NICE (National Institute for Heath and Care Excellence) have finally said No to Otezla for the treatment of psoriatic arthritis, it's been heading that way for a while but now it's official.

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NICE has published final draft guidance today which does not recommend apremilast (Otezla, Celgene) for adults with active psoriatic arthritis that has either not responded to disease-modifying antirheumatic drug (DMARD) therapy, or where such therapy is not tolerated.

Psoriatic arthritis is an inflammatory disease affecting the joints and connective tissue, and is associated with psoriasis of the skin or nails. It is a lifelong, progressive disorder, ranging from mild synovitis (inflammation of the tissue lining joints such as the hip or shoulder) to severe progressive erosion of the joints.

People with psoriatic arthritis are usually treated initially with non-steroidal anti-inflammatory drugs (NSAIDs) and disease-modifying antirheumatic drugs (DMARDs) such as methotrexate. Most people whose disease doesn’t respond to these drugs will be treated with a tumour necrosis factor alpha inhibitor (TNF-alpha inhibitor) starting with the lowest-cost drug as recommended in NICE technology appraisal guidance on etanercept, infliximab and adalimumab for the treatment of psoriatic arthritis and golimumab for the treatment of psoriatic arthritis.

Professor Carole Longson, Director of the Health Technology Evaluation Centre at NICE, said: “Psoriatic arthritis is a chronic condition that can have a significant physical and psychological impact on an individual’s life, employment and social activities. Around 10% of patients stop TNF-alpha inhibitor treatment each year, either because it is contraindicated, or because of loss of effectiveness or adverse effects. There is, therefore, a clear clinical need for a range of treatment options.  

“The Committee considered the evidence on the use of apremilast both before and after TNF-alpha inhibitors and for people who aren’t able to take TNF-alpha inhibitors. The Committee concluded that apremilast is clinically effective compared with no other treatment. However, compared with TNF-alpha inhibitors, apremilast was the least clinically effective for treating psoriatic arthritis although some costs were saved by its use. Importantly, there was not enough robust evidence demonstrating that apremilast slows progression of the disease compared to TNF-alpha inhibitors. The Committee concluded that they were unable to recommend apremilast for treating active psoriatic arthritis because the costs saved were not sufficient to justify the health losses.”

This draft guidance does not mean that people currently taking apremilast will stop receiving it. They have the option to continue treatment until they and their clinicians consider it appropriate to stop.

The draft guidance is now with consultees, who have the opportunity to appeal against it. Until final guidance is issued to the NHS, NHS organisations should make decisions locally on the funding of specific treatments. Once NICE issues its final guidance on a technology, it replaces local recommendations across the country.

Following on from the announcement that Amgen had dumped Brodalumab see here: Amgen dump brodalumab after some patients had suicidal thoughts. AstraZenaca announced they have granted an exclusive license for Valeant Pharmaceuticals International, Inc to develop and commercialise brodalumab.

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AstraZeneca today announced that it has entered into a collaboration agreement with Valeant Pharmaceuticals International, Inc. under which it will grant an exclusive license for Valeant to develop and commercialise brodalumab.

Brodalumab is an IL-17 receptor monoclonal antibody in development for patients with moderate-to-severe plaque psoriasis and psoriatic arthritis. Under the agreement, Valeant will hold the exclusive rights to develop and commercialise brodalumab globally, except in Japan and certain other Asian countries where rights are held by Kyowa Hakko Kirin Co., Ltd under a prior arrangement with Amgen Inc., the originator of brodalumab. Valeant will assume all development costs associated with the regulatory approval for brodalumab. Regulatory submission in US and EU for brodalumab in moderate-to-severe psoriasis is planned for the fourth quarter of 2015.

Under the terms of the agreement, Valeant will make an up-front payment to AstraZeneca of $100 million as well as additional pre-launch milestones of up to $170 million and further sales related milestone payments of up to $175 million following launch. After approval, AstraZeneca and Valeant will share profits.

