http://dx Authors contributions: AV designed the study, performed statistical analysis, evaluated patients, and wrote the article; VN evaluated patients and published the article; IF, SI, RF, RS, FC, MR, CB, SM, and FC provided intellectual inputs and evaluated patients; MM, IF, FP, FG, MK, RB, GMR, GS, RF, AC, ML, RM, and LT evaluated patients, provided intellectual inputs, and examined the article. Andrea Visentin and Vincenzo Nasillo equally contributed to the work.. in immunocompromised subjects. WNVND can occur as meningitis, encephalitis, or acute flaccid paralysis.8 So far, the knowledge around the clinical course, the rate of central nervous system (CNS) involvement and the outcome of WNV infection in patients with haematological malignancies is scanty, being limited to only a few reports.9 The aim of this multicentre study was to analyse the clinical features and the outcome of WNV infection in patients with malignancies of B-cell lineage. For this purpose, we retrospectively collected clinical data from 21 patients diagnosed with a B-cell lymphoid neoplasm who experienced WNV contamination during the last 7 years at 8 Italian institution. Thirteen patients had chronic lymphocytic leukaemia (CLL), 5 non-Hodgkin lymphomas (3 follicular lymphomas, 1 high-grade lymphoma, and 1 extranodal marginal zone lymphoma), 1 hairy cell leukaemia, 1 Hodgkin lymphoma, and 1 B-cell precursor acute lymphoblastic leukaemia. Anti-WNV antibody and WNV-ribonucleic acid (RNA) were assessed in blood and cerebrospinal fluid (CSF) in all patients. CNS imaging studies (ie brain computer tomography scan and/or magnetic resonance immaging) were performed in all the patients with WNVND, in order to rule out other causes of neurological involvement such as bleeding or lymphoma/leukaemia localization. CNS symptoms associated with the presence of WNV-RNA and/or WNV-IgM in the CSF were applied as diagnostic criteria for WNVND, according to the current guidelines.8 The primary endpoint of the study was to evaluate the rate of WNVND. The secondary endpoints included the median overall survival (OS), calculated as time from WNV contamination to death (event) or last known follow-up (censored), and WNV-related survival. Mann-Whitney and Fisher exact assessments were used to compare continuous and categorical variables. This multicentre retrospective study was approved by the local research ethics committee of Padua Hospital and carried out according to Helsinki declaration. Informed consent was obtained from all alive patients. Authors can share patients data upon affordable request. Clinical and laboratory features of the 21 patients are reported in Table ?Table11 and in Physique ?Figure1A.1A. Sixteen (76%) participants experienced received one previous anti-leukaemia/lymphoma treatment (0C3) and 10 (57%) experienced an active haematological disease at the time of WNV infection, including previously untreated Fenoldopam cases and those with relapsed diseases. The median time from lymphoid neoplasm diagnosis to WNV contamination was 6.5??4.5 years, being longer in patients with WNVND (3.5??2.9 vs 7.4??4.4 in cases without and with WNVND, test. the lower panels report the overall survival of the whole cohort (C) and the WNV-related survival in patients with and without WNVND (D). Patients with WNVND have a short WNV-related survival ( em P /em ?=?0.0463). WNV = West Nile computer virus, WNVND = West Nile computer virus neuroinvasive disease. All the patients offered fever (maximum value range 38.2C40C), while 17 (81%) reported fatigue, 9 (42%) arthralgia, and Fenoldopam 4 (19%) dyspnoea. As shown in Table ?Table1,1, anti-WNV IgM was detected in the blood of 14 patients (67%), with a obvious difference between patients with or without WNVND (53% vs 100%), suggesting that impaired humoral immunity may favour viral diffusion to CNS. Consistently, anti-WNV IgM were unfavorable in CSF of half of WNVND cases. The presence of WNV-RNA in urine was Rabbit Polyclonal to CK-1alpha (phospho-Tyr294) recognized in 4 of 11 assessed patients. Twenty (95%) subjects developed neurological symptoms, such as confusion, amnesia, or headache, but only 15/21 (71%, Physique ?Figure1A)1A) fulfilled the criteria for WNVND. All the six patients without WNVND and 6 of 15 (40%) with WNVND showed complete resolution of the infection without any sequalae. The remaining 9 of 15 Fenoldopam with WNVND manifested gait instability, depressive disorder, or amnesia at 1 year from infection occurrence. Given the lack of a standard therapeutic approach, our patients received different treatments, including polyclonal intravenous immunoglobulins (57%), corticosteroids (33%), antiviral drugs (29%: 24% acyclovir and 5% ganciclovir), and levetiracetam (29%: 15% as prophylaxis and 14% for seizure treatment). Most cases were managed in an inpatient setting, due to high-grade fever and neurological symptoms or clinical manifestations such as tremor and dizziness seizures and coma, requiring intravenous fluids or respiratory support. Among the CLL subgroup, accounting for 62% of all cases, 8 of 13 patients had.