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.

Following on from Lilly's Ixekizumab phase 3 report, Lilly have now published results from the UNCOVER-2 and UNCOVER-3 clinical studies of more than 2,500 psoriasis patients, and the trials look very encouraging.

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Eli Lilly and Company announced today that detailed results of two pivotal Phase III studies for ixekizumab were published by The Lancet. The UNCOVER-2 and UNCOVER-3 clinical studies of more than 2,500 patients found ixekizumab to be statistically superior to etanercept and placebo on all measures of skin clearance. Patients treated with ixekizumab also demonstrated significant and meaningful improvements in health-related quality-of-life measures. Ixekizumab is the company's investigational medicine for the treatment of moderate-to-severe plaque psoriasis.

"These studies show ixekizumab - at two different dosing regimens - performed significantly better than etanercept or placebo, inducing a rapid and high level of psoriasis plaque resolution for patients with moderate-to-severe disease," said Christopher Griffiths, M.D., FRCP, professor of dermatology at The University of Manchester, U.K. and primary study investigator. "Importantly, these clinical results were accompanied by significant improvements to patient quality of life, and were achieved with a safety profile comparable to etanercept in these studies."

In each study, co-primary efficacy objectives assessed whether ixekizumab administered once every two weeks or once every four weeks was superior to etanercept and placebo after twelve weeks, as measured by a Psoriasis Area and Severity Index reduction of at least 75 percent (PASI 75) and a Static Physician Global Assessment score of clear or minimal (sPGA 0/1).

PASI is a measure used by healthcare professionals to determine the severity of psoriasis, including redness, thickness, scaling and the extent of psoriasis coverage. A PASI 75 score signals at least a 75 percent reduction in a patient's psoriasis from their baseline assessment. The sPGA is the physician's assessment of severity of a patient's psoriasis lesions overall at a specific point in time.

"The results of UNCOVER-2 and UNCOVER-3 provide a strong reason to believe that, if approved,  ixekizumab may help patients treat their moderate-to-severe psoriasis quickly and effectively," said Brian J. Nickoloff, M.D., Ph.D., senior medical fellow, Lilly Bio-Medicines. "We saw clinically-meaningful improvements in skin clearance as early as week one of treatment with ixekizumab, and with approximately 40 percent of patients achieving complete skin clearance at 12 weeks, we're hopeful clear skin may be attainable for more people living with this hard-to-treat disease."

Rapid Onset of Efficacy; High Levels of Skin Clearance
In both studies and at both dosing regimens, ixekizumab achieved superiority to etanercept and placebo for PASI 75 at week 12, with statistically significant differences seen as early as the first week of the studies. Approximately 50 percent of all ixekizumab-treated patients achieved PASI 75 by week four.

Patients treated with ixekizumab also achieved higher rates of skin clearance as measured by PASI 90 and PASI 100 compared with etanercept and placebo. PASI 90 reflects at least a 90 percent reduction in psoriasis symptoms, while PASI 100 is the highest possible reduction, representing complete skin clearance. Patients treated with ixekizumab were five to seven times more likely to achieve a PASI 100 score than with etanercept. At the end of the 12-week study period, patients achieved PASI 90 and PASI 100 at the following rates:

Patients receiving ixekizumab every two weeks: 71 percent in UNCOVER-2 and 68 percent in UNCOVER-3 achieved PASI 90; 41 percent in UNCOVER-2 and 38 percent in UNCOVER-3 achieved PASI 100;
Patients receiving ixekizumab every four weeks: 60 percent in UNCOVER-2 and 65 percent in UNCOVER-3 achieved PASI 90; 31 percent in UNCOVER-2 and 35 percent in UNCOVER-3 achieved PASI 100;
Patients receiving etanercept: 19 percent in UNCOVER-2 and 26 percent in UNCOVER-3 achieved PASI 90; 5 percent in UNCOVER-2 and 7 percent in UNCOVER-3 achieved PASI 100.

Quality-of-Life Measures Significantly Improved
Clinical improvements in ixekizumab-treated patients were accompanied by rapid improvements in health-related quality-of-life measures. Nearly 60 percent of ixekizumab-treated patients reported that their psoriasis had no impact on their quality of life by week 12 as measured by the Dermatology Life Quality Index (DLQI). The DLQI is a standardized tool that evaluates how psoriasis affects various aspects of a person's quality of life, including itching, ability to conduct daily activities, and relationships and intimacy.

