Psoriasis, a chronic skin condition, characterized by scaly erythematous plaques, is prevalent in around 2% of the population. Around 25% of psoriasis patients have psoriatic arthritis (PsA), an inflammatory musculoskeletal disease that often leads to progressive joint damage and disability. Psoriatic diseases (PsD) encompassing psoriasis and PsA, are often associated with pathophysiologically related conditions like uveitis and inflammatory bowel disease as well as comorbidities such as cardiovascular disease. Due to the heterogeneous nature of PsD, diagnosis and treatment is a challenge. Biomarkers can objectively measure variables, such as disease state, disease progress, and treatment outcomes, thus offering the possibility for better management of disease. This review focuses on some of the biomarker research that was carried out in PsD in the past year.

Diverse biomarker types ranging from SNPs, mRNA, proteins, metabolites and immune cell profiles have been categorized as per the Biomarkers, EndpointS and other Tools (BEST) resource developed by the FDA/NIH. Some of the latest research has focused on multiomic assays and these along with advanced bioinformatic tools can help in better disease management.

Recent developments in PsA biomarker research show promise in identifying markers that can help in diagnosis, assess disease activity and predict treatment response. However, most studies are in the early discovery and verification state. Large-scale studies to replicate findings and develop and validate predictive algorithms are required.

Psoriasis is a chronic autoimmune skin disorder characterized by keratinocyte hyperproliferation, inflammation, and angiogenesis, significantly impacting patients' quality of life. Current therapeutic strategies, including topical corticosteroids, phototherapy, and systemic biologics, often present limitations such as adverse effects, high costs, and inadequate skin penetration. Transdermal drug delivery offers a promising alternative by enhancing localized drug bioavailability and minimizing systemic side effects. In this study, we investigated the antipsoriatic potential of pemetrexed disodium, a multitargeted antifolate agent, formulated as a transdermal patch in an imiquimod-induced psoriasis mouse model. The patches were prepared using a solvent evaporation technique and optimized for controlled drug release. Mice treated with pemetrexed-loaded transdermal patches exhibited significant dose-dependent reductions in psoriasis severity, as evidenced by improvements in Psoriasis Area and Severity Index (PASI) scores, histopathological analysis, and suppression of inflammatory cytokines (TNF-α, IL-6) assessed via qRT-PCR and ELISA. The highest concentration (0.16 mg/cm2) demonstrated the most pronounced therapeutic effects, comparable to the standard ketoconazole treatment. These findings highlight the potential of pemetrexed disodium-loaded transdermal patches as an innovative, targeted therapy for psoriasis, warranting further clinical investigations.

The Brazilian Unified Health System is an interesting model for international healthcare innovation analysis. Covering over 200 million people, this system stands out as one of the largest purchasers of healthcare technologies worldwide. Our goal in this study was to evaluate how targeted therapies reduce the duration of sick leave for psoriasis patients.

We conducted a retrospective cohort study within the Brazilian National Institute of Social Security. The primary outcome was the return to work (cessation of sick leave) of patients with psoriasis. Factors such as age, sex, and access to targeted therapies were evaluated using a Cox proportional hazards model.

Over the 25-year period from 1998 to 2023, 32,512 benefits were granted for psoriasis, totalling an expenditure of $577,478,002.15. Public access to psoriatic arthritis (PsA)-targeted therapies decreased the average minimum wage granted to psoriasis patients on sick leave by 22%, and public access to psoriasis-targeted therapies reduced the average wage by 7%. The availability of these therapies was associated with earlier cessation of sick leave in our proportional hazards model (targeted therapies for PsA: hazard ratio (HR) = 1.90, 95% confidence interval (CI) = 1.82-2.00; targeted therapies for psoriasis: HR = 1.63, 95% CI = 1.54-1.70).

This study highlights a remarkable reduction in costs and sick leave duration due to the implementation of therapies for psoriatic disease by the Brazilian Unified Health System, which underscores the importance of considering detailed indirect cost data when evaluating new health technologies for large populations.

In recent years, cancer immunotherapy has introduced novel treatments, such as monoclonal antibodies, which have facilitated targeted therapies against tumor cells. Programmed death-1 (PD-1) is an immune checkpoint expressed in T cells that regulates the immune system's activity to prevent over-activation and tissue damage caused by inflammation. However, PD-1 is also expressed in tumor cells and functions as an immune evasion mechanism, making it a therapeutic target to enhance the immune response and eliminate tumor cells. Consequently, immune checkpoint inhibitors (ICIs) have emerged as an option for certain tumor types. Nevertheless, blocking immune checkpoints can lead to immune-related adverse events (irAEs), such as psoriasis and cytokine release syndrome (CRS), as exemplified in the clinical case presented by Zhou et al involving a patient with advanced gastric cancer who received sintilimab, a monoclonal antibody targeting PD-1. Subsequently, the patient experienced exacerbation of psoriasis and CRS. The objective of this editorial article is to elucidate potential immunologic mechanisms that may contribute to the development of CRS and psoriasis in patients receiving ICIs. It is crucial to acknowledge that while ICIs offer superior safety and efficacy compared to conventional therapies, they can also manifest irAEs affecting the skin, gastrointestinal tract, or respiratory system. In severe cases, these irAEs can lead to life-threatening complications such as circulatory shock or multiorgan failure. Consequently, it is recommended that patients receiving ICIs undergo regular monitoring to identify and manage these adverse events effectively.