Brodalumab is supported by data from the three AMAGINE Phase III pivotal studies1 . The results highlighted that brodalumab has an effective mechanism of action that delivers clinical benefit and could help a significant number of moderate-to-severe plaque psoriasis patients achieve total clearance of their skin disease. At the 210 mg dose, brodalumab was shown to be efficacious in total skin clearance of psoriasis compared to placebo and superior to ustekinumab at week 12 in two replicate comparator trials involving over 3,500 patients.

Pascal Soriot, Chief Executive Officer, said: “Our agreement will help to bring brodalumab to patients with psoriasis who need new treatment options through Valeant’s expert focus on dermatology.”

J. Michael Pearson, Chairman and Chief Executive Officer of Valeant, said, “We are delighted we were able to reach a licensing agreement with AstraZeneca to commercialize brodalumab, which is potentially the most efficacious therapy yet for moderate-to-severe plaque psoriasis. We remain fully committed to dermatology and will continue to advance our pipeline of internally developed and acquired products.”

The transaction is expected to complete in the fourth quarter of 2015, subject to customary closing conditions, and it does not materially impact AstraZeneca’s financial guidance for 2015. As AstraZeneca continues to retain a significant interest in brodalumab, the upfront payment and any potential subsequent milestone payments are expected to be reported as Externalisation Revenue.

I have been on a regimen of 0.8 ml MTX (20mg/ml) weekly to control my plaque Psoriasis. It has been wonderful and basically left me symptom free for 4 yrs . Recently I have noticed some recurrence of scalp issues....
I have monitoring labs every 8 wks, and all has remained "normal".
Anyone have any info on relapse in the face of ongoing treatment?
thanks.

Hi-

Brand new to this forum and interested in hearing others' experiences.

I was dx. with PsA Jan. 2014. I immediately went on the auto immune paleo diet and started Mtx8. I have significant shoulder tendon damage and cervical spine degeneration. I was on MtX8 for 14 months, in combination with Humira for 2 of those months. The Humira caused some infections immediately but the combo caused my WBC to tank. I took a break from the meds and have been on low dose naltrexone at varying doses for the past 2 months, at 4.5 mg. for the past 2 weeks. I went up rapidly to try and stay ahead of the increasing pain.

I'm not opposed to trying meds again but am wondering how long I should give LDN on it's own? Does anyone on this site take LDN with MtX8? I'm concerned that the combination of MtX8 and a biologic, in this case looking at Enbrel, will similarly impact my WBC. If so, maybe LDN can be used w/ Enbrel to reduce risk of antibodies?

OK! it has been suggested I start a thread about my Acitretin journey!!.. This is my back now its not as bad as it was because i had just come out of the sun and sea!!!!!I started the medication on Tuesday 18/8/15!  I will post another picture in a few weeks!!   I hope this is of some help to others starting out on this road!!  
[img][/img]

Hi everyone!  My name is Steve but everyone calls me fingers!..even my own son!!
I have had psoriasis for over 15 years! I have been on methotrexate and cyclosporin  over the years but was taken off ...I have just started Acitretin this week and stumbled across this forum while reading about it!!!....I hope I can exchange experiences and information with you good people!
I look forward to talking with you all....best wishes, fingers!

I am posting on behalf of my 76 year old husband. We are having a lot of problems controlling the psoriasis although we are seeing the dermatologist on a regular basis. Ciclosporin did work but sadly blood tests showed that it also affected the liver and kidney function. The Doctor then tried reducing the dose but this did not help. My husband has been started on Fumaderm and took his first tablet on Wednesday night. He felt very sick today but I realise that this might be a side affect and am going to encourage him to keep taking it. He is still on Acetretin because the dermo felt he needed the overlap to prevent flare ups. I would say that the flare ups have been very bad and he has had to have antibiotics due to the infections. He is having a lot of problems walking due to the skin on his heels peeling.
I just wondered how others coped with Fumaderm?  The Dermo did say that around a  third of people have to come off it due to the side affects.....
If it does not work, the next option is injections but my husband is very against these. Also he has anaemia which is being investigated and the dermo wanted to find the cause of the anaemia before going down this route. He also has Lupus which is thankfully dormant at the moment. I do now understand that some of the medications initially used to treat the Lupus may well have made the psoriasis worse or even sparked it.
Thank you for reading. I do feel very out of my depth trying to help my husband - I am his carer, and he does get quite depressed at times especially when he is really struggling to walk or get his shoes on.