In a separate, pre-specified analysis evaluating patients that had achieved PASI 100, 78 percent in UNCOVER-2 and 85 percent in UNCOVER-3 reported the disease had no impact to their quality of life as measured by the DLQI.

"Psoriasis is more than just a condition that affects the skin; it affects a person's relationships with friends and families, their day-to-day activities and, in many cases, other aspects of their health," said Aarti Shah, Ph.D., global brand development leader, Lilly Bio-Medicines. "Based on these study results, we believe ixekizumab, if approved, could offer those with moderate-to-severe psoriasis a treatment choice that may improve both the physical and emotional challenges of psoriasis."

Adverse Events
The overall rates and severities of adverse events observed were comparable to those for etanercept in the two active comparator trials. Most Treatment-Emergent Adverse Events (AEs) were mild or moderate in severity. The most common (≥2 percent) Treatment-Emergent AEs in ixekizumab-treated patients were upper respiratory tract infections, injection site reactions, itching, headache and arthralgia. Serious Adverse Events (SAEs) were reported by < 2 percent of patients, and there were no deaths in either study. Rates of SAEs and discontinuations due to AEs were comparable across treatment groups.

About UNCOVER-2 and UNCOVER-3
UNCOVER-2 and UNCOVER-3 are double-blind, multicenter, Phase III studies evaluating more than 2,500 patients with moderate-to-severe psoriasis in 18 countries. In these comparator studies, patients were assigned to receive either placebo, etanercept (50 mg twice a week) or ixekizumab (80 mg every two or four weeks) for 12 weeks, following a 160 mg starting dose. Patients enrolled in the UNCOVER-2 and 3 studies had a confirmed diagnosis of chronic plaque psoriasis for at least six months prior to randomization. Additionally, at screening and at randomization, they demonstrated at least 10 percent Body Surface Area (BSA) of psoriasis, an sPGA score of at least 3 and PASI score of at least 12.

Following on from the bad news for Otezla (apremilast) Germany says Otezla gives no benefit to psoriasis patients today Celgene looks like taking another knock in the UK.

NICE (National Institute for Heath and Care Excellence) look set to say no to Otezla for England and Wales, (Scotland will be getting it however) it looks set to get rejected for use in England and Wales after not meeting cost effectiveness.

Don't ask me why Scotland gets preferential treatment, as far as I know it's a political thing.

*This report is made up from various pieces of information that have been passed on to me, I've not been able to find any official announcement as yet but it looks very likely this is going to happen.

Another new treatment goes into phase 1 for the treatment of psoriasis, this one is from Prothena a late stage clinical biotechnology company and the treatment is PRX003 a monoclonal antibody for the potential treatment of psoriasis and other inflammatory diseases.

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Prothena Corporation plc, a late-stage clinical biotechnology company focused on the discovery, development and commercialization of novel protein immunotherapy programs, today announced the successful first human dosing in a Phase 1 clinical trial of its proprietary protein immunotherapy, PRX003. PRX003 is a monoclonal antibody targeting melanoma cell adhesion molecule (MCAM) for the potential treatment of psoriasis and other inflammatory diseases.

"PRX003, our third program to advance into clinical development, further demonstrates our commitment to develop a robust pipeline of protein immunotherapies that have the potential to transform patients' lives," said Gene Kinney, PhD, Chief Scientific Officer and Head of Research and Development for Prothena. "MCAM allows disease-causing immune cells to migrate into the surrounding tissues to initiate and/or maintain a pathogenic process and we believe that blocking this process holds tremendous promise for the treatment of inflammatory diseases. We look forward to assessing the safety and tolerability of PRX003 in subjects through this Phase 1 single ascending dose study and also expect to initiate a multiple ascending dose study in patients with psoriasis in 2016."

The Phase 1 clinical trial is a randomized, double-blind, placebo-controlled, single ascending dose study designed to assess the safety, tolerability, pharmacokinetics and immunogenicity of PRX003. Prothena plans to enroll up to 40 subjects in the U.S.

