Do any of you have/had any comorbidities ? I've added the most common to the poll above, if you have others please let me know.

Members and guests can vote in the poll above, and our members are welcome to post in this thread too if they wish.

More Psoriasis Club Polls

UCB today announced the start of BE BOLD, a head-to-head Phase 3b study, comparing Bimzelx (bimekizumab), an IL-17A and IL-17F inhibitor, with Skyrizi (risankizumab), an IL-23 inhibitor, in the treatment of adults with active psoriatic arthritis (PsA). BE BOLD is the first head-to-head study in PsA evaluating the superiority of an IL-17A and IL-17F inhibitor to an IL-23 inhibitor. 

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This is the first Phase 3b head-to-head study in psoriatic arthritis to utilize the primary endpoint of ACR50 at Week 16. This robust assessment is set to provide a meaningful comparison of bimekizumab vs. risankizumab on inflamed joints, one of the areas of most concern for many people living with psoriatic arthritis. We look forward to the results and the implications for future clinical practice.

In moderate to severe plaque psoriasis UCB has conducted three head-to-head Phase 3/3b studies with bimekizumab versus commonly used biologics, and results from these studies showed that bimekizumab was superior to secukinumab, ustekinumab and adalimumab,

BE BOLD represents the fourth head-to-head study in the bimekizumab clinical trial program, the first to be conducted in psoriatic arthritis, and the first versus an IL-23 inhibitor. This study underscores our confidence in the potential of bimekizumab for people living with psoriatic disease. We look forward to communicating the top-line results in 2026.

BE BOLD is a multicentre, randomized, double-blind, risankizumab controlled, parallel-group study designed to evaluate the efficacy and safety of bimekizumab in adult study participants (n=~550) with active psoriatic arthritis. The study population will include adults with active psoriatic arthritis who are biologic treatment naïve or who had previous exposure to one tumour necrosis factor-inhibitor (TNFi) with an inadequate or intolerant response. The primary endpoint will assess American College of Rheumatology 50 (ACR50, i.e., 50 percent or greater improvement in the signs and symptoms of psoriatic arthritis) at Week 16. Key ranked secondary endpoints include minimal disease activity at Week 16, and the composite endpoint, ACR50 and PASI100 (complete skin clearance) at Week 16.

Well a very brief summary of where I am at first. Started on Methotrexate worked well for a number of years until I was taken off it due to poor liver score which is now back to a 0-1. I then went on to Acitretin which nearly killed me! Severe reaction did something to my blood counts and I got called to come off it straight away and stay at home for 2 weeks so I didn't get so much as a cold. Then Apremilast and which didn't work and my consultant had me taking Apremilast with Skilarence. These didn't work either. Lastly for the past 2 years I have been on Cislosporine. 

Now I have to come off Ciclosporine as you can only be on it for 2 years.

Now, my consultant prescribed me Skilarence again and I declined as it didn't work and he said he had not prescribed it and he had no record of it! Great, not keeping proper medical records.

He tried again to get me to go on it but I have insisted on a referral but he has stated I cannot be referred to the biologicals team until I have a PASI. However, I am now not on any medication and I know that in the coming months my psoriasis will flare up again. His secretary stated NICE guidlines which I have read and none of them prevent hinm referring me, what the guidelines are is a PASI of 10 and a DLQI of 10 to be prescribed biologicals.

I will easily hit these when my current medication wears off and not looking forward to a flare up. I am tempted to push to get the referal as there is a wait after he refers me anyway, he can do it immediately and I am in the queue and my take is that I have a condition that will deteriorate and now I am in a position where they are doing nothing about it.

Interestingly I know its about cost and I asked to go back on methotrexate as my liver scores indicate there is no damage, the NICE guidelines he states suggest methotrexate as a first line of defence followed by other treatments.

Today I am at a loss as to escalate via PALs, ask for a second opinion or even go full nuclear and report incorrect records keeping and duty of care.

Any advice greatly appreciated any questions feel free to ask.

Thanks and sorry for the rambling rant.

