Along with my regular psoriasis I now have sebopsoriasis around my nostrils and down the sides of my nose. It is so sore (obviously not helped by having to wear face masks - but not for much longer!), dry, itchy, unslightly. Dermatologist prescribed protopic but that’s not helped. Does anyone else suffer from this and has any tips on how to manage it? I’m really self conscious of it.

This study investigated whether selected clinical/serum biomarkers were associated with remission duration, and psoriasis clearance at the end of phototherapy.

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Background:
Remission duration and treatment response following phototherapy for psoriasis are highly variable and factors influencing these are poorly understood.

Objectives:
Our primary outcome was to investigate whether selected clinical/serum biomarkers were associated with remission duration, and secondly with psoriasis clearance at the end of phototherapy. In addition, we looked at whether early trajectory of UVB clearance was associated with final clearance outcome.

Methods:
We performed a prospective cohort study of 100 psoriasis patients, routinely prescribed Narrowband UVB and measured selected clinical and biochemical biomarkers, including weekly PASI (psoriasis-area-and-severity-index) scores. Patients were followed up for 18-months.

Results:
The median time to relapse was 6-months (95% CI 5-18) if PASI90 was achieved, and 4-months (95% CI 3-9) if less than PASI90 was achieved. Achieving PASI100 did not result in prolonged remission.
On UVB completion, the median final PASI (n=96) was 1.0 (IQR 0.5, 1.6) with 78 (81%) achieving PASI75 and 39 (41%) achieving PASI90. Improved PASI90 response was significantly associated with lower BMI, higher baseline PASI, non-smoking status and lower cumulative NbUVB. Serum levels of C reactive protein (CRP) and vitamin D were not associated with clearance or remission duration.
Early treatment response from weeks 2-3 was predictive of final outcome. For example, achieving PASI30 at week 3 was significantly associated with PASI90 at the end of the course (36/77 (51%) versus 2/24 (8%), p < 0.001).

Conclusions:
Raised BMI and positive smoking-status predicted poorer phototherapy response. For the first time, we have shown that PASI clearance trajectory over the first 2-3 weeks of UVB, can predict psoriasis clearance. This is an important new step towards developing psoriasis personalised prescribing, which can now be formally tested in clinical trials. These simple clinical measures can be used to inform patient treatment expectations; allowing treatment modifications and/or switching to alternative therapies.

This cohort study looked at the effect of methotrexate and targeted immunosuppression on humoral and cellular immune responses to the COVID-19 vaccine BNT162b2

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Background:
Patients on therapeutic immunosuppressants for immune-mediated inflammatory diseases were excluded from COVID-19 vaccine trials. We therefore aimed to evaluate humoral and cellular immune responses to COVID-19 vaccine BNT162b2 (Pfizer-BioNTech) in patients taking methotrexate and commonly used targeted biological therapies, compared with healthy controls. Given the roll-out of extended interval vaccination programmes to maximise population coverage, we present findings after the first dose.

Methods:
In this cohort study, we recruited consecutive patients with a dermatologist-confirmed diagnosis of psoriasis who were receiving methotrexate or targeted biological monotherapy (tumour necrosis factor [TNF] inhibitors, interleukin [IL]-17 inhibitors, or IL-23 inhibitors) from a specialist psoriasis centre serving London and South East England. Consecutive volunteers without psoriasis and not receiving systemic immunosuppression who presented for vaccination at Guy's and St Thomas' NHS Foundation Trust (London, UK) were included as the healthy control cohort. All participants had to be eligible to receive the BNT162b2 vaccine. Immunogenicity was evaluated immediately before and on day 28 (±2 days) after vaccination. The primary outcomes were humoral immunity to the SARS-CoV-2 spike glycoprotein, defined as neutralising antibody responses to wild-type SARS-CoV-2, and spike-specific T-cell responses (including interferon-γ, IL-2, and IL-21) 28 days after vaccination.