About PRX003:
PRX003 is a monoclonal antibody for the potential treatment of psoriasis and other inflammatory diseases. Within the immune system, Th-17 white blood cells initiate the body's response to infections, and are known to be a key participant in both normal inflammatory reactions and autoimmune diseases. MCAM is expressed on the surface of Th-17 cells, and allows certain cells traveling in the blood stream to leave the circulation and enter tissues, primarily to initiate or continue a disease process. PRX003 is designed to block MCAM and not allow the migration of these pathogenic cells into tissues. PRX003 may be useful for treating a variety of inflammatory diseases such as psoriasis, psoriatic arthritis, rheumatoid arthritis, multiple sclerosis, sarcoidosis, uveitis, vasculitis, and Behcet's disease.

About Prothena:
Prothena Corporation plc is a late-stage clinical biotechnology company focused on the discovery, development and commercialization of novel protein immunotherapy programs for the potential treatment of diseases that involve amyloid or cell adhesion. The company is developing antibody-based product candidates that target a number of potential indications including AL amyloidosis (NEOD001), Parkinson's disease and other related synucleinopathies (PRX002), and psoriasis and other inflammatory diseases (PRX003).

Psoriasis trial drug halted due to suicide concerns



According to a statement released last week, one of the makers of brodalumab, a biologic drug currently being tested as a treatment for psoriasis and psoriatic arthritis, will no longer participate in developing the drug. Amgen, which, along with the company AstraZeneca, had been developing brodalumab, has stopped developing the drug based on reports of suicidal thoughts and behavior during clinical trials for the drug, the company stated in a press release.

AstraZeneca is still considering whether to continue with the drug development, according to a statement released by AstraZeneca last week.Brodalumab targets the receptor of a cytokine, or inflammatory protein, involved in psoriasis known as interleukin-17 (IL-17).

Brodalumab is still in the testing phase, and is not available to patients outside of clinical trials.

It differs from Cosentyx (secukinumab), a drug recently approved by the Food and Drug Administration (FDA). While brodalumab targets the receptor of IL-17, Cosentyx targets the inflammatory protein itself, IL-17A. Ixekizumab, which is being developed by Eli Lilly, also targets IL-17A and still is in clinical trials and not available to patients.

So far, there have been few reports of serious side effects from Cosentyx. The most commonly reported side effects are upper respiratory tract infections, the common cold and diarrhea.
“There does not appear to be any concern over suicidal behavior in patients receiving either secukinumab or ixekizumab, two other drugs that also block IL-17A function,” said Dr. Andrew Blauvelt,  a dermatologist and president and investigator at Oregon Medical Research Center, a clinical research center.
Regarding brodalumab, Blauvelt also said that he “did not see any documentation from the trials that the rate of suicidal behavior was higher than expected in the general population.” However, he said, the FDA had asked Amgen to monitor all patients on brodalumab for suicidal behavior.

Bloody weird question, but why does psoriasis on your scalp appear in lumps, but the rest of your body doesn't?  I know sometimes you can get raised plaques on your skin, but not to the extent of the scalp.

Hello!! Fresh meat here! 
I'm recently turned 18, from Ireland, diagnosed in 2007 with psoriasis.
I have, like most, tired various treatments for psoriasis none of which have helped.
The last treatment I tried was another round of light therapy (3rd round) that was a year ago.Safe to say the light therapy didn't work.
After waiting months (7 to be precicise) to see my derm again my psoriasis has slowly but surely managed to spread to even more. My psoriasis is now covering every inch of my body. 
The only good thing about that is my derm now thinks my psoriasis is "serious" enough to try other treatments.
I'm going to start fumaderm in the coming weeks. This site has been great for finding information on it.
So thanks to the members who are using this drug for updating about their progress with it. It's truly helpful for others!
Have a good one

I just got back from a dermatology appointment and I'm a bit disappointed to be honest.

I've been using Ciclosporin without a great deal of success as well as dovobet (and epaderm) so was desperate to try fumaderm which has been so highly regarded by so many in this group but my Dr was massively apologetic and said he just couldn't prescribe it (he's obviously been told he mustn't) so I ended up with MTX.

Now I'm just praying my liver can take it and my skin only needs a low dose. I'm also a bit worried as I can no longer take Naproxen as well as Codydramol (for joint pain not PSA) and have to up my dose of Codydramol but I am allergic to Codeine so don't want to take any more as it makes my whole body itch unbearably. So my options are...

