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Background/Aim: Vitamin D deficiency and vitamin D receptor (VDR) gene polymorphisms are involved in a variety of biological processes including cell proliferation, apoptosis, and adhesion in malignant tumors. This study investigated whether vitamin D levels and genetic variations of VDR are risk factors for thyroid cancer. Patients and Methods: Patients who underwent surgery for differentiated thyroid carcinoma (n=113) and those with benign thyroid pathology (n=150) were genotyped for VDR gene polymorphisms (ApaI, TaqI, FokI, and BsmI) and their 25(OH)D levels were simultaneously measured. Demographic data and histopathologic reports were also acquired for all patients. Results: Vitamin D levels were significantly lower in the thyroid cancer group (p=0.03). FokI and TaqI polymorphisms were more frequent in the thyroid cancer patients (p

Thyroid cancer (TC) has become the most rapidly increasing type of cancer representing 1-1.5% of all cancers diagnosed annually probably due to intensive screening. It is estimated that the death rate of TC has slowly increased from 0.49 to 0.51/100.000 in the last 10 years and 53.990 new cases will be diagnosed in 2018 in the United States. Therefore, efforts are being made in order to stop the increasing incidence and genetic alterations are thoroughly studied. One of the most recent incriminated factors in TC etiology and physiopathology is vitamin D deficiency. Besides the well-known role in bone metabolism, vitamin D has extra-skeletal effects exerted through the vitamin D receptor (VDR) and has been shown to interfere with many cellular functions such as inhibiting cell proliferation, stimulating differentiation and malignant cell apoptosis in different types of cancer. Cross-sectional, retrospective study which included 114 patients (71 with confirmed thyroid cancer and 43 patients in the control group with benign pathology). Preoperative levels of 25(OH)vitamin D, PTH, biochemical and thyroid panel were measured. The histopathologic features were analyzed. Mean values of vitamin D was 16.31 � 7.14 ng/mL with lower levels in patients with thyroid cancer (14.95 � 5.91 ng/mL) in comparison to patients with benign thyroid pathology (18.55 � 8.41 ng/mL), with a p value of 0.008. Majority of the cases were papillary thyroid cancer (97.18%) in stage 3 (45.07%). Vitamin D levels also correlated negatively with TNM staging. The necessity of further studies is a reality in order to establish if vitamin D deficiency is a possible risk factor for thyroid cancer and its correction can be considered an additional therapy.

Vitamin D deficiency is a global health problem, its role as an immune modulator being recently emphasized. Recent studies are increasingly suggesting that vitamin D plays a significant role in reducing the incidence and progression of autoimmune diseases. Furthermore, it was reported that patients with Hashimoto’s thyroiditis, an autoimmune thyroid disease had lower vitamin D levels [1]. We initiated a prospective study, for a period of 6 months with a study group represented by 160 patients admitted to the National Institute of Endocrinology “CI Parhon” in the period 2013 -2014. Patients were divided into 3 groups: 121 patients without thyroid pathology, 22 patients diagnosed with chronic autoimmune thyroiditis, who received 2000 IU cholecalciferol daily, 17 patients diagnosed with chronic autoimmune thyroiditis, which did not receive cholecalciferol. We found that patients with chronic thyroiditis have a poor vitamin D status with ATPO values negatively correlating with 25 (OH) vitamin D levels. Treatment with cholecalciferol not only improves vitamin D status but also lowers antithyroid antibodies titres. Keywords: vitamin D deficiency, chronic

Primary hyperparathyroidism is a common endocrine disorder that is mostly caused by solitary tumors within the parathyroid glands. Characterized by early debut and higher frequency of multiple parathyroid masses, familial forms of primary hyperparathyroidism are caused by the already known mutations of: menin (MEN1 syndrome), RET proto-oncogene (MEN2 syndrome), HRPT2-parafibromin (hyperparathyroidism-jaw tumor syndrome), calcium sensing receptor gene (familial hypocalciuric hypercalcemia). A specific mutation in FIHP has not been identified in the majority of affected families. Recent studies revealed menin, HRPT2 and calcium-sensing receptor mutations in patients with FIHP. Whether FIHP is a variant or an early stage of MEN1 syndrome or hyperparathyroidism-jaw tumor syndrome is yet to be established. We present three siblings with familial isolated hyperparathyroidism due to solitary parathyroid adenoma and favorable evolution post-parathyroidectomy. Genetic tests revealed HRPT2 mutation.