Findings:
Between Jan 14 and April 4, 2021, 84 patients with psoriasis (17 on methotrexate, 27 on TNF inhibitors, 15 on IL-17 inhibitors, and 25 on IL-23 inhibitors) and 17 healthy controls were included. The study population had a median age of 43 years (IQR 31–52), with 56 (55%) males, 45 (45%) females, and 85 (84%) participants of White ethnicity. Seroconversion rates were lower in patients receiving immunosuppressants (60 [78%; 95% CI 67–87] of 77) than in controls (17 [100%; 80–100] of 17), with the lowest rate in those receiving methotrexate (seven [47%; 21–73] of 15). Neutralising activity against wild-type SARS-CoV-2 was significantly lower in patients receiving methotrexate (median 50% inhibitory dilution 129 [IQR 40–236]) than in controls (317 [213–487], p=0·0032), but was preserved in those receiving targeted biologics (269 [141–418]). Neutralising titres against the B.1.1.7 variant were similarly low in all participants. Cellular immune responses were induced in all groups, and were not attenuated in patients receiving methotrexate or targeted biologics compared with controls.

Interpretation:
Functional humoral immunity to a single dose of BNT162b2 is impaired by methotrexate but not by targeted biologics, whereas cellular responses are preserved. Seroconversion alone might not adequately reflect vaccine immunogenicity in individuals with immune-mediated inflammatory diseases receiving therapeutic immunosuppression. Real-world pharmacovigilance studies will determine how these findings reflect clinical effectiveness.

Hi all. I have a question for those who are familiar and have personal experience with TALTZ. I got on TALTZ because I have inverse psoriasis in the under carriage area. My face (though it’s flared in the past) had been clear for about 6 months before getting on TALTZ. I have had 2 injections. My face is now flaring pretty bad. Is that a temporary side affect? Should I press on? Or quit immediately?

As I reported in my introduction topic, I would talk to my rheumatologist about starting Mtx. His assistant nurse had called me a few weeks back, about de Mri results, and she had said that they would start with Mtx and if that didn't help they would switch to Humira.

But why start with Mtx if you're not sure what it does for PsA? I also told in my introduction topic, that I had found a video on Youtube in which my rheumatologist himself indicates that it is unknown whether Mtx actually works for PsA. 
Given the many negative reports, but also positive reports about Mtx, I myself had a hesitant attitude towards it. Why start with Mtx if you, as a rheumatologist, don't support it yourself? And why not immediately start on the Humira?

So last Tuesday I went for a consultation with my rheumatologist and told him what my reluctance was towards starting Mtx. 
Of course he indicated that it is an insurance policy thing and also the guidelines within the Netherlands, so Mtx is the first choice of treatment, blabla bla bla...

To which I indicated: Yes that's a good story, but not enough for me, because I read that several studies indicate that Mtx does not do much for PsA, that they do not know what it does anyway. And besides, there is a video of you on Youtube in which you indicate that you also do not know whether it really works. So how do you substantiate the choice to start with Mtx?

He looked at me in surprise 
I said: I told you that I have Autism and that I am not a patient like others, I research everything in advance, down to the semicolon, so substantiate your story  

He started laughing really hard and he said “shit, I'm getting caught on my own words here, very good!.
 
He didn't mind at all that I confronted him about the research end video and was impressed that I had sorted out so much information.
He said, “As a rheumatologist I can bound the rules, my assitent nurse is not allowed to do that. I understand that she stated to start with Mtx. But I can deviate from the rules. Obviously is by Mri and also diagnosed, you have axial PsA, and if you don't want to use Mtx, I immediately will let you start with Humira, which I also think is the best option for you.
So I said: that's what I want, no Mtx, but the Humira.

And today I will start with the Humira. I have to pick up the injections at the pharmacy of the hospital later this day. Than go to the rheumatism nurse for a injection instruction and my first injection of Humira will be immediately made.

I'm glad I got into the discussion with my rheumatologist and he went along with it. I'm realy glad I chose him as my rheumatologist. When I told him that the pain is sometimes unbearable, my quality of life is really F.ckedup , that I sometimes couldn't stand it anymore, he also indicated that he understood that very well. (sometime it's very nice to be heard).

