Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Ther+Umsch 2007 ; 64 (5): 277-80 Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Hungriger Knochen nach Parathyreoidektomie--Das "Hungry Bone Syndrome" #MMPMID17685087
Farese S
Ther Umsch 2007[May]; 64 (5): 277-80 PMID17685087show ga
The Hungry Bone Syndrome (HBS) represents an important cause of prolonged hypocalcemia after parathyreoidectomy (PTX) due to primary, secondary or tertiary hyperparathyreoidism. The sudden postoperative withdrawal of parathyroid hormone (PTH) induces a stop in osteoclastic bone resorption without affecting the osteoblastic activity. Consequently, an increased bone uptake of calcium, phosphate and magnesium is observed. Risk factors for the development of HBS include: Large parathyroid adenomas, age > 60 years, high preoperative levels of serum PTH, calcium and alkaline phosphatase. In these patients a careful monitoring of clinical symptoms of hypocalcemia as well as the laboratory parameters are warranted during the immediate postoperative period. Treatment with oral calcium, and especially in patients with renal failure, additionally active vitamin D should be started as soon as possible after PTX. In severe cases of HBS, the administration of intravenous calcium is necessary. The duration of therapy is governed by symptoms and severity of the HBS and may last for up to 12 or more months. While prevention of HBS in high risk patients includes preoperative Vitamin D, the role of bisphosphonates has yet to be established.
Ther+Umsch 2007 ; 64 (5): 277-80
