Aug 2026· International Journal of Molecular Sciences· Vol 27, pp. 7221· 0 citations· 88 references
Medicine
TL;DR
Although inflammatory biomarkers provide a biologically grounded framework for assessing treatment response, their clinical implementation remains limited and further large-scale, standardized studies are required to validate candidate markers and support the development of integrated, multi-omics approaches for personalized management.
Abstract
Psoriasis vulgaris is a chronic immune-mediated inflammatory disease in which treatment response is assessed using clinical indices such as the Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index (DLQI), despite their limited ability to capture systemic inflammation and underlying immunological activity. This narrative review aims to summarize current evidence on inflammatory biomarkers for monitoring treatment response and to evaluate their potential clinical utility. A structured, non-systematic literature search was performed in April–May 2026 across PubMed, Cochrane Library, Scopus, and ClinicalTrials.gov, focusing primarily on literature published during the preceding 10 years, with selected earlier studies being retained when directly relevant. Emerging data indicate that multiple biomarker domains may reflect therapeutic outcomes, including cytokines and chemokines, acute-phase proteins, complete-blood-count (CBC)-derived inflammatory indices, genetic markers, micro(mi)RNAs, metabolomic and lipidomic profiles, and tissue-based markers. These biomarkers may serve as severity-associated, baseline-predictive, pharmacodynamic, or prognostic markers, and these roles should not be interpreted interchangeably. Nevertheless, discrepancies between biomarker dynamics and clinical improvement occur, reflecting the partial dissociation between local and systemic inflammation, disease heterogeneity, and differences in response kinetics. Although inflammatory biomarkers provide a biologically grounded framework for assessing treatment response, their clinical implementation remains limited. Further large-scale, standardized studies are required to validate candidate markers and support the development of integrated, multi-omics approaches for personalized management.
It is concluded that precision medicine in RA will require integrated biomarker panels combining clinical, pharmacological, molecular, and synovial tissue data, and the development of scalable, externally validated, and clinically interpretable models capable of assigning synovial endotypes and supporting mechanism-based therapeutic selection.
N. A. Batashkov, E. Gerasimova, D. Gerasimova et al.· Frontiers in Immunology· 0 citations
Background: Psoriasis is a chronic inflammatory skin disorder affecting approximately 2-4% of the global population, characterized by immune dysregulation and keratinocyte hyperproliferation. Although multiple investigations have identified potential biomarkers, no validated panel exists for assessing disease severity. Objectives of the study were to determine levels of serum uric acid (SUA), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), CRP/albumin ratio (CAR), neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR) in psoriasis patients versus controls, and assess their correlation with disease severity using psoriasis area severity index (PASI).
Methods: This case-control study included 50 psoriasis patients and 50 age- and sex-matched controls. Participants underwent complete blood count, CRP, ESR, serum albumin, and SUA measurements. Disease severity was categorized as mild (PASI <7), moderate (PASI 7-15), or severe (PASI >15).
Results: ESR was significantly elevated in cases versus controls (33.24±22.75 versus 19.44±11.50 mm/hour, p<0.001). CAR distribution differed significantly (p<0.001), with 56% of cases having CAR ≤0.1 mg/l versus 2% of controls. SUA showed no overall difference between groups (p=0.468) but significantly correlated with disease severity (p=0.028), increasing from mild (4.76±0.97 mg/dl) to moderate (5.47±1.50 mg/dl) to severe disease (5.77±1.01 mg/dl). CRP, albumin, NLR, and PLR showed no significant differences.
Conclusions: ESR and CAR significantly differentiate psoriasis patients from controls. SUA, while not discriminating between cases and controls, correlates with disease severity. These cost-effective biomarkers can complement clinical assessment in psoriasis management.
Akhila Pandigunta, H. Yadalla· International Journal of Res...· 0 citations
Psoriasis is a chronic, immune-mediated inflammatory skin disease affecting
approximately 2–3% of the global population and is associated with significant
physical, psychological, and socioeconomic burden. Moderate-to-severe psoriasis is
characterized by extensive skin involvement, recurrent disease activity, impaired
quality of life, and increased risk of multiple systemic comorbidities, including
psoriatic arthritis, cardiovascular disease, metabolic syndrome, obesity, diabetes
mellitus, and depression. Advances in the understanding of psoriasis
immunopathogenesis have transformed therapeutic strategies through the development
of biologic agents targeting specific inflammatory cytokines involved in disease
progression. Tumor necrosis factor-alpha (TNF-α), interleukin-12/23 (IL-12/23),
interleukin-17 (IL-17), and interleukin-23 (IL-23) inhibitors have demonstrated
remarkable efficacy in achieving sustained skin clearance, improving patient-reported
outcomes, and reducing systemic inflammation. More recently, precision medicine,
molecular biomarkers, pharmacogenomics, and artificial intelligence have emerged as
promising tools for optimizing biologic selection, predicting treatment response, and
individualizing long-term disease management. This review summarizes the current evidence regarding biologic therapy for moderate-to-severe psoriasis, highlighting
mechanisms of action, clinical efficacy, safety, emerging biologic agents, and future
perspectives in personalized dermatologic care.