If the Humira does not help me, the pain in my neck remains unbearable, he has promised to send me to the pain clinic. So at least he won't let me down and won't send me away like all the other rheumatologists in the past nine years who send me away to the psychologist 

I am curious, I hope the Humira will work for me, that I will hardly get any side effects and that I will finally be freed from stiffness and pain after more than 9 years, I hope so! The most important thing for me is that my quality of life gets better than it is now, that's what I'm going for! 

Y’all, I’m scared!!   

I’m about to do my first auto injection of Taltz and I here it hurts like a mother. I had a regular injection of the stuff at my derm’s office 2 weeks ago and THAT even hurt more than a regular shot. Autoinjecter is supposed to be much worse.

So my questions: 

Which site on the body is best??
Any tips for making it less painful?? 

Thanks all!

Hey, everyone. I’ve never been in a forum before, so I hope I’m doing this right (not over sharing or whatever )  .

My skin issues started in 2019, with scaly crinkly skin under my eyes and around my mouth… and also on the lady bits (hence the concern with over sharing). I had no idea wtf was happening because while I’d dealt with occasional eczema patches between my fingers, at 42 years old I’d never had anything like psoriasis. Also, it’s not in my family. 

I had just stopped using a very strong cortisone cream. I think using it for so long (which apparently I wasn’t supposed to do) and then quitting it is what triggered an autoimmune disorder that most resembles inverse psoriasis down below and plaque psoriasis on my face. Which is why I’m here. 

My latest doc got me on TALTZ. I’ll go to the treatment page to ask questions about that. 

But as far as intros go: I’m 42, married (though I cannot fathom why he hasn’t hit the door yet since my issues have kept us from…. Over sharing again, sorry). I have 3 kids. 

Anyway, I hope to not feel so alone by talking to other people who deal with this, as well as get answers about how to cope. 

New EU and Industry-funded €21 million research project aims to improve diagnostic and therapeutic options for patients living with psoriatic arthritis.

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By looking into the disease mechanisms of psoriatic arthritis an international team of 26 research partners, pharmaceutical companies, SMEs and patient organisations, led by UCD, are collaborating in HIPPOCRATES a new €21 million research project which aims to improve diagnostic and therapeutic options for patients living with psoriatic arthritis.

By gaining a better understanding of the complex interplay between clinical and environmental factors, genotype and molecular pathways, the HIPPOCRATES team aims to enable earlier diagnosis and a more accurate prediction of disease progression. This will revolutionise treatment and deliver profound patient benefits.

The 5-year project, which has just commenced, has been funded by the Innovative Medicines Initiative (IMI 2), a Joint Undertaking (JU) of the European Union (EU) and the European Federation of Pharmaceutical Industries and Associations (EFPIA).

Of the total budget, 50% is being contributed by the EFPIA partners (Novartis [EFPIA lead], UCB [EFPIA Co-lead], Pfizer and BMS) and 50% by the EU.

Psoriatic arthritis (PsA) is a chronic immune-mediated inflammatory disease that affects joints and other components of the musculoskeletal system, together with skin involvement, in an estimated 5-10 million individuals in the EU.

The symptoms of the disease, including pain, joint stiffness and fatigue, can impact on many aspects of life including function and productivity. Overall, it is increasingly recognised that PsA is associated with multiple comorbidities, particularly those affecting mental health such as depression and those which promote the development of accelerated atherosclerosis and contribute to the observed increase in cardiovascular morbidity and mortality.

PsA most commonly develops on a background of established skin and/or nail psoriasis, however it can be difficult to diagnose as there are no diagnostic criteria or laboratory tests available. This can contribute to diagnostic delay and poor outcomes. PsA is characterised by considerable heterogeneity with regards to clinical features, disease progression and response to targeted therapies.

Future treatments will need to focus on earlier disease stages and be selected on the basis of detailed patient molecular profiling so as to limit poor long-term outcomes and possibly prevent the development of PsA altogether.

“We anticipate that the advances provided by HIPPOCRATES will result in significant new developments that improve patients’ quality of life,” said Professor Oliver FitzGerald, Newman Clinical Research Professor, UCD School of Medicine and the UCD Conway Institute of Biomedical and Biomolecular Research, and co-ordinator of the HIPPOCRATES consortium.