Hi I'm new to this and I've had psoriasis for over 14 years. I have tried all the usual creams light treatment, methotrexate and none have worked. I started on fumaderm initial 3 weeks ago and since my uptake has increased to 3 tablets a day I have suffered all of the side affects. The cramps are unbearable and I have a high pain threshold. I have also vomited. I don't want to stop the medication as it's improving slightly. Does anyone know what I can do to ease the cramps or how long they will last? Thanks in advance

I hope this helps one person ill be very happy since it cleared my husbands right up with no flare ups.  simple liquid iodine applied on affected area at night then wash off in morning plus one pill a day of potassium iodide. in 10 days it has disappeared.  please try and share if it helps great, we have battled this for 10 years taking every cream and pill tossed at him.

Does anyone else find that the sun seems to make no difference to their P? My plaques have been slowly but steadily growing this summer and I've been outside a lot.

I'm interested to know if I'm in a minority or perhaps not?

Hi,vim taking humira. After about 3-4 weeks since I started it, I noticed no difference until over the course of about 3 days my skin became completely clear. From 90% coverage to clear! But hen I woke up one day after injecting to see it coming back. And the next day, today, it's almost as bad as originally. I was wondering if this suggests my body will always find a way around it and whether or not I should expect to ever be clear on this again?

Many thanks

Smoking has for a long time been said to be bad for psoriasis, but could passive smoking also increase ones chance of getting psoriasis?

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Background:
Smoking is a potential risk factor for psoriasis. Both psoriasis and smoking habits are partly explained by genetic factors. However, twin studies investigating the association between these traits are limited.

Methods:
Questionnaire-based data on smoking habits and psoriasis were collected for 34,781 twins, aged 20–71 years, from the Danish Twin Registry. A co-twin control analysis was performed on 1700 twin pairs discordant for lifetime history of smoking. Genetic and environmental correlations between smoking and psoriasis were estimated using classical twin modeling.

Results:
After multivariable adjustment, age group (50–71 vs. 20–49 years) and childhood exposure to environmental tobacco smoke (ETS) were significantly associated with psoriasis in the whole population (odds ratio [OR] 1.15, 95% confidence interval [CI] 1.02–1.29 [P = 0.021] and OR 1.28, 95% CI 1.10–1.49 [P = 0.002], respectively). Risk for psoriasis increased substantially (OR 2.18, 95% CI 1.82–2.61; P < 0.001) for smokers with a history of >5 pack-years, even after adjusting for age, sex, and childhood ETS. Among twin pairs discordant for smoking, risk for psoriasis in the ever-smoking twin was lower among monozygotic twins (OR 1.23, 95% CI 0.59–2.56; P = 0.578) than among same-sex dizygotic twins (OR 2.21, 95% CI 1.36–3.58; P = 0.001). Genetic factors explained 20% (14–25%; P < 0.001) of the correlation between psoriasis and smoking, whereas non-shared environmental factors explained 8% (0–22%; P = 0.504).

Conclusions:
Tobacco consumption and childhood ETS are significantly associated with psoriasis. Results indicate shared genetic factors for smoking and psoriasis.

Hi All

Well 9 weeks in the waiting and funding is through, Bupa have called and all kicks off next week.

Skin - pure pants!! using lots of elecon, eumovate, ysp, and Drambuie.

Nurse due next Friday to train me.  So hopefully be easy and manage myself.

I've read to take out of fridge before she comes, and wondering any more tips and what to expect with Stelara?

My derm tells me to not expect it to work quickly and give it 12 weeks.

