ArticleBMC infectious diseases2012
HIV patients treated with low-dose prednisolone exhibit lower immune activation than untreated patients.
Article in BMC infectious diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.
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Who cites it
9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 17 citations in OpenAlex.
- Adjunct Therapy for CD4Frontiers in immunology · 2021Pooled it
- Platelet activation in adult HIV-infected patients on antiretroviral therapy: a systematic review and meta-analysis.BMC medicine · 2020Pooled it
- Pneumocystis jirovecii Pneumonia and HIV-Associated Nephropathy in Acute HIV Infection.Cureus · 2024Article
- Relevance of biomarkers indicating gut damage and microbial translocation in people living with HIV.Frontiers in immunology · 2023Review
- HIV-Related Immune Activation and Inflammation: Current Understanding and Strategies.Journal of immunology research · 2021 · on this mapReview
- Inflammation, HIV, and Immune Quiescence: Leveraging on Immunomodulatory Products to Reduce HIV Susceptibility.AIDS research and treatment · 2020Review
- Rheumatoid arthritis in patients with HIV: management challenges.Open access rheumatology : research and reviews · 2016Review
- Article
- Dimethyl fumarate modulation of immune and antioxidant responses: application to HIV therapy.Critical reviews in immunology · 2013Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHIV-associated general immune activation is a strong predictor for HIV disease progression, suggesting that chronic immune activation may drive HIV pathogenesis. Consequently, immunomodulating agents may decelerate HIV disease progression.
methodsIn an observational study, we determined immune activation in HIV patients receiving low-dose (5 mg/day) prednisolone with or without highly-active antiretroviral therapy (HAART) compared to patients without prednisolone treatment. Lymphocyte activation was determined by flow cytometry detecting expression of CD38 on CD8(+) T cells. The monocyte activation markers sCD14 and LPS binding protein (LBP) as well as inflammation markers soluble urokinase plasminogen activated receptor (suPAR) and sCD40L were determined from plasma by ELISA.
resultsCD38-expression on CD8+ T lymphocytes was significantly lower in prednisolone-treated patients compared to untreated patients (median 55.40% [percentile range 48.76-67.70] versus 73.34% [65.21-78.92], p = 0.0011, Mann-Whitney test). Similarly, we detected lower levels of sCD14 (3.6 μg/ml [2.78-5.12] vs. 6.11 μg/ml [4.58-7.70]; p = 0.0048), LBP (2.18 ng/ml [1.59-2.87] vs. 3.45 ng/ml [1.84-5.03]; p = 0.0386), suPAR antigen (2.17 μg/ml [1.65-2.81] vs. 2.56 μg/ml [2.24-4.26]; p = 0.0351) and a trend towards lower levels of sCD40L (2.70 pg/ml [1.90-4.00] vs. 3.60 pg/ml [2.95-5.30]; p = 0.0782). Viral load in both groups was similar (0.8 × 105 ng/ml [0.2-42.4 × 105] vs. 1.1 × 105 [0.5-12.2 × 105]; p = 0.3806). No effects attributable to prednisolone were observed when patients receiving HAART in combination with prednisolone were compared to patients who received HAART alone.
conclusionsPatients treated with low-dose prednisolone display significantly lower general immune activation than untreated patients. Further longitudinal studies are required to assess whether treatment with low-dose prednisolone translates into differences in HIV disease progression.
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