Wound healing represents a complex and evolutionarily conserved process across vertebrates, encompassing a series of life-rescuing events. The healing process runs in three main phases: inflammation, proliferation, and maturation/remodelling. While acute inflammation is indispensable for cleansing the wound, removing infection, and eliminating dead tissue characterised by the prevalence of neutrophils, the proliferation phase is characterised by transition into the inflammatory cell profile, shifting towards the prevalence of macrophages. The proliferation phase involves development of granulation tissue, comprising fibroblasts, activated myofibroblasts, and inflammatory and endothelial cells. Communication among these cellular components occurs through intercellular contacts, extracellular matrix secretion, as well as paracrine production of bioactive factors and proteolytic enzymes. The proliferation phase of healing is intricately regulated by inflammation, particularly interleukin-6. Prolonged inflammation results in dysregulations during the granulation tissue formation and may lead to the development of chronic wounds or hypertrophic/keloid scars. Notably, pathological processes such as autoimmune chronic inflammation, organ fibrosis, the tumour microenvironment, and impaired repair following viral infections notably share morphological and functional similarities with granulation tissue. Consequently, wound healing emerges as a prototype for understanding these diverse pathological processes. The prospect of gaining a comprehensive understanding of wound healing holds the potential to furnish fundamental insights into modulation of the intricate dialogue between cancer cells and non-cancer cells within the cancer ecosystem. This knowledge may pave the way for innovative approaches to cancer diagnostics, disease monitoring, and anticancer therapy.

It has been reported that the imbalance of gut microbiota is involved in the pathogenesis of psoriasis. We retrieved randomized placebo-controlled trials to evaluate the efficacy and safety of probiotic administration in the treatment of psoriasis.

The outcomes were changes in Psoriasis Area and Severity Index (PASI), Dermatology Life Quality Index (DLQI), and serum inflammatory indicators after treatment, and adverse events (AEs). Risk ratios (RRs) and mean differences (MDs) were calculated using random or fixed effects model.

Seven qualified studies were identified in our study. The pooled percentage of patients with ≥75% reduction from baseline in PASI was higher in the probiotic group than that in the placebo group (33.57% vs. 23.61%; RR 1.40, 95% CI 0.98-1.98, p = 0.06). Compared with the placebo group, the PASI (MD -3.09, 95% CI -5.04 to -0.74, p = 0.01) and CRP level (MD -2.36, 95% CI -2.77 to -1.95, p < 0.0001) were significantly reduced in the probiotic group. There was no significant difference in DLQI (MD -1.45, 95% CI -6.72 to 3.82, p = 0.59) and AEs (RR 0.68, 95% CI 0.37-1.25, p = 0.22) between the two groups.

Oral administration of probiotics can improve psoriasis; however, large randomized controlled trials are needed to support this conclusion.

PROSPERO, identifier CRD42024506286, https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42024506286.

To determine the global burden of psoriasis in young adults, i.e., those aged 15-49, from 1990 to 2019 and predict trends in this burden for 2020 to 2030.

Age-standardized disease burden indicators and their estimated annual percentage changes were assessed and used to compare the estimated burden between regions. In addition, generalized additive models were used to predict the burden in this population from 2020 to 2030.

From 1990 to 2019, the overall burden of psoriasis in young adults worldwide trended downward, as the age-standardized incidence rate and the age-standardized disability-adjusted life year rate decreased. From 1990 to 2019, there were gender differences in the burden of psoriasis between regions with different Socio-demographic index. Specifically, there was a smaller increase in the burden in young men than in young women in middle- and low-middle-Socio-demographic index areas. In 2019, Western Europe, Australasia, and Southern Latin America had the highest age-standardized incidence rate of psoriasis in young adults, whereas age-standardized disability-adjusted life year rates of psoriasis in young adults were highest in high-income North America. In 2019, the psoriasis burden in young adults was the highest in high-Socio-demographic index areas and the lowest in low-Socio-demographic index regions. We predict that from 2020 to 2030, the incidence rate and disability-adjusted life year rate of psoriasis in all age groups of young adults will continue to decline, but the burden in those aged 30-39 will increase.

From 1990 to 2019, the overall burden of psoriasis in each age group trended downward in this period. We predict that from 2020 to 2030, the burden of psoriasis in those aged 30-39 will increase.