Results of a 52 week efficacy and safety study of Cosentyx v Stelara

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Background:
Secukinumab demonstrated superior efficacy over ustekinumab in the treatment of moderate to severe plaque psoriasis over 16 weeks in the CLARITY study and over 52 weeks in the CLEAR study.

Objective:
To compare the efficacy and safety of secukinumab vs ustekinumab over 52 weeks in CLARITY.

Methods:
Analysis of 52‐week data from CLARITY (NCT02826603), a phase 3b study in which patients were randomized to receive secukinumab 300 mg (n = 550) or ustekinumab 45/90 mg (n = 552) per label.

Results:
At week 52, secukinumab was superior to ustekinumab in the proportion of patients who achieved ≥90% improvement in Psoriasis Area and Severity Index (73.2% vs 59.8%; odds ratio [OR], 1.84 [95% CI, 1.41‐2.41]; P < .0001), Investigator’s Global Assessment modified 2011 responses of clear (0) or almost clear (1) skin (76.0% vs 60.2%; OR, 2.12 [95% CI, 1.61‐2.79]; P < .0001), and Dermatology Life Quality Index response of no effect (0/1) (69.9% vs 61.2%; P = .0028). Proportions of patients with any adverse events were comparable between treatment arms.

Conclusions:
This second head‐to‐head study confirmed the superior efficacy of secukinumab over ustekinumab in skin clearance and quality of life through 52 weeks, with safety comparable to that reported in previous trials.

This study compared clobetasol cream and calcipotriol/betamethasone dipropionate foam (Cal/BD‐foam)

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Background:
Treatment response for psoriasis is typically evaluated using clinical scores. However, patients can relapse after clinical clearance, suggesting persistent inflammation. Dermoscopy, reflectance confocal microscopy (RCM) and optical coherence tomography (OCT) can non‐invasively improve treatment response assessment.

Objectives:
To compare the clinical and non‐invasive microscopic features in a psoriatic target lesion treated with clobetasol cream or calcipotriol/betamethasone dipropionate foam (Cal/BD‐foam)

Methods:
Prospective, unicentric, open, randomized clinical trial comparing clinical data (total clinical score [TCS]) and microscopic data (dermoscopy, RCM, OCT) in psoriasis patients treated with clobetasol or Cal/BD‐foam.

Results:
We included 36 adult patients (22 men). At week 4, more patients treated with Cal/BD foam achieved TCS≤1 than with clobetasol (63.2% vs 18.8%, p=0.016). Treatment satisfaction was higher with Cal/BD‐foam (p<0.03). Microscopically, Cal/BD‐foam induced more reduction of epidermal thickness at week 4 (p<0.049). Dilated horizontal blood vessels were more common with clobetasol than with Cal/BD‐foam at week 8 (69.2% vs 31.2%, p=0.159). If epidermal hyperplasia was noted at baseline, the response was poorer with clobetasol (p=0.029).

Limitations:
Small sample size, open study, imaging sampling bias.

Conclusion:
Cal/BD‐foam is more effective than clobetasol, has better patient satisfaction and induces greater reduction of the hyperkeratosis/acanthosis, regardless of baseline epidermal hyperplasia.

This study looked at the usefulness and reliability of insurance databases in psoriasis studies.

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Background:
Psoriasis is one of the most frequent chronic inflammatory dermatoses in the world. Data on the prevalence of psoriasis in adults differ depending on the study.

Objective:
To estimate the prevalence of patients with treatment for psoriasis in France and to identify and characterize patients receiving systemic treatments.

Methods:
This was a French, nationwide cohort study based on health administrative data from the French national health insurance scheme linked to the national hospital discharge database (SNDS‐PMSI). All adults with psoriasis registered in the SNDS between January 1, 2008 and December 31, 2016 were eligible for inclusion. All patients with a new prescription for a systemic treatment for psoriasis were included.

Results:
A total of 874,549 patients were identified as having psoriasis (mean±SD age 53.8±17 years; 52.4% males); 112,969 (13%) had filled at least one prescription for a systemic medication used to treat psoriasis. The prevalence of patients with treatment for psoriasis was estimated at 1.3%. Overall, 73,168 and 16,545 were new users of conventional systemic treatments and biologics, respectively. The most frequent comorbidities associated with psoriasis were hypertension, dyslipidemia, diabetes and chronic obstructive pulmonary disease.

