Glad to be here.  I hope that I can share my 51 years of experience as someone living with Psoriasis.   As my conditioned has worsened, I hope to access the knowledge and experiences you all have.

Hello, fellow flakeys. Long-time sufferer here. Psoriasis and psoriatic arthritis has definitely made a dent in my life. I'm finally in somewhat of a remission, but I tend to develop a tolerance to meds over time. At least with all of the new meds they keep coming up with, it leaves me options for finding new ones.

I used to be married, lived on a farm, and took care of kids, cats, dogs, horses, sheep, rabbits, and a few chickens while working as a kennel attendant in a veterinarian's office. Now I'm divorced, unemployed, on disability, and live in a tiny house with a roommate and her kid. 

I do have two dogs, but I lost my two cats in the last couple of years and haven't found new ones that need homes yet.

I'm finally back to my favorite hobby (cross-stitch) after a bad flare starting last year. The Cosentyx has done wonders, but I'll never be as active as I once was. I've learned to slow down, but it hasn't been easy. 

I hope everyone is doing well and finding what treatment works best for them. Take care and I'll see you around.

Researchers at the University of Copenhagen have developed a patch for easier and more effective treatment of psoriasis.

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We have developed a dry patch, which contains active ingredients for treatment of psoriasis, and which reduces the frequency of use to once a day. It has the potential to make treatment more comfortable for psoriasis patients.

The patch is designed to contain two active ingredients at once and release them onto the skin at different rates.

The two ingredients are released in a controlled manner and at different rates, as they serve different functions: Salicylic acid is released immediately to remove the dead cells that have accumulated on the skin, while hydrocortisone decreases inflammation of the skin – a process that takes more time.

We have tested the prototype on pig skin and human skin cells and compared the results to the creams and ointments available at pharmacies, and our studies show that the patch is just as effective as standard treatments.

The researchers used electrospinning to produce the patch – a method where high voltage is applied to a polymer solution to produce synthetic nanofibers. The fibres are then used to make a fibre mat that may be attached to the skin like a plaster.

The researchers are still working on the patch. More research, product development and clinical trials are needed before the method is ready for use.

Hey everyone,

It's been a very long while. Sorry I have been away. I am struggling for a while with thing going on in my life. Lost my brother in 2021 and lost my dad in 2023. My plaque psoriasis are flaring up. This past July I was diagnosed with psoriatic arthritis and fibromyalgia. Currently onTriamcinolone ointment and methotrexate.
Sarah

Does psoriasis effect the clothes you wear ?

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Management of moderate to severe psoriasis with Kyntheum / Siliq (brodalumab) real world evidence from the LIBERO study.

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Background:
Brodalumab, a fully human monoclonal immunoglobulin IgG2 antibody that binds the human interleukin 17 receptor subunit A, is available for the treatment of moderate-to-severe plaque psoriasis in Europe since September 2017, but so far there are only a few studies on its use in real-world conditions.

Objectives:
To assess the management of moderate-to-severe psoriasis with brodalumab 210 mg in daily practice after 12 and 52 weeks (W). In addition, patient profiles and treatment pathways are described.

Methods:
LIBERO is a prospective, multicenter, non-interventional study including adult patients with plaque psoriasis treated with brodalumab 210 mg.

Results:
In total, 638 patients (65% male, mean age: 49.3 ± 14.4 years) from 148 sites in Germany were enrolled. The majority suffered from severe (51.1%) or very severe (13.1%) psoriasis according to physician global assessment (PGA0-5). When starting with brodalumab, 58.5% were biologic naïve and 41.5% were previously treated with another biologic, mainly adalimumab (18.5%) and secukinumab (17.9%). About 74.0% of patients met the primary endpoint of an absolute PASI ≤3 at ~W12 (n = 618, LOCF). The mean PASI was reduced significantly as of ~W2 from 17.2 (±11.7) to 9.7 (±8.8) and improved further to 3.3 (±6.3) at ~W12 (p < 0.001). At ~W52 85.5% of patients reached a PGA0/1-response (primary endpoint) and 54.1% patients were assessed as completely clear (PGA0) (both n = 399, as observed). Effectiveness of brodalumab was confirmed in relevant subgroup analysis by previous treatment regimen. Most frequently reported adverse events were nasopharyngitis (4.6%), psoriasis (4.6%) and arthralgia (4.1%), new safety signals were not detected.

