This study suggests the Flightless 1 (FLii) could be a new approach for the fight against psoriasis.

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Background:
Psoriasis is a common chronic skin condition characterized by excessive inflammation and aberrant epidermal proliferation. Flightless I (Flii) is an actin-remodelling protein that regulates these processes, suggesting a possible role in psoriasis.

Objectives:
We sought to determine whether a benefit in psoriasiform dermatitis might occur after modulating Flii gene expression or reducing its levels using neutralizing antibodies.

Methods:
Biopsies of psoriatic skin lesions from patients were assessed for Flii levels. Psoriasis-like lesions were induced in Flii heterozygous (Flii+/−), wild-type (Flii+/+) and Flii transgenic (FliiTg/Tg) mice using topical application of imiquimod. Additionally, psoriasis-induced wild-type mice were treated with topical application of Flii neutralizing antibodies and erythema, inflammation and histology were assessed.

Results:
Flii was elevated in psoriatic lesions from patients with psoriasis compared with normal human skin. Reducing Flii decreased erythema, inflammatory cell infiltrate, proinflammatory cytokines and the thickness of the epidermis. Topical application of Flii neutralizing antibodies to wild-type mice treated with imiquimod resulted in significantly reduced psoriasiform dermatitis.

Conclusions:
Flii is a novel target involved in psoriasiform dermatitis and reducing cutaneous Flii could potentially be a new approach for treating patients with psoriasis.

This study looked at anti drug antibodies (ADA) levels and clinical efficacy in psoriasis patients using Humira and Enbrel

Quote:

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Background:
An algorithm based on measurement of a serum tumour necrosis factor antagonists (anti-TNF) and antidrug antibodies (ADA) has been proposed previously to guide dose escalation or therapy switching in the early (i.e. the first months of) treatment of psoriasis by anti-TNF. In long-term treatment of responding patients with psoriasis, it is usual to empirically reduce standard doses of anti-TNF to reduce exposure while maintaining clinical response. The relationship between serum anti-TNF, ADA levels and clinical efficacy in long-term treated patients with psoriasis has not yet been determined, so the potential role of these parameters in guiding dose escalation in this scenario is unknown.

Aims:
To evaluate the relationship between drug/ADA levels and clinical efficacy in a group of patients with psoriasis undergoing long-term treatment with adalimumab or etanercept.

Methods:
This was a single-centre, prospective, cohort study of patients with psoriasis receiving adalimumab or etanercept for a minimum of 48 weeks. All patients were started on the standard dose, but some adalimumab users had a reduced frequency of administration. Clinical efficacy was measured using the Psoriasis Area and Severity Index. Serum concentrations were measured by ELISA. Clinical assessment and blood sample collection were carried out simultaneously within 24 h before the next drug administration.

Results:
In total, 21 patients were enrolled (67 simultaneous clinical and serum determinations: 38 receiving adalimumab, 29 receiving etanercept). We did not find any association between serum anti-TNF levels and clinical response. None of the patients developed ADA.

Conclusions:
ADA and anti-TNF levels are not related to clinical effectiveness in patients with psoriasis undergoing long-term treatment with adalimumab or etanercept.

   Hi!  I am already playing Christmas melodies from the past - to get me in the spirit!  I'm glad that I found this site.  Looking forward to contacts and great advice. 

