has anyone any experience in this? i only have a small patch of flexural psoriasis (groin area) about the size of a hand palm, but it is sore (3 out of 5) and itchy (again 3 out of 5) have tried hydrocortisone (1%) ointments, eumovate (0.05% w/w clobetasone butyrate) Silkis (calcitriol 3 mg / 1gm ointment. emmolients such as Diprobase & Epaderm for moisturing. I still have the pustular rash that i started with about 3 months ago. it wans but never really disappears completely. I am currently on a treatment break as directed by GP. I have read on other forums about increasing Vitamin D3 helps may other psoriasis sufferer's and have seen varying levels of dosage, from 1000mg to 10,000mg. I was looking for thoughts about this from the users here...any advice anyone? thanks in advance

These results follow on from this thread Piclidenoson submits registration plans for psoriasis

Quote:

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Objective:
A3 adenosine receptor (A3AR) is overexpressed in the skin and peripheral blood mononuclear cells of psoriasis patients. We investigated the efficacy/safety of piclidenoson (CF101), an orally bioavailable A3AR agonist that inhibits IL-17 and IL-23 production in keratinocytes, in moderate-to-severe plaque psoriasis.

Methods:
The randomized, placebo- and active-controlled, double-blind phase 3 COMFORT-1 trial randomized patients (3:3:3:2) to piclidenoson 2 mg BID, piclidenoson 3 mg BID, apremilast 30 mg BID or placebo. At Week 16, patients in the placebo arm were re-randomized (1:1:1) to piclidenoson 2 mg BID, piclidenoson 3 mg BID or apremilast 30 mg BID. The primary end point was the proportion of patients achieving ≥75% improvement in Psoriasis Area and Severity Index (PASI) from baseline (PASI-75) at Week 16 versus placebo.

Results:
A total of 529 patients were randomized and received ≥1 dose of study medication (safety population). The efficacy analysis population for the primary end point included 426 patients (piclidenoson 2 mg BID, 127; piclidenoson 3 mg BID, 103; apremilast, 118; placebo, 78). Piclidenoson at 2 and 3 mg BID exhibited similar efficacy. The primary end point was met with the 3 mg BID dose: PASI 75 rate of 9.7% versus 2.6% for piclidenoson versus placebo, p = 0.037. The PASI responses with piclidenoson continued to increase throughout the study period in a linear manner. At week 32, analysis in the per-protocol population showed that a greater proportion of patients in the piclidenoson 3 mg BID arm (51/88, 58.0%) achieved improvement from baseline in Psoriasis Disability Index (PDI) compared to apremilast (59/108, 55.1%), and the test for noninferiority trended towards significance (p = 0.072). The safety/tolerability profile of piclidenoson was excellent and superior to apremilast.

Conclusions:
Piclidenoson demonstrated efficacy responses that increased over time alongside a favourable safety profile. These findings support its continued clinical development as a psoriasis treatment.

I will link my first thread here (or ask Fred to) once it's determined how he wants to handle it.  However, I wanted a bit more uncluttered thread that deals with my experience of actually using Skyrizi.


Today I received my Skyrizi:




It was nicely packaged and as you can see the card has the white dot meaning that the temperature wasn't compromised (it would be red otherwise)

Two pens, Week 0 and week 4 (the next one will be week 16, I'll call for a refill at about 4 weeks before it's due)

Not much paperwork, one page describing how the temperature card works which a simple sentence of white is good and red is bad would have sufficed, but it was an in depth explanation which is expected when it comes to medical stuff.

4 pages of information.  Describing what Skyrizi is, side effects, etc.  Things you'd find on the webpage.

It came in an insulated box with two ice packs,

So, I'm not really ready for some reason but I will inject later today or tomorrow. 

I have psoriasis under 2 finger nails. Luckily for me 1 has cleared up (mostly) but my thumb nail is tough as old boots and I keep it short so I don’t catch it. I now have psoriasis under one toe nail. It’s lifting off and I’m unsure whether to cut it right down as far as possible as it sometimes catches on my sock. It’s only lifting on the left side but it’s nearly down to the bottom and I’m concerned it’ll get ripped off and that’ll hurt! Can anyone advise please.