I've had plaque psoriasis since 1983. In the past year, a rheumatoligist came to believe I have psoriatic arthritis, based on chronic  stiff joint symptoms and xrays showing mild joint space shrinkage. Blood tests to support this were all negative. She also suggested I try Rinvoq and provided a 30 day free trial. I've not taken this drug. Frankly, I'm not sure the pain is bad enough and the side effects for someone my age (over 65) are a bit alarming. I'm curious of what others may have experienced in combating my issues. The score I get on this website is 13 and the psoriasis plaquing bothers me much less than the joint pain.

It is a very long time since I have been here, I kind of lost track of it and searched a few times but didn't manage to find the site but today I have.

So whats new! I was on methotrexate and eventually got taken off it. I was given skilerance that didn't work but my consultant has no record of it so has prescribed it again. I need to get the pharmacy to write to him telling him that I have already tried it! I had acretin that nearly killed me. You know when you have a blood test and within hours your GP and consultant ring you and tell you to stop taking the drug immediately and to go to hospital the next day for tests, I think it was my neutrophils cells had plummeted so I had basically no immune system, something like that anyway. Then I went on cyclosporine which I have just been taken off.

Life is OK learned to cope with psoriasis a long time ago and it has generally been a lot more manageable apart form about 12 months after I was taken off methotrexate. I know I know its a bad drug but worked for me until my liver needed to recover a little.

If I don't end up on the skilerance I will be on biologicals.

Anyway I am glad I found you.

The Health Sciences Authority (HSA) Singapore are advising anyone using Touch Skin by Dermacare Skin Relief Treatment Cream to stop using it immediately.

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The Health Sciences Authority (HSA) is alerting members of the public not to purchase or use “Touch Skin by DermaCare Skin Relief Treatment Cream”. Tests revealed that the cream contained a potent steroid (betamethasone valerate) which should be used under medical supervision. A consumer in her 50s suffered severe skin reactions from the use of the cream.

The consumer had been using the cream for about 8 years for her sensitive facial skin and would experience flare-ups (a sudden worsening of symptoms) whenever she stopped applying the cream. In May 2024, she saw that HSA alerted the public to a similar product found to be adulterated with a steroid, she immediately stopped the use of the cream, two days after stopping use she developed red, sensitive and itchy skin on her face and consulted a doctor. The doctor found her skin to be severely inflamed, sensitive to sunlight, and thinned-out with telangiectasia (spider veins) and reported the adverse event to HSA.

Consumers should be alert to the dangers of purchasing skin creams from dubious, unfamiliar or online sources. From 2022 to July 2024, HSA had detected an increased number of creams marketed for skin conditions (e.g., rash, eczema and psoriasis) adulterated with steroids and other potent medicinal ingredients.

The majority of the creams were used in young children. As young children are more susceptible to the effects of adulterants such as steroids, they suffered serious adverse effects from the use of these creams. The creams were sold on websites, e-commerce platforms, social media platforms, and in one case, by a peddler in a makeshift stall.

Adulterated products are often manufactured under poor conditions with no quality control, and different batches of the same product may contain variable amounts of ingredients and/or different types of adulterants.

All sellers and suppliers must stop selling these products immediately. HSA will not hesitate to take stern enforcement actions against anyone who sells and supplies products found to be adulterated with steroids. Sellers and suppliers are liable to prosecution and if convicted, may be imprisoned for up to 3 years and/or fined up to $100,000.

This large-scale Korean cohort study of children provided evidence that higher BMI was linked to an increased risk of developing AA, AD, and psoriasis among children.

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Whether childhood obesity or weight gain leads to the development of pediatric immune-mediated skin diseases remains unclear. We aimed to determine the associations between body mass index or body mass index changes and the development of 3 main immune-mediated skin diseases—alopecia areata, atopic dermatitis (AD), and psoriasis—by analyzing a longitudinal cohort of 2,161,900 Korean children from 2009 to 2020.

The findings indicated that children who were obese had a higher risk of pediatric immune-mediated skin diseases than those with normal weight (P for trend < .01). An increase in body mass index was associated with a higher risk of AD, whereas a decrease in body mass index was correlated with a reduced risk of AD.