Conclusion:
The prevalence of psoriasis we found was lower than in other studies. It was probably underestimated because we identified only patients with treatment for psoriasis. Our results concerning comorbidities associated with psoriasis patients requiring systemic treatment were similar to those from other published studies using other data sources, highlighting our ability to catch moderate‐to‐severe psoriasis. This study highlights the usefulness and reliability of the use of insurance databases in studies, because they allow for a better application to the general population.

This study looked at heterogenicity using gene expression profiles of lesional skin biopsy specimens in Chinese psoriasis patients.

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Background:
Psoriasis is an immune‐mediated, chronic inflammatory disease with diverse phenotypes. However, its biological diversity has not been well‐characterized in Chinese psoriasis population.

Objectives:
To characterize psoriasis biological heterogenicity using gene expression profiles of lesional skin biopsy specimens in a Chinese psoriasis population.

Methods:
Lesional tissues and blood samples from Chinese psoriasis patients (n = 40), atopic dermatitis (AD) patients (n = 25) and age‐matched healthy controls (n = 19) were investigated by using Real‐Time PCR Array, histological evaluation and flow cytometry. Unsupervised hierarchical clustering was performed using gene expression profiles of patients with psoriasis.

Results:
Two distinct psoriasis clusters were identified. Both clusters indicated high TH17 activation. One cluster (n = 6 of 40 consecutive psoriasis patients) indicated a strong TH2 component in skin lesions, with early onset and low peripheral blood eosinophil level. Significantly higher IL‐4, IL‐13, IL‐25, IL‐31 and TSLP gene induction typified this cluster of psoriasis patients, even compared with AD patients. Both psoriasis clusters were characterized by neutrophilic microabscess formation. Histologically, the TH2 high psoriasis cluster indicated a low percentage of perivascular eosinophils.

Conclusions:
Two distinct psoriasis clusters were identified. One presented early onset and a low eosinophil level, indicating TH17 polarization and a strong TH2 component. These results laid the foundation for further demonstrating the pathogenesis of psoriasis in Chinese population.

Hi I'm new here, just got what turned out to be guttate after a bad strep infection in March. What started out as brown discoloration on my legs turned into tiny red dots all over my legs. I didn't pay much attention until it showed up on my chest. That's when i went to a dermatologist and got a biopsy. My doctor put me on betamethasone, however it doesn't seem to have lasting effect. I started out with tiny dots, now after 3 rounds of topical steroid, it spreads to other areas of my body. It does seem to reduce the inflammation and redness during my 2 weeks treatment, however as soon as i stop, the spots come back with a vengeance. Some spots even joined together and formed a 1inch leisons

I'm hesitantly carrying on with my current round of betamethasone as i know it will get worse and then have to go back to square one again. I heard people saying weening off steroid is the same as quitting cold turkey, since the lest you put on your body the easier it is to quit. I'm tempting to manage my guttate with dietary change and natural sunlight.

People often say that guttate goes away in a couple months. Does that mean I have to keep up with topical steroid until it fades? From my own experience, last time most of my spots seemed to fade, with only some white discoloration but then after a week, they come back redder and more raised and showed up at other places in my body as well. If you have succeed treating your guttate with topical steroid, do you still have to use it for maintenance during remission?

Hi again. After a few years of bad side effects from oral treatment and then starting biological treatments. I am now on My 2nd attempt with injections. I am now on Taltz.
I have just had my 5th injection. My skin is well on the way to perfect. Just my lower legs to clear. Still early days.
No horrendous side effects the all other treatments. There is 2 side effects, 1 of which is listed a lot.
1. Injection site goes red. I mean a large circle if I inject my tummy and lumpy under the skin. It lasts between 1 and 2 weeks. Doesn't bother me.
2. My eyes have ached really badly on 2 occasions. The first time it came on rapidly with gritty eyes. I assumed it was allergy's and just put in eye drops. It was on and off for 1 week but only bad for 1 evening. Didn't think anything of it. Then it happened again 3 weeks later. 
I phoned my GP and she said take anti histamine tablets as allergies can make them also ache. If still bothering me in 24 hours book with opticians as she cant see in the eye.
I phoned the opticians anyway. They said come in and they will look. 
The next day my eyes were fine. The day after I had appointment at opticians.
Note I only have 1 good eye!!
Opticians said he couldn't find anything wrong other than the ware very slightly dry. Also needed prescription for distance. Even though I had them tested 2 month prior. This he found "interesting" As I write this, my eyes feel fine.

Most sites don't list eye problems but some sites do. In total it lists, redness, pain, selling of the eye or inner lining.

