This study provides valuable insights into the role of glucocorticoid receptor (GR) expression in psoriasis and its subtypes.

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Purpose:
Psoriasis is a common, chronic epidermal hyperplastic and inflammatory skin disease. Studies have shown that the reduction of skin-derived glucocorticoids (GC) may be one of the pathogenic factors of psoriasis. However, the clinical significance of the glucocorticoid receptor (GR) in patients with psoriasis remains unclear. This study aims to investigate the immunohistochemical expression of GR in psoriatic lesional tissues and its quantitative correlation with psoriasis severity, as well as to clarify the direction of this association (positive or negative).

Methods:
Skin tissue and corresponding patient information were collected from 15 patients with chronic eczema (CE), 15 patients with lichen planus (LP), 26 patients with psoriasis, and 15 healthy adults. The skin tissue was embedded in paraffin and sectioned, followed by immunohistochemical staining using a GR antibody. The clinicopathological data were then correlated with the staining results. Disease severity was assessed using the Psoriasis Area and Severity Index (PASI), body surface area (BSA), Investigator’s Global Assessment (IGA), and Dermatology Life Quality Index (DLQI) scoring systems.

Results:
We compared GR levels in skin tissues among healthy adults and patients with psoriasis, CE, and LP. Compared with normal skin tissues, GR levels were reduced in lesional skin of both CE and LP, with an even more pronounced decrease observed in psoriasis tissues (p < 0.01). Among the three psoriasis subtypes (ordinary psoriasis [psoriasis], pustular psoriasis [PP], and psoriatic arthritis [PA]), GR expression was the highest in the lesional skin of PA patients, exceeding that found in psoriasis patients, while expression was lower in PP lesions (p < 0.01). Strong positive correlation was found between PASI and BSA (r = 0.8). In comorbidity analysis, psoriasis with obesity (PO) showed increased GR levels (p < 0.01), whereas psoriasis associated with hyperuricemia (PH) did not, confirming GR as a reliable diagnostic marker for psoriasis despite comorbidities.

Conclusion:
GR level shows promise as an immunohistochemical biomarker for identifying psoriasis and assessing its severity. While comorbidities like obesity may affect its utility as a diagnostic marker, in the case of hyperuricemia, GR levels remain a reliable indicator.

Blood based systemic inflammatory biomarkers are an easily accessible and cost effective tool for identifying psoriasis and partially mediating the association between psoriasis and depression.

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Background:
Psoriasis is a chronic relapsing systemic inflammatory disease with a high prevalence of psychiatric comorbidities, especially depression. However, the precise role of inflammation in the relationship between psoriasis and depression remains unclear.

Method:
We explored the association among psoriasis, systemic inflammatory biomarkers, and depression in a large, ethnically diverse sample from the 2009–2014 National Health and Nutrition Examination Survey (NHANES) data. Psoriasis was estimated by the questionnaire. Depression was evaluated using the 9-item Patient Health Questionnaire (PHQ-9). Systemic inflammation response index (SIRI) and neutrophil-to-lymphocyte ratio (NLR) were determined using the examination data. Meanwhile, multivariable logistic and linear regression analyses explored the relationship between psoriasis, systemic inflammatory markers, and depression. On the basis of restricted cubic spline (RCS) regression, we further explored the potential linear relationship between systemic inflammatory biomarkers and depression. Finally, a mediation model was established to explain the intermediary role of systemic inflammatory biomarkers in this relationship.

Result:
Among the 12,734 participants in this study, 1172 participants had a depression score ≥ 10. After full adjustment, psoriasis was positively associated with depression and systemic inflammatory markers (for depression, OR [95% CI]: 2.000 [1.500, 2.668]; for LnSIRI, β [95% CI]: 0.091 [0.033, 0.150]; for LnNLR, β [95% CI]: 0.053 [0.006, 0.099]). Meanwhile, systemic inflammatory marker levels were linearly associated with depression (LnSIRI: Pnon-linear = 0.696; LnNLR: Pnon-linear = 0.921). Further mediation analysis indicated that SIRI and NLR mediated a marginal portion of the potential effects of psoriasis on depression, with proportions of 1.64% and 2.00%, respectively.

Conclusion:
Psoriasis is a risk factor for depression. Blood-based systemic inflammatory biomarkers are an easily accessible and cost-effective tool for identifying psoriasis and partially mediating the association between psoriasis and depression. It may provide important insights into guiding anti-inflammatory treatment strategies to prevent depression.