Hope your all well and will keep updating (or annoying you lot, with questions , ha )

Angie  

This study looked into the use of Kunzia oil formulations in the treatment of psoriasis, Kunzea is a genus of shrub in the myrtle family Myrtaceae native to Australia.

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What is known and objective:
Anecdotally, topical kunzea oil has been used to treat various skin conditions, including psoriasis and eczema, with good results. This study compared the clinical efficacy of kunzea oil (20%)-containing formulations in mild to moderate psoriasis.

Methods:
A randomized, comparative, double-blind, 8-week study was undertaken. Thirty patients (age range: 25–74 years and mean ± SD: 52·8 ± 13·6 years) with mild to moderate psoriasis (affecting at least 10% of one or more body regions: arms, head, legs and trunk) randomly received ointment and/or scalp lotion containing 20% kunzea oil (test group) or control medications not containing kunzea oil (control group). Formulations in both treatment arms also contained 5% liquor carbonis detergens (LCD) and 3% salicylic acid. The clinical responses to the test and control formulations were evaluated using the Psoriasis Area and Severity Index (PASI).

Results and discussion:
After 8 weeks of treatment, both test and control groups demonstrated a significant (P < 0·05) improvement in PASI scores. Subjects in the test group had a decrease in mean±SD PASI score from 12·7 ± 7·9 to 6·7 ± 7·2, whereas the control group showed a decrease in PASI score from 8·1 ± 4·6 to 3·5 ± 4·7. Comparative efficacy analysis between the test and control groups did not reveal any significant difference (P > 0·05).

What is new and conclusions:
The inclusion of kunzea oil made no difference to the efficacy of topical formulations containing LCD and salicylic acid for the treatment of psoriasis.

Here is an abstract that looked to assess the effects and safety of oral fumaric acid esters for psoriasis.

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Background:
Psoriasis is a chronic inflammatory skin condition that can markedly reduce life quality. Several systemic therapies exist for moderate to severe psoriasis, including oral fumaric acid esters (FAE). These contain dimethyl fumarate (DMF), the main active ingredient, and monoethyl fumarate. FAE are licensed for psoriasis in Germany but used off-licence in many countries.

Objectives:
To assess the effects and safety of oral fumaric acid esters for psoriasis.

Search methods:
We searched the following databases up to 7 May 2015: the Cochrane Skin Group Specialised Register, CENTRAL in the Cochrane Library (Issue 4, 2015), MEDLINE (from 1946), EMBASE (from 1974), and LILACS (from 1982). We searched five trials registers and checked the reference lists of included and excluded studies for further references to relevant randomised controlled trials. We handsearched six conference proceedings that were not already included in the Cochrane Skin Group Specialised Register.

Selection criteria:
Randomised controlled trials (RCTs) of FAE, including DMF monotherapy, in individuals of any age and sex with a clinical diagnosis of psoriasis.

Data collection and analysis:
Two review authors independently assessed trial quality and extracted data. Primary outcomes were improvement in Psoriasis Area and Severity Index (PASI) score and the proportion of participants discontinuing treatment due to adverse effects.