I've recently started on Cosentyx - into my second month and I am delighted!  I did take Humira but had a very bad flare up, then lost the good affects.  The problem was - flu shot at work - no one to get advice from - both my Doctors were away.  I read on line that as long as it wasn't a live specimen it was ok to take.  NOT a good idea.  I got very sick, for one thing and then the Humira no longer worked for me.  I have been putting up with extensive psoriasis on my legs (once considered  attractive) and periodically some on my elbows, for many, many years.  I am just grateful that it didn't start in my twenties or thirties.  I would have been even more devastated.  My Mom had it, but not as badly.  She was very upset to find out that I was affected, but didn't live long enough to see it take over like a monster!  So here I am, but there is more to me.  I am a type 2 diabetic in my 60's (I don't want you to think I'm REALLY old, because I have a young spirit and people tell me I look 10 years younger).  Ok, so now I will say that I have two wonderful children that are close to my heart but far away.  My son runs a home appraising business in Calgary and has been very successful.  My daughter is in Markham, Ontario and works as a wildlife conservationist.  She got her Masters in Scotland.  I was born in Germany and immigrated at the age of 5, with my parents.  I am very CANADIAN.  I am a Registered Nurse - once retired very early, but returned to work when I moved here, due to boredom and desire to travel.  I am on my own with two cats.  Life is good, but it could be better.  I look forward to communication with others.  It's lonely being on your own. So, I'll close for now and say "thanks for letting me be a member and Merry Christmas to all!"

We have a few of these studies on Psoriasis Club and this one concludes that patients with periodontitis have a significantly elevated risk of psoriasis.

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Background:
The association between periodontitis and systemic diseases has been increasingly recognized. However, the data on the association between periodontitis and psoriasis are still limited.

Objectives:
To summarize all available data on the association between periodontitis and the risk of psoriasis.

Methods:
Two investigators independently searched published studies indexed in MEDLINE and EMBASE databases from inception to July 2016 using a search strategy that included terms for psoriasis and periodontitis. Studies were included if the following criteria were met: (i) case–control or cohort study comparing the risk of psoriasis in subjects with and without periodontitis; (ii) subjects without periodontitis were used as comparators in cohort studies while participants without psoriasis were used as controls in case–control studies; and (iii) effect estimates and 95% confidence intervals (CI) were provided. Point estimates and standard errors from each study were extracted and combined together using the generic inverse variance technique described by DerSimonian and Laird.

Results:
Two cohort studies and three case–control studies met the inclusion criteria and were included in the meta-analysis. The pooled risk ratio of psoriasis in patients with periodontitis versus comparators was 1.55 (95% CI, 1.35–1.77). The statistical heterogeneity was insignificant with an I2 of 18%. Subgroup analysis according to study design revealed a significantly higher risk among patients with periodontitis with a pooled RR of 1.50 (95% CI, 1.37–1.64) for cohort studies and a pooled RR of 2.33 (95% CI, 1.51–3.60) for case–control studies.

Conclusions:
Patients with periodontitis have a significantly elevated risk of psoriasis.

Valeant Pharmaceuticals  have announced positive results from a Phase 3, multicenter double-blind, randomized, vehicle-controlled clinical study to assess the safety and efficacy of IDP-118 (halobetasol propionate and tazarotene) lotion in the treatment of plaque psoriasis.

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Valeant Pharmaceuticals International, Inc. (NYSE: VRX and TSX: VRX) ("Valeant") today announced positive results from a Phase 3, multicenter double-blind, randomized, vehicle-controlled clinical study to assess the safety and efficacy of IDP-118 (halobetasol propionate and tazarotene) lotion in the treatment of plaque psoriasis.

Within the Phase 3 study of 215 adult subjects with moderate to severe psoriasis, IDP-118 showed statistical significance to vehicle with a treatment success rate of 45.33% and a p<0.001.  The primary endpoint of the 12-week study was achievement of a "clear" to "almost clear" score based on an Investigator Global Assessment (IGA) at 8 weeks, and at least 2 grade improvement in the IGA at weeks 12, 6, 4 and 2 as secondary endpoints.

"We are pleased to share the positive results from the Phase 3 study of this important new formulation," stated Joseph C. Papa, Chairman and Chief Executive Officer.  "Psoriasis is often difficult to treat, and dealing with this life-long condition can significantly impact a patient's quality of life.  Valeant remains committed to continued research into innovative new treatments to improve the lives of those who suffer from psoriasis."

