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Adrenal (Excluding Mineralocorticoids)

SAT-475 - Androgen Levels and Rheumatoid Arthritis Activity: A Systematic Review of Clinical Outcomes and Inflammatory Markers

Saturday, June 13, 2026
9:30 AM - 4:30 PM CT


Introduction: Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease associated with joint destruction and functional disability. It is more prevalent in women, suggesting hormonal influence on its pathophysiology. Androgens such as testosterone and dehydroepiandrosterone sulfate (DHEAS) exert immunomodulatory and anti-inflammatory effects, including suppression of pro-inflammatory cytokines (TNF-α, IL-6) and modulation of T lymphocyte activity. Dysfunction of the hypothalamic–pituitary–adrenal (HPA) axis and relative hypoandrogenism have been implicated in persistent inflammation in RA.

Objective: To evaluate the association between circulating androgen levels and disease activity, inflammatory markers, and clinical severity in patients with rheumatoid arthritis.
Methodology: A systematic review was conducted according to PRISMA guidelines using PubMed, EMBASE, and Cochrane Library, identifying 350 studies. Primary studies involving adult RA patients assessing circulating androgen levels (testosterone, DHEA, DHEAS) and their association with disease activity (DAS28), inflammatory markers (CRP, ESR), or clinical outcomes were included. Study selection was performed by two independent reviewers using Rayyan QCRI. After duplicate removal and eligibility criteria, 16 studies were included. Risk of bias was assessed using the Newcastle–Ottawa Scale, showing overall moderate methodological quality.

Results: A consistent inverse association was observed between androgen levels and inflammatory activity in RA. Reduced levels of DHEAS and testosterone were associated with higher disease activity (DAS28 ranging from 3.43 to 5.5) and increased inflammatory markers (ESR up to 42.72 mm/h; CRP up to 31.74 mg/L). Hypoandrogenism was also associated with worse functional status (HAQ). Longitudinal data suggest that inflammatory control may be associated with partial recovery of androgen levels. Major confounding factors include glucocorticoid use, which suppresses the HPA axis, and DMARD therapy.

Conclusion: Reduced androgen levels, particularly DHEAS, are associated with higher inflammatory activity and worse functional status in rheumatoid arthritis. Hypoandrogenism may act as a biomarker of disease severity; however, this association is influenced by confounding factors, especially glucocorticoid and DMARD use. There is insufficient evidence to recommend hormone replacement as a therapeutic strategy. Longitudinal studies and clinical trials are needed to clarify this relationship.

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