BACKGROUND AND OBJECTIVE: Cytomegalovirus (CMV) infection is a life-threatening condition in patients with diffuse parenchymal lung diseases (DPLDs), who are receiving immunosuppressive therapy. The aim of this study was to describe the clinical features of CMV infection and to propose a strategy for managing CMV infection in patients with DPLD who are receiving immunosuppressive therapy. METHODS: A retrospective longitudinal observational study was performed on 69 patients with DPLDs (39 with acute/subacute onset, 30 with chronic onset) who were receiving immunosuppressive therapy and were positive for CMV pp65 antigen (CMV-pp65Ag) in peripheral blood leukocytes (PBLs). RESULTS: Clinical CMV disease and subclinical CMV antigenaemia developed in 23 and 46 patients, respectively. The cut-off level of CMV-pp65Ag indicating clinical CMV disease, as determined by receiver operator characteristic curve analysis, was 7.5 cells per 5 × 10(4) PBLs. Multivariate analysis revealed that early CMV infection was associated with acute/subacute onset of underlying DPLD and with respiratory dysfunction at the commencement of immunosuppressive therapy. Multivariate analysis also suggested that the acute/subacute onset of underlying DPLD, a CMV-pp65Ag titre of >7.5 cells per 5 × 10(4) PBLs, and C-reactive protein levels ≥ 10 mg/L indicated a poor prognosis. CONCLUSIONS: We recommend that CMV-pp65Ag antigenaemia of >7.5 cells per 5 × 10(4) PBLs in patients with DPLD should be treated with ganciclovir. Patients with lower levels of CMV-pp65Ag antigenaemia should be closely monitored or treated with ganciclovir if the clinical findings suggest a poor prognosis.
BACKGROUND AND OBJECTIVE:Cytomegalovirus (CMV) infection is a life-threatening condition in patients with diffuse parenchymal lung diseases (DPLDs), who are receiving immunosuppressive therapy. The aim of this study was to describe the clinical features of CMV infection and to propose a strategy for managing CMV infection in patients with DPLD who are receiving immunosuppressive therapy. METHODS: A retrospective longitudinal observational study was performed on 69 patients with DPLDs (39 with acute/subacute onset, 30 with chronic onset) who were receiving immunosuppressive therapy and were positive for CMV pp65 antigen (CMV-pp65Ag) in peripheral blood leukocytes (PBLs). RESULTS: Clinical CMV disease and subclinical CMV antigenaemia developed in 23 and 46 patients, respectively. The cut-off level of CMV-pp65Ag indicating clinical CMV disease, as determined by receiver operator characteristic curve analysis, was 7.5 cells per 5 × 10(4) PBLs. Multivariate analysis revealed that early CMV infection was associated with acute/subacute onset of underlying DPLD and with respiratory dysfunction at the commencement of immunosuppressive therapy. Multivariate analysis also suggested that the acute/subacute onset of underlying DPLD, a CMV-pp65Ag titre of >7.5 cells per 5 × 10(4) PBLs, and C-reactive protein levels ≥ 10 mg/L indicated a poor prognosis. CONCLUSIONS: We recommend that CMV-pp65Ag antigenaemia of >7.5 cells per 5 × 10(4) PBLs in patients with DPLD should be treated with ganciclovir. Patients with lower levels of CMV-pp65Ag antigenaemia should be closely monitored or treated with ganciclovir if the clinical findings suggest a poor prognosis.