Lupus & antiphospholipid syndrome
Pathogenetic associations of anti-ribosomal P protein antibody titres and their subclasses in patients with systemic lupus erythematosus
Authors' conclusion
Anti-RibP was associated with clinical manifestations and parameters in SLE, and its index might be a useful indicator of disease severity. Anti-RibP IgG3 was the IgG subclass most strongly associated with the pathogenesis of SLE.
Study context
- Population
- Japanese patients admitted and treated in Niigata University Hospital for new-onset or flare-up of SLE
- Participants
- 80 patients
- Exposure
- Anti-RibP positive vs anti-RibP negative SLE patients
- Anti-RibPn = 30
- Outcome
- Association between anti-RibP titres and disease activity
- Follow-up
- Admission
Methodological detailssingle-centre
- Single-centre
Main finding
As reported in the abstract
- Anti-RibP presence associated with greater prevalence of skin rash and more severe inflammatory responses (higher inflammatory cytokines, hypocomplementemia, accelerated tryptophan metabolism), in younger patients
- Anti-RibP index correlated with age at diagnosis, clinical indicators, initial prednisolone dose, cytokines and tryptophan metabolite levels (univariate)
- Anti-RibP index independently associated with initial prednisolone dose and prevalence of skin rash (multivariate)
Observational data: associations, not effects.
Further findings
Anti-RibP IgG subclasses
- Anti-RibP IgGs mainly IgG2 and IgG3; anti-RibP IgG3 associated with hypocomplementemia, higher DAS, accelerated kynurenine pathway activity and higher proinflammatory cytokine production
- Coexistence of anti-dsDNA IgG and anti-RibP IgG2 or IgG3 accompanied higher IL-10 and IFN-α2 levels; anti-RibP IgG3 with anti-dsDNA contributed to higher initial prednisolone doses and accelerated kynurenine pathway activity
Original publication
Pathogenetic associations of anti-ribosomal P protein antibody titres and their subclasses in patients with systemic lupus erythematosus. Rheumatology (Oxford). Published 12 August 2023. doi:10. 1093/ rheumatology/ kead402
Composed by AI from the published abstract and checked against it. How Briefs are made →