Role of preoperative intact parathyroid hormone levels in predicting the likelihood of multiglandular disease in primary hyperparathyroidism

Head & Neck ◽  
2010 ◽  
Vol 33 (4) ◽  
pp. 543-546
Author(s):  
Emad Kandil ◽  
Kathryn A. Carson ◽  
Anthony P. Tufaro ◽  
Obai Abdullah ◽  
Haytham Alabbas ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Intact Parathyroid Hormone ◽  
Multiglandular Disease ◽  
Hormone Levels

Intact parathyroid hormone levels and primary hyperparathyroidism

2017 ◽  
pp. 1-5 ◽  
Author(s):  
Haidar Al-Hraishawi ◽  
Peter J. Dellatore ◽  
Xinjiang Cai ◽  
Xiangbing Wang
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Intact Parathyroid Hormone ◽  
Hormone Levels

scholarly journals A case of Turner’s syndrome with Graves’ disease and primary hyperparathyroidism

2021 ◽  
Vol 9 ◽  
pp. 2050313X2110590
Author(s):  
Shigeru Nagaki ◽  
Emiko Tachikawa ◽  
Hitomi Kodama ◽  
Takao Obara ◽  
Makiko Osawa ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Serum Calcium ◽  
Clinical Laboratory ◽  
Graves Disease ◽  
Turner's Syndrome ◽  
Intact Parathyroid Hormone ◽  
Turner’S Syndrome ◽  
Laboratory Findings ◽  
Hormone Levels

We report a 21-year-old woman with Turner’s syndrome, Graves’ disease and primary hyperparathyroidism. At 12 years of age, she was of short stature, and was diagnosed with Turner’s syndrome and treated with growth hormone. At the age of 17 years, she was diagnosed with Graves’ disease. On treatment with methimazole, her laboratory findings normalized. At the age of 20 years, her serum calcium and intact parathyroid hormone levels were high. The upper left parathyroid gland showed swelling and was resected, and adenoma was diagnosed pathologically. Then, primary hyperparathyroidism induced by the adenoma was diagnosed. After the parathyroidectomy, the patient’s serum calcium and intact parathyroid hormone levels normalized. Is likely that Turner’s syndrome and Graves’ disease were not associated with primary hyperparathyroidism. Multiple endocrine neoplasia type 1 was unlikely considering the clinical, laboratory, ultrasonographic, and scintigraphic findings.

scholarly journals A novel CASR variant in a family with familial hypocalciuric hypercalcaemia and primary hyperparathyroidism

2020 ◽  
Vol 2020 ◽  
Author(s):  
Satyanarayana V Sagi ◽  
Hareesh Joshi ◽  
Jamie Trotman ◽  
Terence Elsey ◽  
Ashwini Swamy ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Organ Damage ◽  
Urinary Calcium ◽  
Interesting Case ◽  
List Type ◽  
Loss Of Function ◽  
Clearance Ratio ◽  
Hormone Levels ◽  
Severe Hypercalcaemia

Summary Familial hypocalciuric hypercalcaemia (FHH) is a dominantly inherited, lifelong benign disorder characterised by asymptomatic hypercalcaemia, relative hypocalciuria and variable parathyroid hormone levels. It is caused by loss-of-function pathogenic variants in the calcium-sensing receptor (CASR) gene. Primary hyperparathyroidism (PHPT) is characterised by variable hypercalcaemia in the context of non-suppressed parathyroid hormone levels. Unlike patients with FHH, patients with severe hypercalcaemia due to PHPT are usually symptomatic and are at risk of end-organ damage affecting the kidneys, bone, heart, gastrointestinal system and CNS. Surgical resection of the offending parathyroid gland(s) is the treatment of choice for PHPT, while dietary adjustment and reassurance is the mainstay of management for patients with FHH. The occurrence of both FHH and primary hyperparathyroidism (PHPT) in the same patient has been described. We report an interesting case of FHH due to a novel CASR variant confirmed in a mother and her two daughters and the possible coexistence of FHH and PHPT in the mother, highlighting the challenges involved in diagnosis and management. Learning points: Familial hypocalciuric hypercalcaemia (FHH) and primary hyperparathyroidism (PHPT) can coexist in the same patient. Urinary calcium creatinine clearance ratio can play a role in distinguishing between PHPT and FHH. Genetic testing should be considered in managing patients with PHPT and FHH where the benefit may extend to the wider family. Family segregation studies can play an important role in the reclassification of variants of uncertain significance. Parathyroidectomy has no benefit in patients with FHH and therefore, it is important to exclude FHH prior to considering surgery. For patients with coexisting FHH and PHPT, parathyroidectomy will reduce the risk of complications from the severe hypercalcaemia associated with PHPT.

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.

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