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Lal Babu Gupta, MD, DM; Ashish Kumar, MD, DM; Ashish Kumar Jaiswal, MD; Jamal Yusuf, MD, DM; Vimal Mehta, MD, DM; Sanjay Tyagi, MD, DM; Deepak K. Tempe, MD; Barjesh Chander Sharma, MD, DM; Shiv Kumar Sarin, MD, DM

Arch Intern Med. 2008;168(16):1820-1823.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Hepatopulmonary syndrome (HPS) is characterized by a triad of liver disease, hypoxemia, and intrapulmonary vascular dilations (IPVDs).¹ Its prevalence is 4% to 47% in patients with cirrhosis.^1-2 Patients with HPS demonstrate a significant reduction in exercise capacity due to abnormal pulmonary circulation. Anatomic arteriovenous shunts in the lung are used during exercise and lead to exercise-induced impairment in gas exchange and exercise-induced arterial hypoxemia.

The pathogenesis of HPS is unclear. Cytokine-mediated injury is alleged to play a key role. Endothelin-1 and tumor necrosis factor (TNF) interaction, occurring in the lung vasculature, contribute to the development of experimental HPS.³ Overproduction of TNF, due to endotoxin stimulation of Kupffer cells, might be a . . . [Full Text of this Article]

Methods

Patients

Pentoxifylline Treatment

Investigations

Response to Therapy

Statistical Analysis

Results
Patients

Response to Pentoxifylline

Clinical

PaO₂ Levels

TNF Levels

Adverse Effects

Comment

AUTHOR INFORMATION


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