The aim of this prospective study was to confirm whether and when a fall in gas transfer occurs following heart transplantation (HT); and to examine the potential relationship between gas transfer and haemodynamic change, immunosuppression, and cytomegalovirus (CMV) infection.The lung physiology of 34 heart transplant recipients (HTR) and 14 control patients undergoing coronary artery bypass grafting (CABG) were studied. The absolute and standardized residual values of forced expiratory volume in one second (FEV1), forced vital capacity (FVC), residual volume (RV), forced residual volume (FRC), total lung capacity (TLC), transfer factor of the lungs for carbon monoxide (TL,CO) and carbon monoxide transfer coefficient (KCO) were measured before and at 30, 60, 90, 120 and 150 days after HT. These data were compared to haemodynamic status, graft rejection, cyclosporin levels and episodes of CMV infection. Lung function was studied in a group of patients before and 4 weeks after CABG.There was a significant fall in mean KCO after HT (pre-HT=1.29 and post-HT= 1.06 mmol·min -1 ·kPa·L -1 ) but not after CABG (pre-CABG=1.49, post-CABG=1.5 mmol·min -1 ·kPa·L -1 . No relationship was observed between gas transfer and CMV.At the latest stage following HT (150 days) there was a positive correlation between TL,CO (absolute value and standardized residual) and mean cyclosporin level (r=0.48 and r=0.44, respectively) and also between the absolute KCO and actual (r=0.56) and mean (r=0.55) cyclosporin levels. Following HT, there is an early fall in gas transfer, which is independent of the effects of surgery and bypass, implicating early immunosuppression (e.g. antithymocyte globulin/cyclosporin).
A Al ll le er rg gi ic c b br ro on nc ch ho op pu ul lm mo on na ar ry y a as sp pe er rg gi il ll lo os si is s i in n l lu un ng g a al ll lo og gr ra af ft t r re ec ci ip pi ie en nt ts s J.J. Egan * , N. Yonan ** , K.B. Carroll * , A.K. Deiraniya ** , A.K. Webb * , A.A. Woodcock * Allergic bronchopulmonary aspergillosis in lung allograft recipients. J.J. Egan, N. Yonan, K.B. Carroll, A.K. Deiraniya, A.K. Webb, A.A. Woodcock. ERS Journals Ltd 1996. ABSTRACT: Following lung transplantation for end-stage cystic fibrosis, two male patients presented with shortness of breath, peripheral blood eosinophilia and segmental lung collapse.At bronchoscopy, each had bronchial mucous plugging containing Aspergillus fumigatus. This finding was associated with a systemic eosinophilia and skin test positivity to Aspergillus. Augmented steroid therapy resulted in the successful resolution of the symptoms.We believe that these are the first reported cases of allergic bronchopulmonary aspergillosis in lung allograft recipients. Eur Respir J., 1996, 9, 169-171. Aspergillus fumigatus (Asp f) infection is associated with high morbidity and mortality following lung transplantation [1]. A spectrum of infection has been described ranging from colonization to invasive disease [1], but to date this has not included Aspergillus-induced allergymediated pulmonary dysfunction in lung transplant recipients. We describe two cases of allergic bronchopulmonary aspergillosis (ABPA) following lung transplantation for cystic fibrosis (CF). They provide insights into the pathogenesis of allergy-mediated airways disease. Case Reports Patient No. 1A 20 year old, 42 kg male patient received a double sequential lung transplantation for CF. The 15 year old donor had mild asthma requiring salbutamol on a p.r.n. basis and had previously been prescribed oral antihistamines for allergic rhinitis. The recipient was atopic with positive skin tests to Dermatophagoides pteronyssinus, grass pollen and Asp f extracts (8 mm weal, as an immediate type reaction). Prior to transplant, Aspergillus was not isolated from his sputum and he was Aspergillus precipitins negative. Four months following transplantation, the recipient underwent a routine surveillance transbronchial biopsy (TBB) which demonstrated moderate (A3a) rejection. He received 500 mg of methylprednisolone on three consecutive days. Twelve days later, he presented in respiratory failure (arterial oxygen tension (Pa,O 2 ) 4.6 kPa, arterial carbon dioxide tension (Pa,CO 2 ) 4.2 kPa) with collapse of the left lower lobe, which progressed over 24 h to show complete collapse
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