Icotyde (icotrokinra) 200 mg is a pill that selectively blocks the IL-23 receptor and is indicated for the treatment of moderate to severe plaque psoriasis in adults and paediatric patients 12 years of age and older who weigh at least 40 kg.

Dosage: 200 mg orally once daily on an empty stomach with water upon waking.

• Wait at least 30 minutes after taking before eating food.
• For patients who have difficulty swallowing tablets, Icotyde can be dispersed in water.

Tell your doctor if you have or ever had:

• have an infection that does not go away or that keeps coming back;
  
• have tuberculosis (TB) or have been in close contact with someone with TB;
  
• have recently received or are scheduled to receive an immunisation (vaccine). Avoid receiving live vaccines during treatment;
  
• have kidney problems;
  
• are pregnant or plan to become pregnant;
  
• are breastfeeding or plan to breastfeed;
  

• Prescription medicines
  
• Over-the-counter medicines
  
• Vitamins
  
• Herbal supplements
  

• Fever, sweat, or chills
  
• Muscle aches, weight loss or a cough
  
• Warm, red, or painful skin or sores on your body different from your psoriasis
  
• Diarrhoea or stomach pain
  
• Shortness of breath
  
• Blood in your mucus or phlegm 
  
• burning when you urinate or urinating more often than normal
  

This retrospective, observational cohort study assessed longitudinal changes in serologic and virologic hepatitis B virus  (HBV) markers and evaluated the incidence of HBV reactivation in patients with moderate-to-severe plaque psoriasis undergoing long-term biologic therapy.

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Background:
Psoriasis vulgaris is a chronic immune-mediated inflammatory disease frequently requiring long-term biologic therapy. Although biologics targeting TNF-α and interleukin pathways have revolutionized disease management, they may disrupt antiviral immune surveillance and trigger hepatitis B virus (HBV) reactivation in individuals with prior HBV exposure. Data on the long-term safety of newer agents—particularly IL-17 and IL-23 inhibitors—in patients with prior HBV exposure remain limited.

Objectives:
To evaluate longitudinal changes in HBV serological and virological markers and determine the frequency of HBV reactivation among patients with psoriasis vulgaris receiving biologic therapies in routine clinical practice.

Methods:
This retrospective, single-center study included adult patients treated with biologics between December 2019 and January 2025. HBV serology (HBsAg, anti-HBs, and anti-HBc) and HBV-DNA were assessed at baseline and every 6 months, with 3-monthly monitoring for anti-HBc–positive patients from electronic hospital records.

Results:
A total of 345 biologic treatment episodes in 311 patients, corresponding to 534.3 patient-years of exposure, were analyzed. Biologic therapies included secukinumab (33%), risankizumab (24.6%), guselkumab (17.7%), ixekizumab (15.4%), adalimumab (4.1%), certolizumab pegol (2.9%), and ustekinumab (1.7%). Anti-HBc positivity was identified in 42 treatment episodes (12.2%), of whom 93% received antiviral prophylaxis. Four HBV reactivation events (9.5%) were observed—two during ixekizumab, one during secukinumab, and one during risankizumab therapy—without progression to clinical hepatitis. The incidence of HBV reactivation among anti-HBc–positive patients was 5.42 per 100 patient-years.

Conclusions:
In this real-world cohort, HBV reactivation occurred in a clinically meaningful proportion of patients with prior HBV exposure (9.5%), presenting exclusively virologic or serologic reactivation without clinical hepatitis despite widespread antiviral prophylaxis. These findings underscore the need for individualized risk assessment and continuous virologic monitoring during biologic therapy and highlight the importance of further prospective studies to inform future clinical guidelines.

This study demonstrated that at the time of generalized pustular psoriasis (GPP) diagnosis, patients with GPP have a high burden of both psoriasis-related complications and non–psoriasis-related comorbidities.

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Generalized pustular psoriasis (GPP) is a rare, chronic, inflammatory skin disease characterised by widespread eruption of sterile, macroscopic pustules. Patients with GPP can present with multiple comorbidities that may influence treatment. This study aimed to assess the frequency of psoriasis-related complications and non–psoriasis-related comorbidities, and clinical laboratory findings, at the time of GPP diagnosis among patients with GPP.

This was a retrospective, longitudinal medical chart review of data from patients with a documented GPP diagnosis attending 29 GPP referral hospitals in Japan. Demographics and clinical characteristics were assessed at baseline (within 6 months prior to and 3 months after GPP diagnosis), including psoriasis-related complications, non–psoriasis-related comorbidities, and clinical laboratory findings.

