This cohort study from Taiwan looked at infections in patients with psoriasis.

Quote:

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Background:
The risks of serious infections that lead to hospitalisation and mortality in patients with psoriasis in Asia have not been comprehensively studied.

Objectives:
We examined the incidence of serious infection and infection mortality in patients with psoriasis.

Methods:
This population-based retrospective cohort study used the Taiwan National Health Insurance claims database from 2000 to 2017. Adult patients with psoriasis were identified by a relevant International Classification of Diseases (ICD) code and matched to six comparators without psoriasis on age and sex. Psoriasis patients were categorised as having moderate-to-severe disease once exposed to systemic therapies, phototherapy or biologic therapies. The incidence of serious infection and infection mortality were identified by ICD codes from inpatient hospitalisation and death registration. Cox proportional hazard models were used to compare the risk, and the results were adjusted for covariates and presented as adjusted hazard ratios (aHR) and 95% confidence interval (95%CI).

Results:
Overall, 185,434 psoriasis patients and 1,112,581 comparators were included. A higher rate of serious infection (aHR:1.21, 95%CI: 1.19-1.22) was found in patients with psoriasis compared to matched comparators without psoriasis, and the risk was enhanced when patients had moderate-to-severe psoriasis (aHR:1.30, 95%CI: 1.27-1.34). Specifically, there was an increased risk of serious infection due to respiratory infections (aHR:1.11, 95%CI: 1.09-1.13), skin/soft-tissue infections (aHR:1.57, 95%CI: 1.52-1.62), sepsis (aHR:1.23, 95%CI: 1.19-1.27), urinary tract infections (aHR:1.11, 95%CI: 1.08-1.14), hepatitis B (aHR:1.18, 95%CI: 1.06-1.30), and hepatitis C (aHR:1.49, 95%CI: 1.32-1.69). Furthermore, psoriasis patients were associated with a higher risk of infection-related mortality (aHR:1.15, 95%CI: 1.11-1.18) compared to matched comparators.

Conclusion:
Patients with psoriasis had a higher risk of serious infection and infection mortality, which was enhanced by moderate-to-severe psoriasis. Practitioners should be aware of the increased risk in patients with psoriasis, but it should not be a barrier to offering effective treatment.

Hi there,

Ive had psorasis since my teenage years, I'm 35 now. Over 50% covered, tried light treatment, steroids, etc. About a month ago, my psoriasis started peeling like sunburn. Its very red, flat and itchy - the itching has subsided a bit recently. I currently have a brain tumour grade 3 - which I've had for coming up 3 years - but i'm not receiving any cancer medication. Only Brivaracatam for my epilepsy, which is a result of the tumour. Last MRI June 2023 - "sound and stable." I'm currently using - Enstilar foam and Zeroveen, which I alternate with.

I remember reading that for it to be Erythemarodermic Psoriasis, it would need to be covering almost my entire body. Not sure how true that is.

Any help would be much appreciated.

Thanks.

Got a little bit of psoriasis flared up on my left hand, it's not bleeding but I had forgotten how sometimes it used to weep.

I've tried Coconut Oil, Aveeno, Dexeryl  but as it's been so long I've forgotten what works best for the weeping, I'm thinking just leaving it open to the air may be the best way to go and it will form a crust.

Here's a photo, it's not great but if you zoom in you can see it's just a clear fluid.



Tips anyone ?

Any thoughts on how to safely moisturize or care for flaky eyelids?

This study assessed the persistence, effectiveness and safety of Tremfya (guselkumab) in patients with moderate-to-severe psoriasis in real clinical practice in Spain.

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Background:
Guselkumab is a monoclonal antibody that blocks the IL-23 pathway with proven efficacy and tolerability in the treatment of moderate-to-severe plaque psoriasis.

Objectives:
To assess the persistence, effectiveness and safety of guselkumab in patients with moderate-to-severe psoriasis in real clinical practice in Spain.

Methods:
SPRING was a phase IV, retrospective and non-interventional study analysing patients with moderate-to-severe plaque psoriasis who had initiated guselkumab under clinical practice conditions at least 12 months before inclusion in the study. The primary endpoint was persistence (non-persistence: discontinuation or interruption ≥90 days). Effectiveness was assessed using the Psoriasis Area Severity Index (PASI) and Investigator Global Assessment (IGA). Dermatology Life Quality Index (DLQI) and safety were also evaluated.