Obviously I will be talking to my dermatologist but I know all she will say is "do you want to continue on it"
I will now be  taking the injection every month instead of every 2 weeks. So if it is Taltz I will soon find out.

HAS ANYONE ELSE HAD EYE ACHE USING TALTZ !! 

Sorry for ranting on. Its just I was so pleased to have found something that works without side effects after all this time 
Duncan

I am new to the Board; I’m 70 and live in California. I first broke out with Psoriasis at age 31 when my dad got Cancer at age 52; I broke out over 80% of my body almost everywhere but my face, hands, and feet. After my father passed at age 55 my psoriasis cleared mainly except for a few spots of my lower legs and an occasional spot here and there. I would say less than 2% of body.

I quit smoking 35 years ago and drink a bit of alcohol albeit know more than 7-8 drinks per week. I exercise 2x per week playing ? tennis. I take several supplements including Turmeric, D 3, Vitamin C, Vitamin E, etc

I’m concerned about possibly getting cancer which is my greatest fear but I understand if we have Psoriasis are likelihood is increased!! There are many studies that indicate this.

Anyone know of anything we can do to lower the probability?

hello, everyone

after 50 years of suffering with psoriasis, I was eventually put on  Methotrexate and it really works.       over the years,  I tried so many steroid ointments, nothing worked.  hope this is useful

This study looked at the impacts of gene polymorphisms on Methotrexate in Chinese psoriasis patients.

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Background:
Methotrexate (MTX) is the first‐line treatment for psoriasis in China. The metabolic processes of MTX include various proteins and genes. Previous studies have shown that gene polymorphisms had significant impacts on the efficacy of MTX. However, the influence of gene polymorphisms has not been reported in the Chinese psoriatic patients.

Objective:
The aim of this study was to verify the impacts of candidate genes polymorphisms on the effectiveness of MTX in a Chinese psoriatic population.

Methods:
In this study, we enrolled 259 psoriasis patients from two clinical centres. Each of them received MTX treatment at 7.5‐15 mg/week for at least 8 weeks. Patients were stratified as responders and nonresponders according to whether the Psoriasis Area and Severity Index score declined more than 75% (PASI75). According to previous reports, 16 single‐nucleotide polymorphisms (SNPs) were selected and genotyped for each patient using the Sequenom platform. Fisher’s exact test, the χ2 test, Mann‐Whitney tests, and ANOVA analyses were used for statistical analysis.

Results:
Among 259 patients, there were 182 males and 77 females, 63 patients with psoriatic arthritis and 196 patients without arthritis phenotype, and the age of all patients ranged from 19 to 70 years (49.7±13.6). The baseline PASI value of patients was 13.8±8.5, and 33.2% of patients achieved a PASI75 response after MTX treatment. Patients carrying the ATP‐binding cassette subfamily B member 1 gene (ABCB1) rs1045642 TT genotype were associated with more severe psoriasis skin lesion (P=0.032). Furthermore, the ABCB1 rs1045642 TT genotype was found to be more frequent in nonresponders (P=0.017), especially in moderate‐to‐severe patients (P=0.002) and patients without psoriatic arthritis (P=0.026) after MTX treatment.

Conclusion:
We have demonstrated for the first time that polymorphism of the ABCB1 rs1045642 TT genotype is predictive of a worse clinical response of skin lesions to MTX therapy in a Chinese psoriatic population.

This study evaluated the effectiveness, safety, and drug survival of Otezla (apremilast) at 52 weeks in patients with moderate to severe plaque psoriasis or palmoplantar psoriasis in routine clinical practice.

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Background:
Little has been published on the real‐world effectiveness and safety of apremilast in psoriasis.

Objectives:
To evaluate the effectiveness, safety, and drug survival of apremilast at 52 weeks in patients with moderate to severe plaque psoriasis or palmoplantar psoriasis in routine clinical practice.

Methods:
Retrospective, multicenter study of adult patients with moderate to severe plaque psoriasis or palmoplantar psoriasis treated with apremilast from March 2016 to March 2018.