Children who gained weight, transitioning from normal to overweight, exhibited a higher AD risk than those who maintained a normal weight (adjusted hazard ratio = 1.15, 95% confidence interval = 1.11–1.20). However, those who shifted from being overweight to achieving a normal weight (adjusted hazard ratio = 0.87, 95% confidence interval = 0.81–0.94) had a lower AD risk than children who were overweight who maintained their weight.

In summary, early childhood obesity may increase the risk of pediatric immune-mediated skin diseases like psoriasis. Weight gain may increase AD risk, whereas weight loss may lower the risk.

Early results from an ongoing study have found there is a high level of psoriatic arthritis (PsA) amongst patients with psoriasis.

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Early results of an international study examining the risk of arthritis for people with psoriasis have shown a high burden of joint symptoms in 712 patients – 25% of the total studied so far.

The study led by researchers at the Universities of Oxford, University College Dublin and supported by The University of Manchester has recruited almost 3,000 patients so far.

The 25% figure results confirms existing knowledge that up to a third will go on to develop psoriatic arthritis (PsA), which causes joints and tendons to become inflamed and painful.

At the moment there is no way to predict which patients with psoriasis are likely to go on to develop joint problems but this research will help us to design ways to prevent people with psoriasis developing arthritis, by offering potential drug treatments or lifestyle interventions such as exercise or stress management.

We know that some patients with psoriasis will go on to develop psoriatic arthritis. If we could identify which patients are at higher risk for arthritis development, it could mean that in the future, those people could receive preventative treatment.

To date, we have baseline data on a total of 2,841 patients, of which 1761 are from Ireland and 1067 are from the UK.

GPs are not always skilled enough to spot the symptoms and they may manifest themselves in a myriad of different ways. Receiving a diagnosis is in many ways a relief, patients can then plan for the future knowing that they do indeed have an ongoing condition.

A cohort study with 474 055 participants looking at long-term exposure to air pollution association with the development of psoriasis.

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Importance: 
Psoriasis is a common autoinflammatory disease influenced by complex interactions between environmental and genetic factors. The influence of long-term air pollution exposure on psoriasis remains underexplored.

Objective: 
To examine the association between long-term exposure to air pollution and psoriasis and the interaction between air pollution and genetic susceptibility for incident psoriasis.

Design, Setting, and Participants: 
This prospective cohort study used data from the UK Biobank. The analysis sample included individuals who were psoriasis free at baseline and had available data on air pollution exposure. Genetic analyses were restricted to White participants. Data were analyzed between November 1 and December 10, 2023.

Exposures: 
Exposure to nitrogen dioxide (NO2), nitrogen oxides (NOx), fine particulate matter with a diameter less than 2.5 µm (PM2.5), and particulate matter with a diameter less than 10 µm (PM10) and genetic susceptibility for psoriasis.

Main Outcomes and Measures: 
To ascertain the association of long-term exposure to NO2, NOx, PM2.5, and PM10 with the risk of psoriasis, a Cox proportional hazards model with time-varying air pollution exposure was used. Cox models were also used to explore the potential interplay between air pollutant exposure and genetic susceptibility for the risk of psoriasis incidence.

Results: 
A total of 474 055 individuals were included, with a mean (SD) age of 56.54 (8.09) years and 257 686 (54.36%) female participants. There were 9186 participants (1.94%) identified as Asian or Asian British, 7542 (1.59%) as Black or Black British, and 446 637 (94.22%) as White European. During a median (IQR) follow-up of 11.91 (11.21-12.59) years, 4031 incident psoriasis events were recorded. There was a positive association between the risk of psoriasis and air pollutant exposure. For every IQR increase in PM2.5, PM10, NO2, and NOx, the hazard ratios (HRs) were 1.41 (95% CI, 1.35-1.46), 1.47 (95% CI, 1.41-1.52), 1.28 (95% CI, 1.23-1.33), and 1.19 (95% CI, 1.14-1.24), respectively. When comparing individuals in the lowest exposure quartile (Q1) with those in the highest exposure quartile (Q4), the multivariate-adjusted HRs were 2.01 (95% CI, 1.83-2.20) for PM2.5, 2.21 (95% CI, 2.02-2.43) for PM10, 1.64 (95% CI, 1.49-1.80) for NO2, and 1.34 (95% CI, 1.22-1.47) for NOx. Moreover, significant interactions between air pollution and genetic predisposition for incident psoriasis were observed. In the subset of 446 637 White individuals, the findings indicated a substantial risk of psoriasis development in participants exposed to the highest quartile of air pollution levels concomitant with high genetic risk compared with those in the lowest quartile of air pollution levels with low genetic risk (PM2.5: HR, 4.11; 95% CI, 3.46-4.90; PM10: HR, 4.29; 95% CI, 3.61-5.08; NO2: HR, 2.95; 95% CI, 2.49-3.50; NOx: HR, 2.44; 95% CI, 2.08-2.87).