Atturos, a UCD clinical diagnostics spin-out company supported by NovaUCD, is among the HIPPOCRATES SME consortium partners. The company is focused on integrating molecular diagnostics into decision making tools to improve the health and quality of life of patients while also increasing the cost-effectiveness of healthcare systems.

Joint co-coordinator, Professor Stephen Pennington, Professor of Proteomics at the UCD School of Medicine and the UCD Conway Institute of Biomedical and Biomolecular Research and founder, Atturos said, “The advances will include the identification of sub-populations and endotypes, the validation of existing and identification of new biomarkers, improved imaging options and the development of a sustainable infrastructure for future PsA research.”

“This public-private partnership is a great opportunity to decipher this highly heterogenous disease, and to enable the development of novel PsA therapies and treatment strategies including precision medicine approaches,” added Dr Christine Huppertz, Senior Principal Scientist in the Disease Area Autoimmunity, Transplantation and Inflammation at Novartis, and EFPIA lead of the consortium.

"HIPPOCRATES offers the great promise of powerful new tools to advance both early diagnosis and treatment of patients with PsA. Additionally, and to further its effectiveness, HIPPOCRATES retains the focus on the patient, involving Patient Research Partner’s within all aspects of the project," added Denis O’Sullivan, Patient Representative Arm of GRAPPA-EU.

In order to achieve its goals, the HIPPOCRATES project will set up a single integrated database combining the cohorts and datasets of the most important European PsA studies and establish a Europe-wide library of relevant clinical biosamples.

HIPPOCRATES will also establish a large, prospective, observational study of 25,000 patients with psoriasis who will be recruited and followed on-line for development of PsA, with patient-centric blood sampling at defined intervals.

Furthermore, the team of experts will evaluate and validate newly discovered biomarker signatures for the early diagnosis of PsA, for the identification of psoriasis patients at risk of developing PsA, for the identification of PsA patients at highest risk of damage progression and for personalised or stratified treatment strategies so as to maximise treatment response.

Overall, HIPPOCRATES places particular emphasis on the involvement of patients, clinicians, primary care practitioners, regulators, SMEs (Oxford Biodynamics Limited and NEOTERYX Limited in addition to Atturos Limited) and relevant large industry to meet the needs of all stakeholders and to maximise the project’s impact.

Formed as a transdisciplinary consortium, the project team comprises 26 partner institutions from Belgium, Denmark, Germany, Ireland, Italy, Spain, Sweden, Switzerland, the Netherlands, the United Kingdom and the United States of America. The partners contribute a diverse range of backgrounds including clinical, scientific, data analytics, ethics, patient participation as well as SME and pharmaceutical industry expertise in pursuit of the ambitious goals set for the HIPPPOCRATES project.

Three year outcomes from the CIMPACT (NCT02346240) phase 3, Cimzia (certolizumab pegol) in moderate to severe plaque psoriasis.

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Background:
Certolizumab pegol (CZP) is an Fc-free, PEGylated anti-tumor necrosis factor biologic.

Objectives:
To report three-year outcomes from the CIMPACT (NCT02346240) phase 3, CZP in moderate to severe plaque psoriasis, randomized controlled trial.

Methods:
Adults were randomized 3:3:3:1 to CZP 200 mg every other week (Q2W), CZP 400 mg Q2W, etanercept biweekly, or placebo. At Week 16, CZP- and etanercept-treated PASI 75 responders were re-randomized to CZP 200 mg Q2W, CZP 400 mg Q4W, CZP 400 mg Q2W, or placebo for maintenance treatment; PASI 75 non-responders entered an open-label escape CZP 400 mg Q2W arm. Patients entering the open-label extension (OLE; Weeks 48-144) from blinded treatment received CZP 200 mg Q2W.

Results:
Double-blinded results have been reported previously. 261 patients received 200 mg Q2W upon OLE entry. PASI 75 response was maintained in patients continuing 200 mg Q2W treatment through Weeks 16-144 (Week 144: 96.2%). In patients dosed down at Week 48 (double-blinded 400 to 200 mg Q2W), PASI 75 decreased (Week 48: 98.7%; Week 144: 85.9%). In patients who received placebo through Weeks 16-48, PASI 75 response decreased (Week 48: 60.4%), then increased following Week 48 switch to 200 mg Q2W (Week 144: 95.1%). 48 and 36 patients initially randomized to 200 and 400 mg Q2W, respectively, were Week 16 PASI 75 non-responders and entered the escape arm; at Week 144, 71.8% and 78.2% achieved PASI 75. No new safety signals were identified.