Highlights Why Was the Study Undertaken? Treatment response in psoriasis remains variable despite multiple systemic therapies, and patients often require sequential switching. This systematic review and meta-analysis was undertaken to evaluate whether circulating blood-derived biomarkers can predict response to systemic psoriasis treatments and support more personalized treatment selection. What Does This Study Add? The study identifies recurrent exploratory signals for downstream IL-23/Th17 path-way biomarkers, particularly BD-2, IL-17A, and IL-17F, while upstream IL-23 showed only a non-significant trend. BD-2 showed the largest pooled statistical signal, but these findings remain hypothesis-generating rather than validated predictors. What Are the Implications of This Study for Disease Understanding and/or Clinical Care? The findings are compatible with the hypothesis that amplified downstream pathway activity may better reflect treatment-responsive inflammation than isolated upstream cytokines. However, this interpretation remains exploratory, and no soluble circulating biomarker is currently sufficiently validated for routine treatment selection; prospective multicenter studies using standardized assays and biomarker panels are needed before clinical implementation. Abstract Background/Objectives: Psoriasis is a chronic immune-mediated inflammatory disease primarily driven by the interleukin (IL)-23/T helper 17 (Th17) pathway. Despite multiple systemic therapies, treatment response varies considerably, and many patients require sequential switching. We aimed to evaluate circulating blood-derived biomarkers associated with response to systemic psoriasis therapies. Methods: MEDLINE and Web of Science were searched on 8 August 2025, following PRISMA guidance. The protocol was registered in PROSPERO (CRD420251129182). Eligible studies were original English- or Spanish-language studies published within the previous 10 years that evaluated circulating blood-derived biomarkers associated with cutaneous response to approved systemic psoriasis therapies in patients with psoriasis, with or without psoriatic arthritis. Genetic predictors, therapeutic drug monitoring studies, reviews, editorials, letters, conference abstracts, case reports, and non-original publications were excluded. Risk of bias was assessed using QUIPS and PROBAST. Quantitative synthesis included standardized mean difference meta-analysis and exploratory pooled p-value analysis. Results: Twenty-six studies were included. Most evaluated biologic therapies targeting TNF, IL-17, or IL-23; fewer assessed apremilast or methotrexate. Response definitions and follow-up varied across studies. Most studies showed moderate to high risk of bias, mainly due to small sample sizes, exploratory or post hoc analyses, heterogeneous treatment groups, limited confounding adjustment, multiple testing, and lack of external validation. Random-effects meta-analysis of baseline cytokines from two studies, including 71 patients per biomarker, showed no statistically significant differences between responders and non-responders for IL-17A, TNF-α, IL-6, IL-12, or IL-23. Exploratory pooled p-value analyses showed recurrent signals for downstream IL-23/Th17 biomarkers, particularly β-defensin-2 (BD-2; z = 4.63, p < 0.001), IL-17A (z = 3.27, p = 0.001), and IL-17F (z = 2.92, p = 0.003). Conclusions: Downstream IL-23/Th17 biomarkers, particularly BD-2 and IL-17 isoforms, showed recurrent exploratory associations with systemic treatment response. However, these findings should not be interpreted as evidence of superior predictive performance over upstream biomarkers, and no soluble circulating biomarker is currently ready for routine treatment selection.
J. M. Villa-Gonzalez, I. Arevalo-Ortega, M. González‐Hermosa et al.· Journal of Clinical Medicine· 0 citations
Emerging biomarkers are fundamental for the transition to precision medicine in IBD, aiming to enhance pathogenesis understanding, personalize therapies, and improve patient quality of life, establishing pathways for more effective, individualized management approaches.
Matheus Querino da Silva, João Daniel de Souza Menezes, José Luis Esteves Francisco et al.· PLoS ONE· 0 citations
Psoriasis is a chronic, autoimmune skin disease driven by persistent inflammation and immune dysfunction that severely impairs quality of life and is associated with serious comorbidities, including psoriatic arthritis, cardiovascular diseases (CVDs), and depression. Emerging epidemiological evidence suggests an association between psoriasis and an increased risk of certain malignancies, such as breast cancer (BC) and non-Hodgkin’s lymphoma (NHL), although the strength and consistency of these associations vary across study designs, and the underlying thrombo-inflammatory mechanisms remain incompletely understood. Several therapeutic approaches, including topical therapies, conventional systemic drugs (e.g., methotrexate and cyclosporine), and biological agents have been investigated for their potential associations with malignancy risk. However, the available evidence is heterogeneous and influenced by disease severity, treatment duration, cumulative exposure, and patient-related confounding factors. While some epidemiological studies have reported associations between conventional therapies and selected skin or hematological malignancies, combined or sequential treatment regimens further complicate the interpretation of treatment-related cancer risk. Similarly, Janus kinase (JAK) inhibitors have been associated with higher reported rates of lymphoma and non-melanoma skin cancer than tumor necrosis factor α inhibitors (TNFi-α) in some observational studies. Recent studies also highlight the clinical utility of inflammatory markers, specifically the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte (PLR) ratio, and systemic immune-inflammation index (SII), for monitoring systemic inflammation and treatment response, while certain therapies may additionally influence CVD risk. Despite these advances, substantial heterogeneity across observational studies, meta-analyses, and Mendelian randomization analyses preclude definitive conclusions regarding causality. Overall, this review synthesizes the current epidemiological and mechanistic evidence linking psoriasis, chronic inflammation, therapeutic interventions, cancer risk, and cardiovascular comorbidities, while highlighting the need for large prospective studies and standardized analytical approaches.
Aikaterini Lymperi, Evgenia Lamprianidou, Theodora Adamantidi et al.· International Journal of Mol...· 0 citations
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