Posted a long intro for backstory on my psoriasis.

Saw a dermatologist this week, actually was a good visit despite her solution for me to start methotrexate and the biologics. However I am far from ready for drugs, still hoping to find improvements and ideally remission naturally.

Been off my diet for a while now and off the diet for me is just eating chocolate and regular oats pretty often (baking cookies or banana bread, no refined sugar though), and the odd cheat meal from a restaurant, few pizzas, servings of french fries, dessert here n there otherwise my normal is gluten free, sugar free, processed food free, whole food diet. Lots of protein, healthy fat sources, carbs are brown rice, sweet potatoes, veggies, fruit. Been planning to get back to being very strict but been slacking. 

Anyways, derm was talking about the connection between strep and psoriasis. Wanted to test me for group a (throat) and group b (intestinal/colon) strep. She said if group a is present, then the plan is remove tonsils, if group b is present, go on penicillin (antibiotics). Well no group a for me but tested positive for group b.

I am kind of glad knowing there is possibly something that is a problem that can be targeted and corrected, but nervous to start on antibiotics. I definitely want to kill off the strep in my intestines. You see alot about psoriasis being related to the gut and fix the gut and yada yada which sounds good but what does fix the gut mean. Its kind of like the boogeyman, you don't know what is actually the problem and best solution. Is it the candida diet, is it a whole food diet, is it come sort of short term cleanse? Do you do it for 3 months, 6? What do you take, what do you eat, what DONT you eat. Theres alot of conflicting information available.

I had done strict diet for 5 months, including probiotics and even leaky gut supplements not long ago but didn't find any improvement at all and eventually started being less and less strict to where I am now. I would still say my diet is excellent but I feel like I could be better and more disciplined and focused.

So now I know I have to deal with this strep bacteria. Antibiotics are the easiest answer but I am just a bit concerned. Ive done antibiotics in the past and believe they played a big part and messing up my gut flora in the first place. Maybe I can do it right this time tho. I am looking for any feedback with anyone having similar experience.

Thinking I do the penicillin for 2 weeks, but also take a probiotic and eat completely clean (been wanting to commit to a diet again for 6 months, this is already 90% my diet but making it 100%). No chocolate, nothing like honey, just beef, chicken, quality fish, eggs, presoaked and drained brown rice, sweet potatoes, rutabagas, carrots, beets, presoaked and drained and fermented gluten free organic oats, fruits, homemade coconut milk yogurt, sauerkraut, nuts like cashews, walnuts, almonds, basically the candida diet in regards to spices and foods, little modified for myself. Reason I soak the rice and oats it to remove any possible pesticides or toxins and starch from the rice, i donno if anyone else does this. For the oats i've been wanting to start fermenting them using a probiotic powder (from a pill). Ive been thinking I should cut out coffee, just test it out, tho i love coffee.

So im probably gonna start this immediately, would be nice to hear from anyone with experience regarding antibiotics. Think it will make my psoriasis worse immediately? The idea is that this will start me on a complete reset to correct and fix my gut flora. As long as I prepare myself with an appropriate diet and supplement probiotic pills and foods and that doing so will allow my body to start healing more.

Planning to use the Renew Life brand 50 billion probiotic. Ill take as directed as well as use it to make fermented oat and coconut milk yogurt.

Thoughts?

Hi all - I was looking for any info as to whether or not common side effects of bimzelx - wear off - go away!
Best wishes to Fred - I really hope your treatment makes you better.
My own story is that I am an allergic type - Im the awkward one who always gets those 'rare' side effects! 

I have had 2 loading doses so far of Bimzelx and I have not taken my third one - I am told I can skip a dose and take the next one when I feel better...

mmm...when I feel better....my story is below - not necessary to read! its just a brief history in time - of infections...

My question is lovely people - is there anyone out there who has had similar common side effects with bimzelx - and...did they wear off? Im just getting zero help from the people running the study Im on - or the dermatologists - I feel like Im being kept in the dark...the manufactrures and so called yellow card scheme must surely have data? after all - they state the side effects....maybe I should go to them?
any tips greatly apprecitated - Ive been so ill I just dont know whether to continue this or not...

best wishes


since starting bioligics in february - Ive had 4 loads of anti biotics for infections - one a throat thing the others UTI's. 
Ive been in a lot of pain with un diagnosed stomach and digestion problems so await test results for IBS and coeliac. Oh I also have medication now for oral thrush.... I had an allergic reaction to amgevita and started bimzelx in April this year. Ive felt ill ever since...this is not me!

