Lindholt J S, Heickendorff L, Antonsen S, Fasting H, Henneberg E W
Department of Vascular Surgery, Viborg Hospital, Denmark.
J Vasc Surg. 1998 Aug;28(2):226-33. doi: 10.1016/s0741-5214(98)70158-2.
To study the relation between abdominal aortic aneurysms and chronical obstructive pulmonary disease (COPD), in particular the suggested common elastin degradation caused by elastase and smoking.
A cross-sectional population study and a prospective cohort study of small abdominal aortic aneurysms was performed in a community setting. All previous diagnoses recorded in a hospital computer database were received for 4404 men 65 to 73 years of age who had been invited to a population screening for abdominal aortic aneurysm. One hundred forty-one men had AAA (4.2%). They were asked to participate in an interview, a clinical examination, and collection of blood sample. Men with an abdominal aortic aneurysm 3 to 5 cm in diameter were offered annual ultrasound scans to check for expansion.
Among patients with COPD 7.7% had abdominal aortic aneurysms (crude odds ratio=2.05). The adjusted odds ratio, however, was only 1.59 after adjustment for coexisting diseases associated with abdominal aortic aneurysm (P=.13). The mean annual expansion was 2.74 mm per year among patients with COPD, 2.72 among patients without COPD, and 4.7 mm among patients who used oral steroids compared with 2.6 among patients who did not use steroids (P < .05). Concentration of serum elastin peptide and plasma elastase-alpha1-antitrypsin complexes correlated negatively with forced expiratory volume in the first second (FEV1) among patients with COPD. However, multivariate regression analysis showed that concentration of serum elastin peptide, therapy with beta-agonists, and FEV1 correlated positively with degree of expansion but that concentration of plasma elastase-alpha1-antitrypsin complexes and serum alpha1-antitrypsin did not influence expansion, suggesting that elastase plays an important role in the pathogenesis of COPD but not of abdominal aortic aneurysm.
The high prevalence of abdominal aortic aneurysm among patients with COPD is more likely to be caused by medication and coexisting diseases rather than a common pathway of pathogenesis.
研究腹主动脉瘤与慢性阻塞性肺疾病（COPD）之间的关系，特别是由弹性蛋白酶和吸烟导致的常见弹性蛋白降解。
在社区环境中对小型腹主动脉瘤进行了一项横断面人群研究和前瞻性队列研究。从医院计算机数据库中获取了4404名65至73岁男性的所有既往诊断记录，这些男性被邀请参加腹主动脉瘤的人群筛查。141名男性患有腹主动脉瘤（4.2%）。他们被要求参加访谈、临床检查并采集血样。直径为3至5厘米的腹主动脉瘤患者每年接受超声扫描以检查是否扩张。
COPD患者中7.7%患有腹主动脉瘤（粗比值比=2.05）。然而，在对与腹主动脉瘤相关的共存疾病进行调整后，调整后的比值比仅为1.59（P=0.13）。COPD患者的平均年扩张率为每年2.74毫米，无COPD患者为2.72毫米，使用口服类固醇的患者为4.7毫米，未使用类固醇的患者为2.6毫米（P<0.05）。COPD患者血清弹性蛋白肽和血浆弹性蛋白酶-α1-抗胰蛋白酶复合物的浓度与第一秒用力呼气量（FEV1）呈负相关。然而，多变量回归分析表明，血清弹性蛋白肽浓度、β-激动剂治疗和FEV1与扩张程度呈正相关，但血浆弹性蛋白酶-α1-抗胰蛋白酶复合物浓度和血清α1-抗胰蛋白酶不影响扩张，这表明弹性蛋白酶在COPD的发病机制中起重要作用，但在腹主动脉瘤的发病机制中不起作用。
COPD患者中腹主动脉瘤的高患病率更可能是由药物治疗和共存疾病引起的，而非共同的发病途径。
