Abstract

ObjectiveSevere acute pancreatitis (SAP) is a highly morbid condition in general population as well as in solid organ transplant (SOT) recipients. The present study aimed to investigate the effect of continuous renal replacement therapy (CRRT) with different anticoagulation methods on the expression levels of cytokines in SAP. MethodsA total of 120 patients with SAP, admitted into our hospital between September 2017 and July 2020, were enrolled as the research subjects and randomly divided into a control group (60 cases) and a study group (60 cases). CRRT with low molecular weight (LMW) heparin‑calcium anticoagulation was conducted on patients in the control group, and CRRT with topical citrate + low-dose LMW heparin‑calcium anticoagulation was conducted on patients in the study group. The expressions of cytokines in the two groups were compared after treatment. ResultsThere was no significant difference in white blood cells (WBC), C-reactive proteins (CRP), and procalcitonin (PCT) before treatment between the two groups (P > 0.05). After treatment, the levels of WBC (P = 0.006), CRP (P < 0.001), and PCT (P < 0.001) were significantly lower in the study group when compared with those in the control group. There was no significant difference in the concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α) between the two groups before treatment (P > 0.05). After treatment, the concentrations of IL-6, IL-8, and TNF-α were significantly lower in the study group when compared with those in the control group. The APACHEII, SOFA and Ranson scores of the two groups were analyzed, and there was no difference between the two groups before treatment (P > 0.05). After treatment, the score of the study group was lower than that of the control group (P < 0.05). ConclusionCRRT with topical citrate + low-dose LMW heparin‑calcium anticoagulation in the treatment of patients with SAP reduces the levels of WBC, CRP, and PCT and the concentrations of cytokines, including IL-6, IL-8, and TNF-α. This inhibits the release of inflammatory mediators in patients with SAP and reduces damage to the body caused by the inflammatory response, thus effectively improving the patients' condition.

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