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甲状腺功能对脂蛋白(a)浓度的影响。

Effect of thyroid function on concentrations of lipoprotein(a).

作者信息

Engler H, Riesen W F

机构信息

Institute of Clinical Chemistry and Hematology, State Hospital, St. Gallen, Switzerland.

出版信息

Clin Chem. 1993 Dec;39(12):2466-9.

PMID:8252717
Abstract

The effect of thyroid hormones on concentrations of lipoprotein(a) [Lp(a)] was analyzed in 60 patients with active thyroid dysfunction (hyperthyroidism 30 cases, hypothyroidism 32 cases, and 2 cases with opposite changes) and after normalization of the thyroid state. Treatment of hyperthyroidism increased the mean Lp(a) concentrations by 60% (from 73 to 102 mg/L, P < 0.002); at the same time, low-density lipoprotein cholesterol (LDL-C) increased by 53% (from 2.6 to 3.7 mmol/L, P < 0.0001) and apolipoprotein B (apo B) by 35% (from 0.91 to 1.17 g/L, P < 0.0005). In hypothyroidism, the opposite changes were observed: mean Lp(a) decreased from 136 to 114 mg/L (10%, P < 0.02), LDL-C from 4.6 to 3.9 mmol/L (13%, P < 0.01), and apo B from 1.51 to 1.20 g/L (14%, P < 0.01). Although the changes in Lp(a) concentrations did correlate with changes of LDL-C during treatment of hyperthyroidism (r = 0.43, P < 0.05), and with changes in apo B during thyroxine-substitution therapy for hypothyroidism (r = 0.46, P < 0.05), we observed no associations between Lp(a) and LDL-C or apo B in the euthyroid state. These data cannot rule out the possibility that the thyroid hormone-induced increase in LDL-C receptor activity was responsible for the decreased concentrations of Lp(a) in hyperthyroidism. Given that LDL-C is approximately 30% of the Lp(a) molecule but the changes in Lp(a) concentrations are comparable with those in LDL-C (60% vs 53%), and given that Lp(a) is metabolized by an LDL-C-receptor-independent pathway, the present data suggest a direct effect of thyroid hormones on Lp(a) synthesis.

摘要

对60例活动性甲状腺功能障碍患者(甲状腺功能亢进症30例、甲状腺功能减退症32例以及2例有相反变化的患者)以及甲状腺状态恢复正常后,分析甲状腺激素对脂蛋白(a)[Lp(a)]浓度的影响。甲状腺功能亢进症的治疗使Lp(a)平均浓度升高了60%(从73mg/L升至102mg/L,P<0.002);与此同时,低密度脂蛋白胆固醇(LDL-C)升高了53%(从2.6mmol/L升至3.7mmol/L,P<0.0001),载脂蛋白B(apo B)升高了35%(从0.91g/L升至1.17g/L,P<0.0005)。在甲状腺功能减退症中,观察到相反的变化:Lp(a)平均浓度从136mg/L降至114mg/L(降低10%,P<0.02),LDL-C从4.6mmol/L降至3.9mmol/L(降低13%,P<0.01),apo B从1.51g/L降至1.20g/L(降低14%,P<0.01)。尽管在甲状腺功能亢进症治疗期间Lp(a)浓度的变化确实与LDL-C的变化相关(r=0.43,P<0.05),并且在甲状腺功能减退症的甲状腺素替代治疗期间与apo B的变化相关(r=0.46,P<0.05),但我们在甲状腺功能正常状态下未观察到Lp(a)与LDL-C或apo B之间存在关联。这些数据不能排除甲状腺激素诱导的LDL-C受体活性增加是甲状腺功能亢进症中Lp(a)浓度降低原因的可能性。鉴于LDL-C约占Lp(a)分子的30%,但Lp(a)浓度的变化与LDL-C的变化相当(60%对53%),并且鉴于Lp(a)通过一条不依赖LDL-C受体的途径代谢,目前的数据表明甲状腺激素对Lp(a)合成有直接影响。

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