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While most cases (95%) occur sporadically, about 5% are associated with a hereditary syndrome: multiple endocrine neoplasia syndromes (MEN-1, MEN-2A, MEN-4), hyperparathyroidism-jaw tumour syndrome (HPT-JT), familial hypocalciuric hypercalcaemia (FHH-1, FHH-2, FHH-3), familial hypercalciuric hypercalcaemia, neonatal severe hyperparathyroidism and isolated familial hyperparathyroidism. Recently, molecular mechanisms underlying possible tumour suppressor genes (\n                    <jats:italic>MEN1, CDC73\/HRPT2, CDKIs, APC, SFRPs, GSK3\u03b2, RASSF1A, HIC1, RIZ1, WT1, CaSR, GNA11, AP2S1<\/jats:italic>\n                    ) and proto-oncogenes (\n                    <jats:italic>CCND1\/PRAD1, RET, ZFX, CTNNB1, EZH2<\/jats:italic>\n                    ) have been uncovered in the pathogenesis of hyperparathyroidism. While bi-allelic inactivation of\n                    <jats:italic>CDC73\/HRPT2<\/jats:italic>\n                    seems unique to parathyroid malignancy, aberrant activation of cyclin D1 and Wnt\/\u03b2-catenin signalling has been reported in benign and malignant parathyroid tumours. Clinicopathological correlates of primary hyperparathyroidism include parathyroid adenoma (80\u201385%), hyperplasia (10\u201315%) and carcinoma (&lt;1\u20135%). Secondary hyperparathyroidism generally presents with diffuse parathyroid hyperplasia, whereas tertiary hyperparathyroidism reflects the emergence of autonomous parathyroid hormone (PTH)-producing neoplasm(s) from secondary parathyroid hyperplasia. Surgical resection of abnormal parathyroid tissue remains the only curative treatment in primary hyperparathyroidism, and parathyroidectomy specimens are frequently encountered in this setting. Clinical and biochemical features, including intraoperative PTH levels, number, weight and size of the affected parathyroid gland(s), are crucial parameters to consider when rendering an accurate diagnosis of parathyroid proliferations. This review provides an update on the expanding knowledge of hyperparathyroidism and highlights the clinicopathological correlations of this prevalent disease.\n                  <\/jats:p>","DOI":"10.1136\/jclinpath-2015-203186","type":"journal-article","created":{"date-parts":[[2015,7,10]],"date-time":"2015-07-10T22:45:08Z","timestamp":1436568308000},"page":"771-787","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":111,"title":["Clinicopathological correlates of hyperparathyroidism"],"prefix":"10.1136","volume":"68","author":[{"given":"Kai","family":"Duan","sequence":"first","affiliation":[{"name":"Department of Pathology, University Health Network, Toronto, Ontario, Canada"},{"name":"Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen","family":"Gomez Hernandez","sequence":"additional","affiliation":[{"name":"Endocrine Oncology Site Group, Princess Margaret Cancer Centre, Toronto, Ontario, Canada"},{"name":"Department of Medicine, University Health Network, Toronto, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ozgur","family":"Mete","sequence":"additional","affiliation":[{"name":"Department of Pathology, University Health Network, Toronto, Ontario, Canada"},{"name":"Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada"},{"name":"Endocrine Oncology Site Group, Princess Margaret Cancer Centre, Toronto, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"239","published-online":{"date-parts":[[2015,7,10]]},"reference":[{"key":"2025112109044944000_68.10.771.1","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2014-1413"},{"key":"2025112109044944000_68.10.771.2","doi-asserted-by":"publisher","DOI":"10.1590\/S0004-27302010000200004"},{"key":"2025112109044944000_68.10.771.3","unstructured":"Bilezikian JP , Marcus R , Levine MA , et al . 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