So if some of you were following my aloe vera and vitamins thread, you will know I decided to go back onto medication and tomorrow was when I'm due to talk to them about it. I have now been off medication for about 8 weeks, and my psoriasis has now..calmed down significantly I have had no new pustules appearing on my feet for a good while, my psoriasis on my stomach has cleared and the legs are clearing up as well, and I've only been using double base and some other creams now and again on my feet.

I'm now considering just getting some more creams tomorrow and continuing with them to see if I still stay clear as my crohns and arthritis is doing ok at the moment, so I don't need any medication for them. I'm guessing all the different medications that has been pushed around my body over the past few years were just making everything worse!

More good news for Cosentyx and psoriatic arthritis patients as Novartis announce one year results from the pivotal Phase III FUTURE 2 study, it shows improvements were sustained over one year of treatment in the majority of patients.

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Novartis announced today that new one year results from the pivotal Phase III FUTURE 2 study of secukinumab in psoriatic arthritis (PsA) were published in The Lancet following fast-track review. Secukinumab is the first interleukin-17A (IL-17A) inhibitor to demonstrate efficacy in a Phase III study in adult patients with active PsA. PsA is a long-term, debilitating, inflammatory disease associated with joint pain and stiffness, skin and nail psoriasis, swollen toes and fingers, persistent painful tendonitis and irreversible joint damage.

The new study results published in The Lancet show improvements observed with subcutaneous secukinumab 300 mg and 150 mg were sustained over one year of treatment in the majority of patients (64% for both doses), as measured by the American College of Rheumatology response criteria (ACR 20). Moreover, ACR 50 response rates were also sustained to one year in secukinumab 300 mg and 150 mg (44% and 39% respectively). Secukinumab met the primary endpoint of the study, which was ACR 20 at Week 24 with response rates significantly higher in the secukinumab 300 mg (54%; p<0.0001) and 150 mg (51%; p<0.0001) groups versus placebo (15%), with clinical improvements observed as early as Week 3. ACR 20 and 50 are standard tools used to assess improvement of PsA signs and symptoms, and represent a 20% and 50% improvement from baseline, respectively.

"Secukinumab is the first IL-17A inhibitor to show consistent efficacy through one year in Psoriatic Arthritis, Psoriasis, and Ankylosing spondylitis" said Vasant Narasimhan, Global Head of Development, Novartis Pharmaceuticals. "Novartis has recently filed global regulatory submissions for secukinumab in both psoriatic arthritis and ankylosing spondylitis and will continue to work to bring this important advance to patients with these debilitating diseases."

Secukinumab 300 mg and 150 mg also significantly improved a key secondary endpoint which was improvement in psoriasis symptoms, as measured by 90% improvements in Psoriasis Area and Severity Index score (PASI 90). Achieving PASI 90 means that patients can attain clear to almost clear skin. This is important as the majority of people living with PsA have a history of, or concomitant, psoriasis, another long-term condition which is characterized by thick and extensive skin lesions, called plaques, known to cause itching, scaling and pain.

Although the secukinumab benefits seen in FUTURE 2 were generally higher in patients without previous treatment with standard of care anti-TNF therapy, clinical benefits were observed in both anti-TNF-naïve patients and those with an inadequate response to anti-TNFs. This is important as many patients do not respond to, or tolerate these therapies and approximately 40% of people are dissatisfied with current treatments. There is therefore, a high unmet need for patients with PsA.

Secukinumab was well tolerated in FUTURE 2, with a safety profile consistent with that observed in the psoriasis clinical trial program involving nearly 5,000 patients. The most common adverse events (AEs) were upper respiratory tract infections and the common cold.

OK so I am new here and decided to come along as my psoriasis has been very hit and miss since they stopped making Dovobet cream and I had to use the gel.

Just had my first dermatology consult in about 20 years and given a choice of MTX and something else. Decided to try MTX even though I know its tea total and there are portential side effects. Hopefully it will work.

I had my consult last Wednesday and bloods taken Friday. I get the blood results tomorrow and hopefully start MTX on Wednesday. 5mg first week then 10 and upto 15 with fortnightly bloods. It may not be right for me as I am traveling a lot at present but getting really fed up with the daily ritual of creams and hoovering, well Mrs Pingu does the hoovering!

