Inflammatory phenotypes and clinical outcomes amongst patients with presumed and confirmed Pneumocystis jirovecii pneumonia without underlying human immunodeficiency virus infection.

Abstract

Pneumocystis jirovecii pneumonia (PJP) has significant mortality, especially in immunocompromised hosts without underlying human immunodeficiency virus infection (HIV). Inflammatory phenotypes may influence clinical outcomes. This study examines the relationship between inflammation, as measured by C-reactive protein (CRP), and adverse outcomes in HIV-negative patients with PJP. A retrospective analysis was conducted on 62 HIV-negative patients with presumed or confirmed PJP from 2006 to 2023. CRP measured within 48 hours of admission were used to classify patients into hypo-inflammatory (CRP<30 mg/l), normo-inflammatory (30-135 mg/l), and hyper-inflammatory (>135 mg/l) groups. Composite adverse outcomes (defined as all-cause in-hospital mortality or mechanical ventilation) were compared across groups using univariate and multivariable analyses. The inflammatory groups differed in CRP but not significantly in terms of white cell count, ferritin, or lactate dehydrogenase. Corticosteroid use was similar across groups. Adverse outcomes occurred in 37.5% of the hypo-inflammatory group, 20.0% of the normo-inflammatory group, and 68.8% of the hyper-inflammatory group (P = 0.005). Hyper-inflammation independently predicted adverse outcomes (adjusted OR 6.98, 95% CI 1.81-26.92, P = 0.005). This study raises the possibility of a U-shaped relationship between inflammatory phenotypes and outcomes in PJP, with hypo- and hyper-inflammatory phenotypes associated with worse outcomes.