While halobetasol propionate and tazarotene are both approved and used to treat plaque psoriasis, each has certain attributes that can influence the treatment duration owing to potential adverse events.  Based on existing data from our clinical studies, the combination of these ingredients in IDP-118 with a dual mechanism of action potentially allows for expanded use of these active ingredients with reduced adverse events.

The Phase 3 program was preceded by a successful Phase 2 study where the combination product IDP-118, with a treatment success rate of 52.5%, was superior to each of the actives halobetasol propionate and tazarotene as well as the vehicle. Valeant expects to have data from a second confirmatory pivotal Phase 3 study in 2017.

Dave here.  42 years old, psoriasis symptoms for ~20yrs, arthritis for ~8 years.

I've typically been a medication minimalist as much as possible over the years, but with the arthritis steadily getting worse, I've given in to things I don't want to take.

I have Celebrex for the pain when needed.  DMARDs started as sulfasalazine and then Otezla.

I was in love with Otezla.  Worked great for about a year, then a somewhat spontaneous decline in efficacy.  I have quit the medication for 3 weeks before I go see my Rheumy next week, just so I could get a feel of whether it was actually working period anymore or not.  IMO, it's at about 30-40% of what it was doing for me at its peak, so I'm not sure it's worth taking anymore.  But since being off Otezla, I've felt fairly bad.

As I said, I'm going in next week to likely start a new course of treatment.  I've been reading up just trying to get a sense of what is out there, so I'm fairly well-versed.

Methotrexate - I don't want to take it.  Bad vibes is all... no other reasonable reason.

I've been reading about Cosyntex, which looks like it's at least a more specific biologic than Humira or Enbrel, right?  Not sure if I have that right but I'll see what my doc wants to do with me.  Immune suppressors give me the heebie-jeebies as well. 

Anyone with a significant background in medicine on here, I'd like to throw this little nugget out there:  I'm fully aware this could be coincidence, but since I've been symptomatic with the arthritis, I've not had more than a bad cold in terms of sickness.  If I've had a fever in that time, it's a very short period of time... maybe an evening or something like that.  I haven't had the flu, and I work in an environment with community computer workstations, so decent germ exposure.  Nothing else has really changed in that time.

Anyways, just saying hello and telling my story.  I'm tired of hurting.  I used to run, play softball, hike... just stayed as active as possible.  Now I spend a lot of time in hot baths.  Hopefully I can find a remedy that won't wreck other parts of my body in the process.

This meta-analysis evaluated IL-17 levels in patients with psoriasis. IL-17 is targeted by the new bio's:
Cosentyx (secukinumab) and Taltz (ixekizumab)

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Background:
Emerging evidence indicates that plasma interleukin (IL)-17 levels may be associated with increased risk of psoriasis, but the individual published results are inconclusive.

Aim:
To evaluate IL-17 levels in patients with psoriasis using a meta-analysis of studies comparing IL-17 levels in controls and in patients with psoriasis.

Methods:
All relevant studies were identified by searching pub med, Web of Science and MEDLINE databases before 1 November 2015. Pooled risk estimates were calculated by random-effects models. Crude OR and standardized mean difference (SMD) with corresponding 95% CI were also calculated.

Results:
In total, eight cross-sectional study studies were included in the final analysis. The mean plasma levels of IL-17 were higher in patients with psoriasis than in healthy controls (SMD = 0.47, 95% CI = 0.07–0.86, P < 0.001).

Conclusions:
Based on this literature review, there appears to be a positive association between IL-17 plasma levels and psoriasis.

Lycera has announced it has initiated a phase2 trial of LYC-30937-EC for psoriasis. YC-30937, a first-in-class, oral, gut-directed ATPase modulator, is designed to selectively target and induce cell death (apoptosis) in disease-causing immune cells (T-lymphocytes) based on their unique metabolic features, while sparing normal cells.