Results:
A total of 284 patients were included between September 2020 and June 2021. The 1-year probability of persistence was 89.6% (86.1-93.3%). The 1-year probability of persistence was also calculated according to prior biologic treatment, being 90.3% for biologic-naïve patients and 89.5% for patients who received one or more biologic therapies before guselkumab. Additionally, patients were also classified based on the frequency of the administration of guselkumab treatment; the 1-year probability of persistence was 91.9% in patients receiving guselkumab according to the Summary of Product Characteristics and 89.3% in patients with lengthened intervals of administration. After one year, PASI 90 was achieved by 56.4% of patients, IGA 0/1 response and BSA <3% were achieved by 65.5% and 77.8% of patients, respectively, and 65.8% achieved a minimal clinically significant difference (>4-point reduction) in the DLQI score at one year. Twenty-six adverse reactions (4 of them serious) were reported in 16 patients.

Conclusions:
This study suggests that guselkumab has high persistence in real clinical practice in Spain, independently of the previous biologic treatments and changes in the frequency of treatment. Effectiveness and safety are consistent with previously published data.

I just saw an ad for Sotyktu (deucravacitinib)

The FDA approved Sotyktu for use in the US at the end of 2022.  Another oral medication.  Their website says unsure if it can harm unborn baby and unsure if it can cause harm while breastfeeding.  Also could cause liver problems and not for use with people who have rheumatoid arthritis. 

First ad I've seen for it and I tend to look it up if it's new to me.  It's always difficult to read the side effects and warnings. 

(I saw where there was a post showing it was approved in the US but it had been removed but the one showing approval in England was still up. Not sure I'd be a fan of trying it but thought I'd put it out there anyway.)

This study looked at atopic like dermatitis induced by IL-17A inhibitors used for psoriasis.

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Background:
Atopic-like dermatitis (ALD) is a common side-effect of IL-17A  inhibitors.

Objective:
To determine the prevalence, risk factors, outcomes and treatment of ALD in a cohort of psoriasis patients treated with IL-17A inhibitors.

Methods:
This retrospective study included 226 psoriasis patients treated with an IL-17A inhibitor in our dermatology department between July 2020 and July 2022. The patients were reviewed over 2 years. A logistic regression model in rare events data (relogit) was used to predict the risk factors for ALD.

Results:
Of the 226 patients, 14 had ALD. Data including age, body mass index, IL-17A inhibitor use, personal and family history of atopic disease, pet ownership history, and immunoglobulin E (IgE) levels were analysed using the relogit regression model. It indicated a personal history of atopic disease (odd ratio [OR] 27.830, 95% confidence interval [CI] 3.801-203.770; P = 0.001) and elevated IgE levels (OR 5.867, 95% CI 1.131-30.434; P = 0.035) as independent predictors of incident ALD. In one patient, anti-IL-17A therapy was discontinued, and treatment was switched to tofacitinib. Thirteen patients who continued with IL-17A inhibitor were treated with topical therapy and/or antihistamines, and their ALD was partially or completely resolved.

Conclusion:
In this study, the incidence rate of ALD was 6.19%. Elevated IgE levels and a personal history of atopic disease were found to be the risk factors for ALD. Our study findings suggest that treatment should be provided based on the severity of psoriasis and incident ALD. Prior to treatment, psoriasis patients who have the risk factors for ALD should be informed of the possible development of ALD, and alternative psoriatic therapeutic options should be considered if severe ALD develops.

I lost a friend on July 13, was with him when he passed, and the grief is likely to be lasting a while.  In the meantime, I'm shedding more flakes around the house than previously (and have more patches due to this stressful life event).  So it got me wondering about flaking and the residue of our scratching or shedding.  It'd be weirdly fun to read about where fresh flakes are likely to be found.

I found some while vacuuming, yesterday.  They were on the arm of the couch where I sit.  This was expected.  But they were also on the table cloth of the side table where the lamp sits.  This was not expected.  These fresh flakes were from my scalp and my vacant scratching while watching tv.

Where would you find Fresh Flakes in your home or places you frequent?

