Efficacy and Safety of Pentoxifylline in Improving Oxygenation in Hepatopulmonary Syndrome
Status:
Not yet recruiting
Trial end date:
2023-04-30
Target enrollment:
Participant gender:
Summary
The triad of liver disease, arterial hypoxia, and extensive pulmonary vascular dilatation is
known as the hepatopulmonary syndrome (HPS). The prevalence of this syndrome ranges from 10%
to 30% in people with chronic liver disease.
The exact cause of HPS is unknown. Previous research has shown that eicosanoids function as
vasoconstrictors and cause an increase in the number of intravascular macrophage-like cells.
Cirrhosis has been linked to increased NO generation in the lungs, which has been linked to
intrapulmonary venous dilation. Increased pulmonary NO production is attributed to increased
expression of pulmonary vascular endothelial NO synthase (eNOS) and inducible NO synthase.
Increased hepatic synthesis and release of low levels of endothelin 1 (ET-1) has been
established in recent investigations to function as a trigger for increasing eNO levels. TNF
(tumor necrosis factor) and ET-1 have both been linked to the onset of experimental HPS.
Increased CO generation and heme oxygenase expression have been linked to the progression of
HPS in recent investigations. HPS increases mortality in cirrhotic patients and may affect
the frequency and severity of portal hypertension consequences.
To the best of our knowledge there have been only three pilot studies in humans which checked
the effect of pentoxifylline in hepatopulmonary syndrome and they showed highly contrasting
results. The outcome was also measured in a short interval. Investigator hypothesize that
pentoxifylline would improve the oxygenation in patients with hepatopulmonary syndrome