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Lycera Corp., a privately held biopharmaceutical company developing breakthrough immune modulatory medicines, announced today the initiation of a Phase 2 clinical trial of the Company’s lead therapeutic candidate, LYC-30937-Enteric Coated, in patients with psoriasis. Psoriasis is often a debilitating skin disease that is estimated to affect as many as 7.5 million people in the United States, with approximately 1.5 – 3 million cases being diagnosed as moderate.  Current systemic therapeutics for the treatment of moderate-to-severe psoriasis result in 75% improvement in the Psoriasis Area Severity Index (PASI) in approximately 80% of patients, but require injections and often lead to side effects, including pronounced immune suppression.  A significant need exists for more convenient, orally dosed psoriasis treatments that provide high PASI scores and low rates of adverse events.

“We continue to make substantial progress with our development of novel immune modulators and are very pleased to have initiated our second Phase 2 clinical trial with our first-in-class ATPase modulator this year. Moreover, this study marks a major accomplishment for the investigation of a gut-directed therapy to target the treatment of peripheral autoimmune disease,” said Paul Sekhri, President and CEO of Lycera. “Based upon the results of our preclinical studies, we believe LYC-30937-EC can impact pathogenic lymphocytes that traffic through the human gastrointestinal tract before these lymphocytes can migrate to distal tissues, such as the skin, causing psoriasis.  If successful, this trial may lead the way to exploring LYC-30937-EC in other diseases, such as rheumatoid arthritis and multiple sclerosis.”

“Psoriasis can pose a significant burden for patients, i.e., chronic itching, stinging, and pain, having a profound negative impact on daily functions and diminished quality of life,” stated Jerry Bagel, M.D., Medical Director for the Psoriasis Treatment Center of Central New Jersey and an investigator in the Phase 2 study. “In addition, many patients experience depression, decreased self-esteem, and anxiety, and new oral therapies would be helpful. I believe LYC-30937-EC represents a unique mechanism of action and a promising approach to targeting the cells that cause inflammation and are the hallmark of psoriasis.”

Lycera’s Phase 2 study UPRISE (gUt-directed LYC-30937-EC study in Psoriasis as oRal treatment for autoImmune diseaSE) is a randomized, double-blind, placebo-controlled parallel group trial designed to assess the efficacy and safety of LYC-30937-EC given orally once daily in subjects with moderate psoriasis. The study is expected to enroll up to 30 patients, randomized on a 2:1 basis to receive either treatment with LYC-30937-EC or placebo. Subjects will be treated for 12 weeks, with an additional 2-week safety follow-up. The primary efficacy endpoint will be the change in mean PASI Score and Investigator global assessment; safety will be measured over 14 weeks.

Hi I'm new I have been suffering from psoriasis for about 25 yrs it's not to bad at the moment i just wanted to share with everyone the way I have gotten mine under control. I have been taken vitamin D about 4000 iud a day and magnesium 1 a day I also use a Philips hand held Uvb device which I use once a day and I went cold turkey and came off steiod cream and use coconut oil instead o and also a 20 billion probiotics one a day it has made a big difference 
I hope this helps someone as I know how dis stressing this horrible thing is x

  Hi all.   I am waiting for a nurse to arrive from Oxford ( I am in Somerset) to give me training on how to use cosentyx, it will be my first injection today after an incredibly long wait.  I feel very anxious. She should be here within the hour and I have taken the syringes out if the fridge.  Please wish me luck!   

I first had psoriasis about 20 years ago, in my ears, which developed into chronic plaque psoriasis over time.   I have tried many treatments, all the usual creams and moisturisers. Light therapy, acitretin, methotrexate for past 6 years and it stopped working about 6  onths ago.

My worst time ever came in 2008.     I had phototherapy with such a bad reaction resulting in third degree burns after (5 low dose treatments)  I was extremely ill when everywhere got infected,  bedridden and then hospitalised. Housebound for 5 months.   ( the consultant I was under threatened me not to take legal action - there was suspicion that the nurse set the machine wrong, we did later take legal action ) anyway, the outcome was It left me in a wheelchair for a year with severely damaged and scarred backs of both legs. I still cannot walk far and still need a wheelchair. 