Conclusions and Relevance: 
In this prospective cohort study of the association between air pollution and psoriasis, long-term exposure to air pollution was associated with increased psoriasis risk. There was an interaction between air pollution and genetic susceptibility on psoriasis risk.

Elafin, also known as peptidase inhibitor 3 or skin-derived antileukoprotease (SKALP), is a protein that in humans is encoded by the PI3 gene.

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Background:
Eczema and psoriasis are common diseases. Despite both showing active epidermal contribution to the inflammatory process, their molecular aetiology and pathological mechanisms are different.

Objective:
Further molecular insight into these differences is therefore needed to enable effective future diagnostic and treatment strategies. The majority of our mechanistic and clinical understanding of psoriasis and eczema is derived from RNA, immunohistology and whole skin biopsy data.

Methods:
In this study, non-invasive epidermal sampling of lesional, perilesional and non-lesional skin from diseased and healthy skin was used to perform an in depth proteomic analysis of epidermal proteins.

Results:
Our findings confirmed the psoriasis-associated cytokine IL-36γ as an excellent protein biomarker for lesional psoriasis. However, ELISA and ROC curve analysis of 53 psoriasis and 42 eczema derived samples showed that the sensitivity and specificity were outperformed by elastase-specific protease inhibitor, elafin. Of note, elafin was also found upregulated in non-lesional psoriatic skin at non-predilection sites demonstrating inherent differences between the non-involved skin of healthy and psoriatic individuals. Mass spectrometry and ELISA analysis also demonstrated the upregulation of the anti-inflammatory molecule IL-37 in psoriatic perilesional but not lesional skin. The high expression of IL-37 surrounding psoriatic plaque may contribute to the sharp demarcation of inflammatory morphology changes observed in psoriasis. This finding was also specific for psoriasis and not seen in atopic dermatitis or autoimmune blistering perilesional skin. Our results confirm IL-36γ and add elafin as robust, hallmark molecules distinguishing psoriasis and eczema-associated inflammation even in patients under systemic treatment.

Conclusions:
Overall, these findings highlight the potential of epidermal non-invasive sampling and proteomic analysis to increase our diagnostic and pathophysiologic understanding of skin diseases. Moreover, the identification of molecular differences in healthy-looking skin between patients and healthy controls highlights potential disease susceptibility markers and proteins involved in the initial stages of disease.

This cohort study comprised 7,029,160 patients over 20 years old explored the relationship between psoriasis and chronic obstructive pulmonary disease (COPD) to determine whether patients with psoriasis are at increased risk for developing COPD.

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Background:
Understanding the relationship between psoriasis and chronic obstructive pulmonary disease (COPD) may enhance disease management.

Objectives:
We aimed to determine the prevalence and incidence and risk of COPD in psoriasis patients.

Results:
The COPD prevalence was 9.64 % in psoriasis patients and 6.94 % in psoriasis-free patients. The COPD incidence was 10.74 per 1000 person-years in psoriasis patients and 6.36 per 1000 person-years in psoriasis-free patients. Multivariable Cox regression showed no association between psoriasis and COPD development (HR 0.99, p = 0.271).

Conclusions:
Our findings suggest that psoriasis is not an independent risk factor for COPD development.

