{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T00:12:54Z","timestamp":1793059974717,"version":"4.5.0"},"reference-count":35,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2012,7,10]],"date-time":"2012-07-10T00:00:00Z","timestamp":1341878400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Endocrinology"],"published-print":{"date-parts":[[2012,8]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>The pathogenesis of basal ganglia calcification (BGC) in hypoparathyroidism is not clear. Its occurrence in hypocalcaemic milieu of hypoparathyroidism is believed to be due to high serum calcium\u2013phosphorus product and poor calcium control.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To report details of BGC in patients with idiopathic hypoparathyroidism (IH) and factors determining its progression during follow\u2010up.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method<\/jats:title>\n                    <jats:p>\n                      Clinical, biochemical characteristics and a meningioma\u2010expressed antigen\u20106 (MGEA6) gene polymorphism were analysed in 145 patients with IH, recruited since 1998, to determine the factors associated with BGC. The progression of BGC and its relationship with metabolic control of serum calcium, phosphorus, serum 25(OH)D and 1,25(OH)\n                      <jats:sub>2<\/jats:sub>\n                      D were assessed after a mean of 6\u00b79\u00a0\u00b1\u00a03\u00b75\u00a0years in 49 of them.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Basal ganglia calcification was present in 73\u00b78% (95% CI: 66\u00b76%\u201381\u00b70%) of subjects affecting the globus pallidus (68\u00b78%) putamen (55\u00b79%) and caudate nucleus (54\u00b78%). The other sites calcified were grey\u2013white junction (39\u00b78%), cerebellar parenchyma (31\u00b72%), thalamus (29\u00b70%) and dentate nuclei (24\u00b77%). Parkinsonism and dystonic symptoms were present in three cases. The presence of BGC at presentation was associated with calcification of the choroid plexus, cataract and an increased risk of seizures but not tetany. The progression of BGC during follow\u2010up was related to calcium\/phosphorus ratio. For every 1% increase in this ratio, the odds of progression decreased by 5% (OR: 0\u00b795, 95% CI: 0\u00b793\u20130\u00b799,\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00\u00b7001). A MGEA6 polymorphism, serum 25(OH)D and 1,25(OH)\n                      <jats:sub>2<\/jats:sub>\n                      D did not affect progression of BGC.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Basal ganglia calcification occurs in 73\u00b78% of patients with IH and correlates with the duration of hypocalcaemia, choroid plexus calcification, seizures and cataract. The progression of BGC is related to the calcium\/phosphorus ratio during follow\u2010up. This brings forth the importance of adequate phosphorus control in the management of hypoparathyroidism.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/j.1365-2265.2012.04353.x","type":"journal-article","created":{"date-parts":[[2012,1,30]],"date-time":"2012-01-30T14:43:10Z","timestamp":1327934590000},"page":"200-206","source":"Crossref","is-referenced-by-count":177,"title":["Prevalence and progression of basal ganglia calcification and its pathogenic mechanism in patients with idiopathic hypoparathyroidism"],"prefix":"10.1111","volume":"77","author":[{"given":"Ravinder","family":"Goswami","sequence":"first","affiliation":[{"name":"Departments of Endocrinology and Metabolism New Delhi India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raju","family":"Sharma","sequence":"additional","affiliation":[{"name":"Radiodiagnosis New Delhi India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vishnubhatla","family":"Sreenivas","sequence":"additional","affiliation":[{"name":"Biostatistics All India Institute of Medical Sciences New Delhi India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nandita","family":"Gupta","sequence":"additional","affiliation":[{"name":"Departments of Endocrinology and Metabolism New Delhi India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arthi","family":"Ganapathy","sequence":"additional","affiliation":[{"name":"Departments of Endocrinology and Metabolism New Delhi India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sathi","family":"Das","sequence":"additional","affiliation":[{"name":"Departments of Endocrinology and Metabolism New Delhi India"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,7,10]]},"reference":[{"key":"e_1_2_7_2_1","first-page":"458","article-title":"Ossification des capillaries du cerveau","volume":"2","author":"Delacour A.","year":"1850","journal-title":"Annales medico\u2010psychologiques"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1001\/archneurpsyc.1939.02270170059003"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.32.7.779"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1007\/s10072-011-0514-7"},{"key":"e_1_2_7_6_1","doi-asserted-by":"crossref","first-page":"371","DOI":"10.1542\/peds.77.3.371","article-title":"Carbonic anhydrase II deficiency syndrome: recessive osteopetrosis with renal tubular acidosis and cerebral calcification","volume":"77","author":"Ohlsson A.","year":"1986","journal-title":"Pediatrics"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1007\/s12031-010-9445-7"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1097\/MAJ.0b013e3181cc3c9d"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00839209"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1530\/eje.0.1500009"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1530\/EJE-09-0303"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMcp0803050"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1148\/radiology.135.2.7367628"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2990.1986.tb00137.x"},{"key":"e_1_2_7_15_1","doi-asserted-by":"crossref","first-page":"251","DOI":"10.1152\/ajplegacy.1951.165.1.251","article-title":"Phosphate transport and turnover in the Brain","volume":"165","author":"Sacks J.","year":"1951","journal-title":"American Journal of Physiology"},{"key":"e_1_2_7_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(88)90832-3"},{"key":"e_1_2_7_17_1","doi-asserted-by":"crossref","first-page":"1322","DOI":"10.1523\/JNEUROSCI.02-09-01322.1982","article-title":"Regulation of calcium entry into the extracellular environment of the rat brain","volume":"2","author":"Barkai A.I.","year":"1982","journal-title":"The Journal of Neuroscience"},{"key":"e_1_2_7_18_1","first-page":"233","article-title":"The equilibrium between cerebrospinal fluid and blood plasma; 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