SPECT/CT Imaging in Hyperparathyroidism and Benign Thyroid Disorders
SPECT/CT optimizes interpretation and diagnostic confidence, thereby enriching the nuclear physician's role in guiding clinical management of endocrine tumors. SPECT/CT has become an increasingly important tool in the preoperative evaluation of hyperparat
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SPECT/CT Imaging in Hyperparathyroidism and Benign Thyroid Disorders Nicolas Aide, Elif Hindié, Stéphane Bardet, and David Taieb
3.1
Hyperparathyroidism
3.1.1
Embryology
The superior parathyroid glands (also called P4) are derived from the fourth branchial pouch. The third branchial pouches give rise to the inferior parathyroid glands (also called P3) and the thymus. The superior parathyroid glands are most commonly found at the upper and middle third of the thyroid lobes. The inferior parathyroid glands are more varied in location and are usually found near the lower pole of the thyroid lobe below the lobe in the thyrothymic ligament. In some cases, the migration patterns are aberrant (insufficient or excessive), with clinical implications.
3.1.2
Pathophysiology, Treatment Goals and Strategies
3.1.2.1 Primary Hyperparathyroidism Sporadic primary hyperparathyroidism (pHPT) is only rarely diagnosed before the age of 50 and is mostly caused by solitary parathyroid adenomas. Parathyroid adenomas are monoclonal tumours which are probably related to defects in a set of N. Aide, MD, PhD • S. Bardet, MD Department of Nuclear Medicine, François Baclesse Cancer Centre, Caen, France E. Hindié, MD, PhD Department of Nuclear Medicine, Haut-Lévêque Hospital, University of Bordeaux, Bordeaux, France D. Taieb, MD, PhD (*) Department of Nuclear Medicine, La Timone University Hospital, European Center of Research in Medical Imaging (CERIMED), Aix-Marseille University, Marseilles, France e-mail: [email protected] H. Ahmadzadehfar, H.-J. Biersack (eds.), Clinical Applications of SPECT-CT, DOI 10.1007/978-3-642-35283-6_3, © Springer-Verlag Berlin Heidelberg 2014
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specific genes that control parathyroid cell growth. Double adenomas are seen in about 5% of cases. Diffuse parathyroid hyperplasia may occur in up to 10 % of sporadic cases and in all patients with MEN1 disease or with familial hypocalciuric hypercalcaemia. Carcinomas are rare and frequently related to mutations in HRPT2 gene. In sporadic cases, a clear indication for surgery is most obviously for symptomatic patient. The controversy arises with the asymptomatic patient, and criteria have been defined by International Workshops by the NIH taking into account patient’s age, renal function and bone mineral density.
3.1.2.2 Secondary Hyperparathyroidism Secondary hyperparathyroidism (sHPT) is a frequent and major complication for patients on long-term haemodialysis or peritoneal dialysis. With the decline of kidney function, sHPT develops due to a cascade of metabolic abnormalities: (1) phosphate retention, (2) increased FGF23 (fibroblast growth factor-23) which inhibits 1α-hydroxylase and calcitriol synthesis [1], (3) the negative net calcium balance stimulates PTH release and (4) chronically stimulated parathyroid cells lose their expression of VDR (vitamin D receptor), CaR (calciumsensing receptor), klotho and FGFR1–3 and become resistant to the inhibitory effect of vitamin D, calcium and FGF23 [1]. In patients on long-standing dialysis,
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