The serum level of soluble CXCL16 is increased in preeclampsia and associated with hepatic/renal damage

Abstract

Objective To compare the serum level of the chemokine, CXCL 16, in preeclamptic and healthy pregnant patients. Methods This prospective case control study was conducted between January and December 2018 in a tertiary level hospital. The study group was formed of 70 pregnant women diagnosed with preeclampsia, and the control group was formed of 70 healthy pregnant women matched to the study group in respect of age, gestational week and body mass index (BMI). The study group was separated into two subgroups of mild preeclampsia (n = 35) and severe preeclampsia (n = 35). The groups were compared in terms of demographic and clinical parameters and the levels of serum CXCL 16. Results No statistically significant difference was determined between the study and control groups in respect of maternal age, gravida, parity, BMI, and gestational age at sampling. Neonatal birth weight was significantly lower in the study group than in the control group. Mean serum alanine aminotransferase (ALT), aspartate amino transferase (AST) and creatinine levels of the study group were significantly higher than those of the control group (p < .05 for all). There was a statistically significant difference between the study and control groups regarding the mean platelet count. Compared to the control group, the severe and mild preeclampsia groups had a significantly higher serum level of CXCL 16. The serum level of CXCL 16 was significantly higher in patients with severe preeclampsia than in patients with mild preeclampsia (2.94 ± 3.89 pg mL−1 vs. 1.08 ± 1.87 pg mL−1, p = .14). Correlation analysis revealed a significant positive correlation of serum CXCL 16 level with serum ALT level (r = 0.320, p ≤ .001) and serum AST level (r = 0.373, p ≤ .001) and serum creatinine level (r = 0.279, p = .01) in both groups. High values indicated presence of preeclampsia, with a diagnostic cut-off point of 0.225, sensitivity of 75.7% and specificity of 72.9% for CXCL 16 (area under curve: 0.820, p < .001 CI: 0.753–0.888). Conclusions This is the first study in literature to show a significantly higher level of CXCL 16 in patients with severe preeclampsia compared to those with mild preeclampsia. The study can also be considered of value in respect of showing that CXCL 16 could play a role in the etiopathogenesis of preeclampsia and the emergence of renal-hepatic damage. Blocking the CXCL 16/CXCR six axis in preeclampsia treatment could lay the ground for the development of new drugs which could be used in the treatment of preeclampsia.