1. Take a chemotherapy drug and risk going insane through itching.
2. Take a chemotherapy drug and never leave the house cos I'm in agony.
3. Don't take a chemotherapy drug and hide at home without pain or itching but with horrible flakey skin.

Hmmm...decisions decisions lol.

I'm gonna go with secret option 4.Stop over thinking it, hope for the best and eat chocolate.

Anyway just thought I'd catch you up cos you've all been so nice to me xxx

Hi! My name is Connie.  I am 48 and I have had psoriasis since I was 12.  The psoriasis on my skin has never been that bad, I am happy to say.  Over the years I have put up with it for a while then decide to try a new medicine, none of which really had helped.  Like I said it is not very bad and not a worry really.  I had gotten a couple of places by my ears, which was really noticeable but usually it will clear up when I get out in the sun in the summer time. 

I was finally diagnosed with psoriatic arthritis last June but I have had symptoms of it for years.   I had a hard time getting doctors to listen to me and I finally had to demand a referral to a rheumatologist.   It had finally gotten to where I could hardly walk and could not even turn the ignition key in my car.  I could not go on like that and keep working.   Things are getting better and I am hopeful it will continue to get better.  So that's the short version of my story.

This Danish cohort study investigated the risk of psoriasis in subjects with childhood asthma, it concludes that there is a significantly increased risk of psoriasis and further studies are warranted to determine the clinical significance and effects of therapeutic interventions.

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Background:
Psoriasis and asthma are disorders driven by inflammation. Psoriasis may carry an increased risk of asthma, but the reverse relationship has not been investigated.

Objectives:
To investigate the risk of psoriasis in subjects with childhood asthma in a nationwide Danish cohort.

Methods:
Data on all Danish individuals aged 6–14 years at study entry between 1 January 1997 and 31 December 2011 (n = 1 478 110) were linked at an individual level in nationwide registers. Incidence rates per 10 000 person-years were calculated, and incidence rate ratios (IRRs) adjusted for age, sex, concomitant medication and comorbidity were estimated by Poisson regression models.

Results:
There were 21 725 cases of childhood asthma and 6586 incident cases of psoriasis. There were 5697 and 889 incident cases of mild and severe psoriasis, respectively. The incidence rates of overall, mild and severe psoriasis were 4·49, 3·88 and 0·61 for the reference population, and 5·95, 5·18 and 0·83 for subjects with childhood asthma, respectively. The IRRs for overall, mild and severe psoriasis were 3·94 [95% confidence interval (CI) 2·16–7·17], 5·03 (95% CI 2·48–10·21) and 2·27 (95% CI 0·61–8·42) for patients with childhood asthma.

Conclusions:
Childhood asthma was associated with a significantly increased risk of psoriasis. Further studies are warranted to determine the clinical significance and effects of therapeutic interventions on this association.

Hi everyone

I'm Simone and been suffering from P since 2007, woke up one morning and it started to appear. I have p on the tops of my feet, patches on my elbows, knees and other patches appearing more recently. I lost my mum on Boxing Day, so half expected I would get more. I'm using topical steriods but would like to see what others are using.

Look forward to chatting ?

This study looked at the use of TNF-α inhibitors for psoriasis and pregnancy, The aim of this study was to evaluate the risk of major birth defects, spontaneous abortion, preterm birth and reduced birth weight after first trimester exposure to Humira (adalimumab) Remicade (infliximab) Enbrel (etanercept) Cimzia (certolizumab pegol) and Simponi (golimumab)

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Aims:
TNF-α inhibitors are considered relatively safe in pregnancy but experience is still limited. The aim of this study was to evaluate the risk of major birth defects, spontaneous abortion, preterm birth and reduced birth weight after first trimester exposure to TNF-α inhibitors.

Methods:
Pregnancy outcomes of women on adalimumab, infliximab, etanercept, certolizumab pegol or golimumab were evaluated in a prospective observational cohort study and compared with outcomes of a non-exposed random sample. The samples were drawn from pregnancies identified by institutes collaborating in the European Network of Teratology Information Services.