Hello,

Just found this forum, have had psoriasis for about ten years but never really looked for a forum before. But in the past few years its progressed to an intolerable point and ive been struggling.

Bit of background on me, 29 y/o male, live in Ontario, Canada. I consider myself very fit and healthy. 

I has psoriasis start around the ears and nose at first. That was easily remedied with any lotion. I really first noticed persistent psoriasis on my elbows and then knees. Then my belly button as well. I had a few spots pop up here and there on torso and arms but just adjusted my diet to eat more healthy meals (not eating a cookie for breakfast) and was able to control it pretty well with just a little steroid cream and basic 80/20 kind of diet (eat healthy 80% of time, eat junky food 20% of time), and no restrictions. Sometimes it would flare and be extra flaky but some diet correction and salt baths would get it under control. Over the years a new spot would develop here and there, on my fore arms, shins, torso, the forearms and shins would come on as a result of damage to the skin (cuts) that despite my "healthy lifestyle" wouldn't go away. Admittedly I did smoke on and off and drink from time to time for many years and often eat anything i felt like but I was active and felt like anytime i could reel it in and control flares. It was annoying but i could deal with it and enjoy going to the beach and wearing shorts and t shirts.

In the past 2ish years my psoriasis kind of exploded. It basically covered my forearms, spots popped up all over the inside of my forearms, all over my upper arms, all over my stomach and lower back, my entire lower legs, not just on my shins but all over my calves, and my upper legs as well. Id often get flares and spots on my forehead and other spots on my face around my eyes. I had already quit smoking by this time but was drinking every week or two in the summer before this happened.

I am still not sure why it got so bad. I shortly there after decided I needed to completely revamp my diet. I was eating a pretty carb heavy diet before, oats or gluten free hot cereal with fruit, peanut butter & jelly sandwiches, sweet potatoes, beats, beans, quinoa, rice. Only protein I was eating really was chicken or fish for dinner and paired with rice usually, or made into tacos with cheese and other goodies you'd eat with tacos. All sorts of things but always "healthy". Often having snacks/dessert too though. Chocolate, cookies, peanut m&m's. But I felt I needed to become more strict and get in more protein as well as I have always been very active and lean and muscular. I got diet guidance from the "REMOVED" mostly. I started eating eggs for breakfast with avocado, usually chicken for lunch with rice or potatoes, started eating beef after having pretty much avoided it for years, raw and unsalted nuts, yogurt, whey protein. I decided to give it some time to adjust. It didn't really accelerate my psoriasis but it kind of just stayed pretty bad and spots grew and grew. About a year ago I even went on a probiotic and did a few rounds of gut supplements for leaky gut. Not really any affect on the PSO.

I always felt tired and bogged down before. Since eating like this I feel stronger and more on it. I feel like a beast mostly. But my psoriasis isn't getting better. I still pretty much eat like this except now I eat oats again, less eggs, cut the yogurt, but always try to balance carbs, protein and fats with all my meals. Its the best I have felt physically. I always do coffee in the morning after water. For breakfast I do a big bowl of oats with some fruit, lunch is beef or chicken or sardines with rice usually (just switched from basmati to brown), dinner is chicken or beef with potatoes (did white and yellow potatoes for a long time, just switched to sweet potatoes), i get snacks in, usually fruit, or banana bread i make with oats, banana, eggs, coconut oil or butter, little maple syrup or dark chocolate. 

1 - 3 months ago I've found a bit of healing happening. Spots cleared on my lower legs, forearms, face. And alot of spots became less flaky and scally. Stopped waking up to loads of skin in my bed. I was eating whey protein everyday and gluten by way of oats and loads of potatoes and nuts. But it seems to have gone back to being not great again. Think its cause I started having a few whiskeys on saturday nights watching ufc for too many weeks in a row. Still, ive stopped but over a month ago but still find it to be very irritated. I also stopped the whey and try to do gluten free oats. Ive also started eating more veggies as well.

I am just not sure where to go from here. Thinking of cutting the coffee and beef. Already have been upping the veggie intake. I definitely enjoy and need alot of protein though so i don't know what ill replace the beef with. I have a very very strong appetite. I eat loads of food. Im still super lean and muscular. I also hate leafy greens and veggies like brocolli. They tear up my stomach.

