scholarly journals Incidental Parathyroid Disease during Thyroid Surgery: Should We Remove Them?

ISRN Surgery ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
S. Helme ◽  
A. Lulsegged ◽  
P. Sinha
Keyword(s):  
Primary Hyperparathyroidism ◽  
Parathyroid Gland ◽  
Thyroid Surgery ◽  
Parathyroid Tissue ◽  
Neck Surgery ◽  
Safe Procedure ◽  
Preclinical Phase ◽  
Abnormal Parathyroid Gland ◽  
Parathyroid Disease ◽  
History Of

Aim. Despite an incidence of parathyroid “incidentalomas” of 0.2%–4.5%, only approximately 135 cases have been reported in the literature. We present eight patients in whom an incidental abnormal parathyroid gland was found during routine thyroid surgery. We have reviewed the literature and postulate whether these glands could represent further evidence of a preclinical stage of primary hyperparathyroidism. Methods. A retrospective analysis of all 236 thyroid operations performed by a single surgeon was performed to identify patients in whom abnormal parathyroid tissue was removed at surgery. Results. 8/236 patients (3.39%) had a single macroscopically abnormal parathyroid gland removed and sent for analysis. Seven patients were found to have histological evidence of a parathyroid adenoma or hyperplasia. None of the patients had abnormal serum calcium detected preoperatively. Postoperatively, four patients had normal calcium, three had temporary hypocalcaemia and one refused followup. No patients had recurrent laryngeal nerve impairment. Conclusions. Despite the risk of removing a histologically normal gland, we believe that when parathyroid “incidentalomas” are found during surgery they should be excised and sent for histological analysis. We have found this to be a safe procedure with minimal morbidity to the patient. As the natural history of primary hyperparathyroidism is better understood, these glands found in normocalcaemic patients may in fact represent the early or preclinical phase of the disease. By removing them at the original operation, the patient is saved redo neck surgery with its high complication rate as or when clinically apparent primary hyperparthryoidism develops in the future.

Primary hyperparathyroidism after thyroid surgery and autotransplantion of parathyroid gland

2018 ◽  
Author(s):  
Bernardo Marques ◽  
Raquel Martins ◽  
Joana Couto ◽  
Jacinta Santos ◽  
Teresa Martins ◽  
...  
Keyword(s):  
Primary Hyperparathyroidism ◽  
Parathyroid Gland ◽  
Thyroid Surgery

scholarly journals Preoperative parathyroid harpoon localisation: a new technique helpful in reoperative patients with persistent hyperparathyroidism

2013 ◽  
Vol 95 (2) ◽  
pp. e1-e2
Author(s):  
J Gómez-Ramírez ◽  
D Tagarro ◽  
JM Bravo ◽  
E Martín-Pérez ◽  
E Larrañaga
Keyword(s):  
Primary Hyperparathyroidism ◽  
Parathyroid Gland ◽  
Conservative Surgery ◽  
New Technique ◽  
Reoperative Surgery ◽  
Abnormal Parathyroid Gland ◽  
Persistent Hyperparathyroidism ◽  
A New Technique ◽  
Ultrasonography Guidance ◽  
Inexpensive Technique

Surgery for persistent primary hyperparathyroidism remains a major challenge for surgeons and these reoperative procedures require an experienced parathyroid surgeon. The goal of reoperative surgery is to excise the abnormal parathyroid gland(s) and limit exploration to help minimise the potential complications. At least two positive and concordant localising studies should be available before reoperation because the technical difficulties in these cases make an exact localisation necessary before surgery. We describe the placement of a metallic harpoon under ultrasonography guidance as a safe, simple and inexpensive technique for localisation of the enlarged gland prior to conservative surgery.

scholarly journals MANAGEMENT OF ENDOCRINE DISEASE: Postsurgical hypoparathyroidism: current treatments and future prospects for parathyroid allotransplantation

2021 ◽  
Vol 184 (5) ◽  
pp. R165-R175
Author(s):  
Radu Mihai ◽  
Rajesh V Thakker
Keyword(s):  
Thyroid Surgery ◽  
Case Reports ◽  
Prospective Trial ◽  
Significant Proportion ◽  
Parathyroid Tissue ◽  
Major Complication ◽  
Neck Surgery ◽  
Parathyroid Cell ◽  
Healthcare Provision ◽  
Complex Needs

