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Parathyroid disordersHyperparathyroidismHyperparathyroidism is related to an overactivity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH). In primary hyperparathyroidism (HPT1), an autonomous overproduction of PTH is observed, due to the ability of parathyroid cells to proliferate into large hyper-functioning glands. Secondary hyperparathyroidism (HPT2) refers to the excessive secretion of PTH by the parathyroid glands in response to hypocalcemia from any cause. It is mainly observed in patients with Chronic Kidney Disease [CKD]. HPT2 progresses as renal function deteriorates and most people with End-Stage Renal Disease [ESRD] will have HPT2 to varying degrees. ● Primary hyperparathyroidism [HPT1] The consequences of untreated HPT1 can range in severity from no demonstrable health effects to major lifethreatening problems. The most likely risks are progressive silent bone loss that increases the future risk of occurrence of fractures and nephrolithiasis or nephrocalcinosis with impairment of renal function. The treatment of HPT1 aims to respectively normalize serum PTH level and serum calcium level. Surgery was recognized as the only definite therapy for HPT1 and was acknowledged to be the appropriate course of action. Alternative solutions are today available such as minimally invasive surgery and non-invasive surgery. ● Secondary hyperparathyroidism [HPT2] In CKD patients, long-lasting hypocalcemia and coincidental hyperphosphatemia lead to the stimulation of parathyroid glands and subsequent HPT2, which causes decalcification of bones. Moreover, hyperphosphatemia has been recognized as an important risk factor for cardiovascular disease [CVD] mortality in patients with CKD. These complications markedly and negatively affect the prognosis and quality of life of patients with CKD. The standard care for patients with HPT2 consists of medically controling the level of parathyroid hormone, serum phosphorus and calcium in the blood. It includes dietary restrictions, phosphorus binders and administration of activated vitamin D analogues. |
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Thyroid
Anatomy and Physiology
Fibroadenoma
