ArticlePathogens and disease2025
Inflammatory phenotypes and clinical outcomes amongst patients with presumed and confirmed Pneumocystis jirovecii pneumonia without underlying human immunodeficiency virus infection.
Article in Pathogens and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Non-HIV Pneumocystis jirovecii pneumonia-associated immune reconstitution inflammatory syndrome: a case report and systematic review.BMC infectious diseases · 2026Pooled it
- Antiviral Resistance in Influenza: Clinical and Public Health Implications.Influenza and other respiratory viruses · 2026Review
- Pneumonia caused by co-infection with Mycobacterium tuberculosis and Pneumocystis jirovecii leading to acute respiratory distress syndrome in an HIV-negative immunocompromised patient: a case report and literature review.BMC infectious diseases · 2026Review
- Corticosteroids in bacterial severe community-acquired pneumonia: lessons from recent trials.Frontiers in medicine · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
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.
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