Primary hyperparathyroidism (PHPT) is characterised by autonomous overproduction of parathyroid hormone (PTH), resulting in hypercalcemia and multisystem complications. Although routine calcium screening has reduced advanced skeletal disease in many regions, severe manifestations such as osteitis fibrosa cystica (OFC) still occur in resource‐limited settings. We report a case of a woman in her 30s who presented with profound disability after 4–5 years of progressive bone pain, fatigue, proximal myopathy and eventual loss of independent ambulation, requiring her to drag herself on the ground. Imaging revealed generalised osteopenia, subperiosteal bone resorption, a ‘salt and pepper’ appearance of the skull, codfish vertebrae, anterior bowing of long bones and multiple lytic lesions consistent with advanced OFC. Laboratory investigations revealed marked hypercalcemia (14.3 mg/dL), hypophosphataemia (1.49 mg/dL), elevated alkaline phosphatase (781 U/L) and elevated intact PTH (iPTH) (1110 pg/mL), confirming PTH‐dependent hypercalcemia. A 4D‐CT scan localised a left inferior parathyroid adenoma (LIPA), and a renal ultrasound showed bilateral nephrocalcinosis. Following preoperative stabilisation with saline diuresis and intravenous zoledronic acid, she underwent minimally invasive parathyroidectomy (MIP) with an immediate postoperative fall in PTH, indicating biochemical cure. However, she developed hungry bone syndrome (HBS), requiring intensive intravenous and oral calcium supplementation along with active vitamin D therapy. This case highlights the catastrophic skeletal consequences of delayed PHPT diagnosis. It underscores the importance of early recognition of metabolic bone disease to prevent irreversible disability and systemic complications, particularly in low‐resource settings.
Ara et al. (Thu,) studied this question.