Two studies concluded that MBL deficiency was associated with an increased incidence of AECOPDs and one concluded that it was not. The age, spirometry, and smoking histories of the subjects in these three studies were similar to those we evaluated, with the exception that none of the three studies selected patients who were at increased risk of experiencing acute exacerbations as we did. Yang et al 30 found that 24 of 82 (29%) subjects with COPD had MBL-deficient genotypes. These subjects had lower MBL concentrations than those with the wild-type genotype (107 ng/mL, IQR 30-246, range 21-7675 versus 920 ng/mL, IQR 398-1355, range 21-2256, P , 0.001). MBL concentrations were not presented in a fashion that allowed determination of the prevalence of MBL deficiency based on the definitions used in the literature. Forty of the 82 patients (49%) had one or more admissions for AECOPDs during a two-year follow-up period and 18 of these (45%) had MBL-deficient genotypes. Forty-two patients had no AECOPDs and only six (14%) of these had MBL-deficient genotypes (odds ratio 4.9 95% CI 1.7-14.4, P = 0.0037). We did not determine MBL genotypes but genotypes do not COPD (P = 0.23 and P = 0.10, respectively). No association between MBL concentration and a history of AECOPDs was observed, but no information was provided with respect to how AECOPDs were defined. Eagan et al 31 also noted that subjects with GOLD stage 3 disease had a higher prevalence of MBL deficiency (defined as #100 ng/mL). We found no demographic or COPD severity indicators that were more or less common in subjects with MBL deficiency, regardless of how deficiency was defined ( Table 1) . The strengths of our study include the large sample size, the multicenter design, and the prospective ascertainment of AECOPDs using an event-based (ie, health care utilization) definition. Our study population was enriched by enrolling subjects whom we anticipated would be at increased submit your manuscript | www.dovepress.com risk of experiencing an AECOPD within the one-year follow-up period, based on previous predictors identified by Niewoehner et al. 34 This should have increased the likelihood of finding a higher prevalence of MBL deficiency, regardless of how deficiency was defined, compared with the prevalence in healthy controls. Our study has a number of limitations. First, we only measured MBL concentrations on one occasion. Several groups have demonstrated that MBL is an acute phase reactant. [41] [42] [43] However, in clinically stable patients, MBL concentrations are constant over time, 42, 44 and our patients had to be free of AECOPDs for at least 4 weeks before meeting inclusion criteria. In addition, even during acute phase responses, MBL concentrations in patients with low concentrations only increase by 1.5-4.3-fold and do not reach normal values. 45, 46 Accordingly, we suggest that there is a low likelihood of our data being confounded by spuriously elevated concentrations of MBL resulting in an underestimate of the prevalence of MBL deficiency.