Conclusions:
This representative, non-interventional study confirms the short- and long-term effectiveness and safety profile of brodalumab in the management of psoriasis in daily practice as well as in relevant treatment pathways.

Not aimed specifically at psoriasis, but phase 1 was on patients with psoriasis. In early 2025, Calluna plans to advance CAL101 into Phase 2 studies in fibrotic and fibro-inflammatory indications.

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Calluna Pharma AS (Calluna), a clinical stage biotechnology company pioneering first-in-class antibodies to treat inflammatory and fibrotic diseases, today announced the completion of Phase 1 clinical study for CAL101, Calluna’s lead product candidate. The study demonstrated a favorable safety, pharmacokinetic (PK) and immunogenicity profile for the mAb.

CAL101 is a first-in-class mAb that targets S100A4, a damage-associated molecular pattern (DAMP) protein implicated in serious and life-threatening diseases, such as idiopathic pulmonary fibrosis and systemic sclerosis. Preclinical studies have demonstrated the ability of CAL101 to prevent and treat fibrosis and modify the disease-specific activation of fibroblasts – the key effector cells driving progression of fibrosis.

Jonas Hallén M.D., Ph.D., Co-Founder and Chief Medical Officer of Calluna Pharma, commented: “We are encouraged by the findings from the Phase 1 study. These results are an important step forward in the development of our lead asset, CAL101, particularly for fibrotic and fibro-inflammatory diseases where there remains a critical need for innovative therapeutic options. We are excited as we now move into the next phase of clinical development.”

The first-in-human, randomized, double-blind, placebo-controlled Phase 1 study in 57 subjects was designed to evaluate safety, tolerability, immunogenicity and PK, and was led by Professor Dave Singh at the Medicines Evaluation Unit in Manchester, UK. The study tested single ascending doses of CAL101 in healthy volunteers and multiple ascending doses in patients with mild to moderate chronic plaque psoriasis.

Summary of key CAL101 Phase 1 study results:

• CAL101 demonstrated a favorable safety profile and was well tolerated with no Serious Adverse Events across all doses tested.
  
• Adverse Events were all mild to moderate and balanced between CAL101 and placebo.
  
• CAL101 demonstrated a favorable PK profile with dose-dependent increases in exposure, supporting once monthly dosing.
  
• In participants with anti-drug antibodies, titers were very low and with no impact on PK and safety.
  
• Target engagement data supports complete target coverage at clinically relevant doses.
  

Currently you need two shots at 160mg each, but soon in the USA and EU you will be able to get one shot at 320mg

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UCB  today announced that the U.S. Food and Drug Administration (FDA) has approved a 2 mL pre-filled syringe and pre-filled autoinjector, each containing 320 mg of BIMZELX® (bimekizumab-bkzx).

These new device presentations add to the currently available 1 mL administration options, each containing 160 mg of bimekizumab-bkzx, and mean that patients requiring a 320 mg dose of bimekizumab-bkzx will have options for single-injection administration.

“Our goal with these single-injection regimens is to strengthen and expand administration options, increase convenience and enhance the individual patient experience,” said Emmanuel Caeymaex, Executive Vice President, Head of Patient Impact, Chief Commercial Officer, UCB. “With the new device presentations, people with moderate-to-severe plaque psoriasis who receive a bimekizumab-bkzx maintenance dose of 320 mg will have the option of a single-injection every eight weeks.”

The approval of the 320 mg device presentations is supported by data from studies evaluating the bioequivalence of bimekizumab-bkzx 320 mg given as one 2 mL subcutaneous injection, and bimekizumab-bkzx 320 mg given as two 1 mL subcutaneous injections, in healthy study participants. This is the second worldwide approval for the 320 mg single-injection administration options for bimekizumab-bkzx, following approval by the European Commission in August 2024.

These new device presentations will be available in the U.S. in Q1 2025.

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.

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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.