Langén Ville L, Niiranen Teemu J, Puukka Pauli, Sundvall Jouko, Jula Antti M
Department of Health, National Institute for Health and Welfare, Helsinki, Finland.
Heart Centre, Turku University Hospital, Turku, Finland.
Clin Endocrinol (Oxf). 2017 Jan;86(1):120-127. doi: 10.1111/cen.13151. Epub 2016 Aug 2.
Scant data exist on the longitudinal association between thyroid function and lipid concentrations. We investigated associations of TSH and lipid concentrations cross-sectionally and longitudinally in a nationwide population sample.
A total of 5205 randomly sampled participants representative of Finns aged ≥30 years were examined in 2000-2001 and included in cross-sectional analyses. A total of 2486 were re-examined 11 years later and included in longitudinal analyses. With linear regression models adjusted for age, gender, smoking and body mass index, we assessed the associations of baseline TSH and TSH categories (low, reference range and high) with total, high-density lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol; apolipoprotein A1 and B; and triglycerides at baseline and follow-up.
At baseline, higher TSH associated with higher total cholesterol (β = 0·025, standard error [SE] = 0·007, P < 0·001), LDL cholesterol (β = 0·020, SE = 0·007, P = 0·002), apolipoprotein B (β = 0·006, SE = 0·002, P < 0·001) and log triglycerides (β = 0·008, SE = 0·003, P = 0·004), but not with other lipid outcomes. Higher baseline TSH associated with higher total cholesterol (β = 0·056, SE = 0·026, P = 0·033), LDL cholesterol (β = 0·057, SE = 0·023, P = 0·015) and apolipoprotein B (β = 0·012, SE = 0·006, P = 0·028) at follow-up in women, but not with any lipid outcomes in men. Participants with high TSH at baseline had a 0·22 mmol/l (95% confidence interval 0·02-0·41 mmol/l) higher LDL cholesterol at follow-up (P = 0·028) than participants with TSH in the reference range (0·4-3·4 mU/l). However, exclusion of participants with high-risk baseline lipid values rendered these positive longitudinal associations nonsignificant (P ≥ 0·098).
We could confirm a modest association between higher TSH and an adverse lipid profile cross-sectionally but not indisputably longitudinally.
关于甲状腺功能与血脂浓度之间的纵向关联的数据很少。我们在全国范围的人群样本中,对促甲状腺激素(TSH)与血脂浓度进行了横断面和纵向关联研究。
2000 - 2001年对总共5205名年龄≥30岁、具有芬兰人代表性的随机抽样参与者进行了检查,并纳入横断面分析。11年后,对其中2486人进行了重新检查,并纳入纵向分析。通过对年龄、性别、吸烟和体重指数进行校正的线性回归模型,我们评估了基线TSH及TSH类别(低、参考范围和高)与基线及随访时的总胆固醇、高密度脂蛋白(HDL)和低密度脂蛋白(LDL)胆固醇;载脂蛋白A1和B;以及甘油三酯之间的关联。
在基线时,较高的TSH与较高的总胆固醇(β = 0·025,标准误[SE] = 0·007,P < 0·001)、LDL胆固醇(β = 0·020,SE = 0·007,P = 0·002)、载脂蛋白B(β = 0·006,SE = 0·002,P < 0·001)和甘油三酯对数(β = 0·008,SE = 0·003,P = 0·004)相关,但与其他血脂指标无关。较高的基线TSH在随访时与女性较高的总胆固醇(β = 0·056,SE = 0·026,P = 0·033)、LDL胆固醇(β = 0·057,SE = 0·023,P = 0·015)和载脂蛋白B(β = 0·012,SE = 0·006,P = 0·028)相关,但与男性的任何血脂指标无关。基线时TSH高的参与者在随访时的LDL胆固醇比TSH在参考范围(0·4 - 3·4 mU/l)的参与者高0·22 mmol/l(95%置信区间0·02 - 0·41 mmol/l)(P = 0·028)。然而,排除具有高风险基线血脂值的参与者后,这些正向纵向关联变得不显著(P≥0·098)。
我们可以证实在横断面研究中较高的TSH与不良血脂谱之间存在适度关联,但在纵向研究中并非无可争议。