Primary hyperparathyroidism-related giant parathyroid adenoma (Review)

xlomafota13 shared this article with you from Inoreader Primary hyperparathyroidism-related giant parathyroid adenoma (Review) Via Experimental and therapeutic medicine Exp Ther Med. 2022 Jan;23(1):88. doi: 10.3892/etm.2021.11011. Epub 2021 Nov 26. ABSTRACT Primary hyperparathyroidism (PHPT), an endocrine condition caused by a parathyroid adenoma (PTA) in 80-85% of the cases, has shifted in the modern era to a mildly symptomatic phenotype due to the prompt recognition of hypercalcemia and to a minimally invasive surgical approach which has a curative potential. Clinical complications of PHTH are either related to high calcium or parathyroid hormone [also parathormone (PTH)] or both, while the originating tumor typically is small, without local mass effects. A distinct entity is represented by giant PTA (GPTA) which is considered at a weight of more than 3 (3.5) grams. The present article is a review of the literature involving practical points of non-syndromic PHPT-related GPTA. Most authors agree that pre-operatory calcium and PTH are higher in GPTA vs. non-GPTA. However, the clinical presentation of PHPT may be less severe, probably due to local mass effects that bring the patient to an early medical evaluation. Age distribution, sex ratio, rate of successful pre-operatory location do not differ from non-giant PTA. Hypovitaminosis D is more frequent in PTA of higher dimensions. Post-operative hypocalcemia, but not recurrent/persistent PHPT, is expected, even hungry bone disease. A higher rate of atypia is described although the tumor is mostly benign. Unusual presentations such as cystic transformation, initial diagnosis during pregnancy or auto-infarction have been reported. The ectopic localization of PTA presented in almost 15% of all cases may also be found in GPTA. What are the exact cutoffs for defining GPTA is still an open issue. PMID:34934453 | PMC:PMC8652388 | DOI:10.3892/etm.2021.11011 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.