Overall, 205 patients with GPP were included; 48.3% were female, and median age at initial diagnosis was 53 years. Similar proportions of patients had mild (36.1%), moderate (30.7%) and severe (33.2%) GPP at baseline, using Japanese Dermatological Association-GPP severity criteria. Most patients (69.8%) had psoriasis-related complications at baseline, with the most common being psoriasis vulgaris (42.9%) and psoriatic arthritis (26.8%). Non–psoriasis-related comorbidities were present in 69.3% of patients with GPP at baseline, with the most common being hypertension (28.3%), dyslipidaemia (16.6%) and diabetes mellitus (16.1%).

There was large variability in laboratory test values between patients. These results demonstrated that, at the time of GPP diagnosis, patients with GPP have multiple burdens of both psoriasis-related complications and non–psoriasis-related comorbidities.

Bimzelx better than Skyrizi in psoriatic arthritis first head to head study.

• Primary endpoint showing superiority met: Bimekizumab achieved statistically significant superiority over risankizumab in reducing disease activity, as measured by the stringent ACR50 endpoint, at Week 16 in adults living with active psoriatic arthritis 
  
  
• Landmark psoriatic arthritis (PsA) study: Bimekizumab is the first licensed biologic therapy to demonstrate superiority in psoriatic arthritis over an IL-23 inhibitor 
  
  
• Fourth bimekizumab study showing superiority: BE BOLD is the fourth head-to-head study demonstrating superiority in the bimekizumab clinical trial program across psoriatic disease, and the first conducted in PsA
  

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UCB today announced positive topline data from the BE BOLD trial assessing Bimzelx (bimekizumab) versus Skyrizi (risankizumab) in adults living with active psoriatic arthritis (PsA). Bimekizumab, the first and only approved medicine to selectively inhibit both interleukin 17A (IL-17A) and interleukin 17F (IL-17F), demonstrated statistically significant superiority in the ACR50 primary efficacy endpoint at Week 16. Treatment with bimekizumab was generally well tolerated, with no new safety signals observed to Week 16.

“Our landmark BE BOLD study provides the first head-to-head evidence of superiority versus an IL-23 inhibitor in psoriatic arthritis. These topline results reinforce bimekizumab’s potential to deliver clinically meaningful improvements using the stringent ACR50 measure of disease activity, indicating more complete control of joint inflammation,” said Emmanuel Caeymaex, Executive Vice President, Head of Patient Evidence, UCB. “BE BOLD represents the fourth head-to-head study demonstrating bimekizumab superiority, supporting physicians to make informed treatment decisions and advancing our ambitions to raise the standard of care for people living with psoriatic disease.”

The results of BE BOLD add to the breadth of data for bimekizumab across a range of immune-mediated inflammatory diseases.

This study provides a mechanistic foundation for luteolin-based interventions in psoriasis.

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Psoriasis, a chronic inflammatory skin disease, arises from a dysregulated interaction between keratinocytes (KCs) and dendritic cells (DCs).

We previously identified Rh family C glycoprotein (RHCG) as a key mediator of KC inflammation and DC activation. Here, we demonstrate that luteolin, a bioactive compound derived from the traditional Chinese formula cooling blood and detoxicating formula (CBDF), directly binds to RHCG, as confirmed by multiple computational methods and in vitro experiments.

In vitro, luteolin suppressed RHCG expression in KCs, reducing CXCL14 secretion and subsequent DC activation. Spatial transcriptomics (STs) revealed that luteolin preferentially targets DC–enriched spatial domains and restores desmosomal protein expression (e.g., DSC2), which is dysregulated in psoriasis. In vivo, luteolin ameliorated psoriasis-like inflammation in imiquimod-induced mice, lowering Psoriasis Area and Severity Index (PASI) scores and normalizing pathological markers.

Our findings indicate that luteolin disrupts KC–DC communication through multiple modes of action, thereby reversing tissue-level pathology and demonstrating its potential as a targeted therapy for psoriasis.

This study demonstrated that strenuous exercise is associated with enhanced cutaneous, systemic, and enthesis-related inflammatory changes in an imiquimod (IMQ) induced psoriasis mouse model.