In this case-report, we describe an Human immunodeficiency virus positive patient with generalised pustular psoriasis (GPP) possible triggered by monkeypox vaccination and eventually successfully treated with spesolimab, an interleukin-36 inhibitor.

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A man in his thirties with well-controlled Human immunodeficiency virus (HIV) infection (CD4 cell count of 841 cells/mm3) and without previous skin disease developed a rash 7 days after monkeypox vaccination (Imvanex, Lot. No.: FDP00007). His regular medications (abacavir/dolutegravir/lamivudine, desloratadine and melatonin) were unchanged for years. The rash gradually worsened with pustules, fever and systemic symptoms, and he was admitted to the Infectious diseases department. Initially, Herpes simplex virus (HSV) type 2 was detected from the skin, and he was treated with intravenous acyclovir and dicloxacillin. Repeated blood cultures, viral and bacterial skin swabs were negative. After 1 week of treatment, there was no improvement in either the rash or his general condition and he was transferred to the department of Dermatology.

Upon admission, he presented with a generalised erythematous rash with widespread pustules. As the fever and leukocytosis were interpreted to be secondary to the skin inflammation, antibiotics and antiviral therapy were paused and he was treated with intravenous fluids, acetaminophen and topical hydrocortisone butyrate 0.1%. However, his condition rapidly declined with persistent fever above 39°C, tachycardia, hypotension, and an elevated respiratory rate.

Clinically, we first considered AGEP possibly triggered by monkeypox vaccination. The morphological picture could not distinguish between AGEP and GPP and as the rash did not improve, we considered GPP as a differential diagnosis. Treatment with acitretin 0.75 mg/kg was initiated but discontinued after 2 days due to a threefold elevation in liver enzymes.

A comprehensive reassessment for infections came out negative, also test for serum anti-HSV immunoglobulin (Ig) M. A chest & abdomen computer axial tomography revealed basal lung infiltrates and hepatomegaly. To cover Gram-negative bacteria causing a nosocomial pneumonia, he received intravenous treatment with a third-generation cephalosporin, and his condition improved rapidly concomitantly with resolution of the rash.

Due to a relapse, he was readmitted 10 days later. Recalcitrant AGEP was considered, and a second biopsy was taken. As soon as his liver enzymes were normalised, acitretin was re-initiated in a lower dose (0.35 mg/kg). In addition, he was given oral cyclosporin 4-5 mg/kg. His rash and overall condition responded well to this combined treatment. The second biopsy showed similar findings, but the number of eosinophils was substantially decreased. Four weeks later, his renal function deteriorated (serum creatinine 189 µmol/L, ref 60–105 µmol/L). His blood lipids also increased considerably (total cholesterol 10 mmol/L (ref 3.3-6.9 mmol/L) prompting an alternative treatment strategy.

Due to the lack of clinical improvement, as we would have expected with AGEP, we finally considered GPP as the most likely diagnosis. A third biopsy showed similar findings as the previous biopsies; the epidermis was acanthotic with increased basal proliferation, pronounced hypogranulosis and compact parakeratosis with small collections of neutrophilic granulocytes. In the dermal papillae small, tortuous capillaries were seen.

Intravenous treatment with spesolimab was administered approximately 4 months after onset of symptoms. Encouragingly, this led to rapid clearance of his rash and clinical improvement within the first few days. Clinical scorings revealed a GPP Physician Global Assessment (GPPGA) score of 3 and Dematology Life Quality Index (DLQI) of 30 before treatment. One week after treatment, GPPGA was reduced to 1 and DLQI to 4. The treatment had no impact on regular CD4 cell counts, or on HIV-, Cytomegalovirus- and EBV-DNA level quantification. He is still in remission 8 months after treatment, back to work with a GPPGA score and DLQI of 0.

Not sure it proves a lot as I would have thought some countries are happier than others but it's a study.

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Background:
Dermatological research has traditionally concentrated on evaluating mental comorbidities, neglecting positive concepts like happiness. Initial studies indicate that psoriasis and atopic dermatitis (AD) impair the happiness of those affected. Considering global happiness variations, this study aimed to explore the disease- and country-specific differences in disease-related quality of life and happiness, and potential influential factors on heuristic happiness among psoriasis and AD patients in Europe.