Does anyone notice psoriasis, and dupytren’s at ring finger and palm, and female hyperplasia? Or psoriasis started in one location, then collagen overgrowth of skin cells in another location some years later, like it spreads over several years? He’s anyone used gene therapy. Has anyone had genetic mapping to find alleles or amino acid sequences that are not normal. Gene mapping is about $700.00 in the Los Angeles, California area clinics and San Francisco clinics. Currently gene mapping is commonly used to find breast cancer such as Brac. I read up to 25%of people in Great Britain have collagen overgrowth issue in the palm of one of their hands during their lifetime.

This study investigated the association between serine metabolism and psoriatic skin inflammation.

Quote:

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Background:
Serine metabolism is crucial for tumor oncogenesis and immune responses. S-adenosyl methionine (SAM), a methyl donor, is typically derived from serine-driven one-carbon metabolism. However, the involvement of serine metabolism in psoriatic skin inflammation remains unclear.

Objectives:
To investigate the association between serine metabolism and psoriatic skin inflammation.

Methods:
Clinical samples were collected from patients with psoriasis and the expression of serine biosynthesis enzymes was evaluated. The HaCaT human keratinocyte cell line was transfected with small interfering RNA (siRNA) of key enzyme or treated with inhibitors. RNA sequencing and DNA methylation assays were performed to elucidate the mechanisms underlying serine metabolism-regulated psoriatic keratinocyte inflammation An imiquimod (IMQ)-induced psoriasis mouse model was established to determine the effect of the SAM administration on psoriatic skin inflammation.

Results:
The expression of serine synthesis pathway enzymes, including the first rate-limiting enzyme in serine biosynthesis, phosphoglycerate dehydrogenase (PHGDH), was downregulated in the epidermal lesions of patients with psoriasis compared with that in healthy controls. Suppressing PHGDH in keratinocytes promoted the production of proinflammatory cytokines and enrichment of psoriatic-related signaling pathways, including the tumor necrosis factor-alpha (TNF-α) signaling pathway, interleukin (IL)-17 signaling pathway, and NF-κB signaling pathway. In particular, PHGDH inhibition markedly promoted the secretion of IL-6 in keratinocytes with or without IL-17A, IL-22, IL-1α, oncostatin M, and TNF-α (mix) stimulation. Mechanistically, PHGDH inhibition upregulated the expression of IL-6 by inhibiting SAM-dependent DNA methylation at the promoter and increasing the binding of myocyte enhancer factor 2A. Furthermore, PHGDH inhibition increased the secretion of IL-6 by increasing the activation of NF-κB via SAM inhibition. SAM treatment effectively alleviated IMQ-induced psoriasis-like skin inflammation in mice.

Conclusions:
Our study revealed the crucial role of PHGDH in antagonizing psoriatic skin inflammation and indicated that targeting serine metabolism may represent a novel therapeutic strategy for treating psoriasis.

In his first time trying to make a new dish, my husband inadvertently added 1.5 teaspoons of black pepper to a recipe that made four small crabcakes.  Additionally, another seasoning in the recipe, Old Bay Spice, has a mix of ground peppers in its ingredients.  I ate one of the cakes (smothered in plain yogurt to cool it down).  

Very soon, patchy areas that rarely itch began to itch like crazy.  And this morning, several patches are a little more active.  

I think the excessive pepper caused this reaction.  Has anything like this ever happened to you?

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.

I have been contacted by someone (not a member) that it is no longer possible to read Psoriasis Club's posts on what was once known as Twitter but now just a dead bird without logging-in. I have checked it for myself and it is true.

Why am I bothered and posting this ?

#1 We have had a lot of followers on Twitter (some of you found us that way) and some still prefer reading the links I post to the forum rather than joining us here.

#2 I used to encourage our members to check out Twitter if you ever see the forum down as I will post updates there, and the best thing about it was that you could read my posts without needing an account.

#3 I did and still do post links to new threads on the public boards at Psoriasis Club as it does did bring us new members.

Obviesly there is nothing I can do about it and I will be keeping our account open, but I suggest you check out the bottom right of this page where it says "Social" I have put the official places that I post.

You will see we have 3 accounts Mastodon, PostNews and Twitter all have the same content, with the first two you don't need an account to read our posts but for the third one you now will.

I will continue to post on all three for now.

It's your choice if you want to use or follow Psoriasis Club, but I would say if you ever want to know what is going on if the forum is down or you want to know about new threads in the public boards Mastodon would be my choice as it's just like us "Independent" 

*Thank you to the person that contacted me about the change on the dead bird, I wouldn't have known as I have to log-in to post.

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.

Quote:

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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.

Quote:

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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.

Quote:

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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.”