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Background and Aim:
Psoriasis is a skin disorder complicated by arthritis and enthesitis. The cytokines interleukin (IL)-17, IL-23, and tumor necrosis factor (TNF)-α are reportedly key effectors of psoriasis. Additionally, gamma delta (γδ) T cells exacerbate inflammation by producing inflammatory cytokines such as IL-17 and TNF-α. However, details regarding the mechanisms linking pathogenesis and mechanical stress remain unclear. This study aimed to investigate the effect of strenuous exercise on the pathology of psoriasis using mouse models of imiquimod (IMQ)-induced psoriasis.

Methods:
Twenty mice were randomly assigned to four groups: IMQ − TRED− (control), IMQ − TRED+ (treadmill running mice), IMQ + TRED− group (IMQ treated mice), and IMQ + TRED+ group (IMQ treated and treadmill running mice). The tissue sections from back skin and thymus were immunostained with antibodies against IL-17, IL-23, and γδ T cells. Shoulder sections were stained using hematoxylin and eosin, and Toluidine Blue and Picrosirius Red. Additionally, the shoulder tissue sections were immunostained with antibodies against TNF-α and matrix metalloproteinase (MMP)-13. Serum cytokine level was measured to evaluate systemic inflammation.

Results:
Strenuous exercise exacerbated pathological changes associated with psoriasis, including increased γδ T cell infiltration and upregulated IL-17 and IL-23 expression in the skin, as well as enhanced γδ T cell development and IL-17 expression in the thymus. Although strenuous exercise did not further worsen the modified PASI scores, histological and immunological markers of inflammation were significantly enhanced. Serum levels of TNF-α and IL-17 were significantly elevated in IMQ-induced psoriasis model mice. Moreover, pathological changes induced by strenuous exercise were observed in the enthesis, including angiogenesis and upregulated expression of TNF-α and MMP-13.

Conclusion:
This study revealed that strenuous exercise exacerbates pathological changes in IMQ-induced psoriasis model mice.

This study found a non-linear positive relation between body roundness index (BRI) and Psoriasis (Pso)

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Background and Aims:
The prevalence of psoriasis (Pso), a chronic immune-mediated inflammatory skin disease, is high in patients with obesity. This study investigates the mediating role of the systemic immune-inflammation index (SII) in the association between body roundness index (BRI) and Pso prevalence.

Methods and Results:
This study included 14,669 participants from the National Health and Nutrition Examination Survey (NHANES) (2003–2006, 2009−2014). The presence or absence of obesity was identified using the BRI, and Pso was assessed using the Pso questionnaire. The association of BRI with Pso was explored by weighted multivariate logistic regression analyses and restricted cubic spline (RCS) analyses, and the threshold effect was further examined using two-stage linear regression models. Mediation analyses assessed SII’s role in the BRI-Pso association. The Pso group included 445 out of 14,669 participants. Logistic regression analyses indicated a positive association between BRI and Pso after adjusting for potential confounders. RCS analyses showed a nonlinear relation between BRI and Pso (Pnonlinear = 0.018), with a point of inflection at 5.103 (odds ratio [OR] = 1.09, 95% CI: 1.04, 1.14). BRI and Pso were positively correlated on the left side of the point of inflection (OR = 1.25, 95% CI: 1.09, 1.45), whereas such an association was not detected on the right side (OR = 1.04, 95% CI: 0.97, 1.11). Mediation analysis showed SII partially mediated this association, accounting for 9.48% of the effect (p < 0.001).

Conclusion:
BRI is positively associated with Pso, with SII playing a mediating role. These findings highlight the importance of visceral fat management and SII monitoring in addressing Pso and its metabolic comorbidities.

Ocadusertib is a potent and selective allosteric inhibitor of receptor-interacting serine/threonine-protein kinase 1 (RIPK1) that blocks inflammatory cell death downstream of death receptors. RIPK1 inhibitors have shown potential for the treatment of psoriasis but thus far, none have been approved.

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Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) inhibitors are being investigated for chronic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, and psoriasis.

Ocadusertib is a potent and selective allosteric inhibitor of RIPK1 and is currently being studied in clinical trials. Here, we present data on the development of ocadusertib, including preclinical studies and pharmacokinetic, safety, and target engagement results from phase 1 trials.

Preclinically, ocadusertib inhibited RIPK1 enzymatic activity with high potency (half-maximal inhibitory concentration [IC50] = 12–38 nM) and inhibited necroptotic responses in multiple cell-based assays. Ocadusertib was highly selective for RIPK1, showing no significant inhibition of more than 100 other kinases representative of the full kinome. In mouse studies, ocadusertib treatment prevented RIPK1-dependent hypothermia in response to tumor necrosis factor (TNF) challenge and significantly reduced disease severity in a model of chronic proliferative dermatitis.