I am at a point where I question if diet even has much to do with this. There were plenty of times I went off the diet and ate lots of chips or processed chocolate or other "bad" things and my skin got lighter and less irritated. Obviously diet is a huge component but I just question worrying about little things like will tomatoes make it worse or will eating chips and salsa one day or eating one kind of nut or skin on chicken actually cause all of this on my skin? I know alot of people say beef is bad, but I just don't know I buy that. I certainly think the fat in beef isn't great but I eat lean beef. I obviously get a little fat but just don't know I believe that a few grams per say of beef fat in my body is causing this.

For about 2 years now, little by little ive cleaned up my diet and lifestyle and intuitively corrected and made changes to optimize my overall healthy but I haven't seen it translate to my psoriasis like I hoped. I don't let it get my down or depressed, maybe the odd day here and there I have that hopeless feeling but i pull myself out. Im pretty positive and motivated. I just don't understand this disease, still.

My plan is keep making adjustments. Like I said I feel its time to cut coffee and eat less beef, just to try. I switched out the potatoes for sweet potatoes and im adjusting to get more veggies. I see it as process of various trials. At this point ive had this so long that the way I see it my only way to beat the disease is to find the formula that works for me. Just cutting this one thing or adding this one supplement or following a basic protocol won't do it for me I don't think.

In addition to diet I know that stress is a factor, as they say, lol.

I certainly have stress in my life. Wife had a baby late last year, we also bought a house last year. Ever since she got pregnant life has changed and my responsibilities have grown. I love it, but it is alot, It was a big life change. That being said, it certainly could be a major factor for me. But I feel like my ability to manage stress is greater than ever. I don't suffer from or experience anxiety. I did very badly in my early 20's but figured that out. Though my psoriasis was easy to manage then even though i ate like crap, smoked, and experienced bad anxiety and depression at times. I feel more fit than ever, sleep better, eat better, have better emotional stability but the psoriasis persists. 

Im covered in ugly red spots, often scaly and flaky. I feel embarrassed to take my shirt off around my family and enjoy the lake. I wouldn't want to go to the beach, one of my favorite things to do all my life. Ive always been a person who loves summer and being outside, wearing shorts and a tank top or being shirtless and enjoying the sun. I wear pants everyday though and often put a long sleeve on to go in public. I just seem to have psoriasis pretty badly but i have a healthier diet and lifestyle than most people I know. I know that comparing myself to other people won't do my any good and I just need to look at what I can do to change and what else I can try but its just a tough thing to deal with. I believe that this must be possible to heal naturally. I fear going on biologic drugs.

Anyways, thats alot so thanks to anyone who makes it through, lol. Psoriasis is a strange thing and its tough and noone I know really understands.

A real-world study of Stelara (ustekinumab) and Tremfya (guselkumab)  in adult patients with moderate-to-severe plaque psoriasis in Germany.

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Background:
PERSIST was a prospective, non-interventional, real-world study of guselkumab and ustekinumab in adult patients with moderate-to-severe plaque psoriasis in Germany.

Objectives:
To examine effectiveness, safety and quality-of-life (QoL) outcomes to Week (W) 104 of treatment with guselkumab and ustekinumab in patients with moderate-to-severe plaque psoriasis.

Methods:
Patients (≥18 years of age) received guselkumab or ustekinumab as per routine clinical practice. Outcomes to W104 were examined separately in guselkumab and ustekinumab recipients. An ad hoc exploratory analysis of outcomes with guselkumab versus ustekinumab was also performed following propensity score matching.

Results:
Overall, 302 and 313 patients received guselkumab and ustekinumab, respectively. Patients in both cohorts experienced improvements in disease activity and QoL that were maintained to W104, with 64.7% and 63.6% of guselkumab- and 54.6% and 64.4% of ustekinumab-treated patients achieving a Psoriasis Area and Severity Index (PASI) 90 response and a Dermatology Life Quality Index (DLQI) 0/1 score, respectively. Propensity score matching yielded well-balanced baseline characteristics except for prior biologic use, which was higher in guselkumab versus ustekinumab recipients (51.7% vs. 32.0%). Achievement of PASI ≤1 at W104 was more common in guselkumab versus ustekinumab recipients (58.7% vs. 49.7%). The W104 PASI90 response rate was 65.6% with guselkumab and 56.0% with ustekinumab; corresponding rates for PASI100 were 44.3% and 28.5%. In guselkumab recipients, response rates were higher in biologic-naïve versus biologic-experienced patients (PASI90, 77.1% vs. 53.4%; PASI100, 55.0% vs. 33.0%). A high level of response for QoL outcomes was observed for both treatments.

