The Effect of Exenatide on Thyroid-Stimulating Hormone and Thyroid Volume.

OBJECTIVE: Glucagon-like peptide-1 (GLP-1) analogues are now widely used for the treatment of type 2 diabetes mellitus (DM). Many binding sites for GLP-1 have been demonstrated in the specific tissue compartments of organs in-cluding the brain and thyroid. The aim of this study was to investigate the effect of exenatide treatment on thyroid-stimulating hormone (TSH) and thyroid volume in diabetic patients without thyroid disease. MATERIAL AND METHODS: The study included 46 diabetic patients without thyroid disease who were receiving exenatide treatment. Comparisons were made of total thyroid volume and serum concentrations of TSH at baseline and after 6 months of follow-up. RESULTS: Of the 46 patients, 13 were excluded from the study, as they were unable to complete the treatment or left the follow-up process. After 6 months of exenatide treatment, the serum TSH concentration decreased significantly (from 2.3 [0.7-5.4] to 1.8 mIU/L [0.3-4.2], p= 0.007). There were no significant differences in thyroid volume (11.6 ± 9.0 vs. 12.1 ± 8.8 cm3, p = 0.19), free thyroxine (fT4), free tri-iodothyronine (fT3), and calcitonin levels before and after treatment. Thyroid volume was not affected by decreased TSH level (p:= 0.141) or a reduction in body mass index (BMI) (p > 0.05), and no correlation was detected between variation in TSH level and change in BMI (p > 0.05). CONCLUSIONS: Exenatide treatment for 6 months significantly decreased serum TSH concentration but did not affect thyroid volume in diabetic patients without thyroid disease.

Evaluation of the JAK2-V617F gene mutation in Turkish patients with essential thrombocythemia and polycythemia vera.

An activating mutation of Janus kinase 2 (JAK2-V617F) was previously described in chronic myeloproliferative disorders (MPD). In previously published studies, the frequency of the JAK2-V617F mutation was determined to be 80-90 % for patients with polycythemia vera (PV) and 40-70 % for essential thrombocythemia (ET). In this study, we analyzed the relationship between the JAK2-V617F mutation and clinical-hematological parameters in Turkish patients with MPD and compared these findings with published studies from other geographic regions. A total of 148 patients were studied; of which, 70 were diagnosed with PV and 78 with ET. The mutation status of JAK2 was determined using a tetra-primer polymerase chain reaction. We found that 80 % of the PV group and 42 % of the ET group were positive for the JAK2-V617F mutation. When all patients were analyzed, the levels of white blood cells, hemoglobin and splenomegaly were significantly different in patients with the JAK2-V617F mutation (p < 0.05). To our knowledge, this study is the first to evaluate the relationship between MPD and JAK2-V617F in Turkish patients. The JAK2-V617F mutation is frequently detected in the Turkish patients with MPD, and especially in patients with PV. Hence, it would be useful to include JAK2 mutation screening in the initial evaluation of patients suspected to have MPD.

Relation of resistin levels with C-reactve protein, homocysteine and uric acid in smokers and non-smokers.

BACKGROUND: The association between C-reactive protein, homocysteine, uric acid levels and cardiovascular risk have been debated for decades. Resistin is a newly discovered adipocyte derived cytokine. Smoking besides its effect on atherosclerosis, is shown to alter adipocytokine levels. Bearing in mind, these complex relationship of resistin with smoking, C-reactive protein, homocysteine and uric acid, we planned to investigate the association of resistin and these cardiovascular risk factors in smoker and non-smoker subjects. METHODS: We conducted a cross-sectional randomized study including 52 smoking and 33 non-smoking men. After making comparisons of C-reactive protein, homocysteine, uric acid and resistin between the two groups, we classified the subjects according to their insulin resistance and body mass and made again the comparisons.. RESULTS: Resistin levels were higher in smokers than in non-smokers (p<0.001) and also in insulin resistant than in non-insulin resistant smokers (p<0.05). Resistin levels were indifferent in non-smokers as insulin resistance was concerned and in smoker or non-smokers as body mass index was concerned. As all subjects were grouped based on homeostasis model assesment index and body mass index, neither C-reactive protein nor homocysteine and uric acid levels differred. CONCLUSIONS: We found that smoking may have influence on resistin levels and in smokers, insulin resistance is related to resistin levels, but in smoker and non-smokers body mass may not have any association with resistin. Resistin also may not have a role in C-reactive protein, homocysteine and uric acid levels both in smokers and non-smokers.