I changed hospitals and was started on methotrexate which has kept thing mainly in check with occasional blips.  This year I have another serious outbreak which has led to me being started on the cosentyx.  I have been housebound since August, and can only wear very very soft clothes.  As you will all know, the pain and soreness can be unbearable especially when completely covered in psoriasis.  The wired thing is that this time my outbreak was the guttate type, she had then all joined up to make huge areas like the plaques.  

I have a wonderful husband   who helps me, and some lovely neighbours and friends.   I often wonder what would of happened to me without their help. I feel very lucky.   I am so glad to have found this group, everyone is very friendly.  I no longer feel alone with others who understand.

Thank you for taking the time to read my post, you all have a good day 

Hey guys, I'm Nick. I first started with rosacea on my face, which became much worse and led to eczema and seborrheic dermatitis after some dermatologists tried to help. I fixed it myself with herbs and supplements, but after a few years I had issues and went back to the dermatologist, got worse...anyway, that's the cycle I've done 5 or 6 times now, with the latest problem being plaque and guttate psoriasis on my neck and arms that got much worse when my derm suggested (before doing a biopsy) athlete's foot cream in case it was fungal, and I took a lot of B vitamins and zinc (probably unbound copper dumping, but the biochemical angle gets technical real quick).  Otezla helped at first but not so much now, but because I work at a hospital with all sorts of nasty diseases, I don't really want to take anything that decreases my immunity. I took my first, tiny dose of dimethyl fumarate today and tolerated it well, and am trying to slowly increase my zinc levels too. Nice to meet you all.

Hi, I've been battling this since 2013, induced by stress.  After trying every kind of topical option, I was approved for Stelara with my insurance in Dec 2015.  After undergoing initial blood tests, I had two TB Gold tests come back "indeterminate".  Both my physician and dermatologist had never seen this before. They are usually either positive or negative, right?   We first thought it was a lab error but after the second one they wanted me to go to an infectious disease specialist.  I could not find one to except me so I put it on hold until the new year....and then I got a cold, then I got a sinus infection, then I got busy, then an event of extreme stress and constant anger causaed an outbreak of Shingles on my forehead! (Ocular nerve from eye to brain was affected. I was 39 years old!).  That virus and the 3,000 mg a day of anti-viral medicine for 10 days knocked me down for a month. Anxiety and anger was replaced with withdrawal, depression and a massive outbreak of psoriasis. Celexa changed my life emotionally,  that's another topic.  I'm so thankful for my physician.  In November 2016 I felt better than I had in over a year, so I decided to start the process of Stelara again. TB Gold negative!  I believe everything happens for a reason. Those two tests that didn't make sense happened because I was not meant to be on this injection yet. I am scared to think of how bad it. I have been if I had been on Stelara during that time. So as we started the process again, in the meantime they gave me Enstilar, luckily at no cost to me, due to a manufacturer incentive and a specialty pharmacy.   Four weeks later I got my first Stelara injection, Dec 1st.  I am anxious to see how well this works!

Side note - Enstilar is AMAZING, short term. On the 2nd day my skin was peeling and feeling very smooth.  On the 4th day the redness went away! On week 3, the week to take a break from it, it  started to come back and spread.  That was the first topical that ever made a difference to me.  I am happy to share a day 4 "before and after" picture if I can figure out how. Ha! 

hello I'm on acetretin 25mg my nails r so brittle does anyone else have this prob. thanks Linda

After a patch of psoriasis has faded, do the white patches that are sometimes left behind fade and disappear over time or do they generally stay?

I have very mild psoriasis and the patches I get are never very big and certainly not very thick yet I've been left with  2-3 small white circles on my arms where I've had psoriasis come and go. Will they disappear?