Conclusions:
Response to CZP was durable over three years; no new safety signals were identified.

This months poll asks: How embarrassing do you find psoriasis

*Thank you to Jim for the suggestion

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

*Members usernames will not be shown in the poll.

This might be a silly question, but I'm going to ask it anyway  
Hopefuly users of Methotrexate can tell me more.

If you use Methotrexate, it has an effect on your immune system, the chance of contracting viruses and bacteria and resulting infections is greater.
But what about saying hello to people? Do you have to take this into account? I mean shaking hands and kissing? 

Unfortunately, here in the Netherlands we give eachother three kisses when we see eachother and also when we leave... 
For me thats on a weekend with friends, and there are always around 30 men, it will be 90 kisses when i see them and then usually also 90 when I leave. .. I also try to sneak out ... but thats not always possible  

But have you received any advice about this when using Methotrexate? I can't find anything about this form of contact.

I've been reading on this Forum for a while now, it was Caroline who told me about this Forum, so thanks Caroline!  And now I'll introduce myself. My name is Yvon and I come from the Netherlands.

I have psoriasis since I was a child and I got physical complaints when I was 38, I am now 48 years old.
Complaints like back pain, terrible fatigue, painful knees, all my joints hurt, at least the attachments/tendons.

Hospital in and out. I got diagnoses like fibromyalgia, osteoarthritis and the worst "it must be psychological go see the psychiatrist".
Last year the pain became so bad, that I once again went to visit the general pratitioner, who wanted to send me away again, she said that it would be muscle overload. At my insistence, I was referred to the rheumatologist (the fourth), this time a rheumatologist who specializes in psoriatic arthritis.

During the first conversation he immediately confirmed my own suspicion, I also have psoriatic arthritis. He found it unimaginable that I was sent away so much in those 10 years because the signals for PsA were obvious.

Because here in the Netherlands it has to be demonstrated on the basis of redness and swelling and possibly confirmation via an ultrasound and this was all absent with me, I could only get the nsaids/painkillers.
This didn't work and I kept calling the rheumatologist, also because I got an unbearable nerve compression in my neck. Then they did an MRI of my neck and pelvis. It showed that the vertebrae were inflamed, deformities on my vertebrae and there were many spots on my pelvis and sacrum that indicated that there had been inflammation in the past.

In a week I will start with Methodextrate by injection, which I am not looking forward to. But Mtx is also the first choice in the Netherlands for treating PsA, only if that does not work well or you get too many side effects, you can switch to biologicals such as Humira. That's an insurance story here. While research here in the Netherlands indicates that MTX does not work sufficiently for PsA.

Anyway, I hope it will work, because the pain is driving me crazy. And in the meantime, I enjoy reading this Forum, to read your experiences. It's nice for me to see so much recognition, then you're not alone.

Bimzelx (bimekizumab) gets a positive recommendation for psoriasis in the EU.

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UCB, announced today that the European Medicines Agency’s (EMA) Committee for Medicinal Products for Human Use (CHMP) has adopted a positive opinion recommending granting a marketing authorization for BIMZELX®* (bimekizumab), an investigational IL-17A and IL-17F inhibitor, for the treatment of moderate to severe plaque psoriasis in adults who are candidates for systemic therapy.

“This positive CHMP opinion is a significant regulatory milestone towards approval of bimekizumab in Europe. We’re delighted by today’s decision which recognizes the strength of the psoriasis clinical development program. Bimekizumab is testament to our commitment to advancing science in immuno-dermatology, addressing unmet needs and improving patient outcomes,” said Emmanuel Caeymaex, Executive Vice President, Immunology Solutions and Head of U.S., UCB.

