Basal ganglia calcification is associated with local and systemic metabolic mechanisms in adult hypoparathyroidism.

Abstract

CONTEXT\nHypoparathyroidism is characterized by low serum calcium, increased serum phosphorus, and inappropriately low or decreased serum parathyroid hormone, which may be associated with soft tissue calcification in the basal ganglia of the brain.\n\n\nOBJECTIVE\nTo assess the prevalence and factors involved in the pathophysiology of basal ganglia calcification (BGC) in the brain in chronic hypoparathyroidism, and to evaluate proposed pathophysiologic mechanisms.\n\n\nDESIGN\nCase-control study with retrospective review of medical records over 20 years.\n\n\nSETTING\nSingle academic medical center.\n\n\nPATIENTS\n142 patients with chronic hypoparathyroidism and CT head scans followed between 1/1/2000 and 7/9/2020, and 426 age- and sex-matched controls with CT head scans over the same interval.\n\n\nINTERVENTIONS\nNone.\n\n\nMAIN OUTCOME MEASURES\nDemographic, biochemical, and CT head imaging findings, with semi-quantitative assessment of volumetric BGC.\n\n\nRESULTS\nThe study found that 25.4% of 142 patients followed for a median of 17 years after diagnosis of chronic hypoparathyroidism had BGC, which developed at a younger age than in controls. BGC was 5.1-fold more common in nonsurgical patients, and less common in postsurgical patients. Low serum calcium and low calcium/phosphate ratio correlated with BGC. Neither serum phosphorus nor calcium x phosphate product predicted BGC. Lower serum calcium was associated with greater volume of BGC. The extent of BGC varied widely, with nonsurgical patients generally having a greater volume and distribution of calcification.\n\n\nCONCLUSIONS\nBGC is associated with low serum calcium and low serum calcium/phosphate ratio, which may be related to severity of the disease, its etiology, or duration of treatment.