In a first-in-human study of ocadusertib in healthy participants, single oral doses exhibited linear pharmacokinetics and dose-proportional exposure, with a time to maximum concentration of 1–4 h and a half-life of 13–15 h. Steady state was attained at 4–6 days after multiple once-daily dose administrations. Ocadusertib was well tolerated, with no deaths, serious adverse events, or significant treatment-emergent adverse events reported. In a phase 1, double-blind, randomized, multiple-dose study in healthy participants, greater than 90% RIPK1 target engagement was achieved at Day 14 with ocadusertib treatment.

Taken together, these findings support further assessment of ocadusertib for the treatment of chronic inflammatory diseases.

Balinatunfib is being developed as a potential new treatment for patients with psoriasis and other inflammatory diseases, it is the first oral medicine that selectively inhibits TNFR1 signalling to potentially stop or slow the disease-causing processes, while preserving signals initiated through TNFR2.

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Background:
Activation of tumour necrosis factor receptor 1 (TNFR1) promotes inflammation in several autoimmune diseases.

Objectives:
To evaluate safety, tolerability and clinical efficacy of balinatunfib versus placebo in patients with mild-to-moderate psoriasis.

Methods:
Phase-1, 4-week, randomized, double-blind, placebo-controlled pilot study, including patients aged 18–65 years with chronic plaque-type psoriasis with mild-to-moderate severity as defined by Psoriasis Area Severity Index (PASI ≤16) and ≥2 lesions with a Target Lesion Severity Score (TLSS) ≥4 at both screening and baseline. The primary endpoint was safety and tolerability of balinatunfib as assessed by the incidence of adverse events (AEs), treatment-emergent AEs (TEAEs) and AEs of special interest. Secondary endpoints were the percent change in TLSS from baseline to Weeks 2 and 4. Serum biomarkers, interleukin-22 (IL-22), IL-17F and percent change in PASI from baseline to Weeks 2 and 4, were also evaluated.

Results:
38 male patients (age [mean ± SD], 43 ± 10.6) were randomized to receive 200-mg balinatunfib (N = 26) or placebo (N = 12). No serious or severe TEAEs or adverse events of special interest were observed during the study. Dysgeusia (61.5% vs. 0%) and nausea (19.2% vs. 0%) were the most frequently reported TEAEs in the balinatunfib versus the placebo groups. Balinatunfib showed improvements from baseline in TLSS vs. placebo at Week 2 (17.06% vs. 6.29%, p = 0.032) and Week 4 (38.18% vs. 20.44%, p = 0.012). Exploratory analyses suggested an improvement in the total PASI scores at Week 2 (17.73% vs. 4.12%, nominal p = 0.005), Week 4 (35.09% vs. 15.71%, nominal p = 0.009) and decreased serum levels of IL-22 (nominal p = 0.0001) and IL-17F (nominal p = 0.0025) with balinatunfib treatment.

Conclusion:
Patients with mild-to-moderate psoriasis treated with balinatunfib reported no severe or serious TEAEs and showed promising clinical responses, suggesting that further evaluation of TNFR1 signal inhibition in inflammatory diseases is warranted.

These results suggest that the LIGHT/TNFSF14 axis may play a key role in regulating cytokine production by autoimmune cells and related pathways in psoriasis.

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Background:
The pathogenesis of psoriasis is associated with abnormalities in immune pathways. HVEM is known as a receptor of LIGHT (homologous to lymphotoxins, inducible, and competes with HSV glycoprotein D), which is a newly identified member of the TNF superfamily. The expression of HVEM and LTBR (another LIGHT receptor) has been found to be increased in the skin of psoriasis patients. This indicates the potential role of LIGHT and its receptors in the pathogenesis of psoriasis. Therefore, the objective of this study was to examine the effect of LIGHT on keratinocyte proliferation and its therapeutic potential in the treatment of psoriasis.

Methods:
We used immunohistochemistry to examine their expression in psoriasis-affected and normal tissue samples. We treated cells of the keratinocyte cell line HaCat with LIGHT protein, anti-HVEM and anti-LTβR antibodies, HVEM interference and LTβR interference RNA vectors, and NF-κB and JNK/AP-1 inhibitors at various concentrations and for various times, separately or simultaneously. The expression of NF-κB was examined by immunofluorescence staining, and the expression of inflammatory proteins was measured with ELISA. Further, the viability of HaCat cells was examined with a CCK-8 kit. In addition, flow cytometry was used to detect the expression of HVEM and LTBR on HaCat cells.

