Karlsson Lars, Gnarpe Judy, Bergqvist David, Lindbäck Johan, Pärsson Håkan
Institution of Surgical Sciences, Uppsala University Hospital, Uppsala, Gävle, Sweden.
J Vasc Surg. 2009 Jul;50(1):23-9. doi: 10.1016/j.jvs.2008.12.048.
The aim of the study was to evaluate the effect of azithromycin on the expansion rate of small abdominal aortic aneurysms (AAAs), and to determine whether or not a correlation exists between serological markers for Chlamydophilia pneumonia (Cpn) infection and AAA expansion.
Nine vascular centers were included and 259 patients were invited to participate. Ten patients declined and 2 patients had chronic kidney failure, leaving a total of 247 patients. Inclusion criteria were: AAA 35-49 mm and age <80 years. Patients were randomized to receive either azithromycin (Azithromax, Pfizer Inc, New York, NY) 600 mg once daily for 3 days and then 600 mg once weekly for 15 weeks, or placebo in identical tablets. The ultrasound scans were performed in a standardized way within a month before inclusion and every 6 months for a minimum follow-up time of 18 months. Cpn serology was analyzed in blood samples taken at inclusion and 6 months later. Serum was analyzed for Cpn IgA and IgG antibodies by microimmunofluorescence (MIF). Computed tomography (CT) scans were done in 66 patients at inclusion and at 1 year for volume calculations.
Thirty-four patients were excluded, ie, could not be followed for 18 months, 20 in the placebo group and 16 in the active treatment group. A total of 211 patients had at least two measurements and all were analyzed in an intention-to-treat analysis. Detectable IgA against Cpn was found in 115 patients and detectable IgG against Cpn in 160 patients. No statistically significant differences were found between the groups regarding median expansion rate measured by ultrasound scan (0.22 cm/year, interquartile range [IQR]: 0.09 to 0.34 in the placebo group vs 0.22, IQR: 0.12 to 0.36 in the treatment group, P = .85). Volume calculation did not change that outcome (10.4 cm(3)/year in the placebo group vs 15.9 cm(3)/year in the treatment group, P = .61). No correlation was found between serological markers for Cpn infection and the expansion rate. Patients taking statins in combination with acetylsalicylic acid (ASA) had significantly reduced expansion rate compared to patients who did not take statins or ASA, 0.14 cm/year vs 0.27 cm/year, P < .001.
Azithromycin did not have any effect on AAA expansion. No correlation was found between serological markers for Cpn and AAA expansion, indicating no clinical relevance for Cpn testing in AAA surveillance. However, a significant reduction in AAA expansion rate was found in patients treated with a combination of ASA and statins.
本研究旨在评估阿奇霉素对小腹部主动脉瘤(AAA)扩张率的影响,并确定肺炎衣原体(Cpn)感染的血清学标志物与AAA扩张之间是否存在相关性。
纳入9个血管中心,邀请259例患者参与。10例患者拒绝参与,2例患者患有慢性肾衰竭,最终共有247例患者。纳入标准为:AAA直径35 - 49 mm且年龄<80岁。患者被随机分为两组,一组接受阿奇霉素(希舒美,辉瑞公司,纽约,纽约)治疗,600 mg每日1次,共3天,然后600 mg每周1次,共15周;另一组接受相同片剂的安慰剂治疗。在纳入前1个月内以标准化方式进行超声扫描,之后每6个月进行一次,最少随访18个月。在纳入时和6个月后采集血样分析Cpn血清学。通过微量免疫荧光法(MIF)分析血清中的Cpn IgA和IgG抗体。66例患者在纳入时和1年后进行计算机断层扫描(CT)以计算体积。
34例患者被排除,即无法随访18个月,其中安慰剂组20例,积极治疗组16例。共有211例患者至少有两次测量数据,所有患者均采用意向性分析。115例患者检测到针对Cpn的可检测IgA,160例患者检测到针对Cpn的可检测IgG。两组间超声扫描测量的中位扩张率无统计学显著差异(安慰剂组为0.22 cm/年,四分位间距[IQR]:0.09至0.34;治疗组为0.22,IQR:0.12至0.36,P = 0.85)。体积计算结果未改变该结果(安慰剂组为10.4 cm³/年,治疗组为15.9 cm³/年,P = 0.61)。未发现Cpn感染的血清学标志物与扩张率之间存在相关性。与未服用他汀类药物或阿司匹林(ASA)的患者相比,同时服用他汀类药物和ASA的患者扩张率显著降低,分别为0.14 cm/年和0.27 cm/年,P < 0.001。
阿奇霉素对AAA扩张无任何影响。未发现Cpn的血清学标志物与AAA扩张之间存在相关性,表明在AAA监测中Cpn检测无临床意义。然而,接受ASA和他汀类药物联合治疗的患者AAA扩张率显著降低。