Conclusions:
Ustekinumab and guselkumab led to improvements in physician-assessed and patient-reported outcomes that were sustained for up to 2 years, with no new safety signals identified. Following propensity score matching, greater improvements in PASI outcomes were observed with guselkumab versus ustekinumab. Improvements with guselkumab were highest in biologic-naïve patients, highlighting the value of early treatment.

Heard of an interesting new project that is starting in the Netherlands. It is called NGID.

They received funding for a 6 year project. And they are going to investigate the skin with optometric instruments and biopts with the purpose of finding markers that define the psoriasis in a personal way.
The idea is to do so much research into that markers and combined with that the treatments that work for that markers, that in the future it will become possible to measure the markers for a patient and then to be immediately able to prescribe a treatment that will probably work.

I think it will be a complex project and I see that a lot of well-known names in the medical world over here are involved. People from Radboud Medical Centre in Nijmegen, specialised in psoriasis, and people from Leiden University. The project is executed by CHDR (Centre for Human Drug Research) also located in Leiden. Even psychologists are involved to find the psychological markers, like stress or depression.

I will try to keep an eye on this project and see if they make progress. Unfortunately for me for now there are no references to Psoriatic Arthritis.

If I have a smallish area of psoriasis which maybe I’ve scratched and is a bit sore, I’ve found good old antiseptic cream helpful because it moisturises and stops infection but also seems quite soothing unlike normal moisturisers. I am not sure but there’s probably limits to how big an amount you can use each day.

It sounds like a very obvious thing to try but I have to admit I hadn’t thought of trying it until recently, probably because you get a barrage of different creams from the doctor..

Ok so this isn’t usually a prescribed drug, you can just buy it over the counter - but I didn’t put it in natural treatments because it isn’t that either.,

I recently read that regular use of both paracetamol and ibuprofen can raise your blood pressure.

I had no idea of this before now and it’s not something the doc told me, different sources vary as to the extent - some say a slight rise and others that it can be significant - so it’s something to bear in mind.

I am on a bio but although my skin is doing well it’s hard to tell how well it’s working for my psa. I use painkillers on the advice of my rheumy for when I get stiff neck and shoulders and I can feel it bringing on a headache, or for my Achilles when it’s playing up.

I was wondering if anyone else knew more?

JNJ-2113 is an oral IL-23R antagonist peptide that binds to the IL-23 receptor with single-digit picomolar affinity and demonstrated potent, selective inhibition of IL-23 signaling in human T cell.

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Johnson & Johnson today announced positive topline results from its Phase 2b FRONTIER 1 clinical trial evaluating the novel, first and only oral interleukin-23 receptor (IL-23R) antagonist peptide JNJ-2113 in adult patients with moderate-to-severe plaque psoriasis (PsO). The trial achieved all primary and secondary efficacy endpoints. A greater proportion of patients who received JNJ-2113 achieved PASI 75 (primary endpoint) as well as PASI 90 and PASI 100 (75, 90 and 100 percent improvement in skin lesions as measured by the Psoriasis Area and Severity Index, respectively)a compared to placebo, at week 16. Trial results for JNJ-2113 demonstrated a profile that supports its advancement into Phase 3 clinical development for moderate-to-severe plaque PsO in adult patients.

JNJ-2113 is a novel oral IL-23R antagonist peptide that binds with high affinity to the IL-23R and has properties that allow it to be absorbed with oral dosing. The IL-23/IL-23R signaling pathway plays a critical role in the pathogenesis of immune-mediated inflammatory diseases, including PsO. JNJ-2113 selectively and potently blocks IL-23 signaling and downstream inflammatory cytokine production.