The positive CHMP opinion is supported by results from three Phase 3 studies – BE VIVID, BE READY and BE SURE – which evaluated the efficacy and safety of bimekizumab in adults with moderate to severe plaque psoriasis.  All studies met their co-primary and all ranked secondary endpoints. Patients treated with bimekizumab achieved superior levels of skin clearance (PASI 90 and IGA 0/1**) at week 16 compared to those who received adalimumab, placebo and ustekinumab.1,2,3 Clinical responses achieved with bimekizumab at week 16 were maintained up to one year in all studies. The most frequently reported treatment emergent adverse events in bimekizumab-treated patients were nasopharyngitis, oral candidiasis, and upper respiratory tract infection.

If marketing authorization is granted by the European Commission, bimekizumab will become the first approved treatment for patients with moderate to severe plaque psoriasis in the European Union that is designed to selectively and directly inhibit both IL-17A and IL-17F, two key cytokines driving inflammatory processes. The positive CHMP opinion is a scientific recommendation which is shared with the European Commission for the adoption of a decision on an EU-wide marketing authorization. A European Commission marketing authorization through the centralized procedure is valid in all European Union Member States, as well as the European Economic Area countries Iceland, Liechtenstein and Norway.

UCB is committed to bringing bimekizumab to patients worldwide. Bimekizumab is currently under review by the U.S. Food and Drug Administration for the treatment of adults with moderate to severe plaque psoriasis. Regulatory reviews are also underway in Japan, Australia and Canada. The efficacy and safety of bimekizumab are also being evaluated in Phase 3 trials in psoriatic arthritis,  ankylosing spondylitis, non-radiographic axial spondyloarthritis, and hidradenitis suppurativa.

Following on from this thread Could covid vaccine affect efficacy of psoriasis treatments I thought this may be of interest.

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A 46-year-old Caucasian man presented with psoriasis flare-up, which occurred a day after second dose of COVID-19 Pfizer-BioNTech BNT16B2b2 mRNA vaccine. The patient had been suffering from plaque psoriasis for 24 years. During the last 21 months, his psoriasis was completely clear (PASI 0 points) due to deucravacitinib treatment in the clinical trial. Before entering the clinical trial two years ago, the severity of his psoriasis was assessed as PASI 18 points. For the last 48 weeks, he has been in the open-label phase of above-mentioned trial receiving deucravacitinib 6 mg orally once daily.

Regarding COVID-19 vaccination, the patient received his first dose of Pfizer-BioNTech BNT16B2b2 mRNA vaccine and experienced only pain at the site of vaccine injection lasting for 24 hours. Five days after the second dose (administered 3 weeks after the first shot), he noticed psoriatic lesions on his lower legs, which quickly spread with time extending to the whole lower extremities and trunk. He presented again with pain at the injection site accompanied with fever up to 39°C and malaise lasting for 48 hours. On admission, one week after the disease exacerbation, physical examination revealed highly inflammatory, psoriatic plaques with gross, silver scaling localized mostly on patient’s lower legs. Moreover, multiple, smaller lesions were visible on patient’s back and chest. The patient did not complain of neither associated itch nor pain. The PASI score was 18.5 points.

Treatment of chronic inflammatory disorders changed drastically during COVID-19 pandemic. Problems with drugs availability and irregular consultations with dermatologist caused many patients to suffer from exacerbations. Moreover, the pandemic triggered insecurity about the use of novel treatment modalities. Yet, it is important to emphasize that psoriatic patients may present higher risk of respiratory diseases because of systemic inflammation. Therefore, and due to the lack of data on safety of novel, mRNA COVID-19 vaccines, concern on its impact on patients suffering from inflammatory diseases has been raised.

Vaccination, in general, is an uncommon factor triggering psoriasis flares; nevertheless, the association of vaccination with the new development or exacerbation of this skin disease has been reported. The available reports include mostly cases of psoriasis flare-ups after vaccination for influenza (H1N1), pneumococcal pneumonia and yellow fever. However, until now, there was no well-described association with novel mRNA COVID-19 vaccines. Possible cutaneous reactions after COVID-19 vaccination were characterized recently in a registry-based study of 414 cases by McMahon et al.