Main results:
We included 6 studies (2 full reports, 2 abstracts, 1 brief communication, and 1 letter), with a total of 544 participants. Risk of bias was unclear in several studies because of insufficient reporting. Five studies compared FAE with placebo, and one study compared FAE with methotrexate. All studies reported data at 12 to 16 weeks, and we identified no longer-term studies. When FAE were compared with placebo, we could not perform meta-analysis for the primary outcome of PASI score because the three studies that assessed this outcome reported the data differently, although all studies reported a significant reduction in PASI scores with FAE. Only 1 small study designed for psoriatic arthritis reported on the other primary outcome of participants discontinuing treatment due to adverse effects (2 of 13 participants on FAE compared with none of the 14 participants on placebo; risk ratio (RR) 5.36, 95% confidence interval (CI) 0.28 to 102.1; 27 participants; very low-quality evidence). However, these findings are uncertain due to indirectness and a very wide confidence interval. Two studies, containing 247 participants and both only reported as abstracts, allowed meta-analysis for PASI 50, which showed superiority of FAE over placebo (RR 4.55, 95% CI 2.80 to 7.40; low-quality evidence), with a combined PASI 50 of 64% in those given FAE compared with a PASI 50 of 14% for those on placebo, representing a number needed to treat to benefit of 2. The same studies reported more participants achieving PASI 75 with FAE, but we did not pool the data because of significant heterogeneity; none of the studies measured PASI 90. One study reported significant improvement in participants' quality of life (QoL) with FAE, measured with Skindex-29. However, we could not compute the mean difference because of insufficient reporting in the abstract. More participants experienced adverse effects, mainly gastrointestinal disturbance and flushing, on FAE (RR 4.72, 95% CI 2.45 to 9.08; 1 study, 99 participants; moderate-quality evidence), affecting 76% of participants given FAE and 16% of the placebo group (representing a number needed to treat to harm of 2). The other studies reported similar findings or did not report adverse effects fully.

One study of 54 participants compared methotrexate (MTX) with FAE. PASI score at follow-up showed superiority of MTX (mean Difference (MD) 3.80, 95% CI 0.68 to 6.92; 51 participants; very low-quality evidence), but the difference was not significant after adjustment for baseline disease severity. The difference between groups for the proportion of participants who discontinued treatment due to adverse effects was uncertain because of imprecision (RR 0.19, 95% CI 0.02 to 1.53; 1 study, 51 participants; very low-quality evidence). Overall, the number of participants experiencing common nuisance adverse effects was not significantly different between the 2 groups, with 89% of the FAE group affected compared with 100% of the MTX group (RR 0.89, 95% CI 0.77 to 1.03; 54 participants; very low-quality evidence). Flushing was more frequent in those on FAE, with 13 out of 27 participants affected compared with 2 out of 27 given MTX. There was no significant difference in the number of participants who attained PASI 50, 75, and 90 in the 2 groups (very low-quality evidence) whereas this study did not measure the effect of treatments on QoL. The included studies reported no serious adverse effects of FAE and were too small and of limited duration to provide evidence about rare or delayed effects.

Authors' conclusions:
Evidence suggests that FAE are superior to placebo and possibly similar in efficacy to MTX for psoriasis; however, the evidence provided in this review was limited, and it must be noted that four out of six included studies were abstracts or brief reports, restricting study reporting. FAE are associated with nuisance adverse effects, including flushing and gastrointestinal disturbance, but short-term studies reported no serious adverse effects.

Hi There! 

I was diagnosed with Guttate this past June. (Some turned into Plaque and some went Inverse. Yay.) I am not only a newbie to the board but also to Psoriasis. My dermatologist didn't tell me much - Like it's an autoimmune disorder or... Chronic... Needless to say, I've been soaking up as much info as possible from the internet while trying to avoid the quackery/rip-offery stuff. Altho', the itching has driven me to not care too much about self-experimenting. I don't care about the spots so much, even the ones on my face, it's the itching I can't stand.

My heart goes out to everyone with this condition. I'm only on my second flare up and I'm already searching for a cure! 

Take care!
-Beezie

My Dr is thinking of changing me from Acitretin which is working extremely well for me, to Otezla because my hair is getting a little thin (this was a problem before I was ever diagnosed with psoriasis, Acitretin is just making it a bit more noticeable).

Anyone here on Otezla?

Ok, has anyone heard of Cetraben ?

It's cream here in england used for red, inflammed, chapped, dry skin.

Because of my P, my skin splitting etc, i got a 500g pump dispenser bottle.

I've used it for the first time this evening & noticed straight away it was cool & soothing.

Also, i have found since putting it on, it's non greasey !!!

Most of the other creams i get prescribed tend to make feel wrapped up in treacle !

But, this stuff is the dog's doh da's !