Results:
We found that LIGHT treatment of HaCat cells promoted the nuclear translocation of NF-κB. Further, the expression of p-c-Jun, IL-6, IL-8, PGI2, and PTGS2 was increased in response to LIGHT treatment, but the expression of these factors was decreased when the LIGHT receptors were blocked or NF-κB and JNK/AP-1 expression was inhibited. We also found that the viability of HaCat cells was consistent with the expression of pro-inflammatory factors.

Conclusions:
The present findings indicate that the JNK/AP-1-HVEM-LIGHT pathway played a role in the viability of human keratinocytes and the expression of IL-6, IL-8, PGI2, and PTGS2. Thus, the JNK/AP-1-HVEM-LIGHT pathway might be a potential target for the treatment of psoriasis.

This study identifies a novel role for G protein-coupled receptor 108 (GPR108) as a negative regulator of TLR7 signalling in psoriasis and may yield new therapeutic principles for managing psoriatic diseases.

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Objective:
Psoriasis, a common chronic inflammatory skin disease, is characterized by epidermal hyperplasia and inflammatory cell infiltration. While endosomal Toll-like receptors (TLRs), particularly TLR7, are key drivers of psoriatic exacerbations, the regulatory mechanisms governing TLR7 activity in psoriasis remain incompletely understood. This study aims to investigate the role of G protein-coupled receptor 108 (GPR108) in regulating TLR7 activity during imiquimod (IMQ)-induced psoriasiform dermatitis.

Methods:
We established IMQ-induced psoriasiform lesions in Gpr108-null mice, as well as IMQ-treated GPR108-deficient keratinocyte and macrophage models. The psoriasis-like phenotype was assessed in vivo using PASI scoring and H&E staining. Protein expression was examined by Western blotting, immunohistochemistry, and immunofluorescence. Additionally, RNA-seq and flow cytometric analyses were performed to verify the involvement of the TLR7/NF-κB signaling in regulating GPR108-deficient macrophage polarization.

Results:
We found that Gpr108 deficiency exacerbates IMQ-induced psoriatic lesions in mice. Mechanistically, GPR108 deficiency enhances TLR7/MyD88/NF-κB signaling in both keratinocytes and macrophages following imiquimod stimulation. This increased TLR7 activation promotes keratinocyte hyperproliferation and dysregulated differentiation, and alters the M1/M2 macrophage balance, leading to elevated production of cytokines, including TNF-α and IL-6.

Conclusion:
GPR108 functions as a negative regulator of TLR7 signaling in psoriasis.

This review aims to examine the alterations in neural innervation within psoriatic skin and delineate the functional contributions of sensory neuron-derived mediators—including ion channels, receptors, and neuropeptides—in modulating psoriasis-associated immune dysregulation.

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Psoriasis is a chronic inflammatory skin disease characterized by abnormal proliferation of epidermal cells induced by an overactive immune system. In addition to the interaction between immune cells and keratinocytes, emerging research highlights the indispensable role of peripheral sensory neurons in the initiation and progression of psoriatic inflammation.

Sensory neurons not only perceive various external stimuli but also participate in skin immune regulation and barrier repair through the release of neuropeptides and neurotransmitters.

This review systematically compiles current research advancements concerning the altered neural innervation patterns in psoriatic lesions, the pathophysiological functions of sensory neuron-specific receptors and ion channels, and the regulatory mechanisms of neuropeptides in disease pathogenesis.

By elucidating the precise contributions of sensory neurons to the development of psoriasis, this work seeks to further clarify their specific role in the disease and provide new insights for enhancing the understanding of its pathogenesis, thereby informing the development of more targeted therapeutic strategies.

In this cross-sectional analysis of a large, real-world Canadian cohort, G2-PASE demonstrated very strong correlation and excellent reliability compared with PASI.

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Background:
The Psoriasis Area and Severity Index (PASI), a composite measure of plaque psoriasis disease severity, is commonly used to determine treatment eligibility and response, but is time consuming for every-day clinical use. The Gulliver-Gestalt-Psoriasis Area Severity Estimate (G2-PASE) was developed to approximate PASI scores using Physician Global Assessment (PGA) and body surface area (BSA) measures.

Objectives:
To determine the reliability and validity of G2-PASE compared to PASI using data from a multi-center, Canadian cohort of patients with plaque psoriasis.

