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Background &Aims: Heme oxygenase (HO) catalyzes he-moglobin into bilirubin, iron, and carbon monoxide (CO), a known vasodilator. HO expression and CO produc tion as measured by blood carboxyhemoglobin (COHb) levels increase in experiment al hepatopulmonary syndrome (HPS) and contribute to vasodilatation. Whether CO c ontributes to HPS in humans is unknown. Our aim was to assess if arterial COHb l evels are increased in cirrhotic patients with HPS relative to those without HPS . Methods: We collected data prospectively in stable nonsmoking outpatients with cirrhosis. Demographic and clinical data and room-air arterial blood gases wer e collected and analyzed. HPS was diagnosed using established criteria.Results: A total of 159 patients were studied. HPS was present in 27 (17%) patients. Mea n age was 52 ±9 years, 54%were men, and hepatitis C and/or alcohol were the mo st common causes (53%). Fourteen percent were Child-Pugh class A, 53%were Chi ld-Pugh class B, and 33%were Child-Pugh class C.Demographic and clinical feat ures were similar between HPS and non-HPS patients except for the Child-Pugh s core, which was lower in patients with HPS. Arterial Pao2 levels were lower and the alveolar-arterial oxygen gradient was higher in patients with HPS (P <. 001 ). COHb levels were increased in HPS relative to non-HPS (P <. 001) and correla ted with PaO 2 (P<. 001) and Aapo2 (P <. 001) levels. Conclusions: COHb levels a re increased in cirrhotic patients with HPS and correlate with gas exchange abno rmalities. These results are consistent with findings in experimental HPS and su ggest that CO may contribute to human HPS.
Background & Aims: Heme oxygenase (HO) catalyzes he-moglobin into bilirubin, iron, and carbon monoxide (CO), a known vasodilator. HO expression and CO produc tion as measured by blood carboxyhemoglobin (COHb) levels increase in experiment al hepatopulmonary syndrome HPS) and contribute to vasodilatation. Whether CO c ontributes to HPS in humans is unknown. Our aim was to assess if arterial COHb l evels are increased in cirrhotic patients with HPS relative to those without HPS. Methods: We collected data prospectively in stable nonsmoking Outpatients with cirrhosis. Demographic and clinical data and room-air arterial blood gases wer e collected and analyzed. HPS was diagnosed using established criteria. Results: A total of 159 patients were studied. HPS was present in 27 (17%) patients. Mea 54% were men, and hepatitis C and / or alcohol were the common mothers (53%). Fourteen percent were Child-Pugh class A, 53% were Chi ld-Pugh class B, and 33% were Child-Pugh c lass C. Demographic and clinical feat ures were similar between HPS and non-HPS patients except for the Child-Pugh s core, which was lower in patients with HPS. Arterial Pao2 levels were lower and the alveolar-arterial oxygen gradient was higher in patients with HPS (P <.001). COHb levels were increased in HPS relative to non-HPS (P <.001) and correla ted with PaO2 (P <.001) and Aapo2 COHb levels a re increased in cirrhotic patients with HPS and correlate with gas exchange abno rmalities. These results are consistent with findings in experimental HPS and su ggest that CO may contribute to human HPS.