I know already what Fred will say! But I think its a process, eliminate certain tried and tested drugs before we get to the new expensive ones! It might work and I have no ill effects. I may be sick as a dog.

I have read peoples experiences, the good, the bad and the ugly but one question is how soon should I start to notice any effect, besides throwing up the morning after I take them?

I was going to say "Hi, my names Pete I'm an alcoholic" but a) its getting old b) its the wrong club.

I am a 48 year old male who has had psoriasis for about 35-40 years. Thoroughly fed up with it and as my last year has been massively stressful with work it has got a little worse. Probably the worst it has been for a long tiime but I could if I had to live with it but decided to see whats out there.

I am self employed and my partner (GF) has 4 children all grown up and she keeps me sane. Two dogs live in the north west and travel extensively with work. Cirrently spending far to much time away from home.

Hi

Had psoriasis since I was 24 I'm 39 now. I firmly believe in the theory (well for me anyway) it's a stress based illness, as when I am happy it slowly goes away on it's own. I have however tried a couple of creams.. Dovonex was excellent! one application lasted 6 months at one time another 8 months, while Dovobet is a hard slog for me.. it works..kinda, takes ages and many many applications, I can finish a tube in under a week if i'm not careful (my psoriasis is quite extreme, covering I'd guess 16th of my body). I asked the doctor for Dovonex again a few years ago..but he said the NHS don't prescribe it anymore because it's too expensive. He offered me Dovobet.. I tried to insist but no. Then in 2011 I got confused between them and asked for Dovobet.. I was so surprised when he agreed! Using it.. ahh it reduces my plaque but I need to keep using it but then I have to go back.. pay for a taxi..you get the idea. I have sleep apnoea also (which is stress related) so my memory is junk, and im not awake at the same time + remember to get to the doctors. They get quite annoyed if you miss appointments ..not so much with me, but i wouldn't like to let anyone down. 

I bought Dithrocream online to give it a go.. my fiancee is always telling me to look after myself and im starting to think she's right. I just wish I could get that Dovonex again.. that was brilliant for me!

feel free to chat and share experience and info

Dava

Hi guys

New here, thought i'd say hi.

trying to find some info..but ill make a proper post.

thanks

Dava

An interesting one for the DMF gang, this study looked at the effectiveness of Dimethyl Fumarate (DMF) in modulating the Th17, Th1 and Th2 helper cells. We have a lot of members using DMF in it's various forms (Fumaderm, Psorinovo, and even Bill using it raw) so I thought you may find this interesting.

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Background:
Fumaric acid esters such as dimethyl fumarate (DMF) have proven to be effective in the treatment of psoriasis.

Objectives:
In view of the role of Th17 in the pathogenesis of psoriasis, the present study was conducted to investigate the effects of DMF on Th1, Th2, and Th17 responses in patients.

Methods:
Peripheral blood mononuclear cells (PBMCs) were isolated from psoriasis patients and healthy individuals and were cultured in the presence or absence of phytohemagglutinin and DMF. The cell supernatants were removed to measure cytokine secretion, and the lymphocytes were used for real-time polymerase chain reaction to establish gene expression.

Results:
An increase in gene expression of interferon-γ (IFN-γ), as a marker for Th1 activity, and interleukin-17 (IL-17), granulocyte macrophage colony-stimulating factor (GM-CSF) and IL-22 representing the Th17 subset in the PBMCs of patients in comparison with those of control subjects was observed. Culture of PBMCs from psoriasis patients and controls in the presence of DMF decreased IFN-γ and increased IL-4 gene expression in both groups. Treatment with DMF could significantly decrease IL-17, GM-CSF, and IL-22 mRNA levels in the PBMCs of patients. Decreased release of IFN-γ and GM-CSF cytokine secretion after DMF treatment was also observed in PBMC cultures of patients and controls.

Conclusions:
These data show the effectiveness of DMF in modulating Th17 cells in addition to Th1/Th2 cells and reflect one of the underlying mechanisms of action of DMF in psoriasis. These findings may also support the possible benefits of using fumarate in the treatment of other autoimmune diseases in the pathogeneses of which Th1 and Th17 cells play major roles.