Methods:
Canadian patients with a history of moderate to severe plaque psoriasis enrolled in the first cohort of the Psoriasis Longitudinal Assessment and Registry (PSOLAR 1; a global, prospective, longitudinal, disease-based registry) were included. The G2-PASE for each patient was calculated by applying baseline PGA and BSA values available from PSOLAR patient data at enrollment. The correlation and reliability of G2-PASE compared to PASI for each patient at enrollment was then assessed. A similar analysis was conducted to test the reproducibility of results previously published by a participating PSOLAR clinical trial site.

Results:
Of the 1896 Canadian patients in PSOLAR 1, 1803 had PASI data and were included in this analysis. The average baseline PASI score was 5.52 (SD 6.44, range 0.00–64.30), and the mean calculated G2-PASE score was 8.37 (SD 7.51, range 0.00–45.00). The Pearson's correlation coefficient was 0.83 (p < 0.0001), indicating very strong and significant correlation between PASI and G2-PASE scores. The standardized Cronbach coefficient alpha was 0.91. Results from the Canadian PSOLAR cohort are similar to those of patients enrolled at the New Lab Clinical Research Inc. site and complement findings previously reported from this site.

Conclusions:
This study validates G2-PASE as a reliable measure of plaque psoriasis severity when compared to PASI among a large cohort of patients with predominantly moderate to severe disease.

A team of researchers from the Department of Medicine 3 – Rheumatology and Immunology at Uniklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), have now discovered which cells migrate from the skin of psoriasis patients to the joints and how they trigger inflammation there.

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Firstly: How inflammatory cells travel from the skin to the joints:
Psoriasis triggers the production of special precursor cells from the immune system in the inflamed skin. “These cells can migrate from the skin to the bloodstream and from there to the joints,” explains Dr. Simon Rauber, head of the working group at Department of Medicine 3. “It is interesting that the mere migration of immune cells into the joint is not sufficient to trigger inflammation there.”

Secondly: How inflammatory cells infiltrate the joint:
It is crucial to examine the processes that take place in the joint. Here, the migratory immune cells encounter connective tissue cells known as fibroblasts that are usually less than pleased to encounter these new arrivals. “The protective function of these connective tissue cells is usually considerably reduced in people who develop psoriatic arthritis,” says Prof. Dr. Andreas Ramming, team leader and deputy head of department at Department of Medicine 3. “As a result, the inflammatory cells that enter the joint cannot be brought into check, and go on to trigger an inflammatory reaction in the joint.” The results provide an explanation for why some psoriasis patients go on to develop joint disease as well.

Early detection and prevention before the disease affects the joints:
As the migratory immune cells can already be detected in the blood before triggering inflammation in the joints, this could act as an early warning signal in future, allowing patients at risk to be identified in time. In future, treatment strategies could be aimed specifically at intercepting these inflammatory cells and preventing them from triggering inflammation in the joints.

Apologies if this has been covered before but I wasn't able to find anything recent.

Following recent knee pain my Rheumy refereed me to an Orthopedic Surgeon. X-rays etc later it shows my left knee joint is totally messed up. I had a previous surgery on it in 2007 but now the PsA has done a number on the ACL tendon where it joins the bone, which is almost completely pulled loose and is ripping my meniscus. So I have a total knee replacement scheduled for a couple of weeks from now.

Does anyone have a real world experience that they can share? Especially on how the recovery period went.

This study explored the global prevalence of obesity, abdominal obesity, and being overweight in patients with psoriatic arthritis (PsA).

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Background:
Although the risk of psoriatic arthritis (PsA) and obesity comorbidities is increasing, only a few systematic global prevalence studies have been conducted.

Objective:
This study explored the global prevalence of obesity, abdominal obesity, and being overweight in patients with PsA.

Methods:
We examined eight databases from their inception to November 20, 2024. The R language was used for the data analysis. Meta-regression and subgroup analyses were used to evaluate the heterogeneity of the pooled studies. Funnel plots and Egger's tests were used to assess publication bias in the included studies, and the trim-and-fill method was used to correct for bias.

Results:
Twenty-seven studies were included. The overall prevalence of obesity in patients with PsA was 35% (95% CI, 0.30 to 0.40). The prevalence of obesity in adults with PsA was 35% (95% CI, 0.28 to 0.42), and it was 27% (95% CI, 0.11 to 0.46) in children and adolescents. Africa had the highest prevalence (57%; 95% CI, 0.43 to 0.69). In contrast, the prevalence was the lowest in Europe at 31% (95% CI, 0.25 to 0.38). In terms of countries, China had the highest prevalence (65%), followed by Egypt (57%) and Norway (55%). The lowest prevalence was observed in the United States (20%).

