Aims The sequential organ failure assessment (SOFA) score has been a widely used predictor of outcomes in the intensive care unit, whereas short‐term and long‐term survivals of heart failure (HF) patients are predicted by the American Heart Association Get With the Guidelines–Heart Failure (GWTG‐HF) risk score. The purpose of present study was to examine whether the SOFA score on admission is more useful for predicting long‐term mortality in acute HF patients than the GWTG‐HF risk score. Methods and results A total of 269 patients (mean age, 78.5 ± 10.9 years; all‐cause mortality, 53.9%) seen in a single facility from January 2007 to December 2016 were enrolled retrospectively. They were followed up for a mean of 32.1 ± 22.3 months. All‐cause death was associated with higher SOFA and GWTG‐HF risk scores. However, no significant difference was observed in the area under the curve value between the scores. Kaplan–Meier survival analysis indicated that higher SOFA scores (P < 0.001) and GWTG‐HF risk scores (P < 0.001) were related to increased probabilities of all‐cause death. On multivariate Cox proportional hazard model analysis, the SOFA score (P < 0.001) and GWTG‐HF (P < 0.001) score were independent predictors of all‐cause death. Incorporating the SOFA score into the GWTG‐HF risk score yielded a significant net reclassification improvement and integrated discrimination improvement. On decision curve analysis, the net benefit of the SOFA score model when compared with the reference model was greater across the range of threshold probabilities. Conclusions In acute HF patients, long‐term all‐cause mortality can be predicted by the SOFA score. Discriminative performance metrics, such as net reclassification improvement, integrated discrimination improvement, and decision curve analysis, for predicting mortality were improved when the SOFA score was incorporated.

Hemophagocytic syndrome (HPS) is a rare but potentially fatal complication of viral infections. Epstein-Barr virus (EBV) and cytomegalovirus (CMV) often infect patients receiving TNF-alpha inhibitors (TNF-α inhibitors). While EBV and CMV are well established infections for the development of infectious mononucleosis, coinfection with EBV and CMV is common among immunosuppressed patients and can result in a fatal course. In addition, such viral infections can cause HPS. To the best of our knowledge, we present here the first report of HPS induced by EBV and CMV coinfection during anti-TNFα inhibitor use. A 23-year-old man hospitalized with fever, elevated liver enzymes, lymphadenopathy, and hepatosplenomegaly was diagnosed with HPS associated with EBV and CMV coinfection while using adalimumab. No clinical improvement was observed after discontinuation of adalimumab. HPS complicated by EBV and CMV coinfection was finally diagnosed, and immediate administration of ganciclovir and prednisone was considered to have prevented a lethal clinical outcome. For cases showing unexplained fever, elevated liver enzymes, and lymphadenopathy while using anti-TNFα inhibitors, screening for EBV and CMV coinfection should be encouraged. In addition, HPS should be considered in patients with EBV and/or CMV infection receiving anti-TNFα inhibitors to facilitate early definitive therapy.