I started seeing a new dermatologist. As we were going over medical history stuff, I mentioned that I had been diagnosed with NAFLD (nonalcoholic fatty liver disease) and she replied that was common for people with psoriasis. Which surprised me a bit as I hadn't heard that before, nor had it been mentioned to me so I did a little looking up on the internet to see what I could find. I found the following information which seemed to explain it best:

Although many people think of psoriasis primarily as a skin disease, it is a systemic condition that affects other organs as well. People with psoriasis have increased inflammation throughout the body, which increases the risk of developing comorbid conditions (more than one chronic disease at the same time). For example, people with psoriasis have a higher prevalence of fatty liver disease compared to the general population.

Psoriasis is associated with a higher risk for developing obesity (high body mass index), insulin resistance, and metabolic syndrome — factors that can also increase the risk of NAFLD. A person may be diagnosed with metabolic syndrome if they have three of the following:

Abdominal obesity
High triglyceride levels
Low HDL cholesterol levels
High glucose levels
Hypertension (high blood pressure)
People with metabolic syndrome and severe psoriasis are at a higher risk of developing NAFLD.

I tick quite a few of those. Also with inflammation being mentioned it has made me wonder about other things going on with me and how it all ties in together. Of course having arthritis is a factor for the inflammation as well.

So now I'm really hopeful to see how Skyrizi will work out for me (calling them next week to have them ship to me). Maybe if my psoriasis is calmed down so might some other stuff? It would be nice if it works that way!

Efficacy of long-term Skyrizi (risankizumab) treatment for moderate-to-severe plaque psoriasis over 256 weeks.

Quote:

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Background:
Psoriasis is an inflammatory skin disease that impacts a heterogeneous group of patients and can have multiple clinical manifestations. Risankizumab is approved for the treatment of moderate-to-severe plaque psoriasis.

Objectives:
To evaluate the long-term efficacy of risankizumab according to baseline patient characteristics, and for the treatment of high-impact disease manifestations (nail, scalp and palmoplantar psoriasis), through 256 weeks of continuous treatment in the phase 3 LIMMitless study.

Methods:
This subgroup analysis evaluated pooled data from patients with moderate-to-severe plaque psoriasis who were randomized to risankizumab 150 mg during two double-blind, phase 3, 52-week base studies (UltIMMa-1/2; NCT02684370/NCT02684357) and were enrolled in the phase 3 LIMMitless open-label extension study (NCT03047395). Subgroup assessments included the proportion of patients who achieved ≥90%/100% improvement in Psoriasis Area and Severity Index (PASI 90/100). Among patients with nail, scalp and/or palmoplantar psoriasis in addition to skin psoriasis, assessments included changes from baseline in and resolution of these three psoriatic manifestations.

Results:
Overall, a numerically similar proportion of patients (N = 525) achieved PASI 90/100 through Week 256, regardless of their baseline age, sex, body mass index, weight, PASI or psoriatic arthritis status. Patients with nail, scalp and/or palmoplantar psoriasis experienced substantial improvements in manifestation-specific indices (mean improvement from baseline to Week 256 of >81%, >94% and >97%, respectively); in patients with all three manifestations (N = 121), 44.6% achieved complete clearance of these manifestations at Week 256.

Conclusions:
Risankizumab demonstrated generally consistent efficacy through 256 weeks across patient subgroups and showed durable long-term efficacy for psoriatic disease manifestations.

This study looked at pharmacogenetic biomarkers for Cosentyx (secukinumab) response in psoriasis patients.

Quote:

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Background:
Prediction of the response to a biological treatment in psoriasis patients would allow efficient treatment allocation.

Objective:
To identify polymorphisms associated with secukinumab response in psoriasis patients in a daily practice setting.

