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Background <p>Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by progressive synovial inflammation, joint destruction, and functional impairment. Growing evidence implicates inflammasome activation—particularly the adaptor protein PYCARD (Pyrin domain and the Caspase Activation and Recruitment Domain (CARD)—in driving cytokine maturation and amplifying inflammatory pathways central to RA pathogenesis. Our aim was to evaluate the diagnostic performance of PYCARD in patients with rheumatoid arthritis and to assess its association with disease activity and serological markers.</p> Methodology <p>A case-control study included forty participants, with 30 RA patients and 10 controls matched for age and sex. Data collection included medical history and a clinical examination. Disease activity was assessed using the Disease Activity Score-28 with CRP. Laboratory tests included CBC, CRP, Rheumatoid factor (RF), Anti-cyclic citrullinated peptide antibody (ACPA) and serum PYCARD.</p> Results <p>The mean age was 42.17 ± 11.67 years for the patients group and 38.6 ± 12.44 years for the controls group. Most patients exhibited moderate to high disease activity, with a mean DAS28-CRP score of 5.48 ± 1.13. Serum PYCARD levels were significantly higher in RA patients than in controls (<i>p</i> &lt; 0.001). Patients with high disease activity slowed markedly elevated PYCARD levels compared with those with moderate activity (<i>p</i> &lt; 0.001). PYCARD showed high positive correlations with ACPA (<i>p</i> &lt; 0.001) and the ACR–EULAR score (<i>r</i> = 0.694, <i>p</i> &lt; 0.001), and moderate positive correlations with CRP (<i>P</i> = 0.025), and RF (<i>P</i> = 0.036). ROC analysis identified a PYCARD cutoff point of &gt; 176.2 pg. for differentiating RA patients from controls.</p> Conclusions <p>Serum PYCARD, with a cutoff value of &gt; 176.2 pg/mL, may serve as a valuable biomarker for the diagnosis of RA. Larger multicenter studies are recommended to validate these findings.</p>

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Serum PYCARD level as an activity biomarker in rheumatoid arthritis patients

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月3日

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  • Ehsan Abdelgawad Sayed,
  • Nadia Hamed El Arousi,
  • Nayera Zaghloul Saber,
  • Ahmed Ibrahim Hammad

摘要

Background

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by progressive synovial inflammation, joint destruction, and functional impairment. Growing evidence implicates inflammasome activation—particularly the adaptor protein PYCARD (Pyrin domain and the Caspase Activation and Recruitment Domain (CARD)—in driving cytokine maturation and amplifying inflammatory pathways central to RA pathogenesis. Our aim was to evaluate the diagnostic performance of PYCARD in patients with rheumatoid arthritis and to assess its association with disease activity and serological markers.

Methodology

A case-control study included forty participants, with 30 RA patients and 10 controls matched for age and sex. Data collection included medical history and a clinical examination. Disease activity was assessed using the Disease Activity Score-28 with CRP. Laboratory tests included CBC, CRP, Rheumatoid factor (RF), Anti-cyclic citrullinated peptide antibody (ACPA) and serum PYCARD.

Results

The mean age was 42.17 ± 11.67 years for the patients group and 38.6 ± 12.44 years for the controls group. Most patients exhibited moderate to high disease activity, with a mean DAS28-CRP score of 5.48 ± 1.13. Serum PYCARD levels were significantly higher in RA patients than in controls (p < 0.001). Patients with high disease activity slowed markedly elevated PYCARD levels compared with those with moderate activity (p < 0.001). PYCARD showed high positive correlations with ACPA (p < 0.001) and the ACR–EULAR score (r = 0.694, p < 0.001), and moderate positive correlations with CRP (P = 0.025), and RF (P = 0.036). ROC analysis identified a PYCARD cutoff point of > 176.2 pg. for differentiating RA patients from controls.

Conclusions

Serum PYCARD, with a cutoff value of > 176.2 pg/mL, may serve as a valuable biomarker for the diagnosis of RA. Larger multicenter studies are recommended to validate these findings.