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Furthermore, the authors should perform a stratified analysis by source of control groups.
In the stratified analysis by source of control, IL-18−607C/A significantlyicantly reduced risk in population-based subgroup, and for IL-18 −137G/C only significantly decreased risk was found in the hospital-based subgroup.
In a stratified analysis by source of control, only significantly decreased risk was found in the hospital-based subgroup under recessive model (OR = 0.72, 95% CI = 0.54 0.96, P = 0.03) and homozygous comparison (OR = 0.72, 95% CI = 0.53 0.97, P = 0.03).
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In the subgroup analysis stratified by source of controls, significant associations were observed in the population-based subgroup (CC + TC vs TT ORR = 1.33; 95%CI = 1.03 1.71).
Table S1 provides the characteristics of the studies, including sample size, year, study design, and by source of controls (general population or high-risk).
In the stratified analysis by source of controls, significantly increased risks were also found.
No significant associations were observed in the stratified analyses by source of controls and ethnicity (Table 5).
After subgroup analysis by source of controls, the heterogeneity was also decreased; therefore, it can be assumed that the heterogeneity partly results from difference of source of controls.
Results of the subgroup analyses stratified by source of controls and HWE status for controls were similar to those of the overall analyses.
In the stratified analysis by source of controls, significant associations were found in hospital-based group (dominant model: OR = 0.67, 95% CI = 0.46 0.96).
When stratified by source of controls, we observed a significant relationship with Ile/Val polymorphism and COPD risk among studies recruiting hospital-based controls (AG + GG versus AA: OR = 1.99, CI: 1.37 2.90, P < 0.001; Table 3).
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