This small Japanese study set out to evaluate the efficacy of Humira (adalimumab) in treating joint disease in patients with PsA, using the PsA magnetic resonance imaging scoring system (PsAMRIS)

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Psoriatic arthritis (PsA), a seronegative arthropathy, may often result in progressive joint damage without treatment, leading to disability and impaired quality of life. Early therapeutic intervention of PsA is therefore crucial before the development of irreversible joint damage.

Because psoriatic skin lesions generally precede the onset of PsA, dermatologists occupy an important position in treating patients with early PsA.

This study aimed to evaluate the efficacy of adalimumab in treating joint disease in patients with PsA, using the PsA magnetic resonance imaging scoring system (PsAMRIS). Five adult Japanese male patients with active PsA were treated with adalimumab. Magnetic resonance imaging was obtained at baseline and 8–32 weeks with 2–3 time points following adalimumab treatment and assessed using PsAMRIS. Adalimumab treatment markedly improved clinical symptoms and disease activities of joint disease, which was confirmed by the reduction of PsAMRIS scores in all patients. Bone marrow edema and periarticular inflammation, reflecting the presence of enthesitis, were dramatically improved at week 8, while improvement of synovitis and flexor tenosynovitis was observed later, at week 24 or 32. However, bone erosion was not improved by adalimumab treatment during the follow-up period.

These results indicate that adalimumab treatment is associated with dramatic improvement of enthesitis in patients with PsA, whereas bone erosion may be resistant to such treatment. PsAMRIS appears to be useful for the evaluation of treatment efficacy in PsA.

I'm just wondering what shampoos and treatments that all you guys use. I'm having a nightmare at the minute with mine it's the first place my psoriasis has flared after coming off cyclosporine :( the shampoo the dermo has given me had just caused it to irritate and flake way more than it previously has. Didn't know if you guys can recommend anything? I've booked an earlier appointment with the dermo to try and get something

Any help would be appreciated

Are we the psoriasis patient expecting to much from our treatments? how soon do we expect them to work, how long do we expect them to work, etc. This study evaluated psoriasis patients subjective future expectations regarding health-related quality of life (HRQOL) and life expectancy, and to explore clinical features associated with under- or overestimating behaviour.

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Background:
Unrealistic expectations regarding treatments and clinical outcomes may lead to disappointment about therapy and sub-optimal compliance; nonetheless, these expectations have not been studied in psoriasis patients yet.

Objective:
To evaluate psoriasis patients' subjective future expectations regarding health-related quality of life (HRQOL) and life expectancy, and to explore clinical features associated with under- or overestimating behaviour.

Methods:
A cross-sectional questionnaire survey of consecutive adult patients with moderate to severe psoriasis was conducted. HRQOL expectations were recorded by applying the EQ-5D descriptive system for 6 months ahead and for future ages of 60, 70, 80 and 90 respectively.

Results:
In total, 167 patients (71% males) were included in the analysis with mean age of 50.4 ± 12.4 years and mean EQ-5D score of 0.71 ± 0.30. Overall 65% had chronic plaque psoriasis, 35% nail psoriasis, 35% scalp involvement, 29% psoriatic arthritis, 9% inverse psoriasis and 5% palmoplantar psoriasis respectively (combinations occurred). Participants expected 0.1 ± 0.23 mean improvement in EQ-5D within 6 months (P < 0.001) that achieves the minimum clinically important difference. Overall 37% expected improvement and 13% decline; however, 49% expected no changes in any of the five dimensions of EQ-5D within 6 months. Female gender, inverse or palmoplantar involvement and more severe psoriasis were likely associated with higher expectations. Patients at the initiation of their first biological at the time of the survey expected 0.18 ± 0.24 increase that seems to be realistic compared to the EQ-5D utility gain achieved in randomized controlled trials. Males expected by 2.7 ± 11.1 more, while females expected by 5.2 ± 9.3 less life years compared to the average statistical gender- and age-matched life expectancy (P < 0.05). Patients who expected to be alive at ages of 60, 70, 80 and 90 scored their future EQ-5D at ages of 60 to 90: 0.59 ± 0.46, 0.48 ± 0.41, 0.42 ± 0.41 and 0.22 ± 0.47 respectively.

Conclusion:
Our findings highlight the importance of exploring expectations that might help to increase patients' compliance.

A new assessment called PSOCUBE has been proposed which may be employed by practising dermatologists to perform standardized assessment procedures on psoriatic patients raising the chances of early recognition of patients at risk for comorbidities.

