Endocrine Abstracts

Background: Although high levels of calcitonin suggest neoplastic proliferations such as medullary thyroid carcinoma, C cell hyperplasia and some neuroendocrine tumors, systemic diseases and drugs may also elevate calcitonin. Although calcitonin is not as effective as PTH, it has got a role in calcium hemoastasis. Supraphysiological calcitonin level can lead to hypocalcemia.

Case presentation: A 57-year-old male patient was diagnosed with epilepsy with complaints of contraction in the body at the age of 16. Phenytoin therapy was started. He had no epileptic seizures for 13 years. Basal ganglia calcification was detected in brain CT which had been taken when he had muscle contractions while he had been hospitalized for measles in 1992. Calcium: 6.9 mg/dl phosphorus: 5.3 mg/dl albumin: 4.7 g/dl, parathormone: 499 pmol/l (219–659) calcitonin: 145 (0–50) was measured and hypoparathyroidism was diagnosed. Calcitriol and calcium carbonate treatment had been started. In another medical center it was thought that he had pseudohipoparathyroidism, because calcium was normal, vitamin D and parathormone were high while he was not taking calcium replacement treatment. He came to outpatient clinic in 2018 while he was taking 2000 mg oral calcium carbonate treatment. Calcium: 8.9 mg/dl (8.7–10.4) phosphorus:3.5 mg/dl albumin:4.5 g/dl, parathormone: 41 ng/l (18–80), 25-OH vitamin D: 41 ng/ml (25–80), 1,25OH vitamin D: 24.1 pg/ml (18–64) kalsitonin:117 ng/l (<8.4) was measured. Pseudohipoparathyroidism wasn’t considered with clinical findings. The control calcitonin value was 144, and the highest calcitonin value was 323. Thyroid USG and CEA levels were normal. He had no medullary thyroid carcinoma history in the family. CDKN1B, RET, menin gene analysis were normal. 24-h urinary calcium was 55 mg/day. The heterophile antibody examined by the PEG precipitation method and heterophile antibody-coated tube was negative. No pathological lesions were detected in GA-68 DOTA peptide imaging performed for possible neuroendocrine tumor.

Conclusion: In cases of hypercalcitoninemia, C cell neoplasms should be investigated primarily. In this case, medullary thyroid carcinoma was not considered with the current findings. Due to the coexistence of hypocalcemia and endogenous hypercalcitonemia, the possibility of autosomal dominant hypocalcemia was considered in which calcium sensing receptor activation is playing a role. However, hypocalcuria was interpreted against this possibility. In case of low/normal parathormone in the etiology of hypocalcemia, it is also suggested to measure the calcitonin level.