Background Permanent postsurgical hypoparathyroidism (POSH) is a major complication of anterior neck surgery in general and of thyroid surgery in particular. Depending on diagnostic criteria, up to 10% of patients undergoing bilateral thyroid surgery develop POSH. This leads to a multitude of symptoms that decrease the quality of life and burden the healthcare provision through complex needs for medication and treatment of specific complications, such as seizures and laryngospasm. Methods Narrative review of current medical treatments for POSH and of the experience accumulated with parathyroid allotransplantation. Results In most patients, POSH is controlled with regular use of calcium supplements and active vitamin D analogues but a significant proportion of patients continue to experience severe symptoms requiring repeated emergency admissions. Replacement therapy with synthetic PTH compounds (PTH1-34, Natpara® and PTH1-84, teriparatide, Forsteo®) has been assessed in multicentre trials, but the use of this medication is restricted by costs and concerns related to the risk of development of osteosarcoma. Based on recent case reports of successful allotransplantation of parathyroid tissue between siblings, there is renewed interest in this technique. Data on selection of donors, parathyroid cell preparation before allotransplantation, site and timing of transplantation, need for immunosuppression and long-term outcomes are reviewed. Conclusion A prospective trial to assess the efficacy of parathyroid allotransplantation in patients with severely symptomatic protracted post-surgical hypoparathyroidism is warranted.

scholarly journals SAT-361 Familial Hypocalciuric Hypercalcemia Type 3: AP2S1 Mutation

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Sarah Elizabeth Kerut ◽  
Licy L Yanes Cardozo
Keyword(s):  
Vitamin D ◽  
Primary Hyperparathyroidism ◽  
Parathyroid Gland ◽  
Genetic Mutation ◽  
Urinary Calcium ◽  
Familial Hypocalciuric Hypercalcemia ◽  
Dexa Scan ◽  
High Calcium ◽  
History Of ◽  
Type 3

Abstract Background: Familial hypocalciuric hypercalcemia (FHH) type 3 can appear similar to primary hyperparathyroidism and make the diagnosis of etiology of hypercalcemia challenging. Clinical Case: A 45-year-old man with hypertension and glaucoma was evaluated in clinic for hypercalcemia. His calcium was 12.3 mg/dL (8.4–10.2), PTH 41.9 pg/mL (15–65), Vitamin D 14.8 ng/mL (6.6–49) and phosphorus 1.7 mg/dL (2.7–4.5). He denied history of thiazide diuretic use, fragility fracture, nephrolithiasis and family history of calcium disorders. Further workup revealed normal kidney function, undetectable PTH related peptide and dual-energy x-ray absorptiometry (DEXA) scan with a T-score of -3.3 at spine L1-L4, -2.7 at femoral neck and -2.1 at distal one-third forearm. A 24-hour urine collection revealed a urinary calcium of 42.4 mg/24-hour (100–300) and calcium: creatinine clearance ratio of 0.003. Diagnosis of primary hyperparathyroidism was made despite low urinary calcium as this was thought to be due to vitamin D deficiency. Sestamibi scintigraphy and four-dimensional computed tomography did not localize a parathyroid adenoma, however, the patient was sent to surgery for four gland parathyroid exploration for primary hyperparathyroidism in setting of high calcium and young age with evidence of end-organ failure of osteoporosis. During surgery, three large abnormal parathyroid glands were identified and one normal parathyroid gland. Patient had a three-gland parathyroidectomy with intraoperative drop in PTH by 26.5%. Pathology returned as benign parathyroid tissues. After surgery, patient had persistently elevated calcium level of 12.6 mg/dL and an inappropriately non-suppressed PTH. He was then started on bisphosphonate and cinacalcet for osteoporosis and hypercalcemia, respectively and sent for genetic testing of FHH. His CASR gene was negative but his AP2S1 gene was positive which confirmed the diagnosis of FHH type 3. His calcium responded well to cinacalcet and repeat DEXA scan showed stability of bone mineral density in spine and hip after two years of treatment with bisphosphonate therapy. Conclusion: Familial hypocalciuric hypercalcemia type 3 is caused by an inactivating mutation in the AP2S1 gene. This gene encodes the adaptor-related protein complex 2, sigma 1 subunit which is located downstream from calcium-sensing receptor. This genetic mutation can appear similar to primary hyperparathyroidism in that it produces high levels of calcium and PTH and low phosphorus. Hypercalcemia, however, persists despite removal of parathyroid gland. This genetic mutation can be treated with cinacalcet in patients with high levels of calcium (>1 upper limit of normal) or symptoms of hypercalcemia.

scholarly journals SAT-353 Familial Hyperparathyroidism - Due to a Rare Genetic Mutation

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Adeyinka Taiwo ◽  
Joseph Stephen Dillon ◽  
Jennifer Stinson
Keyword(s):  
Family History ◽  
Primary Hyperparathyroidism ◽  
Parathyroid Adenoma ◽  
Gene Mutation ◽  
Parathyroid Tissue ◽  
Clinical Manifestations ◽  
Young Age ◽  
Parathyroid Cancer ◽  
History Of ◽  
Familial Hyperparathyroidism