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Background:
There is increasing awareness of the clinical relevance of psoriasis comorbidities and of the importance of timely and effective screening for such comorbidities in the management of psoriatic patients. Previous works have focused on assessing evidence for prevalence of comorbidities and on the best available evidence for sensitivity in diagnosing suspected comorbidities. No algorithms are available, which have been tested on large numbers of physicians concerning the acceptance of such algorithms both by practicing clinical dermatologists and by their consulting specialists from other fields.

Objective:
To propose a multidimensional assessment algorithm for psoriasis comorbidities which may prove at the same time enough sensitive and practically sustainable in daily clinical practice.

Methods:
After an exhaustive literature search, we performed a Delphi procedure involving 50 dedicated dermatological centres to obtain a standardized assessment algorithm, which would meet requirements of sustainability and acceptability both from the point of view of Evidence-Based Medicine as well as from the point of view of practical and clinical feasibility: to meet both requirements, results from the Delphi procedure were elaborated and modified by a restricted panel of experts.

Results:
The procedure has yielded PSOCUBE, a three-dimensional table comprising 14 clinical examination and history taking items, 32 screening laboratory and instrumental exams and 11 clinimetric scores.

Conclusion:
PSOCUBE, a simple algorithm, may be employed by practising dermatologists to perform standardized assessment procedures on psoriatic patients raising the chances of early recognition of patients at risk for comorbidities, thus fostering more effective prevention; PSOCUBE may therefore contribute to reduce the overall impact of this chronic, widespread disease.

This Egyptian cohort study set out to determine whether inter-ethnic differences exist in the genetic susceptibility to psoriasis, it genotyped single-nucleotide polymorphism variations in the vicinity of candidate genes in 132 Egyptian patients and 175 healthy controls.

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Background:
Psoriasis vulgaris is a common chronic inflammatory skin disease. Development of early onset psoriasis is, to some extent, genetically determined and a strong association with the major histocompatibility complex HLA-Cw6 has been demonstrated. The use of genome-wide association studies has highlighted novel genes associated with the development of psoriasis as IL12B, IL23R, TNFAIP3 and IL13 for instance. The majority of these studies were performed on cohorts of European descent.

Objective:
To determine whether inter-ethnic differences exist in the genetic susceptibility to psoriasis, we genotyped single-nucleotide polymorphism variations in the vicinity of candidate genes in 132 Egyptian patients and 175 healthy controls.

Methods:
Blood samples of patients and controls were screened for nucleotide polymorphisms in four candidate genes by TaqMan single-nucleotide polymorphisms Genotyping Assays.

Results:
We found a significant association between psoriasis and the single-nucleotide polymorphism rs610604, within the TNFAIP3 gene. The TNFAIP3 gene is involved in the TNF-α signalling cascade (P-value: 0.004952), a key step in the pathogenesis of psoriasis. Although there was no significant association found between rs610604 (IL12B) and rs11209026 (IL23R) in this population, the interaction of these two genes showed a significant association with psoriasis (P-value: 0.025). Moreover, when selecting the patients with early disease onset (less than 30 years), we also found that the association of IL12B and psoriasis was highly significant (P-value 1.14 × 10−12). No association between rs20541 (IL13) and psoriasis was observed in our Egyptian cohort.

Conclusion:
Replicating the association of single-nucleotide polymorphisms in the TNFAIP3, IL12B and IL23R genes with psoriasis vulgaris, in subjects from different ethnic backgrounds, underlines their importance in the pathogenesis of the disease. In contrast, the lack of any association between rs20541 (IL13) and psoriasis in our Egyptian cohort suggests the existence of important inter-ethnic genetic differences in psoriasis susceptibility.

Hi everyone, I am Ando Urukwe 37 years old from Nigeria Africa. I have psoriasis for 4 years running. Initially, I thought it was sort a spiritual attack not until the patches spread all over my body. My skin is dilapidated..Contacted a dermatologist, he said no cure that is a rare skin condition in the tropic...mostly common in the developed world. He recommended some cream for me..Nothing work. Went to another skin clinic in Zaria Nigeria, clinic was established in 1920 ...try no improvement. Try dieting...cut nightshade, sugar, alcohol, ..less improvement...now iam using coconut oil.the skin is getting darker but the flaring and small scaling is still there. Notice this days that I need to shower at least 3 times a day and rob coconut oil to have small relive . It's frustrating sometimes. I'm tired. Any assistance in the forum is heartily well..My question is has any one cure of Psoriasis?

