C1-esterase inhibitor in graft failure after lung transplantation

• Published in: Intensive care medicine Vol. 25; no. 11; pp. 1315 - 1318
• Main Authors: STRÜBER, M, HAGL, C, HIRT, S. W, CREMER, J, HARRINGER, W, HAVERICH, A
• Format: Journal Article
• Language: English
• Published: Heidelberg Springer 01.11.1999; Berlin Springer Nature B.V
• Subjects: Biological and medical sciences; Capillary Leak Syndrome - drug therapy; Capillary Leak Syndrome - etiology; Complement C1 Inactivator Proteins - therapeutic use; Extracorporeal Membrane Oxygenation; Graft Rejection - complications; Graft Rejection - drug therapy; Heart surgery; Humans; Lung Transplantation; Lung transplants; Male; Medical sciences; Middle Aged; Nitric oxide; Patients; Pleural Effusion - drug therapy; Pleural Effusion - etiology; Postoperative Complications; Surfactants; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases; Surgery of the respiratory system; Ventilators; Germany; Human; Lung disease; Serine endopeptidases; Respiratory disease; Enzyme; Complement subcomponent C1s; Lung; Enzyme inhibitor; Transplantation; Homotransplantation; Case study; Peptidases; Chemotherapy; Reperfusion; Treatment; Surgery; Hydrolases; High dose; Failure
• ISSN: 0342-4642; 1432-1238
• DOI: 10.1007/s001340051065

Graft failure after lung transplantation may occur immediately after transplantation due to reperfusion injury or later due to rejection and infection. Although the pathological mechanisms are not completely known, the clinical findings are similar to the adult respiratory distress syndrome. In this condition, the blood coagulation contact system and the complement system are activated, leading to a capillary leak syndrome. Activation of the contact as well as the complement system is regulated by a common inhibitor, C1-esterase inhibitor (C1-INH). We report on two patients who received high doses of C1-INH for 2 days during graft failure either due to reperfusion injury immediately after transplantation or due to an acute rejection 2 months after double-lung transplantation. In both cases of graft failure, a capillary leak syndrome occurred with pleural effusions of 7 l to more than 10 l per day. In case 1 disturbance of gas exchange during severe reperfusion injury could not be treated effectively with other treatment modalities like nitric oxide ventilation or surfactant administration. With the use of C1-INH, pleural effusions reduced within 12 h, leading to normal graft function within 4 days. In the second recipient, acute rejection forced the use of extracorporeal membrane oxygenation (ECMO) within 24 h despite immunosuppressive therapy. After administration of C1-INH, pleural effusions reduced from 19 l per day to 300 ml within 3 days of treatment. ECMO was discontinued after C1-INH treatment and the patient extubated 2 weeks later. This experience indicates that C1-INH may play a role in the management of capillary leak syndrome after lung transplantation.