PASI 75 Results – Primary Endpoint

The proportions of adult patients receiving JNJ-2113 (n=212)1 who achieved PASI 75 demonstrated the following dose responses at week 16 compared to 9.3 percent of patients receiving placebo (n=43) (nominal p ≤0.002 for all comparisons):

    37.2 percent at 25 mg daily (n=43)
    51.2 percent at 25 mg twice daily (n=41)
    58.1 percent at 50 mg daily (n=43)
    65.1 percent at 100 mg daily (n=43)
    78.6 percent at 100 mg twice daily (n=42)

PASI 90 Results – Secondary Endpoint

The proportions of adult patients receiving JNJ-2113 who achieved PASI 90 demonstrated the following dose responses at week 16 compared to 2.3 percent of patients receiving placebo (n=43) (nominal p ≤0.002 for all comparisons):

    25.6 percent at 25 mg daily (n=43)
    26.8 percent at 25 mg twice daily (n=41)
    51.2 percent at 50 mg daily (n=43)
    46.5 percent at 100 mg daily (n=43)
    59.5 percent at 100 mg twice daily (n=42)

PASI 100 Results – Secondary Endpoint

The proportions of adult patients receiving JNJ-2113 who achieved PASI 100 also demonstrated the following dose responses at week 16 compared to 0 percent of patients receiving placebo (n=43) (nominal p ≤0.05 for all comparisons):

    11.6 percent at 25 mg daily (n=43)
    9.8 percent at 25 mg twice daily (n=41)
    25.6 percent at 50 mg daily (n=43)
    23.3 percent at 100 mg daily (n=43)
    40.5 percent at 100 mg twice daily (n=42)

Treatment was generally well tolerated, and the proportions of patients with adverse events were comparable between patient groups. The proportion of participants experiencing one or more adverse events (AEs) was 52.4 percent (n=111) in the combined JNJ-2113 group and 51.2 percent (n=22) in the placebo group. Although there was variability across the treatment groups, there was no evidence of a dose-dependent increase in the occurrence of specific AEs across the JNJ-2113 treatment groups. The most frequent system organ class involved in AEs in all groups was infections and infestations, which were 30.2 percent (n=64) vs. 27.9 percent (n=12) in the combined JNJ-2113 group vs. placebo group, respectively; of these, the most common were comparable between groups: COVID-19 (10.8 percent [n=23] vs. 11.6 percent [n=5]), nasopharyngitis (7.1 percent [n=15] vs. 4.7 percent [n=2]) and upper respiratory tract infection (2.4 percent [n=5] vs. 2.3 percent [n=1]).

“The development of a novel oral therapy that specifically targets IL-23R could potentially change the treatment paradigm for patients living with moderate-to-severe plaque psoriasis,” said Lloyd Miller, M.D., Ph.D., Vice President, Immunodermatology Disease Area Stronghold Leader, Janssen Research & Development, LLC. “Until now, advanced psoriasis treatments have been largely limited to injectable biologics. An oral therapy that can uniquely inhibit the IL-23 pathway by directly targeting the IL-23 receptor could help address the needs and preferences of patients, and may offer greater freedom, with the aim of driving greater adoption of advanced treatment.”

Sotyktu (deucravacitinib) is an oral prescription medicine approved by some countries to treat moderate to severe plaque psoriasis in adults.

Dosage: The recommended dose is one 6 mg once daily with or without food. Do not split, break, crush, or chew the tablet.

Tell your doctor if you have or ever had:

• liver or kidney disease;
  
• hepatitis B or C;
  
• high blood levels of fat (triglycerides);
  
• any type of cancer;
  
• tuberculosis or have been exposed to tuberculosis;
  
• if you have an infection that keeps returning or does not go away;
  
• if you are being treated for an infection;
  
• if you have recently received or are scheduled to receive a vaccine;
  
• if you have high blood pressure, high cholesterol, diabetes, menopause, family history of coronary artery disease, being overweight, or being over 50, or if you smoke;
  
• if you are pregnant or breastfeeding.
  