Results:
We studied 292 patients with plaque psoriasis and 85 patients with palmoplantar psoriasis. The mean (SD) Psoriasis Area and Severity Index (PASI) score was 10.7 (7.0) at baseline and 3.0 (4.2) at 52 weeks. After 12 months of treatment, 73.6% of patients had a PASI score of 3 or less. In terms of relative improvement by week 52, 49.7% of patients achieved PASI‐75 (≥ 75% reduction in PASI score) and 26.5% achieved PASI‐90. The mean physician global assessment score for palmoplantar psoriasis fell from 4.2 (5.2) at baseline to 1.3 (1.3) at week 52. Overall drug survival after 1 year of treatment with apremilast was 54.9 %. The main reasons for treatment discontinuation were loss of efficacy (23.9%) and adverse events (15.9%). Almost half of the patients in our series (47%) experienced at least one adverse event. The most common events were gastrointestinal problems.

Conclusions:
Apremilast may be a suitable alternative for the treatment of moderate to severe psoriasis and palmoplantar psoriasis. Although the drug has a good safety profile, adverse gastrointestinal effects are common.

I’ll be taking my third dose tonight and just wondering when I could be seeing results? Pretty sure my dermatologist said it could take 3 months but obviously I want instant results (yes I’m impatient!). Luckily I’ve had no side effects. My slight concern is my GP may not do my 4 week blood test due to the coronavirus but guess have to see when the time comes.

Taltz is now approved by the FDA (U.S. Food and Drug Administration) for use in children over 6 years.

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Eli Lilly announced today the U.S. Food and Drug Administration (FDA) has approved a supplemental Biologics License Application (sBLA) for Taltz® (ixekizumab) injection, 80 mg/mL for the treatment of pediatric patients (ages 6 to under 18) with moderate to severe plaque psoriasis who are candidates for systemic therapy or phototherapy.

Xeljanz (Tofacitinib) is sometimes precribed to treat psoriatic arthritis.

The UK have issued a drug safety update for it's use:

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Tofacitinib: New measures to minimise risk of venous thromboembolism and of serious and fatal infections.

Caution should be used in patients with known risk factors for venous thromboembolism in addition to the underlying disease. Patients older than 65 years of age are at an increased risk of serious infections and should be treated with tofacitinib only if there is no alternative treatment.

After starting this thread Covid-19 (aka Coronavirus) and psoriasis and one member saying they have been advised to stop Cosentyx I thought it would be a good idea to run a poll about psoriasis treatments and covid.

Some treatments can weaken our immune systems and I wondered how many people will be thinking of stopping their treatment during the threat of covid-19.

*I have not found any official advice about stopping a treatment, but you should all discuss the matter with your own healthcare professional if you have concerns.

This poll is open to guests and our members are welcome to vote and post in this thread too if they wish.

Hi all, l've had a thought recently about my upcoming meds.

I am due to start Skillarence next month which as you know has an effect on your immune system. Will this make me more susceptible to complications from the coronavirus?

However I also read that a lot of the fatalities come from an overreaction of the immune system causing widespread inflammation, so conversley if Skillarence is supposed to help reduce inflammation will it actually help prevent complications by reducing the likelihood of the immune system overreacting?

Does all of that make sense or am i barking up the wrong tree with this?

Hi..my name is Mary from New York. Have had psoriasis since 1980 but it got better as I got older. 2 months ago I had a horrible flare up and have eczema as well. I’m 68 and can’t believe this! Dr. gave me creams,etc. My hands cleared up with the steroid cream but had to stop for 2 weeks and it is back. Can start again this week. It’s the itch that’s driving me nuts. Any suggestions? Thanks everyone.

I have seen a few posts on Psoriasis Club recently about the ongoing Covid-19 virus. We do have a thread in the members only board [Group Specific] and most members seem to be saying carry on as usual.

However it is something that is going to get asked so let's have this thread where we can put information for those with psoriasis.

First off I should point out that none of us at Psoriasis Club are medical professionals and you should follow the advice from your own healthcare system, we are just people like you living with psoriasis.

I have spent a lot of time looking for information as it's starting to worry some of our members, and as far I can see there is no reason for anyone taking a treatment for their psoriasis to stop.

Yes we have a recognised immune problem and this can be made worse with some treatments, but as far as I can find the recommendation is to continue with our current treatments.

I will continue to monitor the Covid-19 and Psoriasis news and update this thread if I have anything official to tell you.

*Members are welcome to post in [Group Specific] if they have any supported official information about Covid and Psoriasis, but I will close this thread and update it if necessary to avoid it getting information overload.

• Inflammatory rheumatism and autoimmune diseases are not among the proven risk diseases to date.
  
• Do not change the treatment for your disease ; it does not increase the risk of getting the infection.
  
• Some treatments used in inflammatory rheumatism (hydroxychloroquine, JAK inhibitors, corticosteroids) have even been used or proposed for their potential anti-viral effect and to treat excess inflammation in severe forms of pneumonia complicating COVID-19.
  