The odd thing is that I've had stubborn patches disappear after months and not leave any trace they were ever there but then, for example, I had a small patch appear on my right arm about 3 months ago, I applied Dovobet to it for about 3 days and it disappeared and never came back yet it has left a little white patch where it was.

They don't particularly bother me and are certainly preferable to a psoriasis patch but I was just wondering whether they tend to stick around or disappear eventually?

Thanks.

This study shows that Taltz (ixekizumab) gave significant improvements in fingernail psoriasis.

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Background:
Fingernail psoriasis is difficult to treat.

Objective:
The objective was to evaluate the effect of ixekizumab, a monoclonal antibody selectively targeting IL-17A, on fingernail psoriasis.

Methods:
This Phase 3, double-blind trial (UNCOVER-3) randomized patients to placebo, etanercept (50-mg twice weekly), or 80 mg ixekizumab as one injection every 4 (IXE Q4W) or 2 weeks (IXE Q2W) after a 160-mg starting dose. At Week 12, ixekizumab patients received open-label IXE Q4W through Week 60; placebo patients received a 160-mg starting ixekizumab dose and etanercept patients a 4-week placebo washout before starting IXE Q4W. Efficacy was assessed by mean per cent Nail Psoriasis Severity Index (NAPSI) improvement at Weeks 12 and 60.

Results:
Of 1346 patients in the UNCOVER-3 trial, this subgroup analysis included only patients with baseline fingernail psoriasis: 116 (60.1%) placebo, 236 (61.8%) etanercept, 228 (59.1%) IXE Q4W and 229 (59.5%) IXE Q2W. At Week 12, greater mean per cent NAPSI improvements were achieved in IXE Q4W (36.7%) and IXE Q2W (35.2%) vs. placebo (−34.3%, P < 0.001 each comparison) and etanercept (20.0%, P = 0.048 vs. Q4W, P = 0.072 vs. Q2W). At Week 60, mean per cent NAPSI improvement was >80% regardless of initial treatment. At Week 12 (nonresponder imputation), complete resolution (NAPSI = 0) was achieved in 19.7% (IXE Q4W), 17.5% (IXE Q2W), 4.3% (placebo, P < 0.001 each comparison) and 10.2% (etanercept, P < 0.05 each comparison) of patients. By Week 60, >50% of patients achieved complete resolution.

Conclusions:
At Week 12, significant improvements in fingernail psoriasis were achieved with ixekizumab therapy. With IXE Q4W maintenance dosing, additional improvement was demonstrated through 60 weeks, and >50% of patients achieved complete resolution.

Hi everyone I am new here, I live in Somerset and have had psoriasis for about 20 years. On Monday I am starting cosentyx. Rather nervous, but excited at the same time.

Has anyone ever had a look at this website?  I found it somewhat informative.  Just posting in case it is helpful to someone.  
I'm having a hard time with the psoriatic arthritis today (if that's really what it is...), damn knee won't stop throbbing.  Might just be old age or a faulty knee, but because my psoriasis is so bad, the doc thinks it MAY be psoriatic arthritis.  Great, now I get to have both!

Anyway, here's the website that a friend forwarded to me today.  I had not seen it myself.  LINK REMOVED  

Of course, the only REAL positive and helpful site of LASTING value, is right here, folks!  Step right in!!!!  (And thanks to all of you that talk and listen and post and reply and help and encourage and make others laugh...)

I don't often have time to get online, but I must admit that I do love THIS site...the psoriasis club!

This study is suggesting that Stelara (ustekinumab) could be aiming at the wrong target. The study from Researchers at the University of Zurich and the Center of Allergy and Environment in Munich suggests that IL-12 could actually be beneficial to patients with psoriasis.

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Abstract:

Neutralization of the common p40-subunit of IL-12/23 in psoriasis patients has led to a breakthrough in the management of moderate to severe disease. Aside from neutralizing IL-23, which is thought to be responsible for the curative effect, anti-p40 therapy also interferes with IL-12 signalling and type 1 immunity.

