Background The effects of cryptococcemia on patient outcomes in those with or without HIV remain unclear. Methods One hundred and seventy‐nine cryptococcemia patients were enrolled in this retrospective study. Demographic characteristics, blood test results and outcome were compared between the two groups. Results The diagnosis time of Cryptococcus infection was 2.0(0‐6.0) days for HIV‐infected patients, 5.0 (1.5‐8.0) days for HIV‐uninfected patients (p = .008), 2.0 (1.0‐6.0) days for cryptococcal meningitis (CM) patients and 6.0 (5.0‐8.0) days for non‐CM patients (p < .001). HIV infection [adjusted odds ratio (AOR) (95% confidence interval): 6.0(2.3‐15.9)], CRP < 15 mg/L [AOR:3.7(1.7‐8.1)) and haemoglobin > 110 g/L [AOR:2.5(1.2‐5.4)] were risk factors for CM development. Forty‐six (25.7%) patients died within 90 days. ICU stay [AOR:2.8(1.1‐7.1)], hypoalbuminemia [AOR:2.7(1.4‐5.3)], no anti‐cryptococcal treatment [AOR:4.7(1.9‐11.7)] and altered consciousness [AOR:2.4(1.0‐5.5)] were independent risk factors for 90‐day mortality in all patients. HIV infection did not increase the 90‐day mortality of cryptococcemia patients when anti‐Cryptococcus treatment was available. Non‐Amphotericin B treatment [AOR:3.4(1.0‐11.2)] was associated with 90‐day mortality in HIV‐infected patients, but age ≥ 50.0 years old [AOR:2.7(1.0‐2.9)], predisposing disease [AOR:4.1(1.2‐14.2)] and altered consciousness [AOR:3.7(1.1‐12.9)] were associated with 90‐day mortality in HIV‐uninfected patients who accepted anti‐Cryptococcus treatment. Conclusion HIV infection increased the incidence of CM rather than mortality in cryptococcemia patients. The predictive model was completely divergent in HIV‐infected and HIV‐uninfected patients, suggesting that novel strategies for diagnosis and treatment algorithms are urgently needed.

The roles of cytokines and chemokines in HIV-associated cryptococcal meningitis (HCM) and HIV-associated tuberculous meningitis (HTBM) are debatable. In sum, 34 HIV-infected patients without meningitis, 44 HCM patients and 27 HTBM patients were enrolled for study. The concentrations of 22 cytokines/chemokines in cerebrospinal fluid (CSF) were assayed at admission. Principal component analysis (PCA), Pearson's and logistic regression analyses were used to assess the role of cytokines/chemokines in HCM and HTBM. We found the levels of T helper (Th)17, Th1 [interleukin (IL)-12p40, interferon (IFN)-γ, tumor necrosis factor (TNF)-α and TNF-β and Th2 (IL-2/4/5/6/10)] cytokines were elevated in patients with meningitis compared with those in HIV-infected patients without central nervous system (CNS) infection. Furthermore, the IL-1Ra, IL-12p40, IL-17α and monocyte chemotactic protein-1 (MCP-1) levels were higher in HCM patients, while the IFN-γ, regulated upon activation, normal T cell expressed and secreted (RANTES) and interferoninducible protein-10 (IP)-10 levels were higher in HTBM patients. Elevated CSF concentrations of IL-17a, TNF-β, IL-5, IL-12p40 and IL-1Rα were closely related to meningitis, but elevated IP-10, MCP-1, RANTES and IFN-γ levels and CSF white blood cells (WBCs) were protective factors against HCM. Our study suggested that HIV-infected patients with low CSF WBCs have a high risk of HCM. Th1, Th2 and Th17 cytokines/chemokines mediate differences in the pathogenesis of HCM and TBM. Overexpressed proinflammatory MCP-1, RANTES, IFN-γ and IP-10 in CSF are protective factors against HCM but not HTBM.

The differences in the clinical features and outcomes of respiratory adenovirus infection (RAI) between immunocompetent and immunocompromised adult patients remain unclear. Thirty-nine adult RAI patients, including 28 (71.8%) immunocompetent patients and 11 (28.2%) immunocompromised patients were enrolled in this retrospective study. Demographic characteristics, symptoms, laboratory tests, radiographic findings, therapies and clinical outcomes were compared between the two groups. We found fever (94.9%), cough (66.7%) and sputum production (56.4%) were the most frequent symptoms. Compared with immunocompetent RAI patients, the immunocompromised RAI patients were more likely to experience anemia (g/L; 90.8 ± 24.0 vs 134.3 ± 14.6, P ＜ 0.001), thrombocytopenia (×10 9 /L; 116.9 ± 92.7 vs 178.4 ± 74.6, P = 0.037), hypoalbuminemia (g/L; 29.6 ± 5.5 vs 36.9 ± 5.2, P ＜ 0.001), hyponatremia (mmol/L; 134.8 ± 5.6 vs 138.5 ± 3.9, P = 0.026) and low levels of cholinesterase (U/L; 2650.5 ± 1467.4 vs 5892.8 ± 1875.1, P ＜ 0.001). Chest computed tomography (CT) scans indicated that lung infiltrate was the most common finding (64.1%).Immunocompromised patients had a higher likelihood of bilateral lung involvement (72.7%) and lower lobe involvement (81.8%) of both lungs. The hospitalized mortality rate was 27.3% in immunocompromised RAI patients, but no deaths

Background: The effect of HIV infection on the clinicopathological characteristics of diffuse large B-cell lymphoma (DLBCL) remains debatable. Methods: Fifty-three HIV-infected and ninety-three HIV-uninfected DLBCL patients were enrolled in the retrospective study by propensity score matching for sex, age, body mass index and international prognostic index (IPI) at a ratio of 1:2. The clinicopathological characteristics were compared between the two groups. Results: HIV-infected DLBCL patients had lower white blood cell counts [×109/L; 4.4(3.4–5.6) vs. 6.1(4.2–8.2), p < 0.001], platelet counts ((×109/L; 184.7 ± 89.3 vs. 230.0 ± 113.9, p = 0.014) and serum albumin (g/L; 37.3 ± 6.9 vs. 41.3 ± 6.2, p < 0.001) but higher incidences of central nervous system (CNS) involvement (9.4% vs. 1.1%, p = 0.014), bone marrow involvement (24.5% vs. 11.5%, p = 0.044) and Epstein–Barr viremia (61.1% vs. 26.7%, p = 0.002) than HIV-uninfected patients. In terms of histopathology, HIV-infected patients had higher positivity of Epstein–Barr virus-encoded small RNA (EBER) (41.7% vs. 6.7%, p = 0.002), but lower CD20 (90.2% vs. 98.7%, p= 0.029) and CD79a (23.1% vs. 53.7%, p < 0.001) expression. The overall response rate (ORR) at the end of chemotherapy (70.2% vs. 87.8%, p= 0.012) and 1-year overall survival (OS) (61.7% vs. 84.2%, log-rank p = 0.006) in HIV-infected patients were significantly lower than those in HIV-uninfected patients. Multivariate analysis suggested IPI ≤2.0 [adjusted odds ratio (AOR) (95% confidence interval): 5.0 (1.2–21.2), p = 0.030] was associated with ORR, hypoalbuminemia [AOR: 3.3(1.3–9.1), p = 0.018] and CNS involvement [AOR: 3.3(1.0–10.5), p = 0.044] were associated with reduced 1-year OS in HIV-infected patients. Conclusions: HIV-infected DLBCL patients have unique blood profiles and phenotypic markers. Low ORR and 1-year OS were observed in HIV-infected DLBCL patients in our study, even in the HAART era.