If you have been following the development of ASP015K which we first reported here in 2012 Janssen & Astellas to develop ASP015K (JAK) inhibitor you may be interested in these phase 2a results that show ASP015K has demonstrated dose-dependent improvements in clinical and histological measures of severity over 6 weeks of treatment. And t all doses, ASP015K was well tolerated, with no reported serious adverse events (AEs).

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Background:
Many immune-mediated disorders, including psoriasis, involve cytokine signalling via Janus kinase (JAK) enzymes. ASP015K (also designated JNJ-54781532), a novel oral JAK inhibitor, has shown moderate selectivity for JAK3 over JAK1 and JAK2 in enzyme assays.

Objectives:
The objective of this study was to evaluate the efficacy and safety of escalating, sequentially grouped, doses of ASP015K vs. placebo in patients with moderate-to-severe psoriasis.

Methods:
This phase 2a multicentre, double-blind, randomized, placebo-controlled study (NCT01096862) enrolled 124 patients with moderate-to-severe plaque psoriasis. Five sequential ASP015K cohorts were enrolled, consisting of four twice-daily dosing groups (10, 25, 60, 100 mg) and one once-daily dosing group (50 mg) for 6 weeks.

Results:
The primary efficacy end point [mean change in Psoriasis Area and Severity Index score from baseline to end of treatment (EOT; day 42)] significantly favoured ASP015K (overall treatment effect; P < 0·001) vs. placebo, with greater improvements at higher doses. By EOT, the secondary end points [Physician Static Global Assessment (PSGA) score, percentage of patients achieving PSGA success, and change in percentage, body surface area (BSA)] also improved with ASP015K vs. placebo (P < 0·001 for PSGA score and BSA; P < 0·01 for PSGA success). Epidermal thickness and proliferation decreased from baseline with ASP015K vs. placebo. ASP015K was generally well tolerated, with no serious adverse events (AEs) reported.

Conclusions:
In patients with moderate-to-severe psoriasis, ASP015K demonstrated dose-dependent improvements in clinical and histological measures of severity over 6 weeks of treatment. At all doses, ASP015K was well tolerated, with no reported serious AEs.

This is another one of the those systematic review and meta-analysis articles that looked into prevalence of undiagnosed psoriatic arthritis (PsA) among psoriasis patients, it concluded that there is a high prevalence of undiagnosed PsA in patients with psoriasis and recommended that dermatologists need to screen all patients with psoriasis for PsA.

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Background:
Skin psoriasis precedes the onset of psoriatic arthritis (PsA) in 84% of patients with psoriasis. Dermatologists have an important role to screen psoriasis patients for PsA. The efficiency of PsA screening remains unknown.

Objective:
We sought to determine the point prevalence of undiagnosed PsA in patients with psoriasis using a systematic search of the literature and meta-analysis.

Methods:
pub med, Cochrane, and Embase database searches yielded 394 studies for review. No study aimed to determine the prevalence of undiagnosed PsA in patients with psoriasis. We assumed that the prevalence of newly diagnosed PsA in patients with psoriasis at the time they seek medical care could be a sound estimate of this value. Seven epidemiological studies and 5 studies on PsA screening questionnaires allowed us to clearly identify patients with newly diagnosed PsA and were selected for review.

Results:
The prevalence of undiagnosed PsA was 15.5% when all studies were considered and 10.1% when only epidemiological studies were considered.

Limitations:
Data were obtained from studies not designed to address the question at hand. Heterogeneity was high (I2 = 96.86%), and therefore a random effects model was used.

Conclusion:
The high prevalence of undiagnosed PsA in patients with psoriasis adds to the recommendation that dermatologists need to screen all patients with psoriasis for PsA.

This Friday, the 18th, i am going to see the dermatologist for the first time in 42 years. I wonder if you could tell me what types , of creams or ointments most of the members, use . As i have said in previous posts, i only have it mildly, even though it's on different parts of my body.
I would prefer, i think to have a go taking tablets instead of everyday applying different creams. I have had the most success with Dovobet, but it's supposed not to use it for long periods, even though i have used it for years, without the doctor ever telling me to come of it.

