Association of circulating resistin and adiponectin levels with Kawasaki disease: A meta-analysis

The present meta-analysis was performed to examine the association between circulating blood adipokine levels and Kawasaki disease (KD). Studies were identified by searching various databases, including Web of Science, EMBASE, PubMed, Wanfang and China National Knowledge Infrastructure. After the studies were pooled, the mean difference (MD) and corresponding 95% CI were calculated. Subgroup analyses and publication bias detection were also performed. The Cochrane Q test and I-2 statistics were performed using Review Manager software (version 5.3) to test for heterogeneity. A Begg's test was used to assess publication bias and STATA software (version 12.0) was used for statistical analysis. The results revealed that the KD group exhibited higher levels of resistin compared with those in the healthy controls or disease controls (non-KD; MD=20.76, 95% CI=16.16-25.36, P<0.001; MD=21.27, 95% CI=14.24-28.29, P<0.001, respectively). In addition, when compared with those in patients exhibiting non-coronary artery lesions (NCAL), those with coronary artery lesions (CAL) had higher levels of adiponectin and resistin (MD=1.00, 95% CI=0.06-1.96, P=0.04; MD=2.77, 95% CI=1.32-4.22, P<0.001). Furthermore, compared with those in the inactive-phase group, patients in the active-phase group exhibited higher levels of resistin (MD=17.73, 95% CI=12.82-22.65, P<0.001). In conclusion, the present meta-analysis indicated that resistin levels were elevated in patients with KD. It was also revealed that circulating resistin and adiponectin levels in the CAL group were significantly increased compared with those in patients with NCAL. Furthermore, the active group had higher levels of resistin than the inactive group. The results of these meta-analyses indicated that resistin may serve an important role in the pathogenesis of KD and may therefore be used as biomarkers for the diagnosis of KD, whereas adiponectin may only serve an important role in the pathogenesis of CAL and may therefore be used as a biomarker to distinguish CAL from NCAL.