Methods:
We studied 180 SNPs in patients with moderate-to-severe plaque psoriasis recruited from 15 Spanish hospitals. Treatment effectiveness was evaluated by absolute PASI ≤3 and ≤1 at 6 and 12 months. Individuals were genotyped using a custom Taqman array. Multiple logistic regression models were generated. Sensitivity, specificity and area under the curve (AUC) were analysed.

Results:
A total of 173 patients were studied at 6 months, (67% achieved absolute PASI ≤ 3 and 65% PASI ≤ 1) and 162 at 12 months (75% achieved absolute PASI ≤ 3 and 64% PASI ≤ 1). Multivariable analysis showed the association of different sets of SNPs with the response to secukinumab. The model of absolute PASI≤3 at 6 months showed best values of sensitivity and specificity. Four SNPs were associated with the capability of achieving absolute PASI ≤ 3 at 6 months. rs1801274 (FCGR2A), rs2431697 (miR-146a) and rs10484554 (HLCw6) were identified as risk factors for failure to achieve absolute PASI≤3, while rs1051738 (PDE4A) was protective. AUC including these genotypes, weight of patients and history of biological therapy was 0.88 (95% CI 0.83–0.94), with a sensitivity of 48.6% and specificity of 95.7% to discriminate between both phenotypes.

Conclusion:
We have identified a series of polymorphisms associated with the response to secukinumab capable of predicting the potential response/non-response to this drug in patients with plaque psoriasis.

Had my cataracts done recently and got some psoriasis on one eyebrow, I think the sticky tape to keep the eye shield in place has made it flare though it didn't in the first one.

Obviously I can't use anything near the eye at the moment so I'm trying the good old substitute of coconut oil, I'll see how it goes.

This study looked at the effectiveness and safety of Taltz (ixekizumab) over 5 years.

Quote:

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Introduction:
Ixekizumab proved to be effective and safe for psoriasis treatment in several randomized clinical trials and real-life studies. Nevertheless, long-term real-world experiences are still lacking, with little data up to 4 years of treatment.

Objectives:
To analyse survival, effectiveness and safety of ixekizumab in a real-life cohort of patients affected by moderate-to-severe psoriasis or psoriatic arthritis up to 260 weeks (5 years).

Methods:
We included all patients treated with ixekizumab from December 2017 to March 2021. Drug survival (DS) was analysed in patients at risk for up to 5 years. Cox analysis was adopted to evaluate possible predictive factors of discontinuation. Psoriasis Area Severity Index (meanPASI and PASI100, 90, and ≤3) was used as outcomes of effectiveness on observed patients at 16, 52, 104, 156, 208 and 260 weeks. Logistic regression was performed to identify possible predictive factors of response.

Results:
DS was 65.5% at 260 weeks, with being a super-responder patient (achievement of PASI100 at 16 weeks and maintained at 28 weeks) correlated with less risk of discontinuation. PASI100, 90 and ≤3 was achieved by 54.1%, 60.5% and 73% of observed patients, respectively, at 16 weeks, and by 59.1%, 81.8% and 95.5%, respectively, at 260 weeks. High mean BMI was the only factor strongly associated with less achievement of the outcomes at the earlier time points: PASI100 at 16 weeks (OR 0.93, CI 0.87–0.98, p = 0.014) and at 104 weeks (OR 0.91, CI 0.84–0.98, p = 0.019), PASI90 achievement at 16 weeks (OR 0.94, CI 0.88–0.99, p = 0.028) and 104 weeks (OR 0.91, CI 0.83–0.99, p = 0.027), and PASI ≤3 (OR 0.86, CI 0.76–0.97, p = 0.018) at 104 weeks. No severe adverse events were observed.

Conclusions:
Ixekizumab showed high effectiveness and safety for up to 5 years, with survival of 2/3 of treated patients. Rapid response to treatment is predictive of long-term response.

This small study looked at dry eye syndrome (DES) in patients with psoriasis.

Quote:

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Background:
Psoriasis is one of the most common dermatoses associated with a variety of comorbidities. There have been some reports on its possible association with ocular disorders however dry eye syndrome (DES) in such patients has been poorly investigated.

