Factors associated with the platelet count in patients with chronic hepatitis C

Abstract

Background There are many potential causes of thrombocytopenia in patients with chronic hepatitis C (CHC). Aims We sought to determine the association between thrombopoietin (TPO) level, immature platelet fraction (IPF), immunoglobulin G (IgG) level, spleen size, and the platelet count in CHC. Methods We studied a consecutive sample of patients enrolled in an observational study at a referral-based research center, excluding subjects based on eligibility criteria. TPO, glycocalicin, and von Willebrand Factor (vWF) levels were determined using stored sera. Hepatic fibrosis was assessed via transient elastography (TE) when available, and clinical laboratory values and radiologic data were obtained from the medical record. We performed analyses of the relationships between independent variables and the platelet count. Results On univariate analysis, the following variables were significantly associated with the platelet count: age, alanine aminotransferase (ALT), direct bilirubin, total bilirubin, IPF, international normalized ratio (INR), spleen size, vWF, glycocalicin, fibrosis stage on liver biopsy, and TE (P-values all <0.05). A multivariable model determined that imputed TE score, TPO, IPF, and spleen size were independently associated with the platelet count (P-values all < 0.05). Conclusions The platelet count in CHC is significantly associated with fibrosis, TPO level, IPF, and spleen size. Our findings challenge the proposed mechanism of decreased TPO levels or decreased bone marrow production of platelets as a cause of thrombocytopenia in CHC. Future studies focusing on the effects of fibrosis and splenomegaly on platelets may shed more light on the pathophysiology of thrombocytopenia in patients with CHC.

Reticulated Platelets in Egyptian Patients with Chronic Hepatitis C Infection

“…Moreover, there was a highly significant inverse correlation between RP% and platelet count (r = -0.698; P < 0.001). The same association was found between IPF% and platelet count in prior studies reported by Zucker et al [30] and Tana et al [31] , this suggested that peripheral platelet destruction was the main cause of thrombocytopenia in chronic hepatitis C patients.…”

“…Hypersplenism is often implicated in thrombocytopenia in the portal hypertensive or cirrhotic patient. Another possible mechanism of splenic consumption of platelets occurs when platelets are opsonized by immunoglobulin and sequestered in the spleen [31] . Splenomegaly was significantly more common in thrombocytopenic patients than in those with normal platelet counts (P < 0.001).…”

Influencing factors of transient elastography in detecting liver stiffness

“…With the evolvement of liver tissue fibrosis, thrombopoietin levels decrease, while PLT production is reduced (24,25). It is well known that the liver is the only human organ that synthesizes ALB.…”

Adult‐onset cystic fibrosis liver disease: Diagnosis and characterization of an underappreciated entity

“…The demonstration of declining platelet counts, while not previously described in CFLD, is an important finding that has been described in various liver diseases ranging from cirrhosis‐related liver diseases to noncirrhotic portal hypertension. In chronic hepatitis C, platelets have been described to decline with advancing disease even prior to reaching cirrhosis with improvement after sustained viral eradication even at stages prior to cirrhosis . In noncirrhotic portal hypertension, the declining platelet counts over time was associated with mortality .…”