We treated all CMV seronegative recipients irrespective of donor serology with anti-CMV immunoglobulins from the day of transplantation. Arguments for this strategy were that the CMV serology of the donor is not always available at the time of transplantation and that CMV unscreened (although bufly coat poor) blood is used during open heart surgery. Moreover, in the majority (65 percent) of the CMV seronegative heart transplant recipients rejections are treated in the first three months after transplantation, and therefore, these patients will become high risk for CMV disease.
Based on the data from the literature, we expected to find a high incidence (82 percent) of symptomatic CMV infection in CMV seronegative heart recipients from a CMV seropositive donor. In the globulin- treated patients, we found a much lower (13 percent) incidence of CMV disease. Only one patient had to be treated with DHPG, and none of the seronegative patients died because of CMV infection. However, the incidence of CMV excretion was high (50 percent) in these patients. The incidences of CMV isolation (39 percent) and related disease (10 percent) in the nonglobulin-treated CMV seropositive recipients were comparable with those in the globulin-treated CMV seronegative heart recipients from a seropositive donor. In the untreated CMV seronegative recipients from a CMV seropositive donor, the incidence of CMV disease was 50 percent. These observations suggest that passive immunization with anti-CMV immunoglobulin can prevent or mitigate symptomatic CMV infection, and thus induces the same protection against CMV disease as natural acquired anti-CMV resistance. However, virus replication was not reduced by passive immunization, and prophylaxis was only temporarily effective as can be learned from the patient with symptomatic disease after the anti-CMV IgG titer had decreased to pretransplantation levels. The efficacy of prophylactic globulin treatment to reduce CMV disease but not infection is in accordance with the studies in CMV seronegative renal transplant recipients from a seropositive donor.
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In CMV seronegative heart recipients from a seronegative donor, the incidence of isolation was much lower as compared with that in CMV seronegative recipients of a CMV seropositive allograft (6 percent vs 50 percent). In theory, an incidence of 0 percent was expected as transmission with the allograft is unlikely in the situation of a CMV seronegative allograft donor-recipient combination. However, we used CMV unscreened bufly-coat depleted blood during open heart surgery. Apparently, the use of bufly-coat depleted blood did not completely prevent CMV disease in all patients, not even when passive immunization was given.
In conclusion, our study suggests that passive immunization with anti-CMV immunoglobulin prevents CMV disease but not infection in CMV seronegative heart transplant recipients from a CMV seropositive donor. One can argue that definite conclusions on the efficacy of such a strategy can only be drawn from a prospective, randomized, double-blind controlled study. However, the data from the present uncontrolled study in heart transplant recipients and the reports from controlled trials in kidney and bone marrow recipients may make such an approach questionable on ethical grounds in view of the reported high incidence of CMV disease.