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Over the past 25 years, the application of immunomodulating and immunosuppressive agents in the treatment of multiple sclerosis (MS), an autoimmune demyelinating and neurodegenerative disease, has led to improvements in clinical outcomes [[1]]. The induction of diffuse large B cell lymphoma (DLBCL) by methotrexate in arthritis patients and the induction of hepatosplenic T-cell lymphoma by infliximab (anti-human tumor necrosis factor-alfa antibody) in patients with inflammatory bowel diseases are typical examples [[14]]. Patients with primary cutaneous CD30-positive ALCL generally have a good prognosis, and three patients with cutaneous CD30-positive ALCL (no. 2-4) remained alive for 2-18 months (Table 1). Spontaneous regression of tumor-stage cutaneous T-cell lymphoma in a multiple sclerosis patient after discontinuing fingolimod. [Extracted from the article]

Late kidney injury (LKI) in patients with acute heart failure (AHF) requiring intensive care is poorly understood.We analyzed 821 patients with AHF who required intensive care. We defined LKI based on the ratio of the creatinine level 1 year after admission for AHF to the baseline creatinine level. The patients were categorized into 4 groups based on this ratio: no-LKI (< 1.5, n = 509), Class R (risk; ≥ 1.5, n = 214), Class I (injury; ≥ 2.0, n = 78), and Class F (failure; ≥ 3.0, n = 20). Median follow-up after admission for AHF was 385 (346-426) days. Multivariate logistic regression analysis revealed that acute kidney injury (AKI) during hospitalization (Class R, odds ratio [OR]: 1.710, 95% confidence interval [CI]: 1.138-2.571, P = 0.010; Class I, OR: 6.744, 95% CI: 3.739-12.163, P < 0.001; and Class F, OR: 9.259, 95% CI: 4.078-18.400, P < 0.001) was independently associated with LKI. Multivariate Cox regression analysis showed that LKI was an independent predictor of 3-year all-cause death after final follow-up (hazard ratio: 1.545, 95% CI: 1.099-2.172, P = 0.012). The rate of all-cause death was significantly lower in the no-AKI/no-LKI group than in the no-AKI/LKI group (P = 0.048) and in the AKI/no-LKI group than in the AKI/LKI group (P = 0.017).The incidence of LKI was influenced by the presence of AKI during hospitalization, and was associated with poor outcomes within 3 years of final follow-up. In the absence of LKI, AKI during hospitalization for AHF was not associated with a poor outcome.

The fibrinogen-to-albumin ratio (FAR) in the acute phase of acute heart failure (AHF) has seldom been evaluated.A total of 1,402 hospitalized AHF patients were analyzed. We calculated FAR using the following formula: plasma fibrinogen (g/L) /serum albumin (g/L) × 1,000. Patients were divided into 3 groups according to FAR value quartiles (low-FAR [Q1, FAR ≤ 564, n = 352], middle-FAR [Q2/Q3, 565 ≤ FAR ≤ 1,071, n = 700], and high-FAR [Q4, FAR ≥ 1,072, n = 350]). The median (interquartile range) FAR value was 855 (710-1,103). A multivariate logistic regression model showed that C-reactive protein (per 1 mg/dL increase; odds ratio [OR]: 1.307, 95% CI: 1.250-1.3366, P < 0.001), ischemic heart disease etiology (OR: 1.691, 95%CI: 1.227-2.331, P = 0.001), and diabetes mellitus (DM; OR: 1.624, 95%CI: 1.188-2.220, P = 0.002) were independently associated with high FAR values. Kaplan-Meier curve analysis showed that prognosis of all-cause mortality within 730 days was significantly poorer (P = 0.033) in the high-FAR group than in the other 2 groups. Conversely, in the low-albumin group, the prognosis of all-cause mortality was significantly poorer (P = 0.006) in the low-FAR group than in the other groups. A Cox regression model revealed that in the low-albumin group, a low FAR value was an independent predictor of 730-day mortality (hazard ratio [HR]: 0.503, 95% CI: 0.287-0.881, P = 0.016) and HF events (HR: 0.444, 95%CI 0.276-0.712, P = 0.001).Elevated FAR was associated with inflammation, DM, and ischemic etiology, and with adverse outcomes in the whole AHF group, whereas low FAR was independently associated with adverse outcomes in the low-albumin group.