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Objective: 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., Methods: 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., Results: 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., Conclusion: 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.

Chlamydia pneumoniae (Cpn) is a common respiratory pathogen with a biphasic replicative cycle and has a tendency to cause chronic infections. Azithromycin is commonly used for the treatment of Cpn infections, but little is known about the optimal dose and duration of therapy. In this prospective double-blind, randomized study the effects of azithromycin and placebo were compared regarding longstanding airway and/or pharyngeal symptoms in patients with chronic Cpn infection. Further, effects on antibody titres and lung function were assessed. 103 patients were treated with either azithromycin 500 mg daily for 5 d, repeated 3 times with a 23-d interval, or placebo. Patients were examined 4 months and 1 y after completed treatment. Evaluation of symptoms showed general improvement and less hawking in patients treated with azithromycin compared to placebo after 4 months, but there was no sustained difference 1 y after completed treatment. The antibody titres remained stable, and there was no influence on lung function. Adverse events, primarily gastrointestinal, were more frequently reported with azithromycin than placebo. In conclusion, azithromycin was effective for reduction of respiratory symptoms in patients with chronic Cpn infection, but prolonged intermittent treatment with high doses did not eradicate the chronic infection.

Background: An association between Chlamydia pneumoniae (Cp) infection and coronary heart disease (CHD) has already been reported. We investigated the relationship between Cp infection and other risk factors in CHD patients, as well as the effects of azithromycin treatment. Methods: We studied 38 patients with Cp infection (Cp-pos) and 15 without (Cp-neg). Cp-pos patients had, both at inclusion and 2 years prior to inclusion, elevated Cp-specific IgA-antibodies, with or without the presence of pharyngeal Cp by polymerase chain reaction (PCR) detection. Blood was analyzed for Cp-antibodies, interleukin-6, interleukin-1 receptor antagonist (IL-1ra), CRP, orosomucoid, fibrinogen, leukocytes, PAI-1, tPA, von Willebrand factor (vWf), platelet count and aggregation, and lipids. Cp-pos patients were randomized to placebo or oral azithromycin, 500 mg on day 1 and then 250 mg/day for 4 days, with repeated therapy after 3 weeks. Blood was taken immediately, as well as 3 months and 2 years after therapy. Results: CRP and IL-1ra levels were higher in Cp-pos than in Cp-neg patients: median, interquartile range 8.5 (3.0–20) vs. 2.0 (1.0–3.8) mg/l, and 316 (165–404) vs. 178 (118–195) ng/l, p=0.0006 and p=0.002, and platelet aggregation was lower: 4.8 (2.9–6.4) vs. 8.1 (4.7–11.4) Ω, p<0.05. tPA levels increased in azithromycin-treated patients between entry and 3-month follow-up: mean±S.D. 3.7±4.2 vs. 1.0±2.1 μg/l, p<0.05. Other variables did not differ. Conclusions: Cp infection was associated with increased inflammatory activity and lower platelet aggregability, suggesting that inflammation may be of greater pathophysiological importance than platelet activity in these patients. Although an effect on Cp infection was not shown, azithromycin may have a positive effect on fibrinolysis, as increased levels of tPA were observed in the treatment group. [Copyright &y& Elsevier]