Relationship Between Platelet to White Blood Cell Ratio and 30-Day Prognosis of Patients with Acute-on-Chronic Liver Failure

Abstract

Background: Acute-on-chronic liver failure (ACLF) is always associated with thrombocytopenia or leukocytosis. Therefor the platelet to white blood cell ratio (PWR) in ACLF patients is always reduced. Objectives: Here, we assessed the relationship between PWR and prognosis in ACLF patients. Methods: A retrospective cohort of 415 patients, including 100 patients that were diagnosed of chronic hepatitis B, 104 patients suffered of HBV-related liver cirrhosis and 211 patients suffered of HBV-related ACLF, was investigated. Univariate and multivariate COX models were used to investigate the relationship between PWR and 30-day survival in patients with ACLF. Factors affecting PWR in ACLF patients were also analysed using logistic regression analysis. Results: At baseline, the platelet count in patients with HBV-related ACLF was significantly lower than that in patients with CHB and patients suffered of HBV-related cirrhosis. The PWR value was much higher in the survivors of ACLF than in ACLF patients who died. PWR, age, total bilirubine, prothrombin activity, and aspartate transaminase were independent predictors of the 30-day survival rate of ACLF patients. We also found that ascites and infection were independent factors related to the decrease of PWR in ACLF patients. Conclusions: The PWR value was significant declined in ACLF patients. And it was independent risk factors for the survival rate of those patients.

Hematological ratios in patients with acute decompensation and acute-on-chronic liver failure: prognostic factors

“…Platelets are necessary for targeting WBCs at inflammation sites [41]. Platelets also promote liver regeneration by secreting platelet-derived growth factors and hepatocyte growth factors [42]. So, diminished platelet count can hinder hepatocyte regeneration and augment liver failure.…”

Platelet to White Blood Cell Ratio (PWR) to Predict Mortality in Acute on Chronic Liver Failure of Cirrhosis Patient: A Systematic Review

“…This study also identified the plausible factor that decreased the PWR, there were ascites and infection (p = 0.003). 2 Retrospective cohort study from Jia et al included 433 ACLF-related HBV patient and showed significantly lower PWR than healthy control. This study also showed that there was moderate positive correlation between PWR and RBC (r = 0.2348, p < 0.0001) and HBV DNA (r = 0.1887, p < 0.001) in ACLF patient.…”

“…The decrease peripheral platelet count is associated with liver fibrosis, hypersplenism, increased destruction of platelet, decreased platelet production, decreased thrombopoietin production, antiplatelet antibodies, disseminated intravascular coagulation, translocated toxin, and other gut-derived substance. 2,10,11 Additionally, there is additional mechanism for increased platelet destruction in chronic liver disease, which is the effect of elevated portal pressure. Thrombocytopenia can further aggravate liver damage and promote the progression of liver cirrhosis by decreasing the level of platelet-derived growth factor and hepatocyte growth factor.…”

“…The progression to acute-on-chronic liver failure (ACLF) was associated with systemic inflammation response syndrome, compensatory anti-inflammatory response syndrome, and immune paralysis/organ failure. 1,2 The recently score to classify disease severity and predict survival are chronic liver failure-sequential organ failure assessment (CLIF-SOFA) and model of end stage liver disease (MELD). However, the CLIF-SOFA and MELD have complex calculation and online-tools for their assessment.…”

“…Usually, clinical evaluation of the inflammatory state relies on various indicator of routine peripheral blood test, such as leucocyte count, platelet count and distribution, neutrophil-lymphocyte ratio. 2 Thrombocytopenia in cirrhosis patient is often directly proportional to the severity of liver failure. The etiology of thrombocytopenia is multifactorial in cirrhosis, such as the decreased production of thrombopoietin, hypersplenism, and portal hypertension.…”