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Endocrine Abstracts (2025) 110 P1151 | DOI: 10.1530/endoabs.110.P1151

ECEESPE2025 Poster Presentations Thyroid (141 abstracts)

C cell hyperplasia and multifocal papillary thyroid microcarcinoma in a patient with remarkably elevated basal and stimulated calcitonin levels

Nata Joksimovic 1 , Mirjana Stojkovic 1,2 , Bojan Markovic 1 , Tamara Janic 1 , Jovana Babic 1 , Ivana Djurkovic 1 , Biljana Nedeljkovic Beleslin 1,2 & Milos Zarkovic 1,2


1Clinic for Endocrinology, Diabetes and Metabolic Diseases, University Clinical Centre of Serbia, Belgrade, Serbia; 2Faculty of Medicine, University of Belgrade, Belgrade, Serbia


JOINT1764

Introduction: Medullary thyroid carcinoma (MTC) is calcitonin (CT) secreting tumor, originating from parafollicular thyroid cells. Serum basal and stimulated CT levels are helpful for early detection of MTC, while it is still a matter of debate whether it can differentiate between MTC, reactive and neoplastic C cell hyperplasia (CCH). According to the growth pattern CCH is subclassified into focal, diffuse and nodular. Neoplastic CCH -which is mostly nodular- precedes familial MTC, and often accompanies sporadic MTC with uncertain preneoplastic significance. Physiological CCH is associated with various conditions. It is not always possible to distinguish between these two based on C cell morphology. CCH is often found near differentiated thyroid lesions, and hypercalcitoninemia is not shown to be indicative of PTC.

Case Presentation: A 56 years old man was admitted to our hospital due to raised basal CT of 58.6 pg/mL, associated with incidentally discovered hypoechoic thyroid nodule measuring 9 mm by ultrasound. He had history of hypertension and hypokalemia, coxarthrosis, basal cell carcinoma and suspicion of polycythemia vera (PV). He was not obese, denied alcohol consumption and taking PPI. Basal CT in our institution was 34 pg/mL, CEA was normal. Calcium stimulation test was performed and the peak CT value of 893 pg/mL was highly suggestive of MTC. Laboratory analysis were consistent with the diagnosis of PV and hypokalemia with no other abnormalities. Thyroid-specific antibodies were negative and he was euthyroid. Thoracal CT scan, done for 6 mm pulmonary nodule on prior X ray scan, showed voluminous body of left adrenal gland. Autonomous cortisol secretion and catecholamine excess were excluded. Testing for primary aldosteronism was postponed and patient underwent total thyroidectomy. Histopathological examination revealed two bilateral microfoci of papillary thyroid carcinoma (1.5 and 0.5 mm), modest nodular hyperplasia, as well as focal, diffuse and nodular C cell hyperplasia (Calcitonin +) in both lobes of the thyroid. Testing for RET germline mutation is ongoing.

Conclusion: There are still no appropriate cut offs for discriminating MTC and neoplastic CCH from reactive forms, while it is sometimes hard to distinguish between reactive, neoplastic CCH and micro-MTC on histological evaluation. Thorough pathological search of whole specimen in cases with high CT levels is of great importance.

Volume 110

Joint Congress of the European Society for Paediatric Endocrinology (ESPE) and the European Society of Endocrinology (ESE) 2025: Connecting Endocrinology Across the Life Course

European Society of Endocrinology 
European Society for Paediatric Endocrinology 

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