hospital due to the lack of compliance he failed to take his medications and PTH had risen to the initial level. This case demonstrates that severe hyperparathyroidism thought to be therapy resistant responds well to a combination of paricalcitol and cinacalcet however, patient compliance is essential to therapeutic success.]

Hypertension and nephrology

SEPTEMBER 20, 2011

[Role of calcimimetics in the treatment of secondary hyperparathyroidism in dialysed patients ]

[The authors summarize the pathophysiology and main clinical features of the condition which was previously called secondary hyperparathyroidism (sHTP) and renal osteodystrophy (ROD) in chronic kidney disease patients. Recently this entity has been renamed as chronic kidney disease - mineral and bone disorders (CKD-MBD), which more accurately describes the complexity of the condition including changes in laboratory parameters, bone turnover and vascular calcification. The calcium sensing receptor (CaR) plays a central role in the pathophysiology of CKD-MBD. Calcimimetics, which increase the sensitivity of the CaR to calcium, represent a novel and potentially advantageous class of medications for the management of the condition. Currently cinacalcet is the only available calcimimetic for clinical practice. Robust preclinical and human clinical trials have demonstrated that calcimimetics increase the expression of calcium sensing and the vitamin D receptors, attenuate parathyroid hyperplasia, decrease all four laboratory parameters (iPTH, Ca, P and Ca × P), optimize bone turnover and may slow down vascular calcification. As a results, cinacalcet based therapy is preferable and beneficial strategy in the treatment of CKD-MBD in patients on maintenance dialysis.]

Ca&Bone

NOVEMBER 20, 2004

[The pathophysiological role of the cell surface calcium-sensing receptor New clinical entities and drugs, potential therapeutic targets]

TÓTH Miklós

[The extracellular calcium-sensing receptor (CaSR) was recognized and cloned a decade ago. It is a G-proteincoupled receptor that plays an essential role in the regulation of extracellular calcium homeostasis. Diseases known as familial hypocalciuric hypercalcemia, neonatal severe primary hyperparathyroidism and autosomal dominant hypocalcemia are the consequences of naturally occurring mutations of the CaSR. However, the spectrum of the CaSR diseases became more complex with the recognition of both hypo- and hypercalcemic states caused by anti-CaSR autoantibodies. Activating anti-CaSR autoantibodies have been implicated in the pathogenesis of isolated idiopathic hypoparathyroidism and of hypoparathyroidism associated with autoimmune polyglandular syndromes. Inactivating CaSR autoantibodies may cause fluctuating hypercalcemic disorder that resembles primary hyperparathyroidism. The CaSR recently became one of the most intensively investigated target of potential new drugs. Cinacalcet has been approved for the treatment of secondary hyperparathyroidism associated with chronic renal insufficiency and for the management of inoperable or metastatic parathyroid carcinoma.The CaSR may be one of the main molecular target of strontium ranelate, wich is a new antiosteoporotic compound.]