Hypocalcaemia Across the Adult Lifespan: Divergent Etiologies, Organ System Vulnerability, and Irreversible Sequelae — A Case Series

Abstract

Hypocalcaemia is a common biochemical finding that rarely receives clinical attention beyond acute intravenous or oral replacement [1,2]. However, its downstream systemic manifestations vary widely depending on underlying pathophysiology, chronicity, the calcium-phosphate (Ca \times P) product, and ambient parathyroid hormone (PTH) dynamics [1,3]. We describe three distinct presentations across the adult lifespan: (1) severe vitamin D deficiency and osteomalacia complicated by acute necrotizing pancreatitis; (2) idiopathic primary hypoparathyroidism with extensive neurocognitive and cerebellar manifestations secondary to bilateral basal ganglia calcification; and (3) neglected post-thyroidectomy hypoparathyroidism culminating in irreversible Fahr syndrome decades after surgery. This series highlights that hypocalcaemia is a multi-system metabolic disorder rather than an isolated biochemical target, where delayed etiological characterization leads to permanent structural and neurological damage [2,4].