Abstract Introduction: Hyperparathyroidism occurs most commonly in middle age patients, predominantly in women. It can be caused by parathyroid adenoma, hyperplasia or parathyroid carcinoma. Genetic predisposition can be found in about 10% of primary hyperparathyroidism due to certain gene mutations. This case emphasizes the importance of taking a detailed family history when patients present with hyperparathyroidism at a young age, so that familial hyperparathyroidism, if present, can be detected and relatives screened. Clinical case: A 26 y.o. male presented with symptoms of fatigue and polydipsia for several years. He was noted to have a serum calcium of 12.4 mg/dL(8.5–10.5), with parathyroid hormone of 213 pg/ml (15–65). He denied any history of kidney stones, fractures and no palpable neck masses. The patient’s family history was significant for his paternal half-sister who had parathyroidectomy for hyperparathyroidism at 20yrs old and paternal grandmother died of parathyroid cancer in her 50s. The patient’s father died of pancreatic cancer at 41yrs old. A neck ultrasound revealed a mass posterior to the left inferior thyroid. A Sestamibi parathyroid scan revealed a parathyroid adenoma at the posteroinferior aspect of the left hemithyroid. Labs for free metanephrines and normetanephrine, prolactin and gastrin levels were all normal. Due to his young age and the possibility of having familial hyperparathyroidism, he underwent bilateral neck exploration and parathyroidectomy, with removal of his left inferior, right superior, left superior parathyroid glands and left upper thymus. Surgical pathology revealed, hypercellular parathyroid tissue. Post operatively, his calcium and vitamin D remained within the normal range. Genetic studies revealed a mutation in the parafibromin gene - CDC73 (also called HRPT2), a tumor suppressor gene, which is on chromosome 1q25. The patient currently has 6 children ranging from age 5 months to 6 years. He was advised to have his children tested any time from age 7 years for the gene mutation. The patient has remained stable 4yrs post operatively, with normal calcium and PTH levels. He does not have any history of jaw tumor. He never had an ultrasound kidney done. He is being monitored with yearly lab tests. Conclusion: CDC73 gene mutation-associated disorders are inherited as an autosomal dominant fashion, with variable penetrance. This gene mutation can be found in conditions such as hyperparathyroidism jaw tumor, familial hyperparathyroidism and parathyroid cancer. Reference: 1. CDC73-Related Disorders: Clinical Manifestations and Case Detection in Primary Hyperparathyroidism. J Clin Endocrinol Metab. 2017 Dec 1;102(12):4534–4540.

‘From Felix to the helix, and from the cradle to the grave – Semon's contribution to thyroid surgery’, Royal Society of Medicine, 1 November 2019, London, UK

2020 ◽  
Vol 134 (5) ◽  
pp. 381-386
Author(s):  
J C Watkinson
Keyword(s):  
Head And Neck ◽  
Conflict Of Interest ◽  
Thyroid Surgery ◽  
Royal Society ◽  
Neck Surgery ◽  
Head And Neck Surgery ◽  
History Of ◽  
President Elect

Mr President, Mr President Elect, Fellows and Members, Ladies and Gentleman, it is a pleasure to address the Section of Laryngology this morning and deliver the 94th Semon Lecture. I would like to thank the Semon Committee for their kind invitation. My lecture will discuss Sir Felix Semon (the man himself), highlight the history of head and neck surgery, and then discuss the requirements of a modern-day thyroid surgeon. I have no conflict of interest and nothing to declare.

scholarly journals Parathyroid Elastography―Elastography Evaluation Algorithm

2020 ◽  
Vol 2020 (1) ◽  
pp. 1
Author(s):  
Laura Cotoi ◽  
Daniela Amzăr ◽  
Ioan Sporea ◽  
Andreea Borlea ◽  
Oana Schiller ◽  
...  
Keyword(s):  
Primary Hyperparathyroidism ◽  
Secondary Hyperparathyroidism ◽  
Muscle Tissue ◽  
Thyroid Tissue ◽  
Parathyroid Tissue ◽  
Parathyroid Glands ◽  
Cervical Lymph Nodes ◽  
Cardiovascular Morbidity And Mortality ◽  
Parathyroid Lesions ◽  
Parathyroid Disease