The last time i saw the docs and asked to try a different ointment he put me on Dovonex, well first of all i didn't think it was doing any good, but secondly it says not to be in contact with the sun, when using it.Well with me spending six months of the year in Tenerife it was impossible not to be in the sun. So i am trying to ask for your advise as to when i see the Dermatologist what ointment you think that most of the members have the greatest success with, or the tablets. As i would like to tell him, what i would like to use with the suggestions of the Moderators. Thank you.

Good Afternoon All,

I stumbled on the site this morning while searching comments on hemp oil.  Just spent the last 2 hours reading all the posts here.  Thank you for taking my mind off the current condition of my skin!  I have plaque psoriasis and use clobetasol ointment for treatment.  I decided to give it a break recently as it was not working effectively.  Bad idea.  Tired of being sticky all the time; tired of my bed looking like a snow globe blew up in it; sorry my wife wakes up every morning with dandruff (she doesn't have dandruff).  It was 100+ degrees outside the other day and this guy (me) was the only one at a pool party fully dressed and sweating my ass off.  Shorts and short sleeves are out of the question, exposing my skin in public is out of the question.  I keep my hands hidden and instead of a handshake, most people get a elbow bump upon introduction.   I know there is no cure, just trying to gain some control!  I appreciate all the posts, hopefully I will find something close to a remedy here. -Joe

This large retrospective cohort study included 205 820 health plan enrollees in Israel, and set out to assess the relationship between adherence to statins and the risk of psoriasis.

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Background:
Statins have been shown to downregulate immune mechanisms activated in psoriasis. However, previous studies on their potential role in preventing psoriasis have yielded conflicting results.

Objectives:
To assess the relationship between adherence to statins and the risk of psoriasis.

Methods:
This retrospective cohort study included 205 820 health plan enrollees in Israel (mean age 55 years; 54·1% women) who initiated statin treatment from January 1998 through to September 2009. Adherence to statins, measured by the proportion of days covered (PDC), throughout the entire follow-up period (mean 6·2 years) was recorded. Diagnosis codes of psoriasis were assigned by a dermatologist or rheumatologist, or at discharge from hospital.

Results:
During 1·28 million person-years (PY) of follow-up (median 5·74 years per person; interquartile range 3·78–8·36), 5615 cases of psoriasis (incidence density rate 4·4 per 1000 PY) were recorded. Compared with patients who did not adhere to statins (PDC < 20%), patients covered by statins for 40–59% of the time had a significantly lower risk of psoriasis (P < 0·05), with hazard ratios (HRs) of 0·84 and 0·74 among men and women, respectively. Among patients who adhered better to statins (PDC ≥ 80%), HRs were 0·88 (95% CI 0·79–0·98) and 1·00 (95% CI 0·90–1·11) among men and women, respectively.

Conclusions:
The results of the current study suggest that high and long-term adherence to statins is not associated with a meaningful reduction in the risk of developing psoriasis.

Good news for palmoplantar psoriasis patients as Novartis announce results of two trials that showed superior efficacy compared to placebo in patients with psoriasis of the palms, soles and nails.

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Novartis announced today that Cosentyx® (secukinumab) met the primary endpoints in two new clinical studies, showing superior efficacy compared to placebo in patients with psoriasis of the palms, soles and nails, all difficult-to-treat locations of plaque psoriasis. Detailed findings were presented for the first time at the 23rd World Congress of Dermatology (WCD) in Vancouver, Canada.

In the GESTURE study in patients with moderate-to-severe palmoplantar psoriasis, Cosentyx (300 mg) was superior to placebo at Week 16 in achieving clear or almost clear palms and soles as assessed using the Palmoplantar Investigator’s Global Assessment (33.3% vs. 1.5%; P<0.0001) Similarly, in the TRANSFIGURE study in patients with significant nail psoriasis, Cosentyx (300 mg) was superior to placebo at Week 16, as assessed by mean improvement (decrease) in the Nail Psoriasis Severity Index (NAPSI) compared to baseline (-45.3% vs -10.8%; P<0.0001) The safety profile of Cosentyx in both studies was comparable to previously reported Phase III clinical trials.