Here we dissect the individual contribution of these two cytokines to the formation of psoriatic lesions and understand the effect of therapeutic co-targeting of IL-12 and IL-23 in psoriasis.

Using a preclinical model for psoriatic plaque formation we show that IL-12, in contrast to IL-23, has a regulatory function by restraining the invasion of an IL-17-committed γδT (γδT17) cell subset.

We discover that IL-12 receptor signalling in keratinocytes initiates a protective transcriptional programme that limits skin inflammation, suggesting that collateral targeting of IL-12 by anti-p40 monoclonal antibodies is counterproductive in the therapy of psoriasis.

This study looked at the increased risk of cardiovascular (CV) problems in psoriatic arthritis patients.

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Objective:
To examine the prevalence and incidence of cardiovascular (CV) risk factors, including hypertension, hyperlipidemia, diabetes mellitus (DM), and obesity among patients with psoriatic arthritis (PsA) and rheumatoid arthritis (RA) compared to the general population, and to examine the treatment of incident CV risk factors in PsA and RA compared to controls.

Methods:
A cohort study was conducted within The Health Improvement Network, a medical record database in the UK, using data from 1994 to 2014. Patients ages 18–89 years with PsA or RA were matched to controls on practice and start date. The prevalence and incidence of CV risk factors identified by diagnostic codes were calculated. Cox proportional hazards models were used to examine the relative incidence of these CV risk factors. Finally, pharmacologic therapies for incident CV risk factors were examined.

Results:
Study subjects included patients with PsA (n = 12,548), RA (n = 53,215), and controls (n = 389,269). The prevalence of all CV risk factors was significantly elevated in PsA. Only the prevalence of DM and obesity was increased in RA. Incidence of hypertension, hyperlipidemia, and DM was elevated in PsA and RA. Receipt of therapy within 1 year following incident diagnosis of CV risk factors was not substantially different between the groups; approximately 85%, 65%, and 45% of patients received prescriptions for hypertension, hyperlipidemia, and DM, respectively.

Conclusion:
Patients with PsA have an increased prevalence of CV risk factors, and both patients with PsA and patients with RA have increased incidence of a new diagnosis of CV risk factors. Pharmacologic treatment of CV risk factors in patients with PsA and RA was similar to controls in the UK.

This study looks at how well medication is used in the long-term topical treatment of psoriasis.

Quote:

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Background:
Most people with psoriasis have limited disease that could be treated with topicals, but topical efficacy is limited by low short-term adherence. Psoriasis is a chronic disease, and long-term adherence is an even bigger problem.

Objectives:
To determine how well medication is used in the long-term topical treatment of psoriasis and to assess the potential of an internet-based reporting intervention to improve treatment adherence and outcomes.

Methods:
An investigator-blinded, prospective study evaluated topical fluocinonide adherence in 40 patients with mild-to-moderate psoriasis over 12 months. Subjects were randomized in a 1 : 1 ratio to standard-of-care or internet-based reporting group. Adherence was objectively monitored with Medication Event Monitoring System® caps.

Results:
Fifty per cent of subjects discontinued the treatment. Greater adherence was seen in the intervention group compared with the standard-of-care group (50% vs. 35%, P = 0·08). Psoriasis Area and Severity Index improved more in the intervention group at month 1 (1·61 vs. −0·12, P = 0·003), month 3 (2·50 vs. 0·79, P = 0·025) and month 12 (3·32 vs. 0·34, P = 0·038) than in the standard-of-care group.

Conclusions:
This study likely underestimates the challenge of long-term adherence, as adherence tends to be better in research studies than in clinical practice. This study also did not fully account for primary nonadherence. Adherence to topical treatment is low in the short term and decreased further in the long term, a considerable challenge for dermatologists to address. A reporting intervention may be one of the ways we can improve our patients’ treatment outcomes.