European multicentre study on outcome of surgery for sporadic primary hyperparathyroidism

2020 ◽  
Author(s):  
A. Bergenfelz ◽  
S. van Slycke ◽  
Ö. Makay ◽  
L. Brunaud
Keyword(s):  
Primary Hyperparathyroidism ◽  
Multicentre Study ◽  
Sporadic Primary Hyperparathyroidism ◽  
Outcome Of Surgery

Chief cell and clear cell parathyroid adenoma do not influence clinical and biochemical expression of the sporadic primary hyperparathyroidism

Endocrine ◽  
2012 ◽  
Vol 43 (2) ◽  
pp. 440-443 ◽  
Author(s):  
Shweta Varshney ◽  
Sanjay Kumar Bhadada ◽  
Uma Nahar ◽  
Viral N. Shah ◽  
Anil Bhansali ◽  
...  
Keyword(s):  
Primary Hyperparathyroidism ◽  
Parathyroid Adenoma ◽  
Clear Cell ◽  
Chief Cell ◽  
Sporadic Primary Hyperparathyroidism

Surgeon-Performed Ultrasound Improves Localization of Abnormal Parathyroid Glands

2005 ◽  
Vol 71 (7) ◽  
pp. 557-563 ◽  
Author(s):  
Carmen C. Solorzano ◽  
Theresa M. Lee ◽  
Marcela C. Ramirez ◽  
Denise M. Carneiro ◽  
George L. Irvin
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Thyroid Tissue ◽  
Parathyroid Tissue ◽  
Initial Step ◽  
Multiglandular Disease ◽  
Venous Sampling ◽  
Sporadic Primary Hyperparathyroidism ◽  
Operative Findings ◽  
Abnormal Tissue

With a secure diagnosis of hyperparathyroidism, preoperative localization of abnormal glands is the initial step toward limited parathyroidectomy (LPX). We investigated whether ultrasonography in the hands of the surgeon (SUS) could improve the localization of abnormal parathyroids when sestamibi scans (MIBI) were negative or equivocal. One hundred eighty patients with sporadic primary hyperparathyroidism (SPHPT) underwent preoperative SUS and MIBI scans before LPX guided by intraoperative parathormone assay. When the sestamibi scans were negative, SUS was used to localize the parathyroid, distinguish parathyroid from thyroid tissue, and to guide the intraoperative jugular venous sampling for differential elevation of parathyroid hormone (PTH). Operative findings, intraoperative hormone dynamics, and postoperative calcium levels determined successful localization. MIBI was negative or equivocal in 36/180 (20%) patients: 1) showed no parathyroid gland in 22 patients, 2) suggested an incorrect location for the abnormal gland in 9, and 3) was insufficient in recognizing multiglandular disease in 5. In these 36 patients, the addition of SUS led to the successful identification of the abnormal tissue in 19/36 (53%). In the remaining 17 patients with negative/equivocal scans, the parathyroid could not be clearly visualized by SUS. In these patients, SUS facilitated LPX by aiding preoperative transcutaneous jugular venous sampling for differentially elevated PTH (n = 3) and identifying questionable thyroid nodule versus parathyroid tissue (n = 1). Overall, SUS was useful in 23/36 (67%) patients with nonlocalizing MIBI scans, thus improving the rate of localization from 80 per cent to 93 per cent ( P < 0.01). Surgeon-performed cervical ultrasonography improved the localization of abnormal parathyroids by MIBI scan, adding to the success of limited parathyroidectomy.

Surgical Therapy for Familial Hyperparathyroidism

2009 ◽  
Vol 75 (7) ◽  
pp. 579-583 ◽  
Author(s):  
Jyotirmay Sharma ◽  
Collin J. Weber
Keyword(s):  
Primary Hyperparathyroidism ◽  
Cure Rate ◽  
Patient Demographics ◽  
Initial Surgery ◽  
Sestamibi Scanning ◽  
Recurrence Patterns ◽  
Sporadic Primary Hyperparathyroidism ◽  
Intraoperative Parathyroid Hormone ◽  
Familial Hyperparathyroidism

Isolated familial hyperparathyroidism (FHPT) not associated with multiple endocrine neoplasia is a rare and aggressive form of primary hyperparathyroidism. The traditional management of FHPT is a bilateral neck exploration with an increased rate of multigland hyperplasia, supernumerary glands, and recurrence. A prospective database was queried, which included 1383 consecutive parathyroidectomies between 1992 and 2008, and 28 patients with FHPT were identified. Patient demographics, pathology, intraoperative parathyroid hormone (IOPTH) kinetics, recurrence patterns, and accuracy of localization studies were analyzed. Twenty-one patients underwent bilateral neck explorations as an initial surgery, and seven patients had nine unilateral neck explorations for recurrent hyperparathyroidism. Overall cure rate was 89.2 per cent with a mean follow-up of 2.9 years (range: 6 months to 9.2 years); 64.3 per cent of patients had multigland disease. IOPTH helped identify supernumerary glands in three (12.5%) patients and accurately lateralized recurrent disease in eight of nine surgeries (88.8%). Tc-99m-Sestamibi failed to identify multigland disease in 11 patients (52.3%). FHPT has a greater prevalence of multigland disease, decreased utility of sestamibi scanning, and a higher recurrence rate than sporadic primary hyperparathyroidism. In FHPT, IOPTH is a useful adjunct in identifying additional tumors and in select cases may play a role in tumor localization.

Clinical update: sporadic primary hyperparathyroidism

The Lancet ◽  
2007 ◽  
Vol 370 (9586) ◽  
pp. 468-470 ◽  
Author(s):  
Antonio Sitges-Serra ◽  
Anders Bergenfelz
Keyword(s):  
Primary Hyperparathyroidism ◽  
Sporadic Primary Hyperparathyroidism

scholarly journals Molecular Alterations in Sporadic Primary Hyperparathyroidism

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Maria Inês Alvelos ◽  
Maria Mendes ◽  
Paula Soares
Keyword(s):  
Primary Hyperparathyroidism ◽  
Molecular Mechanisms ◽  
Benign Lesion ◽  
Protein Overexpression ◽  
Endocrine Disorder ◽  
Molecular Alterations ◽  
Familial Form ◽  
Somatic Alterations ◽  
Sporadic Primary Hyperparathyroidism ◽  
Parathyroid Tumours

Primary hyperparathyroidism (PHPT) is a frequent endocrine disorder characterized by an excessive autonomous production and release of parathyroid hormone (PTH) by the parathyroid glands. This endocrinopathy may result from the development of a benign lesion (adenoma or hyperplasia) or from a carcinoma. Most of the PHPT cases occur sporadically; however, approximately 10% of the patients present a familial form of the disease. The molecular mechanisms underlying the pathogenesis of sporadic PHPT are incompletely understood, even though somatic alterations in MEN1 gene and CCND1 protein overexpression are frequently observed. The MEN1 gene is mutated in about 30% of the parathyroid tumours and the protooncogene CCND1 is implicated in parathyroid neoplasia by rearrangements, leading to an overexpression of CCND1 protein in parathyroid cells. The aim of this work is to briefly update the molecular alterations underlying sporadic primary hyperparathyroidism.

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