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

• Feeling faint
  
• Swelling of your face, eyelids, lips, mouth, tongue, or throat
  
• Trouble breathing or throat tightness
  
• Chest tightness
  
• Skin rash, hives
  

• Fever, sweats, or chills
  
• Muscle aches
  
• Weight loss
  
• Cough
  
• Shortness of breath
  
• Blood in your phlegm (mucus you cough up)
  
• Warm, red, or painful skin or sores on your body different from your psoriasis
  
• Diarrhoea or stomach pain
  
• Burning when you urinate or urinating more often than normal
  
• Feeling very tired
  

The National Institute for Health and Care Excellence (NICE) has recommended Sotyktu (deucravacitinib), for use on the NHS in England for treating moderate to severe plaque psoriasis.

Quote:

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1 Recommendations:

1.1 Deucravacitinib is recommended as an option for treating moderate to severe plaque psoriasis in adults, only if:

• the Psoriasis Area and Severity Index (PASI) score is 10 or more and the Dermatology Life Quality Index (DLQI) score is more than 10
  
• the condition has not responded to other systemic treatments, including ciclosporin, methotrexate and phototherapy, or these options are contraindicated or not tolerated
  
• the company provides deucravacitinib according to the commercial arrangement.
  

1.2 Consider stopping deucravacitinib between 16 weeks and 24 weeks if there has not been at least a 50% reduction in the PASI score (PASI 50) from when treatment started.

1.3 Consider stopping deucravacitinib at 24 weeks if the psoriasis has not responded adequately. An adequate response is defined as:

• a 75% reduction in the PASI score (PASI 75) from when treatment started or
  
• a 50% reduction in the PASI score (PASI 50) and a 5-point reduction in DLQI from when treatment started.
  

1.4 If people with the condition and their clinicians consider deucravacitinib to be 1 of a range of suitable treatments fter discussing the advantages and disadvantages of all the options, use the least expensive. Take account of administration costs, dosage, price per dose and commercial arrangements.

1.5 Take into account how skin colour could affect the PASI score and make any adjustments needed.

1.6 Take into account any physical, sensory or learning disabilities, or communication difficulties that could affect the responses to the DLQI and make any adjustments needed.

1.7 These recommendations are not intended to affect treatment with deucravacitinib that was started in the NHS before this guidance was published. People having treatment outside these recommendations may continue without change to the funding arrangements in place for them before this guidance was published, until they and their NHS clinician consider it appropriate to stop.

Why the committee made these recommendations:

Treatment for moderate to severe plaque psoriasis that has not responded to conventional systemic non-biological treatments or phototherapy includes apremilast, dimethyl fumarate and systemic biological treatments. Deucravacitinib is an alternative to apremilast, dimethyl fumarate and systemic biological treatments.

Clinical trial evidence shows that deucravacitinib improves symptoms of plaque psoriasis compared with placebo and apremilast. Deucravacitinib was indirectly compared with apremilast, dimethyl fumarate and several systemic biological treatments. The indirect comparison suggests it improves symptoms better than apremilast and dimethyl fumarate, and works as well as some biological treatments but not as well as others.
The cost-effectiveness estimates for deucravacitinib compared with apremilast, dimethyl fumarate and most biological treatments are within the range that NICE normally considers an acceptable use of NHS resources. So, deucravacitinib is recommended.

Around the late fall of 2022, I came to understand a family relationship differently and was able to set down what had been a long-standing burden in my way of viewing life.  That resolution brought me unexpected peace and also unexpected improvement in my patches of rashy areas.  My skin began to heal a bit, improve a bit on its own.

And it has stayed pretty good.

During the time of pneumonia recovery in early 2023 when I wasn't skating, my lower ankles and feet were doing better.  Friction from the skate boot and sweat was halted.  Now that I'm skating again, that area of skin is more activated for patches.  

When a little stress comes along, skin still flares up a bit.  But overall, the change has been for the better since late 2022.  

I saw my dermatologist, yesterday.  She thought my skin was looking better than the last time she'd seen me.  She said she hears about stress and skin from her patients often.  

I don't know how to overcome stressful situations in life.  But it's interesting that the skin is so sensitive to stressors.  

How do you deal with stress?  Have you ever had improvement in your skin when you've resolved a stressful matter?

This study analysed the association of CRH-POMC polymorphisms with psoriasis and evaluated transcript expression of lesional psoriatic and normal skin in RNA-seq data.