Methods:
A cross-sectional multicentre study was conducted in dermatology departments of university-affiliated hospitals in eight European countries (Austria, Germany, Italy, Malta, Poland, Portugal, Romania and Ukraine) between October 2021 and February 2023. Adult psoriasis and AD patients completed a standardized questionnaire in their native languages, providing data on demographics, disease-related characteristics, disease-related quality of life (Dermatology Life Quality Index, DLQI), heuristic happiness, positive affect (PA), negative affect (NA) and satisfaction with life (SWL). Descriptive analysis and quantile regression were performed.

Results:
Between psoriasis (n = 723) and AD (n = 316) patients almost no differences were observed in happiness, SWL and NA, except for DLQI and small differences in PA, with AD patients reporting greater impact than psoriasis patients. Country-wise variation emerged in DLQI, heuristic happiness, PA, NA and SWL with Austrian patients displaying the highest levels of happiness, satisfaction and positivity, coupled with higher treatment care and lower disease severity. Quantile regression revealed varying coefficients for predictor variables across quantiles, indicating, for example positive effects on heuristic happiness associated with current or previous receipt of systemic therapies at different quantiles.

Conclusion:
This study shows notable happiness differences across European countries and significant disease-related variations, particularly with AD patients being more impaired than psoriasis patients. The findings highlight the need for equality in treatment access and support the development of targeted positive psychological interventions to enhance happiness considering country-specific distinctions in future research and health policies for psoriasis and AD patients.

This study explored the role of early nutrition as a risk factor for the development of psoriasis.

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Background:
Psoriasis is a genetically determined systemic skin disease, although environmental trigger factors are required for disease manifestation. Some of these triggers, such as stress, infections and drug exposure, have been identified.

Objectives:
To explore the role of early nutrition as a risk factor for the development of psoriasis.

Methods:
Parents in the All Babies in Southeast Sweden (ABIS) prospective birth cohort (n = 16 415) answered questionnaires at birth and when their children were aged 1 and 3 years. A diagnosis of psoriasis was determined from the Swedish National Patient Register and National Drug Prescription Register. Statistical analyses were conducted using custom-written R scripts.

Results:
Individuals breastfed for < 4 months and who received infant formula before 4 months of age had a higher risk of psoriasis [odds ratio (OR) 1.84 (P = 0.02) and OR 1.88 (P = 0.02), respectively]. At the 3-year follow-up, the increased consumption of fish, especially from the Baltic Sea, increased the risk of psoriasis (OR 9.61; P = 0.003). In addition, the risk of psoriasis increased following the consumption of a large volume of milk (OR 2.53; P = 0.04).

Conclusions:
Our study underscores, for the first time, the impact of very early nutrition on the manifestation of psoriasis through early adulthood. Exclusive breastfeeding for 4 months appears to be protective.

Interim analysis results at Week 12 from the GULLIVER study.

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Background:
Facial (FP) and genital psoriasis (GP) significantly affect patients' quality of life. Despite the advances in treatments, limited data on efficacy and safety are available on these difficult-to-treat areas. Guselkumab is an interleukin (IL)-23 inhibitor which has been proven effective in treating patients with moderate-to-severe plaque psoriasis.

Objectives:
The aim of this interim analysis was to report the efficacy and safety of guselkumab in the treatment of patients with FP and/or GP.

Materials and Methods:
GULLIVER is a 52-week Italian observational study to evaluate the effectiveness and safety of guselkumab in a real-life setting in patients with FP and/or GP. Adult patients with facial and/or genital moderate-to-severe psoriasis (sPGA score ≥ 3) were included. The primary endpoint of this analysis was the percentage of patients achieving a facial or genital sPGA score of 0 (clear) or 1 (almost clear), at Week 12. The change in the score of the facial or genital sPGA components in patients with a score ≥3 for each sPGA component was assessed. PASI score in patients with a baseline PASI above or below 10 was evaluated.

