Value of C-reactive protein/albumin ratio in predicting intravenous immunoglobulin-resistant Kawasaki disease- a data from multi-institutional study in China.

BACKGROUND: C-reactive protein/albumin ratio (CAR) is associated with inflammation. However, it prognostic value for intravenous immunoglobulin (IVIG) resistant Kawasaki disease (KD) has scarcely investigated. METHODS: A total of 957 patients with KD including 159 IVIG-resistant patients and 798 with IVIG-responsive patients between Jun 2013 and August 2019 were reviewed and the laboratory records were compared between IVIG-resistant patients and IVIG-responsive patients. Univariate and multivariate logistic analysis were performed to determine the independent predictors of IVIG resistance. A receiver operating characteristic curve analysis was conducted to compare the predictive accuracy between CAR and the combination of neutrophil-to-lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR). RESULTS: High CAR was associated with high the incidence of IVIG-resistance, anemia and coronary artery lesions, and high levels of neutrophils, CRP, aspartate aminotransferase, NLR, PLR, and erythrocyte sedimentation rate, and associated with low levels hemoglobin, albumin and lymphocytes count (all p < 0.05). The CAR (OR: 1.33, CI: 1.09-1.57), NLR (OR: 1.02, CI: 1.002-1.039) and PLR (OR: 1.004, CI: 1.003-1.005) were independent predictors for IVIG-resistance. CAR has superior discriminatory ability for IVIG resistance when compared with combination of NLR and PLR (z = 2.575, p = 0.01). CONCLUSIONS: CAR prior to IVIG treatment could be a novel prognostic marker for IVIG resistant KD. CAR was superior to the combination of NLR and PLR for predicting IVIG resistant KD.

[Preventive and Therapeutic Effects of Exogenous Apelin Regulating Autophagy on the Formation of Pulmonary Artery Hhypertension in Rats].

OBJECTIVE: To investigate the effect of exogenous Apelin on pulmonary artery hypertension (PAH) and its related mechanism. METHODS: 26 male SD rats were randomly divided into Control group ( n=6), Model group ( n=10) and Intervention group ( n=10). The rat model of PAH was established by left pneumonectomy combined with monocrotaline injection (PE+MCT) in the Model group and the Intervention group, while the Control group rats were opened chest cavity and injected the same amount of normal saline. From the 2nd week after operation, the Intervention group was intraperitoneally injected with 10 nmol/(kg·d) Apelin-13 for 3 weeks, while the Control group and Model group were injected the same volume of normal saline. The mean pulmonary arterial pressure (mPAP) was measured and the right ventricular hypertrophy index ( RVHI) was calculated in all three groups of rats at the 5th week after operation. The pulmonary tissue HE staining was performed to observe the pulmonary tissue and pulmonary vascular morphology. Protein LC3 was detected by immunofluorescence staining of lung tissues, the mRNA expression level of P62 and Beclin-1 in lung tissues was measured by RT-PCR, and the protein expressions of LC3, LC3-Ⅱ/LC3-Ⅰ, P62 and Beclin-1 in lung tissues were measured by Western blot. RESULTS: Compared with the Control group, the Model group showed increased mPAP and RVHI ( P<0.05), disordered pulmonary tissue structure and thicker pulmonary vascular wall. In Model group rats, expression of LC3 protein and LC3-Ⅱ/LC3-Ⅰ increased in lung tissues, and the expression of Beclin-1 mRNA and the Beclin-1 protein also increased in lung tissues, while the level of P62 mRNA and the expression of P62 protein decreased ( P<0.05). After Apelin-13 intervention, the above indexes were all improved ( P<0.05, compared with the Model group). CONCLUSION: Exogenous Apelin has a certain preventive and therapeutic effect on the formation of PAH, and the mechanism may be related to its inhibition effect on autophagy.