Abstract | BACKGROUND: METHODS: C4, C4A and C4B GCN were determined by real-time PCR in 427 SLE patients and 301 healthy controls, which underwent a detailed clinical evaluation according to a pre-established protocol. RESULTS: The risk of developing SLE was 2.62 times higher in subjects with low total C4 GCN (< 4 copies, OR = 2.62, CI = 1.77 to 3.87, p < 0.001) and 3.59 times higher in subjects with low C4A GCN (< 2 copies; OR = 3.59, CI = 2.15 to 5.99, p < 0.001) compared to those subjects with normal or high GCN of total C4 (≥4) and C4A (≥2), respectively. An increased risk was also observed regarding low C4B GCN, albeit to a lesser degree (OR = 1.46, CI = 1.03 to 2.08, p = 0.03). Furthermore, subjects with low C4A GCN had higher permanent disease damage as assessed by the Systemic Lupus International Collaborating Clinics - Damage Index (SLICC-DI; median = 1.5, 95% CI = 1.2-1.9) than patients with normal or high copy number of C4A (median = 1.0, 95% CI = 0.8-1.1; p = 0.004). There was a negative association between low C4A GCN and serositis (p = 0.02) as well as between low C4B GCN and arthritis (p = 0.02). CONCLUSIONS: This study confirms the association between low C4 GCN and SLE susceptibility, and originally demonstrates an association between low C4A GCN and disease severity.
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Authors | Kaline Medeiros Costa Pereira, Sandro Perazzio, Atila Granado A Faria, Eloisa Sa Moreira, Viviane C Santos, Marcelle Grecco, Neusa Pereira da Silva, Luis Eduardo Coelho Andrade |
Journal | Advances in rheumatology (London, England)
(Adv Rheumatol)
Vol. 59
Issue 1
Pg. 36
(08 06 2019)
ISSN: 2523-3106 [Electronic] England |
PMID | 31387635
(Publication Type: Journal Article, Observational Study, Research Support, Non-U.S. Gov't)
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Chemical References |
- Complement C4
- Complement C4a
- Complement C4b
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Topics |
- Adolescent
- Adult
- Aged
- Analysis of Variance
- Case-Control Studies
- Complement C4
(genetics)
- Complement C4a
(genetics)
- Complement C4b
(genetics)
- Cross-Sectional Studies
- Disease Progression
- Female
- Gene Dosage
- Genetic Predisposition to Disease
- Humans
- Male
- Middle Aged
- Phenotype
- Young Adult
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