Objectives:
To investigate the frequency of DES symptoms in psoriatic patients, also regarding psoriasis severity in PASI, manifestation and therapy.

Methods:
40 patients with psoriasis and 40 volunteers without dermatoses were enrolled in the study. They completed Ocular Surface Disease Index (OSDI) questionnaire and were objectively examined by IDRA® device to perform automatic interferometry, automatic meibography of lower eyelid glands, non-invasive break-up time (NIBUT), blink quality and tear meniscus height.

Results:
Patients with psoriasis had statistically significantly thicker lipid layer (p = 0.0042 left eye, p = 0.0313 right eye) and greater loss of Meibomian glands compared to controls (p = 0.0128 left eye, p = 0.048 right eye). The patients had lower, although insignificantly, eye blink quality and tear meniscus height than the control group, as well as shorter NIBUT and higher score in OSDI. After the division of patients into two groups–with or without nails involvement/psoriatic arthritis/systemic treatment– we did not observe any significant differences between the groups. PASI did not correlate with any DES parameter.

Conclusions:
This is the first study of DES symptoms with an objective IDRA® analyzer. We managed to observe that patients with psoriasis have thicker lipid layer and higher Meibomian glands' loss in lower eyelids. Based on all assessed objective and subjective parameters psoriatics do not seem to have an increased risk of DES. The presence of psoriatic arthritis or nail involvement does not seem to be a predisposing factor for DES development. PASI probably cannot be a prognostic factor for any of the DES-associated parameters. Nevertheless, DES in psoriasis requires further research on bigger samples to establish reliable recommendations.

This study looked at T-lymphokine-activated killer cell-originated protein kinase (TOPK) as a possible new target for treating psoriasis.

Quote:

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Background:
Psoriasis is an inflammatory skin disease. The pathogenesis of psoriasis has not been fully elucidated. T-lymphokine-activated killer cell-originated protein kinase (TOPK) activity increases in a proinflammatory environment, and inhibiting TOPK blocks inflammation. However, whether TOPK is involved in the pathogenesis of psoriasis remains to be identified.

Objectives:
We aimed to study the role of TOPK in psoriasis and attempted to find a drug targeting TOPK for the prevention and treatment of psoriasis.

Method:
Firstly, the expressions of TOPK in psoriatic patients, psoriatic cell and animal model were analysed by Gene Expression Omnibus database, immunohistochemistry (IHC) staining and western blot (WB). After inhibiting TOPK by chemical or gene knockout, the effect of TOPK on the development of psoriasis was verified in cell and animal model by WB, qRT-PCR, ELISA, haematoxylin–eosin (H&E) and IHC staining. Moreover, phosphoproteomic analysis was performed to explore the signalling pathways regulated by TOPK in the occurrence and development of psoriasis. Then, an in vitro kinase assay was performed to prove TOPK kinase activity was inhibited by worenine. Ultimately, WB, qRT-PCR, ELISA, H&E and IHC staining were used to verify the anti-psoriasis effect of worenine by inhibiting TOPK was in cell and animal model.

Results:
In this study, we found that TOPK was highly expressed in psoriasis patients, psoriatic cell and animal model, which suggests that TOPK might be associated with psoriasis pathogenesis. Interestingly, chemical or genetic inhibition of TOPK alleviated M5- and imiquimod (IMQ)-induced psoriasis-like dermatitis, which further confirmed the role of TOPK in promoting the development of psoriasis. Moreover, we determined that worenine inhibited TOPK kinase activity. In addition, worenine relieved M5- and IMQ-induced psoriasiform dermatitis by inhibiting TOPK activity.

Conclusions:
T-lymphokine-activated killer cell-originated protein kinase promotes the development of psoriasis. Therefore, TOPK might be a promising drug target for the prevention and treatment of psoriasis. Worenine alleviates psoriasiform dermatitis by inhibiting TOPK activity, providing new strategies for clinical intervention.

