Recombinant human TSH associated with radioiodine does not have further effects on thyroid volume and function after 2 years

© 2008 The Authors Journal compilation © 2008 Blackwell Publishing Ltd, Clinical Endocrinology , 69 , 342–346 results by using a stenosis of at least 50% in the coronary segments as the criterion for CAD (data not shown). To investigate whether there is an association between the –420C > G polymorphism and fasting resistin plasma levels (ng/ml) we measured resistin in 1162 randomly chosen probands. 4 There was no significant difference between the three RETN genotypes (CC 4·02 ± 2·04, CG 4·09 ± 2·15, and GG 4·10 ± 1·85, means ± SD), even after adjustment for age, gender, cardiovascular status or type 2 diabetes ( P = 0·778). To examine the relationship of the RETN polymorphism with total mortality and mortality from cardiovascular causes, we calculated hazard ratios and 95% confidence intervals (95% CI) using the Cox proportional hazards model. Regardless of whether or not we adjusted for age, sex and conventional risk factors, the RETN polymorphism showed no association with mortality from all causes (adjusted HR 0·99, 95% CI 0·85–1·15; P = 0·891) nor with cardiovascular mortality (adjusted HR 0·99, 95% CI 0·82–1·20; P = 0·920). The present study is the second one to investigate the association between the RETN –420C > G promoter polymorphism and angiographic CAD. In contrast to Tang et al . 2 who included 225 controls and 225 cases and recommended larger studies for confirmation of his results, we could not find that this polymorphism is a risk factor for cardiovascular disease, at least in Caucasians (698 control subjects and 2553 CAD patients). This is supported by the observation that we were not able to detect any relationship of this polymorphism with total and cardiovascular mortality, in our cohort, which is at an intermediate risk of death. Underlying differences in the study populations may account for the inconsistent results of our study and the one from Tang et al . 2 but in many instances it has been shown that positive associations in smaller studies have been disproven in subsequent studies of larger cohorts. Furthermore, our findings are in line with results from Norata et al . 5 who found no association of the RETN –420C > G promoter polymorphism, neither with MI (300 controls and 300 cases) nor with carotid intima-media thickness, supporting our final conclusion, that this polymorphism is not associated with CAD.