(1) Background: Primary hyperparathyroidism is a common disorder of the parathyroid glands and the third most frequent endocrinopathy, especially among elderly women. Secondary hyperparathyroidism is a common complication of chronic kidney disease, associated with high cardiovascular morbidity and mortality. In both primary and secondary hyperparathyroidism, the need to correctly identify the parathyroid glands is mandatory for a better outcome. Elastography can be an effective tool in the diagnosis of parathyroid lesions, by differentiating possible parathyroid lesions from thyroid disease, cervical lymph nodes, and other anatomical structures. There are currently no guidelines or recommendations and no established values on the elasticity of parathyroid lesions. (2) Material and Methods: In our studies, we have evaluated, by Shear Wave elastography (SWE), both primary and secondary hyperparathyroidism, determining that parathyroid glands have a higher elasticity index than both thyroid tissue and muscle tissue. (3) Results: For primary hyperparathyroidism, we have determined, using 2D-SWE, the parathyroid adenoma tissue (mean elasticity index (EI) measured by SWE 4.74 ± 2.74 kPa) with the thyroid tissue (11.718 ± 4.206 kPa) and with the surrounding muscle tissue (16.362 ± 3.829 kPa). For secondary hyperparathyroidism, by SWE elastographic evaluation, we have found that the mean EI in the parathyroid gland was 7.83 kPa, a median value in the thyroid parenchyma of 13.76 kPa, and a mean muscle EI value at 15.78 kPa. (4) Conclusions: Elastography can be a useful tool in localizing parathyroid disease, whether primary or secondary, by correctly identifying the parathyroid tissue. We have determined that an EI below 7 kPa in SWE elastography correctly identifies parathyroid tissue in primary hyperparathyroidism, and that a cut-off value of 9.98 kPa can be used in 2D-SWE to accurately diagnose parathyroid disease in secondary hyperparathyroidism.

scholarly journals A Challenging Diagnosis of Primary Hyperparathyroidism in an Adolescent Female

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A175-A175
Author(s):  
Patricia Vining-Maravolo ◽  
Ethel Clemente ◽  
Berrin Ergun-Longmire
Keyword(s):  
Abdominal Pain ◽  
Primary Hyperparathyroidism ◽  
Parathyroid Adenoma ◽  
Serum Calcium ◽  
Parathyroid Tissue ◽  
Gastrointestinal Symptoms ◽  
Vital Signs ◽  
Normal Thyroid Function ◽  
Sestamibi Scan ◽  
History Of

Abstract Background: Hypercalcemia secondary to primary hyperparathyroidism (PHPT) is less common in children than adults. Single parathyroid adenoma is commonly the cause of primary hyperparathyroidism in children. Clinical Case: We present a 15-year-old female with one-week history of abdominal pain despite taking over the counter antacids. Her initial work up by her primary care provider revealed serum calcium of 11.8 mg/dL (9.0–11.5) and creatinine of 0.8 mg/dL (0.4–1.2). A week later, she presented to the emergency department with same complaint. In ED, she was found to have hypercalcemia (12.8 mg/dl) with elevated parathyroid hormone (PTH) at 78.5 pg/mL (15–65). Her random urine calcium creatinine ratio was high at 2.1. Her 25OHD was 25 ng/mL (30–100). She had negative urine pregnancy test but had trace ketones, leukocyte esterase, blood and bacteria. CBC and CMP were otherwise unremarkable. She continued to complain abdominal pain with nausea, decrease appetite, fatigue, and general muscle weakness. There was no known family history of calcium or metabolic bone disorders. Her vital signs and physical exam were normal. Subsequent labs showed mild improvement of calcium between (11–12.3 mg/dL), PTH between 54.5 and 77 pg/mL, normal thyroid function. Ionized calcium was mildly elevated 6.0 mg/dL (4.5–5.3) but her repeat 25OHD was low at18 ng/mL. Serum phosphorus levels were relatively normal with lowest level of 2.5 mg/dL (2.7–4.5). Gliadin Deamidated IgA was detectable 15 U/mL (< 15.0 U/). Ultrasound of abdomen was significant for nonspecific mild hepatomegaly; kidneys were normal in size and appearance. Ultrasound of thyroid was significant for probably intrathyroid parathyroid, measuring 6 x 8 x 8 mm. Tc-Sestamibi scan did not confirm a parathyroid adenoma. Genetic testing for MEN-1 was negative. FHH- related genes (i.e. CASR) was positive for p.R990G variant resulting in a mild gain of function of the calcium-sensing receptor. Although previous Tc-Sestamibi scan was unremarkable, an over read of it raised a concern for questionable uptake in the left superior lobe. SPEC-CT demonstrated possible abnormal parathyroid tissue in the upper pole of the left thyroid. FNA of the left thyroid nodule confirmed likely intrathyroidal parathyroid adenoma. Subsequent follow up and treatment, including parathyroidectomy, was done by another institution. She underwent a left parathyroidectomy with normalization of serum calcium and PTH levels post operatively (10.1 mg/dl and 8 pg/mL, respectively) and has complete resolution of her previous abdominal and gastrointestinal symptoms. Conclusion: PHPT is uncommon in children and adolescents and is typically associated with a single parathyroid adenoma. High index of suspicion is key for early diagnosis of PHPT despite a negative Tc-Sestamibi initially.

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