Endocrine Abstracts

JOINT254

Primary hyperparathyroidism (PHPT) is an endocrine disorder characterized by increased parathyroid hormone secretion, leading to hypercalcemia and renal, gastrointestinal, neuromuscular, psychological and skeletal manifestations. We would like to introduce the non-common clinical manifestations of PHPT like Brown tumor and Parkinsonism.

Case report: A 64-year-old female was admitted to the Mikaelyan Institute of Surgery complaining of general weakness, pain in the right lumbar region and fever. The patient was diagnosed with Ureterolithiasis, right-ureteral stone obstruction, right-sided ureter hydronephrosis, and pyelonephritis and was preparing for surgery. A right-sided nephrectomy and right-sided ureterolithotomy were performed. In medical history: Schizophrenia for about 25 years, hemimaxillectomy for a giant cell tumor in the upper jaw 10 years ago. The patient has been on Haloperidol 10mg for more than 25 years and Trihexyphenidyl 2mg for the past 7 years. The patient exhibited reduced interaction during the initial examination and appeared very indifferent. Objective neurological examination revealed the following findings: combined rest and action tremor Tremor observed in the chin, accompanied by noticeable oral dyskinesias. Gait is characterized by wide-based steps with shuffling. The patient was diagnosed Drug-induced Parkinsonism. Blood tests: Hb-76g/l(N 115-152), Creatinine-128umol/l(44-100), Ca ionized-2.20mmol/l(1.13-1.32), PTH-409.6pg/ml (15-65), Vitamin D-10.6ng/ml (30-100), TSH-3.85 uIU/ml (0.3-4.5). Neck ultrasound: tissue formation in the left parathyroid gland and multiple thyroid nodules (TI-RADS 4). The patient refused to do FNA. Dual-energy X-ray absorption: T-score at L1-L4 -5.1, hip T-score -5.4. Full-Body CT Scan: multiple lytic lesions involving bones, probable Brown tumor. Esophagogastroduodenoscopy: atrophic gastritis. The patient started treatment with Vitamin D₃, rehydration and correction of anemia. After 1 month, she underwent left parathyroidectomy and total thyroidectomy. The histology showed parathyroid adenoma and papillary microcarcinoma of the left thyroid. PTH level decreased immediately after surgery (from 551.2 to 69.98). The patient’s neurological condition also improved. After surgery the patient was given Vitamin D₃, Calcium gluconate and Levothyroxine. The patient is currently under the follow-up.

Conclusion: Approximately 90% of cases of hypercalcemia are caused by hyperparathyroidism or malignancy. Our patient had both. Except common manifestations of hypercalcemia and PHPT, the patient had also rare manifestations, such as brown tumor. It is a non-neoplastic, reactive bone lesion resulting from excessive PTH secretion. Hypercalcemia is known to cause neuropsychiatric dysfunction too. Evidence of hyperparathyroidism associated with parkinsonism is rare. In our patient parathyroidectomy provided a significant remission of parkinsonism. Therefore, in this case, Parkinsonism may not only be drug-induced, but also hypercalcemia-induced.