• Any suspension of your usual treatment would expose you to a flare-up of your rheumatism and thus to an episode of frailty.
  

Quote:The recommendations of the ResoPso association, which are addressed to the patients receiving immunomodulatory treatments prescribed in chronic inflammatory dermatoses including psoriasis are the following:

For patients currently under treatment, the French Dermatology Society (Société Française de Dermatologie) recommends in a recent press recent press release "not to interrupt these treatments for a PREVENTIVE purpose".

As far as our group is concerned, and in accordance with the position of the scientific societies involved in the prescription of immunomodulators, it is not advisable to stop a treatment in progress that is well tolerated.

This decision must however be pondered according to the specific pathology, its severity, its control, its risk of relapse, the age and comorbidities of the patient.

It is up to the healthcare professional to assess the situation on a case-by-case basis, in consultation with his patient, and to decide whether to suspend the immunomodulatory treatment temporarily or pursue the treatment.

Quote:To date, the BAD is not aware of any good evidence that people taking drugs that target the immune system are at a greater risk of getting COVID-19 or of having a more severe form of the illness to inform this decision.

What happens if my patient wishes to pause therapy?

When providing advice take the following into consideration:

The views and concerns of the patient

The baseline risk of the person for developing significant COVID infection (for example age >70, co-morbidities)

The need for the drug (or drugs) and likely outcome if stopped (including how easily the treatment could be re-started, alternative options that may be acceptable to the person in this context e.g. topicals, and the clinical impact of a disease flare)

This will be my new thread for my journey on Tremfya.

I've had 3.5 years on Cosentyx but it's now failed in it's job at keeping the psoriatic arthritis away. You can read that journey here: Cosentyx for psoriatic arthritis Fred's journey

Tremfya is only prescribed for psoriasis in France at the moment but it is going for approval to treat psoriatic arthritis soon and I will be one of the first trying it for psoriatic arthritis.

Unlike other bio's Tremfya doesn't have a loading dose as such, you take 1 shot of 100mg followed by another at week 4. Then the maintenance dose is 100mg every 8 weeks. I have been doing bio's for well over 10 years now so it will be a simple task doing the shots myself.

It comes in two types of shot. A pre filled Syringe and an Auto injector (Pen). I prefer using the syringes as seen in this image.



Psoriatic arthritis is more important to me but I shall be using the score systems on Psoriasis Club to keep track of my progress.

NO LINKS ALLOWED

PsAscore

Psoriasis score: 8

Psoriatic arthritis score: 14

Psoriasis on one of my skins:


Psoriatic arthritis middle finger:


Annoying red itchiness on forearm


Notes for reference: Before taking my first shot I feel like I have a mild cold and a bit of upset stomach. Also the annoying red itchiness has come back again. I'm putting this here so I know I had those problems before starting Tremfya.

I will do regular updates and you are welcome to post in this thread, but please keep it On Topic.

Hello. I am posting a broad question but hope some of you can help. I'm now on Tremfya  (after taking all else with no help and got all side effects - mostly upped respiratory infections.)
Psoriasis now is painful psoriatic arthritis and autoimmune issues such as lupus.
I started Tremfya on Sunday. I cannot lift my head from my pillow because of severe exhaustion!. When I do get up I have extreme lower back and leg pain.
I don't want to give up. I'm hoping a second dose in a few weeks will bring clear skin as less pain.  I just want to know if anyone else felt these "side effects" when first taking Tremfya. The nurse at Jannsen had nothing to tell me except I would get a letter from them. 
I'm ending day 3 feeling extreme fatigue, pain and still growing New placque. Not what I expected.
Your help.is appreciated.Thank you.

I was just reading TL's comment about anti drug antibodies in response to biological drugs here: RE: Cosentyx for psoriatic arthritis Fred's journey and it's interesting.

I had often thought my body somehow just gets used to my current treatment and it stops working, but I never understood (and still don't really) exactly what was going on. But there is a lot out there about "Anti drug antibodies" and it does make some interesting reading.

Here is how I see it.

#1 My body is making too much of one cell and I get psoriasis, then as it gets worse I also get psoriatic arthritis.

#2 I take a treatment that bombards me with a cell to try and slow down the process and I feel better.

#3 My body then starts to fight against the treatment as it now sees it as a threat.

So eventually there is a high likelihood that my body will eventually get used to the treatment and stop it working.

Thoughts anyone ?