Smoking and hypoxemia caused by hepatopulmonary syndrome before and after liver transplantation
Article first published online: 30 DEC 2003
Copyright © 2001 American Association for the Study of Liver Diseases
Volume 34, Issue 2, pages 430–431, August 2001
How to Cite
Rolla, G., Brussino, L., Dutto, L., Ottobrelli, A. and Bucca, C. (2001), Smoking and hypoxemia caused by hepatopulmonary syndrome before and after liver transplantation. Hepatology, 34: 430–431. doi: 10.1053/jhep.2001.26791
- Issue published online: 30 DEC 2003
- Article first published online: 30 DEC 2003
- Manuscript Accepted: 5 JUN 2001
- Manuscript Received: 9 MAR 2001
- Ministero Italiano dell'Università e della Ricerca Scientifica e Tecnologica.
Severe hypoxemia may occur in patients with liver disease as a result of abnormal intrapulmonary vasodilatations (hepatopulmonary syndrome, HPS). Liver transplantation (LT) is the only effective treatment of HPS, with a quite variable delay of improvement of oxygenation. Smoking, by decreasing respiratory nitric oxide (NO), apparently contributed to improved oxygenation in a 44-year-old man with alcohol-induced cirrhosis, complicated by HPS, who underwent LT. The patient quit smoking just before LT, when his PaO2 was 29 mm Hg and exhaled NO (eNO) 28 ppb, a value far above the normal limits (9.6 ± 3.2 ppb). After LT, oxygenation remained poor and eNO remained high for more than 4 months, when the patient started to smoke again (blood HbCO going up to 5%). At that time eNO decreased to 6 ppb and PaO2 increased to 67 mm Hg. The strict relationship between eNO and oxygenation observed in this case reinforces the hypothesis that NO is the most important vasodilating mediator in HPS. Smoking may have hastened the resolution of HPS after LT by inhibiting respiratory NO and/or through a generalized impairment of endothelium-dependent vasodilation.