Table 2.
Studies evaluating biomarkers predictive of treatment response in PsV.
| Reference | Outcome measure | Treatment | Biomarker | Outcome |
|---|---|---|---|---|
| Chicharro et al.19 | PASI | TNFi, anti-IL-12/IL-23, anti-IL-17 | miRNA in lesional and non-lesional psoriatic skin | Baseline expression of miRNA-146a in non-lesional skin and miRNA-135b in lesional skin were related to response to treatment |
| De Keyser et al.11 | PASI | UST | HLA-C*06 allele | No statistically significant difference in clinical response between HLA-C*06 positive and HLA-C*06 negative patients |
| Dand et al.8 | PASI90 | ADA, UST | HLA-C*06:02 allele | HLA-C*06:02-negative patients were significantly more likely to respond to ADA than UST |
| Ovejero-Benito et al.15 | PASI75 | ADA, IFX | Genetic polymorphisms | Association between polymorphisms in IVL, IL-12B, NFKBIA, ZNF816A and SLC9A8 genes and treatment response |
| Prieto-Perez et al.10 | PASI75 | TNFi | Genetic polymorphisms | Association between polymorphisms in PGLYR4, ZNF816A, CTNNA2, IL12B, MAP3K1 and HLA-C genes and treatment response |
| Ovejero-Benito et al.16 | PASI75 | ETN | Genetic polymorphisms | Association between polymorphisms in HLA-B/MICA, MAP3K1, PTTG1, ZNF816A genes and response to ETN |
| Lu et al.26 | PASI75 | ETN | Serum cytokines | Baseline IL-12 serum level was a significant factor affecting the clinical response to ETN |
| Masouri et al.9 | PASI | TNFi, UST | Genetic polymorphisms | Rs10484554, a genetic polymorphism in the HLA-C gene showed an association with a good response to TNFi agents but not to UST |
| Nishikawa et al.17 | PASI | ADA, IFX | Genetic polymorphisms (GWAS) | Reported on the 10 SNPs showing the strongest association with response to TNFi treatment |
| Tan et al.22 | PASI75 | TOF | CRP | Baseline CRP was not predictive of treatment response |
| Lima et al.27 | NA | NA | Serum chemokines (CXCL9, CXCL10 and CXCL16) | Levels of serum chemokines do not predict treatment response |
| Hoffman et al.29 | LOR, SSE | ADA, ETN | Anti-dsDNA concentration | Low baseline anti-dsDNA concentrations associated with better outcomes in ADA therapy |
| Kivelevitch et al.18 | PASI | ADA, UST | DEGs | 57 DEGs differentiated UST responders from non-responders |
| Lembo et al.21 | PASI | ADA, ETN, EFZ | MCP-1 levels in plasma and skin | MCP-1 levels not found as a predictor of disease response |
| Ryan et al.12 | PASI75 | ADA, ETN | HLA-C, KIR, VDR genotypes | None of the genotypes examined were predictive of treatment response |
| Strober et al.24 | PASI | ADA | CRP | Baseline CRP was not associated with change in PASI |
| Gedebjerg et al.20 | PASI | UST | mRNA expression in skin | IL-20, IL-21 and p40 mRNA expression in lesional psoriatic skin were upregulated in non-responders compared to responders |
| Jokai et al.30 | PASI | ADA, ETN, IFX | CLA | Responders showed (not significantly) lower initial CLA expression than relapsing patients |
| Shimauchi et al.28 | PASI75 | IFX, ADA, UST | Serum IL-22 & VEGF | Baseline levels of serum IL-22 and VEGF were not significantly different between responders and non-responders |
| Chiu et al.13 | PASI50 | ALC, EFZ, ETN, UST | HLA-B & HLA-C alleles | HLA-C*06 status did not affect PASI 50 response |
| Gulliver et al.14 | PASI75 | ALC | Genetic polymorphisms (GWAS) | HLA-C*06 did not predict response to alefacept |
| Kanelleas et al.25 | PASI75 | ETN | Inflammatory markers | No significant difference at baseline between responders and non-responders |
ADA, adalimumab; ALC, alefacept; CLA, cutaneous lymphocyte-associated antigen; CRP, C-reactive protein; DEG, differentially expressed gene; dsDNA, double stranded DNA; EFZ, efalizumab; ETN, etanercept; GWAS, genome-wide association study; HLA, human leucocyte antigen; IFX, infliximab; IL, interleukin; KIR, killer immunoglobulin receptor; LOR, loss of response; MCP, monocyte chemoattractant protein; miRNA, microRNA; mRNA, messenger RNA; NA, not available; PASI, psoriasis area and severity index; PsV, psoriasis vulgaris; SNP, single nucleotide polymorphism; SSE, serious side effect; TNFi, TNF inhibitors; TOF, tofacitinib; UST, ustekinumab; VDR, vitamin D receptor; VEGF, vascular endothelial growth factor.