Among others, authors described cases of local site reactions, swelling, erythema, urticaria, erythromelalgia and flares of existing dermatologic disorders. Regarding the prevalence of psoriasis flare-ups, amid 414 cutaneous reactions, authors stated that it occurred only in two patients, which seems to be very rare. Moreover, there was no explicit description of skin lesions, nor its association with particular vaccination.6 Therefore, to the best of our knowledge, our case is the first, well-described example of psoriatic flare-up after COVID-19 Pfizer-BioNTech BNT16B2b2 mRNA vaccine. The mechanisms responsible for psoriasis exacerbation after vaccination are yet to be understood. It is possible that similarly to influenza vaccines, it may be caused by both dysregulation of immune system due to viral components and vaccine adjuvants.

Moreover, mRNA vaccines, like BCG or diphtheria, may cause a significant increase in IL-6 production and recruitment of Th17 cells, which play an important role in pathomechanism of psoriasis. Nevertheless, even though psoriasis flares are rare, because of extensive and rapid vaccination, medical professionals should pay close attention to possible adverse effects and counteract the worsening of patient’s clinical condition.

What are your thoughts on the covid vaccine having an affect on the efficacy of your psoriasis treatment. ?

I'm on Tremfya and have noticed the psoriatic arthritis isn't doing so well with my last two shots, and as usual I always try to understand why. But apart from thinking the Tremfya isn't working as well as it did, I'm stumped for an answer.

But I started looking at when I took my Tremfya in comparison with the dates of the Pfizer covid vaccine to see if there could be a link.

Tremfya:

24 April
19 June

Pfizer

05 May
14 June

When I look back at my journal it's 15 May that I said the psoriatic arthritis score had shot up from 7 to 12, since then my score has slowly gone up and it's now on 16.

Here is what I'm wondering.

Tremfya is slowing things down and doing it's job, but then along comes Pfizer which wants to create antibodies. So there is a boxing match going on in my system and both drugs are knocking hell out of each other.

The psoriatic arthritis is getting worse because Tremfya is now having to punch away at Pfizer whilst at the same time fight off psoriasis and psoriatic arthritis.

If this is the case its going to go on for a while as I have my third Pfizer jab on 15 July less than 4 weeks after my Tremfya. 

Thoughts ?

I was wondering what the worst area has been for people for psoriasis.  Not necessarily the longest, but either the area that has been most resistant to clearing or just the area that you feel has bothered you the most.

Mine, definitely ears, scalp area.

The ActiPso tool was used in a prospective study in psoriasis patients.

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Background:
Assessment of psoriasis is exclusively done measuring severity using somatic scores such as the psoriasis area and severity index (PASI) or patient-reported outcomes such as the dermatology life quality index (DLQI). There is no established tool to measure a patient’s individual psoriasis activity over time.

Objectives:
Development of a new tool to classify psoriasis activity types.

Methods:
Open patient interviews were performed and adapted in several steps and by using different groups of patients. Wording of the tool’s axis and description how to use it was optimized with the input of patients. The final ActiPso tool was used in a prospective study in psoriasis patients.

Results:
Four activity types could be identified describing psoriasis intensity (eg. severity, itch, pain) over one typical year and an event/trigger type describing flares.
In the study in 586 psoriasis patients of the 536 patients eligible for analysis 40.9% self-classified as type 1 (“stable”), 22.6 % as type 2 (“unstable”), 30.6 % as type 3 (“winter-type”), and 6.0 % as type 4 (“summer-type”), respectively. Flares of psoriasis as identified by the event/trigger type were reported in 36.1 % of patients with activity type 1, 67.8 % with type 2, 73.8 % of type 3, and 59.4 % of type 4, respectively.

Limitations:
In regions with no seasonal variations ActiPso types 3 and 4 may not apply.

Conclusions:
Interviewed patients were able to describe their course of psoriasis disease and to name potential triggering factors. By doing so activity types of psoriasis were defined for the first time and the importance of events/triggers for flares described and integrated into ActiPso types as a basis for advanced patient-centric management.