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Background:
Skin is a target organ and source of the corticotropin-releasing hormone–proopiomelanocortin (CRH-POMC) system, operating as a coordinator and executor of responses to stress. Environmental stress exacerbates and triggers inflammatory skin diseases through modifying the cellular components of the immune system supporting the importance of CRH-POMC system in the pathogenesis of psoriasis. The aim of this study was to analyze the association of CRH-POMC polymorphisms with psoriasis and evaluate transcript expression of lesional psoriatic and normal skin in RNA-seq data.

Methods:
Samples of 104 patients with psoriasis and 174 healthy controls were genotyped for 42 single nucleotide polymorphisms (SNPs) of CRH-POMC using Applied Biosystems SNPlex™method. The transcript quantification was performed using Salmon software v1.3.0.

Results:
The current study demonstrated the associations between melanocortin 1 receptor (MC1R) polymorphisms rs2228479, rs3212369, dopachrome tautomerase (DCT) polymorphisms rs7987802, rs2031526, rs9524501 and psoriasis in the Tatar population. Very strong association was evident for the SNP rs7987802 in the DCT gene (Pc = 5.95е-006) in psoriasis patients. Additionally, the haplotype analysis provided AT DCT (rs7992630 and rs7987802) and AGA MC1R (rs3212358, 2228479, and 885479) haplotypes significantly associated (Pc ˂0.05) with psoriasis in the Tatar population, supporting the involvement of DCT and MC1R to the psoriasis susceptibility. Moreover, MC1R-203 and DCT-201 expression levels were decreased in psoriasis lesional skin compared with healthy control skin.

Conclusions:
This study is the first to identify genetic variants of the MC1R and DCT genes significantly associated with psoriasis in Tatar population. Our results support potential roles of CRH-POMC system genes and DCT in the pathogenesis of psoriasis.

Hello all, I am interested to know if anyone else has had this experience. The second time I got COVID, I was prescribed Paxlovid. Two days into the medication, every trace of my psoriasis disappeared, but all came back as soon as I finished the medication. If others have had the same experience, we should find a way to make the medical research community aware that they should look into it, but if it was just me, I guess I shouldn't make much of it.

This study evaluated the impact of early disease intervention on clinical responses with Tremfya (guselkumab) treatment in patients with moderate-to-severe plaque psoriasis.

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Background:
Guselkumab is an interleukin (IL)-23 inhibitor with demonstrated efficacy in patients with psoriasis.

Objectives:
Evaluate the impact of early disease intervention on clinical responses following 28 weeks of guselkumab treatment in patients with moderate-to-severe plaque psoriasis. Correlate clinical response and disease duration data with serum biomarker data.

Methods:
GUIDE is a phase IIIb randomized, double-blind, parallel-group, multicentre study of adults with moderate-to-severe plaque psoriasis. In study part 1, patients with a short disease duration (SDD [≤2 years]) or a long disease duration (LDD [>2 years]) received guselkumab 100 mg at Week (W) 0, 4, 12, 20 and 28. Those achieving complete skin clearance from W20–28 were defined as a super responder (SRe). A multivariable logistic regression analysed the association between baseline factors and the likelihood of being an SRe. The relationship between clinical response, disease duration and serum biomarker data was assessed at W0 and 4.

Results:
In total, 880 patients were enrolled (SDD/LDD=40.6%/59.4% patients). More SDD than LDD patients achieved absolute Psoriasis Area and Severity Index (PASI)=0[/b] at W28 (51.8% vs. 39.4%) and were SRes (43.7% vs. 28.1% [overall 34.4%]). SDD patients also achieved PASI=0 quicker than LDD patients (median 141 vs. 200 days). Disease duration and prior biologic use had the greatest impact on becoming an SRe, with no strong association among these independent variables. At baseline, there were no significant differences in the serum biomarker levels of IL-17A, IL-17F, IL-22 and β-defensin 2 between SDD and LDD patients, or between SRe and non-SRe patients. Guselkumab rapidly decreased these markers of systemic inflammation across all patient groups analysed at W4. Guselkumab was well tolerated.

Conclusions:
Guselkumab efficacy was consistent across subpopulations, on the skin and systemically. The proportion of SRes was higher in SDD than LDD patients, indicating early treatment intervention may improve clinical outcomes.