I'm suddenly getting itchy patches in many places, all at once.  I think it's the happy anticipation of adult children coming to stay with us for a couple of nights, trying to make everything ready combined with colder air outside and drier air inside from the furnace.  Whatever the cause, it's irritating.  

It'll soon be like living in a snow globe, all these little flakes falling to the floor or on the backs of chairs.

I believe stress, whether positive or negative, affects my skin.  

Does anyone else feel that way?

A prospective multicentre study of nail psoriasis in China. 

Quote:

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Background:
Data on nail psoriasis (PsO) in China are scarce.

Objectives:
To provide nail PsO-related data regarding epidemiologic characteristics, manifestations, fungal infections, arthritic complaints and treatments that may facilitate improved patient management globally.

Methods:
From August 2021 to August 2022, patients with nail PsO were enrolled in a prospective multicentre observational study at 25 hospitals in China. We collected and analysed data concerning nail PsO demography, clinical signs, fungal detection, arthritic symptoms and treatment.

Results:
A total of 817 patients with nail PsO were involved, with a mean body mass index of 24.13 ± 2.93. In addition, 71.41% of the patients were male. The Nail PsO Severity Index score was weakly positively correlated with body surface area. The percentage of nail involvement was 95.29% for fingernails and 57.18% for toenails, with pitting (67.11%) and subungual hyperkeratosis (60.40%) being the most prevalent manifestations, respectively. Toenails showed a significantly higher frequency of nailfold scales, subungual hyperkeratosis and nail plate crumbling and a lower frequency of splinter haemorrhages, pitting and erythema of the lunula. A total of 13.26% of the PsO patients had onychomycosis, and 77.08% were observed in the toenails. Articular symptoms were reported by 12.17% of the patients, with the peripheral type being predominant. Significant associations between articular symptoms and nailfold swelling, subungual hyperkeratosis, nailfold scales, onycholysis and longitudinal ridges were found. Only 2.30% (20 out of 871) of patients with nail PsO received treatment. The most frequently employed therapy for cutaneous PsO with nail involvement was biologic therapy (n = 366).

Conclusions:
PsO showed distinct manifestations in the toenails and fingernails. Additionally, toenail PsO combined with onychomycosis requires special attention. Articular symptoms in psoriatic patients are associated with specific nail changes. It is important to research and advocate for more potent treatments for nail PsO.

Get your name down for my Psoriasis Club tips.

I will be teaching you something you can do at Psoriasis Club. Some people find it difficult finding their way around and although we have help threads here Help using the forum I thought it may be helpful to drop a few tips to help.

Just watch this space or subscribe to this thread, if you have any questions or would like to know how to use something on the forum please post here.

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I might have posted about this before but I can’t find it - does anyone else suffer from psoriasis up their nose, especially in winter? I find it quite annoying and sometimes sore. You get extra skin growth like elsewhere but up your nose you can really feel it.
When I mention it to the derm they don’t have any advice and of course you can’t really use steroid cream on what they call mucous membranes. Moisturisers don’t do anything to help.

Hi,

My name is Kathy and I'm posting for my daughter. She has what I believe is some form of psoriasis. She has been to her GP about 6 times and 3 times to a Dermatologist who said she has atopic dermatitis but I would stake my life on the fact that he is wrong. I've known people with psoriasis and what she has is worse than anything I've ever seen. This morning her pajamas were stuck to her body from skin weeping and bleeding. Her acupuncture DR her body has damp heat. Last week her GP finally took blood and she is supposed to get the results in the next few days. I feel so helpless. Everything I've tried to do for her has not worked. Does anyone have any advice?

Do any other members of your family have psoriasis ?

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

Why does the Support Psoriasis Club keep showing that it has a new unread post when it doesn't?

A bit premature as it has to go through getting approval and such but thought I'd start the thread here. Let you know when I know.

So, first part of my journey is getting insurance approval and seeing what my costs (if any) will be. Different insurance than when I was on biologics before so a bit different process is involved.