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慢性阻塞性肺疾病中血管紧张素转换酶基因型与强度

Angiotensin converting enzyme genotype and strength in chronic obstructive pulmonary disease.

作者信息

Hopkinson Nicholas S, Nickol Annabel H, Payne John, Hawe Emma, Man William D-C, Moxham John, Montgomery Hugh, Polkey Michael I

机构信息

Respiratory Muscle Laboratory, Royal Brompton Hospital, Fulham Road, London, SW3 6NP, United Kingdom.

出版信息

Am J Respir Crit Care Med. 2004 Aug 15;170(4):395-9. doi: 10.1164/rccm.200304-578OC. Epub 2004 Apr 29.

Abstract

Quadriceps muscle weakness is an important contributor to exercise limitation in patients with chronic obstructive pulmonary disease. The deletion allele of the angiotensin converting enzyme gene polymorphism has previously been associated with a greater response to strength training in healthy subjects and might, therefore, protect against detraining in these patients. In 103 stable outpatients (mean [SD] FEV(1) 34.4 [16.5] % predicted), the angiotensin deletion allele was associated with greater isometric quadriceps strength; mean (SD) 31.4 (10.8) kg for insertion homozygotes, 34.1 (13.0) kg for heterozygotes, and 38.3 (11.6) kg for deletion homozygotes (p = 0.04 linear trend). Adjusted for fat-free mass, the relationship was stronger (linear trend p = 0.007). There was no correlation between strength and genotype in a group of 101 age-matched healthy control subjects. Twitch quadriceps force in response to magnetic femoral nerve stimulation, measured in 39 patients, was also genotype dependent; 8.3 (2.6) kg for insertion homozygotes, 10.1 (3.6) kg for heterozygotes, and 12.4 (3.5) kg for deletion homozygotes (p = 0.002 linear trend). Body mass index and fat-free mass did not differ significantly between genotypes in either group. There was no association in either patients or control subjects between genotype and inspiratory muscle strength. In chronic obstructive pulmonary disease the deletion allele is associated with greater quadriceps strength independent of confounding factors.

摘要

股四头肌无力是慢性阻塞性肺疾病患者运动受限的一个重要因素。血管紧张素转换酶基因多态性的缺失等位基因此前已被证明与健康受试者对力量训练的更大反应相关,因此可能有助于防止这些患者出现废用性肌萎缩。在103名稳定的门诊患者中(平均[标准差]FEV(1)为预测值的34.4[16.5]%),血管紧张素缺失等位基因与更大的股四头肌等长力量相关;插入纯合子的平均(标准差)力量为31.4(10.8)kg,杂合子为34.1(13.0)kg,缺失纯合子为38.3(11.6)kg(线性趋势p = 0.04)。校正去脂体重后,这种关系更强(线性趋势p = 0.007)。在101名年龄匹配的健康对照受试者中,力量与基因型之间没有相关性。在39名患者中测量的股四头肌对股神经磁刺激的抽搐力量也与基因型有关;插入纯合子为8.3(2.6)kg,杂合子为10.1(3.6)kg,缺失纯合子为12.4(3.5)kg(线性趋势p = 0.002)。两组中不同基因型之间的体重指数和去脂体重没有显著差异。在患者或对照受试者中,基因型与吸气肌力量之间均无关联。在慢性阻塞性肺疾病中,缺失等位基因与更大的股四头肌力量相关,且不受混杂因素影响。

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