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J Thorac Cardiovasc Surg 1997;114:285-287
© 1997 Mosby, Inc.
BRIEF COMMUNICATIONS |
Berlin, Germany
Received for publication Dec. 23, 1996. Accepted for publication Jan. 24, 1997. Address for reprints: R. Pfitzmann, MD, Deutsches Herzzentrum Berlin, Cardiac Surgery and Transplant Division, Augustenburger Platz 1, 13353 Berlin, Germany.
The occurrence of acute and chronic graft-versus-host disease (GVHD) has been widely described in the literature, with nearly 50% of cases occurring after bone marrow transplantation. Acute GVHD in thoracic organ transplantation has been observed after experimental lung transplantation in animals
1 but has not been recognized very often in lung and heart-lung recipients, 2-5 although donor cells persist in the lungs for up to 6 weeks after the operation. Altogether we found only four publications with a total of six patients having acute GVHD after heart-lung transplantation worldwide.
We report on a 28-year-old woman with congenital ventricular septal defect and Eisenmenger reaction in whom acute GVHD developed on the tenth postoperative day after successful heart-lung transplantation. Immunosuppressive drug therapy was administered with cyclosporine, azathioprine, and steroids. Additionally, rabbit antithymocyte globulin was administered once at a dose of 1.5 mg/kg body weight for induction therapy. Blood products were not given before, during, or after transplantation.
The cytomegalovirus status of the donor and the recipient were negative. Human leukocyte antigen (HLA) match showed conformity of five HLA specificities. With the patient receiving sufficient immunosuppression, initial manifestations of acute GVHD were a temperature higher than 40° C and a maculopapular rash for the first days. Subsequent manifestations included hematopoietic dysfunction (aplastic syndrome) with leukopenia, anemia and low platelet count, hepatitis, cardiac irregularity with supraventricular and ventricular arrhythmias, and generalized central seizures after a few days. Echocardiographic findings (early diastolic relaxation time and myocardial wall thickness) and the intramyocardial electrocardiogram (IMEG) showed no signs of acute rejection. The concentrations of plasma transaminases, serum bilirubin, creatinine, lactate dehydrogenase, creatinine, and myoglobin were elevated to very high levels, whereas the number of red blood cells, leukocytes, and platelets decreased rapidly, indicating a severe course of unknown disease at that time. The skin rash rapidly progressed to a form resembling toxic epidermal necrolysis (Lyell syndrome). At this point we saw no evidence of localized or generalized viral, bacterial, or fungal infection. After the development of renal failure and acute shortness of breath, leading to a short period of cardiopulmonary resuscitation, continuous controlled mechanical ventilation was necessary. Because of progressive renal failure, the patient required hemodialysis. Diagnosis of acute GVHD was confirmed by clinical implications, skin biopsy from the area of cutaneous lesions, and evidence of more than 50% of donor-specific lymphocytes in peripheral blood by HLA typing. For therapy, additional immunosuppression with rabbit antithymocyte globulin at a dose of 2.5 mg/kg body weight and high-dose steroids were instituted. Although cutaneous and hematologic manifestations of acute GVHD improved during the following days, with augmented quadruple immunosuppressive drug therapy and transfusion of blood products for aplastic syndrome, the patient died on postoperative day 34 of intracerebral bleeding.
Acute GVHD may occur as a result of the infusion of blood products containing viable lymphocytes, but in this case the patient had not received any blood products at the time of manifestation of GVHD. Therefore, the viable lymphocytes were considered transplanted with the donor organs.
Acute GVHD in patients receiving thoracic organ transplants has been recognized rarely until now. Thus, in view of the worldwide increasing numbers of lung and heart-lung transplantation, acute GVHD, as yet uncommon, may become more important in the future.
The first manifestation of acute GVHD can be the development of fever and maculopapular rash, which is frequently mistaken for a viral or allergic rash. In due course the persistent rash begins to scale, and diarrhea, hepatosplenomegaly, jaundice, cardiac irregularity, central nervous system irritability, and pulmonary infiltrates may occur at the height of the acute GVHD.
Once acute GVHD is established, little can be done to modify its course. Corticosteroids merely serve to enhance the susceptibility to infection. Cytolytic therapy (antithymocyte globulin) is necessary to destroy donor lymphocytes. On the other hand, this therapy results in further suppression of immunity. Cyclosporine, a more specific immunosuppressive agent, can also be helpful. After solid organ transplantation, the appearance of acute GVHD is fatal in the majority of immunosuppressed patients. Because treatment is very difficult, immediate early diagnosis of acute GVHD appears to be essential to institute adequate and early therapy and to prevent the severe course of this disease, ultimately with the death of the patient.
When characteristic signs appear, such as fever and rash, acute GVHD should be considered a possible diagnosis. If acute GVHD is clinically suspected, this may be confirmed immediately by skin biopsy and by HLA typing of the peripheral blood lymphocytes. Once GVHD is documented, aggressive cytolytic therapy to destroy donor lymphocytes seems to be the only therapeutic option.
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