Results:
Overall, 351 patients were included in the study; 83.3% of FP and 76.5% of GP patients achieved the primary endpoint. Similar response rates were observed for the facial or genital sPGA components in patients with a baseline facial or genital sPGA score ≥3 in each component. Among patients with a baseline PASI score >10, mean PASI score improved from 19.0 (SD 8.3) to 2.2 (SD 4.8). Forty-four AEs were observed in 32 patients; two mild and transient AEs (fatigue and nausea) were considered treatment related. No SAEs were observed.

Conclusions:
Guselkumab, showing to be effective and safe in treating FP and GP, may be a valid therapeutic option for patients with psoriasis localized in these difficult-to-treat areas.

Exploratory multi-omics analysis reveals host-microbe interactions associated with disease severity in psoriatic skin

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Background:
Psoriasis (Pso) is a chronic inflammatory skin disease that poses both physical and psychological challenges. Dysbiosis of the skin microbiome has been implicated in Pso, yet a comprehensive multi-omics analysis of host-microbe interactions is still lacking. To bridge this gap, we conducted an exploratory study by adopting the integrated approach that combines whole metagenomic shotgun sequencing with skin transcriptomics.

Methods:
This was a cross-sectional study, adult patients with plaque-type Psoriasis (Pso) and healthy volunteers were included. Skin microbiota samples and biopsies were collected from both lesional and non-lesional skin areas on the lower back. Weighted Gene Correlation Network Analysis (WGCNA) was employed for co-expression network analysis, and cell deconvolution was conducted to estimate cell fractions. Taxonomic and functional features of the microbiome were identified using whole metagenomic shotgun sequencing. Association between host genes and microbes was analyzed using Spearman correlation.

Findings:
Host anti-viral responses and interferon-related networks were identified and correlated with the severity of psoriasis. The skin microbiome showed a greater prevalence of Corynebacterium simulans in the PASI severe-moderate groups, which correlated with interferon-induced host genes. Two distinct psoriatic clusters with varying disease severities were identified. Variations in the expression of cell apoptosis-associated antimicrobial peptides (AMPs) and microbial aerobic respiration I pathway may partly account for these differences in disease severity.

Interpretation:
Our multi-omics analysis revealed for the first time anti-viral responses and the presence of C. simulans associated with psoriasis severity. It also identified two psoriatic subtypes with distinct AMP and metabolic pathway expression. Our study provides new insights into understanding the host-microbe interaction in psoriasis and lays the groundwork for developing subtype-specific strategies for managing this chronic skin disease.

Results from a retrospective, multicentric, multi-country, cohort study of drug survival rates of interleukin IL-17 and IL-23 inhibitors in elderly psoriasis patients.

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Background:
Scarce data related to the drug survival of biologic agents in psoriasis patients aged ≥65 years is available.

Objectives:
To evaluate the drug survival of interleukin (IL)-23 or the IL-17 inhibitors approved for the treatment of moderate-to-severe psoriasis in elderly patients (aged ≥65 years), compared with younger adult patients (aged <65 years), and to identify clinical predictors that can influence the drug survival.

Methods:
This retrospective multicentric cohort study included adult patients with moderate-to-severe psoriasis, dissecting two-patient subcohorts based on age: elderly versus younger adults. Kaplan–Meier estimator and proportional hazard Cox regression models were used for drug survival analysis.

Results:
We included 4178 patients and 4866 treatment courses; 934 were elderly (1072 treatment courses), and 3244 were younger patients (3794 treatment courses). Drug survival, considering all causes of interruption, was higher in patients aged <65 years than in elderly patients overall (log-rank p < 0.006). This difference was significant for treatment courses involving IL-23 inhibitors (p < 0.001) but not for those with IL-17 inhibitors (p = 0.2). According to both uni- and multi-variable models, elder age was associated with an increased risk of treatment discontinuation (univariable analysis: HR: 1.229, 95% CI 1.062–1.422; p < 0.006; multivariable analysis: HR: 1.199, 95% CI 1.010–1.422; p = 0.0377). Anti-IL-23 agents were associated with a reduced likelihood of treatment discontinuation after adjusting for other variables (HR: 0.520, 95% CI 0.368–0.735; p < 0.001). Being previously treated with IL-17 inhibitors increased the probability of discontinuation.