“These are the largest trials to prospectively compare an active therapy to placebo in patients with psoriasis affecting the palms, soles, and nails, an area where a high unmet need for an effective treatment still exists,” said Vasant Narasimhan, Global Head of Development, Novartis Pharmaceuticals. “These results add to the growing body of evidence that Cosentyx is setting a new standard of care for patients with even the most challenging types of psoriasis.”

Estimated to affect as many as 90% of all psoriasis patients at some point in their lifetime, psoriasis of the palms, soles and nails is extremely difficult to treat and often requires biologic treatment (a protein based medicine made from cells) to control. Patients with these locations of psoriasis endure significantly greater physical disabilities than those whose psoriasis is limited to other parts of the body. Patients may experience difficulty walking, more pronounced burning sensation and difficulty grasping and handling objects, skin soreness and difficulty participating in recreational activities, social and workplace interactions. Nail psoriasis is a significant predictor of psoriatic arthritis, an important comorbidity of psoriasis.

Cosentyx is the first and only interleukin-17A (IL-17A) inhibitor approved for the treatment of moderate-to-severe plaque psoriasis. It was approved in January 2015 in the United States and European Union, and is also approved in Australia, Canada, Chile, Japan, Singapore and Switzerland.

This matched cohort study looked into the risk of getting psoriatic arthritis (PsA) in psoriasis patients after physical trauma, it concluded that there is an increased risk of PsA among psoriasis patients exposed to physical trauma, particularly when trauma to bone and joints was recorded.

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Background:
Most incident cases of psoriatic arthritis (PsA) present among patients with pre-existing psoriasis, and because of the high absolute prevalence of PsA among psoriasis patients this group offers a unique opportunity for risk modification. Several environmental and genetic factors have been associated with PsA. Trauma has been found to be associated with PsA in case series and cross sectional studies. This observation has led to the idea of a “deep Koebner” phenomenon playing a role in PsA, mirroring the Koebner phenomenon in skin psoriasis. We have performed a population based cohort study to determine the risk of PsA following trauma in psoriasis patients.

Objectives:
To evaluate the risk of incident PsA among psoriasis patients exposed to physical trauma.

Methods:
We performed a matched cohort study within the Health Improvement Network (THIN) database among psoriasis patients with data available between 1995 and 2013. Patients exposed to trauma were randomly matched to up to five unexposed controls based on gender, age, and the date of entry into THIN. Trauma exposure was stratified into subgroups of joint, bone, nerve, and skin trauma. Cox proportional hazard models were used to calculate the hazard ratio of developing psoriatic arthritis among those exposed to physical trauma, and the full model included adjustment for age, gender, date of entry into THIN, duration of psoriasis, BMI, smoking, alcohol consumption and the number of visits to the general practitioner. Missing values for smoking, alcohol use, and BMI were imputed by a sequential regression method. For comparison an identical analysis was performed in the non-psoriasis THIN population to evaluate the risk of developing rheumatoid arthritis (RA) following physical trauma.

Results:
Psoriasis patients exposed to trauma (N=15,416) and unexposed controls (N=55,230) were identified and followed for a total of 425,120 person-years (py) during which 1,010 incident PsA cases were recorded. The incidence rate of PsA among unexposed psoriasis patients was 22 (95% CI 21 to 24) per 10,000 py and 30 (95% CI 26 to 34) per 10,000 py in the exposed group. The results of the fully adjusted cox model analysis showed that psoriasis patients exposed to trauma had an increased risk of PsA compared to controls, with a hazard ratio (HR) of 1.32 (95% CI 1.13 to 1.54). In our subset analysis, bone and joint traumas were associated with multivariate HRs of 1.46 (95% CI 1.04 to 2.04), and 1.50 (95% CI 1.19 to 1.90), respectively, while nerve trauma and skin trauma were not associated with a statistically significant difference in risk compared to controls. Patients without psoriasis exposed to trauma did not have an increased multivariate adjusted risk of developing RA: HR 1.04 (95% CI 0.99 to 1.10) based on an analysis of 551,723 exposed individuals and 2,672,836 unexposed individuals followed for 19,479,771 py.

Conclusions:
We found an increased risk of PsA among psoriasis patients exposed to physical trauma, particularly when trauma to bone and joints was recorded.