This Danish cohort study looked at the bidirectional association between psoriatic disease and uveitis, and suggests increased focus on eye symptoms in patients with psoriasis and psoriatic arthritis and on skin and joint symptoms in patients with prior or current uveitis may be appropriate.

Wikipedia: Uveitis (also known as iridocyclitis) is the inflammation of the uvea, the pigmented layer that lies between the inner retina and the outer fibrous layer composed of the sclera and cornea.The uvea consists of the middle layer of pigmented vascular structures of the eye and includes the iris, ciliary body, and choroid. Uveitis is an ophthalmic emergency and requires a thorough examination by an optometrist or ophthalmologist and urgent treatment to control the inflammation.

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Importance:  
Psoriasis, psoriatic arthritis, and uveitis are inflammatory disorders with significant overlap in their inflammatory pathways. Limited evidence is available about the relationship between psoriatic disease and uveitis.

Objective:  
To investigate the potential bidirectional relationship between psoriatic disease, including psoriasis and psoriatic arthritis, and uveitis.

Design, Setting, and Participants:
We performed a nationwide cohort study of the Danish population from January 1, 1997, through December 31, 2011. We included 74 129 Danish patients with psoriasis who were 18 years or older during the study period. Patients were identified through administrative registries, and information on age, sex, socioeconomic status, medication, and comorbidity was obtained using individual-level linkage of administrative registers. We performed data analysis from January 27 through March 4, 2015.

Exposures:  
Diagnosis of mild or severe psoriasis or psoriatic arthritis for uveitis risk and diagnosis of uveitis for the risk for psoriasis or psoriatic arthritis.

Main Outcomes and Measures:  
Diagnosis of uveitis, mild psoriasis, severe psoriasis, or psoriatic arthritis. We calculated incidence rates (IRs) and estimated IR ratios adjusted for potential confounders using Poisson regression.

Results:  
We identified 74 129 cases of psoriasis and psoriatic arthritis and 13 114 cases of uveitis. The IRs (95% CIs) for uveitis were 2.02 (1.99-2.06), 2.88 (2.33-3.56), 4.23 (2.40-7.45), and 5.49 (3.36-8.96) for the reference population and those with mild psoriasis, severe psoriasis, and psoriatic arthritis, respectively. In the reference population, these IRs (95% CIs) were 9.37 (9.30-9.45), 1.12 (1.10-1.15), and 1.04 (1.01-1.06), and in patients with uveitis, these statistics were 15.51 (12.92-18.62), 2.66 (1.72-4.13), and 4.25 (3.00-6.01) for mild psoriasis, severe psoriasis, and psoriatic arthritis, respectively. Adjusted IR ratios (95% CIs) for uveitis were 1.38 (1.11-1.70 [P = .02]), 1.40 (0.70-2.81 [P = .34]), and 2.50 (1.53-4.08 [P < .001]) for patients with mild psoriasis, severe psoriasis, and psoriatic arthritis, respectively. For patients with uveitis, IR ratios (95% CIs) were 1.59 (1.32-1.91 [P < .001]) for mild psoriasis, 2.17 (1.40-3.38 [P < .001]) for severe psoriasis, and 3.77 (2.66-5.34 [P < .001]) for psoriatic arthritis, respectively.

Conclusions and Relevance:  
We found a bidirectional association between psoriatic disease and uveitis. Increased focus on eye symptoms in patients with psoriasis and psoriatic arthritis and on skin and joint symptoms in patients with prior or current uveitis may be appropriate.

I originally stumbled on this forum trying to find an answer on Google, I never did find any insight. So I'll pose the question here:
Does anyone have an idea how long it takes for a trigger to cause a flare?
I know it's going to be different depending on lots of circumstances, but generally speaking - is it a matter of hours, days, weeks?
I have a few theories about mine, which is flaring pretty heavily now, after being almost totally gone for months. But I wonder what is causing it to flare - I know, the eternal question of all psoriasis sufferers.
Personally I think mine is related to fungus. I've been gluten free for over 3 years, no change. Also alcohol free for 4 years, no change.
Thanks for any comments and or insights!!!