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低密度脂蛋白受体(LDLR)基因常见变异影响早发心肌梗死患者家庭成员对瑞舒伐他汀的反应性。

Prevalent Variants in the LDLR Gene Impair Responsiveness to Rosuvastatin among Family Members of Patients with Premature Myocardial Infarction.

作者信息

Kien Nguyen Trung, Nghia Tran Tin, Hoang Nguyen Minh, Phu Tran Nguyen Trong, Nga Pham Thi Ngoc, Mai Ha Thi Thao, Espinoza J Luis

机构信息

Faculty of Medicine, Can Tho University of Medicine and Pharmacy, Can Tho 900000, Vietnam.

Tra Vinh General Hospital, Tra Vinh 940000, Vietnam.

出版信息

J Pers Med. 2023 Dec 18;13(12):1725. doi: 10.3390/jpm13121725.

Abstract

BACKGROUND

Familial hypercholesterolemia (FH) is an inherited metabolic disorder characterized by high levels of low-density lipoprotein cholesterol (LDL-c) from birth. About 85% of all FH cases are caused by pathogenic variants in the LDLR gene. Individuals with FH have increased cardiovascular risk, including a high risk of premature myocardial infarction (PMI).

METHODS

We conducted an opportunistic exome screening to identify variants in the LDLR gene among Vietnamese patients with PMI treated at a general hospital in southern Vietnam. A cascade testing for LDLR variants was conducted in their relatives within three generations, and the effects of the LDLR variant on the response to rosuvastatin treatment were also studied using a comparative before-and-after study design on those who were eligible.

RESULTS

A total of 99 participants from the three generations of four PMI patients were recruited, mean age 37.3 ± 18.5 years, 56.6% males. Sanger sequencing revealed two variants in the LDLR gene: variant rs577934998 (c.664T>C), detected in 17 individuals within one family, and variant rs12710260 (c.1060+10G>C), found in 32 individuals (49.5%) in the other three families tested. Individuals harboring the variant c.664T>C had significantly higher baseline LDL-c and total cholesterol levels compared to those with variant c.1060+10G>C (classified as benign) or those without LDLR variants, and among the 47 patients subjected to a 3-month course of rosuvastatin therapy, those with variant c.664T>C had a significantly higher risk of not achieving the LDL-c target after the course of treatment compared to the c.1060+10G>C carriers.

CONCLUSIONS

These findings provide evidence supporting the existence of pathogenic LDLR variants in Vietnamese patients with PMI and their relatives and may indicate the need for personalizing lipid-lowering therapies. Further studies are needed to delineate the extent and severity of the problem.

摘要

背景

家族性高胆固醇血症(FH)是一种遗传性代谢紊乱疾病,其特征是从出生起低密度脂蛋白胆固醇(LDL-c)水平就很高。所有FH病例中约85%是由LDLR基因的致病变异引起的。FH患者心血管疾病风险增加,包括早发心肌梗死(PMI)的高风险。

方法

我们进行了一次机会性外显子组筛查,以在越南南部一家综合医院接受治疗的PMI越南患者中鉴定LDLR基因的变异。对其三代以内的亲属进行了LDLR变异的级联检测,并采用前后对照研究设计,对符合条件的患者研究了LDLR变异对瑞舒伐他汀治疗反应的影响。

结果

共招募了来自4例PMI患者三代的99名参与者,平均年龄37.3±18.5岁,男性占56.6%。桑格测序在LDLR基因中发现了两个变异:变异rs577934998(c.664T>C),在一个家族的17名个体中检测到;变异rs12710260(c.1060+10G>C),在其他三个检测家族的32名个体(49.5%)中发现。与携带变异c.1060+10G>C(分类为良性)的个体或无LDLR变异的个体相比,携带变异c.664T>C的个体基线LDL-c和总胆固醇水平显著更高,在接受3个月瑞舒伐他汀治疗疗程的47例患者中,与携带c.1060+10G>C变异的个体相比,携带变异c.664T>C的个体在治疗疗程后未达到LDL-c目标的风险显著更高。

结论

这些发现为越南PMI患者及其亲属中存在致病性LDLR变异提供了证据支持,并可能表明需要对降脂治疗进行个性化。需要进一步研究来明确该问题的范围和严重程度。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8150/10744399/253969fbb310/jpm-13-01725-g001.jpg

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