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转甲状腺素蛋白淀粉样变性:肥厚型心肌病的表型模拟。

Transthyretin amyloidosis: a phenocopy of hypertrophic cardiomyopathy.

机构信息

a Department of Clinical Genetics , Academic Medical Center , Amsterdam , The Netherlands.

b Department of Clinical and Experimental Cardiology, Heart Center , Academic Medical Center , Amsterdam , The Netherlands.

出版信息

Amyloid. 2017 Jun;24(2):87-91. doi: 10.1080/13506129.2017.1322573. Epub 2017 May 5.

Abstract

OBJECTIVES

Hypertrophic cardiomyopathy (HCM) is an inherited cardiac disorder that affects over one in 500 persons worldwide. The autosomal dominant transmission of HCM implies that many relatives are at risk for HCM associated morbidity and mortality, therefore genetic testing and counselling is of great importance. However, in only 50-60% of the patients a mutation is found, which hampers predictive genetic testing in relatives. In HCM patients in whom the causal mutation has not been identified (yet), phenocopies of HCM - i.e. diseases that mimic HCM - could be responsible for the HCM phenotype. One of the HCM phenocopies is transthyretin amyloidosis (ATTR), caused by mutations in the transthyretin (TTR) gene.

METHODS

From 697 HCM index patients referred to our cardiogenetics outpatient clinic and tested for HCM associated genes between January 1997 and December 2012, we selected the ones without a detected causal mutation (n = 345). In these patients, additional DNA analysis of the TTR gene was performed.

RESULTS

In four patients (1.2%), a TTR mutation was detected (E7G, V30M, T119M, V122I). The E7G mutation is probably a non-pathogenic mutation. The T119M mutation is a known TTR mutation, but does not cause a cardiac phenotype. So in two (0.6%) patients, TTR analysis identified the cause of their HCM.

CONCLUSIONS

ATTR should always be considered in patients with unexplained HCM, especially because of the great benefit of an early diagnosis regarding treatment and prognosis.

摘要

目的

肥厚型心肌病(HCM)是一种遗传性心脏病,全球每 500 人中就有 1 人患病。HCM 呈常染色体显性遗传,这意味着许多亲属存在患肥厚型心肌病相关发病率和死亡率的风险,因此基因检测和咨询非常重要。然而,只有 50-60%的患者可发现突变,这阻碍了对亲属的预测性基因检测。在尚未确定病因突变的 HCM 患者(中),肥厚型心肌病的表型可能是由 HCM 表型的类病变引起的,即类病变型肥厚型心肌病。类病变型肥厚型心肌病之一是转甲状腺素蛋白淀粉样变性(ATTR),由转甲状腺素蛋白(TTR)基因突变引起。

方法

从 1997 年 1 月至 2012 年 12 月期间,我们在我们的心脏遗传门诊对 697 名 HCM 索引患者进行了与 HCM 相关基因的检测,选择了未发现病因突变的患者(n=345)。对这些患者进行了 TTR 基因的额外 DNA 分析。

结果

在四名患者(1.2%)中发现了 TTR 突变(E7G、V30M、T119M、V122I)。E7G 突变可能是一种非致病性突变。T119M 突变是一种已知的 TTR 突变,但不会引起心脏表型。因此,在两名(0.6%)患者中,TTR 分析确定了他们 HCM 的病因。

结论

在不明原因的 HCM 患者中,应始终考虑到 ATTR,特别是因为早期诊断对治疗和预后有很大的益处。

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