Role of elevated platelet‐associated immunoglobulin G and hypersplenism in thrombocytopenia of chronic liver diseases

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Abstract
Background and Aim: Thrombocytopenia typically worsens with the progression of liver disease and can become a major clinical complication. Several mechanisms that contribute to thrombocytopenia have been proposed, including hypersplenism accompanied by increased platelet sequestration, platelet destruction mediated by platelet‐associated immunoglobulins (PAIgG), and diminished platelet production stimulated by thrombopoietin (TPO). The purpose of the present study was to evaluate the role of each of these mechanisms in patients with liver disease‐associated thrombocytopenia. Methods: Twenty‐nine patients with liver cirrhosis (LC), 20 of whom were hepatitis C virus (HCV)‐seropositive, 29 chronic hepatitis (CH) patients, 24 of whom were HCV‐seropositive, and 16 control patients without liver or hematopoetic disease were enrolled in this study. Serum TPO levels, PAIgG, and liver‐spleen volumes were determined and correlation analyses were performed. Results: No differences in serum TPO levels were observed among the three groups. The PAIgG levels were significantly elevated in CH and LC patients (mean ± SD: 56.5 ± 42.3 and 144.6 ± 113.6 ng/107 cells, respectively) compared with the controls (18.9 ± 2.5 ng/107 cells, P < 0.001 for both). Spleen volume was significantly higher only in LC (428 ± 239) compared with CH (141 ± 55) and control (104 ± 50 cm3) (P < 0.001), while liver volume was not significantly different between the three groups. Correlation analyses demonstrated a significant negative correlation between platelet count with PAIgG (r = − 0.517, P < 0.001) and spleen volume (r = − 0.531, P < 0.001), and no relationship between platelet count and serum TPO level (r = 0.076). Conclusions: Serum TPO level may not be directly associated with thrombocytopenia in patients with chronic hepatitis and liver cirrhosis. In contrast, spleen volume and PAIgG are associated with thrombocytopenia in such patients, suggesting that hypersplenism and immune‐mediated processes are predominant thrombocytopenic mechanisms.