Hypercalcemic Crisis Due to a Giant Intrathyroidal Parathyroid Adenoma, with Postsurgical Severe Hypocalcemia and Hungry Bone Syndrome: A Case Report

Author:

Papanikos Vasileios1,Papadodima Elli2,Bantouna Dimitra3,Paparodis Rodis D.34ORCID,Livadas Sarantis5,Angelopoulos Nicholaos6ORCID,Karvounis Evangelos7

Affiliation:

1. Department of Otorhinolaryngology, School of Medicine, General University Hospital of Patras, 26504 Patras, Greece

2. Division of Endocrinology, Diabetes and Metabolism, Euroclinic Hospital, 11521 Athens, Greece

3. Endocrinology, Diabetes and Metabolism Clinics, Private Practice, 26221 Patras, Greece

4. Center for Diabetes and Endocrine Research, College of Medicine and Life Sciences, University of Toledo, Toledo, OH 43614, USA

5. Endocrinology, Diabetes and Metabolism Clinics, Private Practice, 11524 Athens, Greece

6. Endocrinology, Diabetes and Metabolism Clinics, Private Practice, 65302 Kavala, Greece

7. Center of Excellence in Endocrine Surgery, Euroclinic Hospital, 11521 Athens, Greece

Abstract

Background: Parathyroid adenoma is the most common cause of hypercalcemia and rarely leads to a hypercalcemic crisis, which is an unusual endocrine emergency that requires timely surgical excision. Case presentation: A 67-year-old male was admitted to the ER of the Euroclinic Hospital, Athens, Greece, because of elevated calcium levels and a palpable right-sided neck mass, which were accompanied by symptoms of nausea, drowsiness, and weakness for six months that increased prior to our evaluation. A gradual creatinine elevation and decreasing mental state were observed as well. The initial laboratory investigation identified severely elevated serum calcium (3.6 mmol/L) levels consistent with a hypercalcemic crisis (HC) and parathyroid hormone PTH (47.6 pmol/L) due to primary hyperparathyroidism. Neck ultrasonography (USG) identified a large, well-shaped cystic mass in the right thyroid lobe. With a serum calcium concentration of 19.5 mg/dL and a PTH of 225.3 pmol/L, the patient underwent partial parathyroidectomy and total thyroidectomy, which decreased serum calcium and PTH to 2.5 mmol/L and 1.93 pmol/L, respectively. Histology revealed a giant intrathyroidal cystic parathyroid adenoma, which was responsible for the hypercalcemic crisis. Postoperatively, the patient developed severe biochemical and clinical hypocalcemia, with calcium concentrations as low as 1.65 mmol/L, consistent with hungry bone syndrome (HBS), which was treated with high doses of intravenous calcium gluconate and oral alfacalcidol, and a slow recovery of serum calcium. After discharge, parathyroid function recovered, and symptomatology resolved entirely in more than one month. Discussion/conclusions: We present a case involving an exceptionally large intrathyroidal parathyroid adenoma that is characterized by clinical manifestations that mimic malignancy. The identification and treatment of such tumors is challenging and requires careful preoperative evaluation and postoperative care for the risk of hungry bone syndrome.

Publisher

MDPI AG

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