Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Meta-Analysis
. 2024 May 26;25(11):5793.
doi: 10.3390/ijms25115793.

The Association between Genetics and Response to Treatment with Biologics in Patients with Psoriasis, Psoriatic Arthritis, Rheumatoid Arthritis, and Inflammatory Bowel Diseases: A Systematic Review and Meta-Analysis

Affiliations
Meta-Analysis

The Association between Genetics and Response to Treatment with Biologics in Patients with Psoriasis, Psoriatic Arthritis, Rheumatoid Arthritis, and Inflammatory Bowel Diseases: A Systematic Review and Meta-Analysis

Rownaq Fares Al-Sofi et al. Int J Mol Sci. .

Abstract

Genetic biomarkers could potentially lower the risk of treatment failure in chronic inflammatory diseases (CID) like psoriasis, psoriatic arthritis (PsA), rheumatoid arthritis (RA), and inflammatory bowel disease (IBD). We performed a systematic review and meta-analysis assessing the association between single nucleotide polymorphisms (SNPs) and response to biologics. Odds ratio (OR) with 95% confidence interval (CI) meta-analyses were performed. In total, 185 studies examining 62,774 individuals were included. For the diseases combined, the minor allele of MYD88 (rs7744) was associated with good response to TNFi (OR: 1.24 [1.02-1.51], 6 studies, 3158 patients with psoriasis or RA) and the minor alleles of NLRP3 (rs4612666) (OR: 0.71 [0.58-0.87], 5 studies, 3819 patients with RA or IBD), TNF-308 (rs1800629) (OR: 0.71 [0.55-0.92], 25 studies, 4341 patients with psoriasis, RA, or IBD), FCGR3A (rs396991) (OR: 0.77 [0.65-0.93], 18 studies, 2562 patients with psoriasis, PsA, RA, or IBD), and TNF-238 (rs361525) (OR: 0.57 [0.34-0.96]), 7 studies, 818 patients with psoriasis, RA, or IBD) were associated with poor response to TNFi together or infliximab alone. Genetic variants in TNFα, NLRP3, MYD88, and FcRγ genes are associated with response to TNFi across several inflammatory diseases. Most other genetic variants associated with response were observed in a few studies, and further validation is needed.

Keywords: Crohns; biomarkers; inflammatory bowel diseases; pharmacogenetics; psoriasis; psoriatic arthritis; rheumatoid arthritits; ulcerative colitis.

PubMed Disclaimer

Conflict of interest statement

N.L. has been an honorary speaker for Eli Lilly, Janssen Cilag, and Sandoz. L.S. has received research funding from Novartis, Bristol-Myers Squibb, AbbVie, Janssen Pharmaceuticals, the Danish National Psoriasis Foundation, the LEO Foundation, and the Kgl Hofbundtmager Aage Bang Foundation, and honoraria as consultant and/or speaker for AbbVie, Eli Lilly, Novartis, Pfizer, and LEO Pharma, Janssen Cilag, UCB, Almirall, Bristol-Myers Squibb, and Sanofi. She has served as an investigator for AbbVie, Pfizer, Sanofi, Janssen Cilag, Boehringer Ingelheim, AstraZeneca, Eli Lilly, Novartis, Regeneron, Galderma, and LEO Pharma. VA has served as an advisory board member for MSD (Merck).

Figures

Figure 1
Figure 1
Prisma flowchart.
Figure 2
Figure 2
Genetic variants significantly associated with response to biologics among patients with psoriasis in the meta-analysis.
Figure 3
Figure 3
Genetic variants significantly associated with response to biologics among patients with rheumatoid arthritis in the meta-analysis.
Figure 4
Figure 4
Genetic variants significantly associated with response to biologics among patients with inflammatory bowel diseases in the meta-analysis.
Figure 5
Figure 5
Genetic variants significantly associated with response to biologics among patients across all indications in the meta-analysis.

References

    1. Parisi R., Symmons D.P.M., Griffiths C.E., Ashcroft D.M., on behalf of the Identification and Management of Psoriasis and Associated ComorbidiTy (IMPACT) Project Team Global Epidemiology of Psoriasis: A Systematic Review of Incidence and Prevalence. J. Investig. Dermatol. 2013;133:377–385. doi: 10.1038/jid.2012.339. - DOI - PubMed
    1. Scotti L., Franchi M., Marchesoni A., Corrao G. Prevalence and incidence of psoriatic arthritis: A systematic review and meta-analysis. Semin. Arthritis Rheum. 2018;48:28–34. doi: 10.1016/j.semarthrit.2018.01.003. - DOI - PubMed
    1. Lees C.W., Barrett J.C., Parkes M., Satsangi J. New IBD genetics: Common pathways with other diseases. Gut. 2011;60:1739–1753. doi: 10.1136/gut.2009.199679. - DOI - PubMed
    1. Li Y., Begovich A.B. Unraveling the genetics of complex diseases: Susceptibility genes for rheumatoid arthritis and psoriasis. Semin. Immunol. 2009;21:318–327. doi: 10.1016/j.smim.2009.04.002. - DOI - PubMed
    1. Rendon A., Schäkel K. Psoriasis Pathogenesis and Treatment. Int. J. Mol. Sci. 2019;20:1475. doi: 10.3390/ijms20061475. - DOI - PMC - PubMed

MeSH terms

Substances