Immunocompromised outpatients, including people living with HIV/AIDS (PLWH), diabetes, cancer, and organ transplant recipients, are at high risk of antimicrobial resistance (AMR) due to their weakened immune systems and use of immunosuppressive therapies. The high prevalence of prophylactic and therapeutic antibiotic use in this vulnerable population, coupled with frequent contact with healthcare facilities and limited outpatient antimicrobial resistance surveillance systems, contributes to the increase in antimicrobial resistance. The majority of available data pertains to inpatients, and there is a lack of comprehensive outpatient information on pathogen distribution, resistance patterns, and diagnostic challenges. Moreover, nonspecific clinical presentations, diminished inflammatory responses, and limitations of traditional diagnostic methods complicate infection diagnosis in this population. Increasing resistance surveillance, developing rapid diagnostic tools, and implementing accurate and personalized approaches are key strategies to reduce the burden of disease, mortality, and healthcare costs in the immunocompromised outpatient population. This study was designed as a narrative review based on a comprehensive search of major databases and guidelines. It aims to examine the available evidence and address the challenges associated with AMR in immunocompromised outpatients.

Differentiating glioma from primary central nervous system lymphoma (PCNSL) can be challenging, and current diagnostic measures such as MRI and biopsy are of limited efficacy. Liquid biopsies, which detect circulating biomarkers such as microRNAs (miRs), may provide valuable insights into diagnostic biomarkers for improved discrimination. This review aimed to investigate the role of specific miRs in diagnosing and differentiating glioma from PCNSL. A systematic search was conducted of PubMed, Scopus, Web of Science, and Embase for articles on liquid biopsies as a diagnostic method for glioma and PCNSL. Sixteen dysregulated miRs were identified with significantly different levels in glioma and PCNSL, including miR-21, which was the most prominent miR with higher levels in PCNSL, followed by glioma, including glioblastoma (GBM), and control groups. The lowest levels of miR-16 and miR-205 were observed in glioma, followed by PCNSL and control groups, whereas miR-15b and miR-301 were higher in both tumor groups, with the highest levels observed in glioma patients. The levels of miR-711 were higher in glioma (including GBM) and downregulated in PCNSL compared to the control group. This review suggests that using these six circulating microRNAs as liquid biomarkers with unique changing patterns could aid in better discrimination between glioma, especially GBM, and PCNSL.

Background: The role of toll-like receptor 4 (TLR4) in schizophrenia remains unclear, with studies reporting conflicting results on its expression and activation in persons with schizophrenia (PwSCZ). This systematic review/meta-analysis compared basal monocytic TLR4 expression, as well as its activation pattern between PwSCZ and healthy controls (HCs). Methods: This study was registered with PROSPERO (CRD42021273858) and adhered to the PRISMA guidelines. A systematic search was conducted through MEDLINE (via PubMed), Web of Science, and Scopus from inception to December 12, 2023. Quantitative syntheses were conducted for (a) basal monocytic TLR4 density, (b) basal percentage of TLR4⁺ monocytes, and (c) basal TLR4 gene expression. Effect sizes were computed using Hedges’ g for mean differences. Random-effect models with restricted maximum-likelihood estimation were used, and subgrouping was conducted based on antipsychotic status. The studies’ risk of bias was assessed using the Joanna Briggs Institute (JBI) tool. Results: Eleven studies (473 PwSCZ, 416 HCs) were included. Pooled analysis revealed a nonsignificant trend toward increased basal monocytic TLR4 density in PwSCZ (Hedges’ g = 0.317 [95% CI: –0.060, 0.694], τ2 = 0.127, I² = 68.91%). The difference became significant after sensitivity analysis and excluding one study (Hedges’ g = 0.469 [0.195,0.742], p = 0.001). No significant difference was found between the groups in terms of TLR4⁺ monocytes percentage (Hedges’ g = 0.235 [–0.245, 0.715], τ2 = 0.31, I² = 87.30%) or TLR4 gene expression (Hedges’ g = 0.179 [–0.502, 0.861], τ2 = 0.29, I² = 79.04%). According to qualitative synthesis, TLR4 stimulation resulted in reduced monocytic activation in PwSCZ compared to HCs. Conclusions: This study suggested a trend toward an increased basal monocytic TLR4 density in PwSCZ, with no difference in the basal percentage of TLR4⁺ monocytes or TLR4 gene expression. However, the limited available data underscores the need for future studies.