Endocrine Abstracts

Introduction: Hungry Bone Syndrome (HBS) is characterized by a profound and persistent state of hypocalcemia, typically observed following parathyroidectomy or thyroidectomy. This syndrome manifests in the postoperative period, and its occurrence is associated with extended exposure to elevated levels of parathyroid hormone (PTH) or thyrotoxicosis. This prolonged exposure results in heightened bone turnover rates, marked by a net loss of bone minerals through resorption. We report three cases of Hungry bone syndrome after parathyroidectomy for primary hyperparathyroidism.

Cases: Three patients, aged 46, 78, and 58, presented with altered general conditions, prompting a work-up revealing hypercalcemia (185 mg/l, 141 mg/l, and 140 mg/ml, respectively), hypophosphatemia (19 mg/l in all cases), and elevated parathyroid hormone levels indicative of hyperparathyroidism (4936 pg/ml, 392 pg/ml, and 420 pg/ml, respectively). Initial medical management included rehydration and intravenous bisphosphonates administration. Following localization workup confirming a parathyroid origin, parathyroidectomy was performed in each case, revealing parathyroid adenomas on anatomopathological examination. Postoperatively, all patients experienced prolonged hypocalcemia and hypophosphatemia with normal PTH levels, consistent with the diagnosis of Hungry Bone Syndrome (HBS). These cases underline the clinical challenges and postoperative complications associated with hyperparathyroidism and emphasize the importance of vigilant management in mitigating adverse outcomes.

Dicussion & Conclusion: Hungry Bone Syndrome (HBS), though infrequent, manifests as a severe and enduring condition characterized by profound hypocalcemia. The severity of hypocalcemia stems from a substantial escalation in calcium utilization by the skeletal system. This heightened demand is a consequence of the abrupt cessation of bone resorption, despite persistently elevated circulating parathyroid hormone (PTH) levels, leading to a rapid and pronounced shift towards increased bone formation. The therapeutic approach to HBS is focused on rectifying the substantial calcium deficit and reinstating normal bone turnover. This is achieved through the administration of high doses of calcium and active metabolites or analogues of vitamin D, aiming to restore the delicate balance of bone metabolism and alleviate the severe hypocalcemic state associated with this syndrome.