Abstract
CMV serotesting by means of ELISA was performed every alternate week in 160 patients receiving renal (n= 117), pancreas (n = 18), liver (n = 17) and heart allografts (n = 8). Prophylactic immunosuppression consisted of Cyclosporin A plus methylprednisone and was identical for the different groups of transplant patients studied. In parallel, urinary neopterin values were studied in these cases. Thirty‐eight CMV infections were observed. Of these, 74% represented secondary infections and approximately 50% were symptomatic. CMV infections preferentially occurred in hyperimmunosuppressed individuals as evidenced by (i) an almost complete lack of early acute rejection episodes in transplant recipients who subsequently experienced infection, and (ii) aggravation of severity of infection after intensification of immunosuppressive treatment. The incidence of CMV infection was also markedly increased in polytransfused organ recipients, and evidence suggests that immunosuppression by blood transfusion rather than transmission of virus is responsible. CMV infection and, in particular, CMV disease, at least in renal transplant recipients, negatively influenced graft survival: this was thought to represent a consequence of CMV‐induced enhancement of alloreactivity as well as a consequence of deliberate reduction of immunosuppression during serious CMV disease. Evaluation of the neopterin marker, although not specific, proved to be clinically useful for three reasons: (i) neopterin in response to CMV infection increases approximately 1 wk earlier than antibodies, (ii) the magnitude of CMV‐induced neopterin responses is related to the severity of the infection, and (iii) normalization of neopterin levels is related to resolution of CMV disease.
Published Version
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