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一种新的低肾素性高血压基因位点:II型家族性醛固酮增多症定位于7号染色体(7p22)。

A novel genetic locus for low renin hypertension: familial hyperaldosteronism type II maps to chromosome 7 (7p22).

作者信息

Lafferty A R, Torpy D J, Stowasser M, Taymans S E, Lin J P, Huggard P, Gordon R D, Stratakis C A

机构信息

Unit on Genetics and Endocrinology, Developmental Endocrinology Branch, National Institute of Child Health and Human Development, Building 10, Room 10N262, 10 Center Drive, MSC1862, Bethesda, Maryland 20892-1862, USA.

出版信息

J Med Genet. 2000 Nov;37(11):831-5. doi: 10.1136/jmg.37.11.831.

Abstract

Familial hyperaldosteronism type II (FH-II) is caused by adrenocortical hyperplasia or aldosteronoma or both and is frequently transmitted in an autosomal dominant fashion. Unlike FH type I (FH-I), which results from fusion of the CYP11B1 and CYP11B2 genes, hyperaldosteronism in FH-II is not glucocorticoid remediable. A large family with FH-II was used for a genome wide search and its members were evaluated by measuring the aldosterone:renin ratio. In those with an increased ratio, FH-II was confirmed by fludrocortisone suppression testing. After excluding most of the genome, genetic linkage was identified with a maximum two point lod score of 3.26 at theta=0, between FH-II in this family and the polymorphic markers D7S511, D7S517, and GATA24F03 on chromosome 7, a region that corresponds to cytogenetic band 7p22. This is the first identified locus for FH-II; its molecular elucidation may provide further insight into the aetiology of primary aldosteronism.

摘要

家族性醛固酮增多症II型(FH-II)由肾上腺皮质增生或醛固酮瘤或两者共同引起,通常以常染色体显性方式遗传。与由CYP11B1和CYP11B2基因融合导致的FH-I型不同,FH-II型醛固酮增多症不能通过糖皮质激素治疗。一个患有FH-II的大家庭被用于全基因组搜索,其成员通过测量醛固酮:肾素比值进行评估。对于比值升高者,通过氟氢可的松抑制试验确诊为FH-II。在排除基因组的大部分区域后,在该家族的FH-II与7号染色体上的多态性标记D7S511、D7S517和GATA24F03之间,于θ=0时确定了遗传连锁,最大两点对数优势分数为3.26,该区域对应于细胞遗传学带7p22。这是首次确定的FH-II位点;对其分子机制的阐明可能为原发性醛固酮增多症的病因学提供进一步的见解。

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