AIM： To study the presence of sustained low diffusing capacity （DLco） after liver transplantation （LT） in patients with hepatopulmonary syndrome （HPS）. METHODS： Six patients with mild-to-severe HPS and 24 with...AIM： To study the presence of sustained low diffusing capacity （DLco） after liver transplantation （LT） in patients with hepatopulmonary syndrome （HPS）. METHODS： Six patients with mild-to-severe HPS and 24 without HPS who underwent LT were prospectively followed before and after LT at mid-term （median, 15 mo）. HPS patients were also assessed at Iong-tem （median, 86 mo）. RESULTS： Before LT, HPS patients showed lower PaO2 （71 ± 8 mmHg）, higher AaPO2 （43 ± 10 mmHg） and lower DLco （54% ± 9% predicted）, due to a combination of moderate-to-severe ventilation-perfusion （VA/Q） imbalance, mild shunt and diffusion limitation, than non- HPS patients （94 ± 4 mmHg and 19 ± 3 mmHg, and 85% ± 3% predicted, respectively） （P 〈 0.05 each）. Seven non-HPS patients had also reduced DLco （70% ± 4% predicted）. At mid- and long-term after LT, compared to pre- LT, HPS patients normalized PaO2 （91 ± 3 mmHg and 87 ± 5 mmHg）, AaPO2 （14 ± 3 mmHg and 23 ± 5 mmHg） and all VA/Q descriptors （P 〈 0.05 each） without changes in DLco （53% ± 8% and 56% ± 7% predicted, respectively）. Post-LT DLco in non-HPS patients with pre- LT low DLco was unchanged （75% ± 6% predicted）. CONCLUSION： While complete VA/Q resolution in HPS indicates a reversible functional disturbance, sustained low DLco after LT also present in some non-HPS patients, points to persistence of sub-clinical liver-induced pulmonary vascular changes.展开更多
基金Supported by Red Respira-ISCIII-RTIC-03/11 and Generalitat de Catalunya, No. 2005SGR-00822
文摘AIM： To study the presence of sustained low diffusing capacity （DLco） after liver transplantation （LT） in patients with hepatopulmonary syndrome （HPS）. METHODS： Six patients with mild-to-severe HPS and 24 without HPS who underwent LT were prospectively followed before and after LT at mid-term （median, 15 mo）. HPS patients were also assessed at Iong-tem （median, 86 mo）. RESULTS： Before LT, HPS patients showed lower PaO2 （71 ± 8 mmHg）, higher AaPO2 （43 ± 10 mmHg） and lower DLco （54% ± 9% predicted）, due to a combination of moderate-to-severe ventilation-perfusion （VA/Q） imbalance, mild shunt and diffusion limitation, than non- HPS patients （94 ± 4 mmHg and 19 ± 3 mmHg, and 85% ± 3% predicted, respectively） （P 〈 0.05 each）. Seven non-HPS patients had also reduced DLco （70% ± 4% predicted）. At mid- and long-term after LT, compared to pre- LT, HPS patients normalized PaO2 （91 ± 3 mmHg and 87 ± 5 mmHg）, AaPO2 （14 ± 3 mmHg and 23 ± 5 mmHg） and all VA/Q descriptors （P 〈 0.05 each） without changes in DLco （53% ± 8% and 56% ± 7% predicted, respectively）. Post-LT DLco in non-HPS patients with pre- LT low DLco was unchanged （75% ± 6% predicted）. CONCLUSION： While complete VA/Q resolution in HPS indicates a reversible functional disturbance, sustained low DLco after LT also present in some non-HPS patients, points to persistence of sub-clinical liver-induced pulmonary vascular changes.