Conclusions:
These findings confirm the association between obesity and PsA. Considering the negative impact of obesity on PsA treatment, the early detection and management of obesity should be prioritized. Further population-based prospective observational studies are required to clarify the mechanisms underlying the coexistence of obesity in patients with PsA.

Curcumin solid lipid nanoparticles (CUR-SLN) represents a promising and safer topical therapeutic strategy for psoriasis.

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Psoriasis is a chronic inflammatory skin disorder in which existing topical and systemic therapies are often limited by adverse effects and poor patient compliance. This study aimed to develop a curcumin-loaded solid lipid nanoparticle CUR-SLN (curcumin solid lipid nanoparticles) loaded nanogel to enhance topical delivery and therapeutic efficacy.

CUR-SLNs were prepared using a solvent diffusion method and characterized for particle size, polydispersity index (PDI), zeta potential, entrapment efficiency, and morphology. The optimized nanoparticles (133.90 ± 2.45 nm; PDI 0.325 ± 0.21; entrapment efficiency 89.50% ± 4.52%) were incorporated into a Carbopol-based gel to formulate the CUR-SLN nanogel.

The nanogel was evaluated for appearance, viscosity, pH, and texture profile, along with in vitro drug release, ex vivo skin permeation, drug retention, and stability. Compared with a conventional curcumin gel, the CUR-SLN-loaded nanogel demonstrated sustained drug release over 48 h and significantly enhanced skin permeation and retention. In vivo studies in a psoriasis-induced mouse model showed a marked reduction in Psoriasis Area and Severity Index scores and significant downregulation of key pro-inflammatory cytokines (interferon-α [IFN-α], IL-23, interleukin-17 [IL-17], tumor necrosis factor-α [TNF-α]) (p < 0.001).

Histological evaluation further confirmed restoration of normal skin structure in treated animals. Overall, the CUR-SLN-loaded nanogel represents a promising and safer topical therapeutic strategy for psoriasis, supporting its potential for further clinical development.

This study was an observational, prospective, multicentre, real-world study in moderate-to severe plaque psoriasis patients treated with Siliq / Kyntheum (brodalumab) in Greece.

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Background:
Prospective, multicenter, real-world studies on brodalumab's effectiveness and safety in patients with moderate-to-severe psoriasis are lacking.

Objectives:
The RESOLVE study was an observational, prospective, multicenter, real-world study in moderate-to severe plaque psoriasis patients treated with brodalumab in Greece. The primary objective was to assess the proportion of patients achieving absolute Psoriasis Area and Severity Index (PASI) ≤ 3 after 12 weeks (W12) of treatment and, in those who continued brodalumab after W12, the percentage achieving static Physician's Global Assessment (sPGA) success (“clear/almost clear”) after 52 weeks (W52). Secondary objectives included patients' profile, Patient Reported Outcomes and adverse events' frequency/severity.

Methods:
Analyses were conducted using the as-observed data. Two imputation methods were applied for the missing data: “last observation carried forward” and “worst-case” scenario. Continuous variables were reported using summary statistics, whereas for categorical variables frequency tables were used.

Results:
One hundred and forty-five patients who initiated treatment with or switched to brodalumab were enrolled. Based on the “as-observed data,” 76.4% of patients achieved absolute PASI ≤ 3 at W12, 97.9% continued brodalumab after W12% and 96.1% achieved sPGA success [“clear” or “almost clear” skin (i.e. 0 or 1)] at W52. At W12 i) 78.5%, 68.1% and 53.5% achieved PASI75/90/100, respectively and ii) 71.5% and 54.2% of patients achieved sPGA0/1 and sPGA 0, respectively. The median time [(95% confidence interval (CI)] to achieve PASI ≤ 3 was 13.1 (13.0, 13.6) weeks. From baseline to W12 and W52 (i) mean DLQI scores decreased by 9.3 ± 6.0 and 12.6 ± 6.2, (ii) 52.6% and 81.9% of patients reported being “free of symptoms” and (iii) 57.4% and 82.7% of patients, responded being “extremely satisfied with treatment,” respectively.

Conclusions:
Brodalumab treatment demonstrated clinically relevant short- and long-term effectiveness in real-world patients with moderate-to-severe psoriasis and improvement in quality of life.