If we pooled all the HIV-uninfected NHL patients together, mixing the rituximab group and the control group, to mimic Greens analysis, the prevalence rate of pneumocystis infection in these patients was 2.33% (284/12, 158). of pneumocystis contamination in the rituximab group (N?=?7,554) was significantly higher than that in the control group (N?=?4,604) (2.95% vs. 1.32%). The onset of pneumocystis contamination occurred between 6 and 16 weeks after chemotherapy. Patients who had pneumocystis prophylaxis, whether or not they had a pneumocystis contamination later in their treatment course, had significantly better first-year survival rates (73% vs. 38%). Regular pneumocystis prophylaxis should be considered in this group of patients. Introduction pneumonia, formerly known as pneumonia (PcP), occurs when immune function is usually suppressed to a certain threshold. Noticeably, once these immunocompromised patients are infected, the mortality rate can be as Lemborexant high as 30 ~ 60%1,2. To make points worse, a delay in diagnosis is not uncommon because its initial manifestations are usually nonspecific and include fever, dry cough and pulmonary interstitial infiltrates. Rituximab is usually a monoclonal antibody that binds to the CD20 antigens on B lymphocytes and leads to B cell elimination from the body. Through this effect, rituximab has been proven effective in many B cell-associated diseases, such as B cell lymphoma and inflammatory autoimmune disorders. The widespread application of rituximab was soon followed by reports linking pneumocystis contamination to rituximab3C5. Thanks to previous studies in HIV/AIDS patients, it is comprehended that pneumocystis contamination is mostly associated with T cell dysfunction. Therefore, when pneumocystis contamination occurs in rituximab-treated patients, rituximab, an anti-B cell agent, appears innocent at first glance. However, recent evidence demonstrates that B cell dysfunction can also lead to pneumocystis contamination. In a murine study, Elsegeiny contamination7. Similar findings were found in a human peripheral blood study8. In addition, rituximab can cause prolonged hypogammaglobulinemia and hinder naive B lymphocyte differentiation into plasma cells, which are Lemborexant crucial for eliminating contamination (PJP, formerly known as PcP) in HIV-uninfected non-Hodgkin lymphoma patients from Jan/2006 to Dec/2013. The pneumocystis-infected cases were identified by codes for pneumocystis contamination (136.3), which had to be recorded during admission, and by the use of intravenous trimethoprim/sulfamethoxazole (TMP/SMX). Patients who had a pneumocystis contamination before the initiation of chemotherapy were excluded. The prescription of oral TMP/SMX at the outpatient clinic prior to the diagnosis of pneumocystis contamination was defined as primary prophylaxis. Cases with another opportunistic contamination, cytomegalovirus (CMV) contamination, were identified by codes for CMV contamination (078.5). Although the NHIRD has the advantage of nation-wide coverage and a large number of patients, its drawback is the lack of medical Lemborexant details for each patient. To assess the impact of this weakness and to validate the reliability of this study, we conducted a pilot study with the same inclusion/exclusion criteria plus a detailed medical record review in our hospital (supplement?1). Statistics The frequencies of each categorical variable were compared with chi-square (2) assessments and/or Fishers exact tests. Propensity score matching was performed to correct Rabbit Polyclonal to RPL39L for sample selection bias. Kaplan-Meier analyses were used to calculate the survival rate of the pneumocystis-infected and pneumocystis-free groups, and log-rank assessments were used to Lemborexant compare the survival differences between these two groups of patients. A multivariate analysis of clinical variables associated with the diseases was performed with Cox regression. Results By examining the NHIRD, we identified 20,961 HIV-uninfected NHL patients from January 2006 to December 2013. After excluding patients who were ineligible for this study, we found 7554 HIV-uninfected NHL patients who received rituximab-based chemotherapy (rituximab group) and 4604 HIV-uninfected NHL patients received chemotherapy without rituximab (control group). The result showed that the prevalence rate of pneumocystis infection was significantly higher in the rituximab group than in the control group (2.95% vs. 1.32%; p? ?0.001) (Table?1). This result was validated by a smaller single-centre study done with the same inclusion/exclusion criteria and included a detailed medical record review of each patient (supplement?1). Importantly, there was no difference in the prevalence rate of another T cell-related opportunistic infection, CMV infection, between these two groups of patients (0.99% vs. 0.98%; p?=?0.9334) (Table?1), indicating that pneumocystis infection is a unique risk to this group of patients. Table 1 Demographic data and prevalence rates of (formerly known as (PcP)) and CMV infection in HIV-uninfected non-Hodgkin lymphoma patients. value(PcP)223 (2.95%)61 (1.32%) 0.0001Cytomegalovirus (CMV)75 (0.99%)45 (0.98%)0.93 Open in a separate window The patients in the rituximab group, when compared to those in the control group, were older and had significantly more comorbidities, such as chronic pulmonary disease, rheumatologic disease, diabetes mellitus and chronic kidney disease (Table?1). A further analysis within the rituximab group revealed that the pneumocystis-infected patients had a similar demographic background as the pneumocystis-free patients except for a proportion of males, which was significantly.