Conclusion:
Elderly patients with psoriasis have an increased risk of biologic treatment discontinuation compared with younger adult patients, particularly, if being treated with IL-23 inhibitors. However, in stratified analyses conducted in elderly patients, IL-23 inhibitors showed higher drug survival rates than IL-17 inhibitors.

Class 4 Medicines Defect Information: Manx Healthcare Ltd., Betamethasone Valerate 0.1% Ointment, EL(24)A/18

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MDR number: 142-05/24

Company name: Manx Healthcare Ltd.

Product name: Betamethasone Valerate 0.1% Ointment, PL 14251/0010

SNOMED Code: 41207211000001102

Batch Number: G0039

Expiry Date: Feb-2027

Pack Size: 30g

First Distributed: April 2024

Active Pharmaceutical Ingredient: Betamethasone valerate

Brief description of the problem
Manx Healthcare Ltd. has informed MHRA that they have identified a problem with the product packaging of the batch indicated in the table. The tamper-evident seal on the outer carton may be missing or deformed on some packs. This is due to an intermittent equipment fault during secondary packaging.

Advice for healthcare professionals
The quality of the ointment is not impacted by the defect. Any packs from this batch of product with missing or deformed seals may be dispensed. Healthcare professionals dispensing this medication may wish to advise patients that the seal on the outer carton may be broken but this will not affect product quality.

Advice for patients
The quality of the ointment is not impacted by the manufacturing issue as it only affects the outer carton. The tube of ointment that the patient receives will be sealed. Patients should continue to take medicines from this batch as prescribed by your healthcare professional.

Source: gov.uk

UChicago Chemistry Prof. Bozhi Tian’s lab has been working on a patch to monitor and improve psoriasis.

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Living bioelectronics is a combination of living cells, gel, and electronics that can integrate with living tissue.

The patches are made of sensors, bacterial cells, and a gel made from starch and gelatin. Tests in mice found that the devices could continuously monitor and improve psoriasis-like symptoms, without irritating skin.

Typically, bioelectronics consist of the electronics themselves, plus a soft layer to make them less irritating to the body. But Tian’s group wondered if they could add new capabilities by integrating a third component: living cells themselves. The group was intrigued with the healing properties of certain bacteria such as S. epidermidis, a microbe that naturally lives on human skin and has been shown to reduce inflammation.

They created a device with three components. The framework is a thin, flexible electronic circuit with sensors. It is overlaid with a gel created from tapioca starch and gelatin, which is ultrasoft and mimics the makeup of tissue itself. Lastly, S. epidermidis microbes are tucked into the gel.

When the device is placed on skin, the bacteria secrete compounds that reduce inflammation, and the sensor monitors the skin for signals like skin temperature and humidity.

In tests with mice prone to psoriasis-like skin conditions, there was a significant reduction in symptoms.

“We’re very excited because it’s been a decade and a half in the making,” said Tian.

The British government will be bringing in new labelling for topical steroids.

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Topical steroids are highly effective for the treatment of inflammatory skin conditions such as eczema and psoriasis, when prescribed and used appropriately. They are available in different potencies:

• mildly potent (for example, hydrocortisone)
  
• moderately potent (for example, clobetasone)
  
• potent (for example, betamethasone)
  
• very potent (for example, clobetasol)
  

The lowest potency topical steroid for effective treatment should be used and this may mean using different potency products for different body areas.

Over the coming year, topical steroids will be labelled with their potencies to aid correct selection and to simplify the advice to patients requiring multiple steroid products of differing potencies. These will be labelled ‘mild steroid’, ‘moderate steroid’, ‘strong steroid’, and ‘very strong steroid’.

Adverse reactions have been reported following long-term (generally 6 months or more) use of moderate or stronger potency topical steroids.

In psoriasis, use of large quantities of topical steroids is associated with a risk of more severe disease such as generalised pustular psoriasis.