This study suggests Siliq / Kyntheum (brodalumab) was associated with higher levels of complete clearance and greater cumulative benefit over time compared with Stelara (ustekinumab)

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Background:
The pathway for treatment of psoriasis is partly dependent upon disease severity and patients may experience inadequate response at any point along the treatment pathway. Patients who repeatedly fail therapy represent a population in whom effective and well-tolerated treatment options are limited.

Objectives:
To investigate and describe patients achieving Psoriasis Area and Severity Index (PASI) 100 and cumulative treatment benefit over time in patients with moderate-to-severe psoriasis receiving brodalumab or ustekinumab by prior treatment.

Methods:
We conducted a post hoc analysis of data from two phase 3, randomized, controlled, 52-week AMAGINE trials of brodalumab to describe patients who achieved complete clearance as measured by PASI 100 by prior treatment subgroup (naïve to systemic and biologic treatment, systemic-treated but biologic-naïve, biologic-treated without failure, and biologic-treated with failure). A competing risk model was used to assess cumulative incidence over a 52-week period with outcomes of PASI 100 or inadequate response. Cumulative clinical benefit of treatment was determined with an area under the curve analysis.

Results:
The 52-week cumulative incidence of patients achieving PASI 100 were consistently higher for brodalumab vs. ustekinumab across treatment pathway subgroups (76% vs. 58% in systemic/biologic-naïve patients, 78% vs. 55% in systemic-treated/biologic-naïve patients, 75% vs. 41% in biologic-treated patients without failure, and 70% vs. 30% in biologic-treated patients with failure). Rates of inadequate response were lower with brodalumab compared with ustekinumab across all subgroups. Cumulative treatment benefit was also higher for all subgroups treated with brodalumab compared with those treated with ustekinumab.

Conclusion:
Treatment with brodalumab was associated with higher levels of complete clearance and greater cumulative benefit over time compared with ustekinumab, in patients with moderate-to-severe psoriasis, regardless of prior treatment experience.

Cosentyx has received U.S. Food and Drug Administration (FDA) approval for treatment of children with psoriasis.

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Novartis today announced the U.S. Food and Drug Administration (FDA) has approved Cosentyx® (secukinumab) for the treatment of moderate to severe plaque psoriasis in pediatric patients six years and older who are candidates for systemic therapy or phototherapy. This is the first approval for Cosentyx in a pediatric population in the US. The Cosentyx clinical profile is supported by five years of adult data showing long-lasting efficacy and a consistent safety profile across moderate to severe plaque psoriasis, psoriatic arthritis and ankylosing spondylitis.

The approved pediatric dosing for Cosentyx is 75 mg or 150 mg depending on the child’s weight at the time of dosing and is administered by subcutaneous injection every four weeks after an initial loading regimen. After initial counseling and proper training in injection technique, Cosentyx can be administered by an adult caregiver outside of a healthcare provider’s office via a single-dose prefilled syringe or Sensoready® pen.

This Cosentyx approval is based on two Phase III studies evaluating the use of Cosentyx in children aged 6 to 18 years with plaque psoriasis. The safety profile reported in these trials was consistent with the safety profile reported in adult plaque psoriasis trials. No new safety signals were observed.

The first study, which evaluated efficacy and safety, was a 52-week (236 weeks total), randomized, double-blind, placebo- and active-controlled study which included 162 children six years of age and older with severe plaque psoriasis. The data showed Cosentyx reduced psoriasis severity at Week 12 compared with placebo as demonstrated by the following efficacy results by baseline weight strata for the approved doses (75mg for <50kg and 150mg for ≥50kg): Psoriasis Area Severity Index (PASI) 75 response (55% 75 mg vs 10% placebo (N=22 and N=20, respectively), 86% 150 mg vs 19% placebo (N=21 and N=21, respectively), 70% total Cosentyx vs 15% total placebo (N=43 and N=41, respectively) and Investigator’s Global Assessment modified 2011 (IGA) “clear” or “almost clear” skin response (32% 75 mg vs 5% placebo, 81% 150 mg vs 5% placebo, 56% total Cosentyx vs 5% total placebo), co-primary endpoints of the study.

The second Phase III study, which assessed safety, was a randomized open-label, 208-week trial of 84 subjects six years of age and older with moderate to severe plaque psoriasis.

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