Hepatic TPO gene expression is maintained at a constitutive transcriptional level in patients with liver diseases regardless of etiology, suggesting elevated serum TPO in viral hepatitis is not due to increased hepatic transcription.
Elevated serum TPO in viral hepatitis is not transcriptionally driven; leaves open post-transcriptional or extrahepatic sources for mechanistic study.
BACKGROUND/AIMS: Platelet production is regulated by thrombopoietin (TPO), which is primarily synthesized in the liver. The TPO in patients with liver diseases could possibly be owing to impaired hepatic TPO production. As we reported previously, TPO serum levels are not decreased in patients with liver diseases compared with healthy controls and do not depend on the stage of cirrhosis or platelet count, but are highly elevated in patients with chronic virus hepatitis. METHODS: To study possible mechanisms, we measured hepatic TPO mRNA levels in liver tissue samples from 31 liver cirrhosis patients by quantitative TaqMan real-time RT-PCR and corresponding serum TPO concentrations by ELISA. RESULTS: Median TPO serum levels were elevated in patients with viral hepatitis (n = 12) compared with patients with a biliary (n = 10), alcoholic (n = 6) or other (n = 3) disease etiology, while hepatic TPO mRNA levels did not differ. The TPO mRNA levels in patients with chronic liver diseases were not different from normal liver tissue sample. The TPO mRNA and TPO serum level did not correlate. CONCLUSIONS: We conclude that hepatic TPO gene expression appears to be maintained on a constitutive transcriptional level in patients with liver diseases and does not change dependent on disease etiology.
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Tacke et al. (2002) studied this question.
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