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Smoking and hypoxemia caused by hepatopulmonary syndrome before and after liver transplantation
Author(s) -
Rolla Giovanni,
Brussino Luisa,
Dutto Luca,
Ottobrelli Antonio,
Bucca Caterina
Publication year - 2001
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1053/jhep.2001.26791
Subject(s) - hepatopulmonary syndrome , medicine , hypoxemia , liver transplantation , oxygenation , cirrhosis , gastroenterology , liver disease , alcoholic liver disease , respiratory system , transplantation , vasodilation , cardiology , anesthesia
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 PaO 2 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 PaO 2 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.