Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2013) 32 P1114 | DOI: 10.1530/endoabs.32.P1114

ECE2013 Poster Presentations Thyroid cancer (64 abstracts)

Prevalence of hypovitaminosis D in patients with papillary thyroid carcinoma (PTC)

Aldona Kowalska 1 , Danuta Gasior-Perczak 1 , Iwona Palyga 1 , Monika Siolek 2 , Anna Sluszniak 1 , Ryszard Mezyk 1 & Stanislaw Gozdz 1


1Department of Endocrinology and Nuclear Medicine, Holycross Cancer Centre, Kielce, Poland; 2Genetic Clinic, Holycross Cancer Centre, Kielce, Poland.


Introduction: The correct 25-hydroxy vitamin D (25(OH)D) level plays a key role in the proper supply of vitamin D for the organism. Vitamin D deficiency may lead to an increased risk of development of various neoplasms, including papillary thyroid carcinoma (PTC).

Aim: Evaluation of the prevalence of vitamin D deficiency in patients with PTC and analysis of the relation between 25(OH)D levels and age, sex, place of living, severity of the disease, and presence of the CHEK2 mutation

Material: The study consisted of 168 patients with PTC; F:149 (88.7%), M: 19 (11.3%), aged 19–78 years. Mean age 52.3 (SD±13.6) years.

Methods: Exams were conducted during autumn. Plasma levels of 25(OH)D were measured by the RIA method. Prevalence of vitamin D deficiency in the studied group and the relation of the 25(OH)D levels, prevalence of 25(OH)D deficiency and age, sex, place of living, severity of the disease, and presence of the CHEK2 mutation.

Results: 25(OH)D<30 ng/ml deficiency was present in 101 patients and extremely low vitamin D <10 ng/ml in three patients.

Vitamin D deficiency was present in 62.1% of inhabitants of cities and 65.1% of inhabitants of villages, 63.3% women and 63.2% men, 63.8% patients in I stadium of the disease, 58.8% – II, 57.7% – III, 85.7% – IV, and 56.2% patients with CHEK2 mutation and 69.5% without mutation.

No correlations were found between 25(OH)D levels, prevalence of 25(OH)D deficiency and age, sex, place of living, severity of the disease, and presence of the CHEK2 mutation.

Conclusions: More frequent 25(OH)D deficiency due to CHEK2 gene mutation or severity of the disease was not found. Results suggest the need for prophylaxis programme of the vitamin D deficiency in patients with PTC, but do not allow to point to vitamin D deficiency as the factor potentially influencing the onset and course of the disease.

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