Results:
In total, 495 exposed and 1532 comparison pregnancies were contributed from nine countries. The risk of major birth defects was increased in the exposed (5.0%) compared with the non-exposed group (1.5%; adjusted odds ratio (ORadj) 2.2, 95% CI 1.0, 4.8). The risk of preterm birth was increased (17.6%; ORadj 1.69, 95% CI 1.1, 2.5), but not the risk of spontaneous abortion (16.2%; adjusted hazard ratio [HRadj] 1.06, 95% CI 0.7, 1.7). Birth weights adjusted for gestational age and sex were significantly lower in the exposed group compared to the non-exposed cohort (P = 0.02). As a diseased comparison group was not possible to ascertain, the influence of disease and treatment on birth weight and preterm birth could not be differentiated.

Conclusions:
TNF-α inhibitors may carry a risk of adverse pregnancy outcome of moderate clinical relevance. Considering the impact of insufficiently controlled autoimmune disease on the mother and the unborn child, TNF-α inhibitors may nevertheless be a treatment option in women with severe disease refractory to established immunomodulatory drugs.

Hello there everybody!

Just introducing myself, if that is okay. I have been reading through the forum for a few days and everybody seems very kind and helpful   !

I don't wish to bore anybody, so will just give a brief recap. I first developed psoriasis four years ago at the grand old age of 36. It advanced fairly aggressively from a few patches on my scalp to fairly large-scale plague psoriasis coverage - including on my face; ye baxtards! - nail psoriasis, and the unfettered joy that is inverse psoriasis. I tried topical steroids for a while but no joy. In fact, I got way slap happy with the fecking things and ended up with some fairly horrible skin damage   .

Anyway, I started on Fumaderm Initial three weeks ago and am beginning the first day of Fumaderm full strength tomorrow. Side effects not terribly nasty yet.... Just wondering if any Fumaderm users recall how long it took to see an improvement? I check all my various scaly bits every day hoping to see a clear bit emerging, but no joy yet!

Thank you in advance for any info or advice. It is so nice to know there are other people who understand the various horrors and embarrassments of the psoriasis sufferer. I had to buy a little hand-held vacuum cleaner to clean up under my work desk at the end of every day. Scarlet for me!

If anybody is kind enough to reply and I do not respond, please forgive me. It might be tomorrow morning before I get a chance to come back!

Hope you are all doing well   .

This study looked at the psoriasis area and severity index (PASI) and the dermatology life quality index (DLQI) on patients taking Bio treatments for psoriasis for up to 6.5 years.

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Background/Objectives:
Patients with psoriasis experience higher rates of depression, anxiety and suicidal ideation than the general population. With effective treatment, there is evidence that with the initial decrease in the psoriasis area and severity index (PASI) score, patients' quality of life (QoL), measured by the dermatology life quality index (DLQI) improves. However, to date, there have been no studies demonstrating that patients' QoL remains improved. We investigated the association between the DLQI and PASI of patients with psoriasis on biologic agents for an extended period of time of up to 6.5 years.

Methods:
The data for this longitudinal, retrospective study was collected from a large tertiary teaching hospital in South Australia. Data was collected from all patients with psoriasis who had been on biologic agents for 2 or more years (n = 54).

Results:
PASI and DLQI were highly correlated over all time points (ρ = 0.50), P < 0.001. DLQI scores significantly decreased by 0.8 (95% CI: 0.30, 1.26) units per year from 12 months to 6.5 years, P = 0.002. After 12 months, PASI scores declined by 0.19 (95% CI: 0.13, 0.52) units per year, P = 0.24.

Conclusion:
This study demonstrates that DLQI and PASI remain low after 12 months, and, in fact, both gradually decline further with time. Patients on biologic agents for prolonged periods maintained their improvement in QoL for up to 6.5 years.

This small study looked at the possible role of Proenkephalin (PENK) in the pathogenesis of psoriasis and to assess if it is related to the severity of psoriatic lesions, and concludes anti-PENK drugs in addition to current psoriasis treatments might be of value in its treatment.

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Background:
Psoriasis is a common chronic skin disease that can also affect the mucous membranes and joints. It is multifactorial in origin, occurring in genetically predisposed individuals, and triggered by various endogenous and exogenous factors. Proenkephalin (PENK) is an endogenous opioid polypeptide hormone that acts on specific opiate receptors found on nerve and mucosal cells, and on various cells in the immune system. PENK receptors are expressed on skin cells, and their activation can regulate keratinocyte and melanocyte activities. PENK expression has been found to be increased in keratinocytes in psoriatic skin, and together with its inflammatory basis, this suggests that PENK may be regulated by inflammatory stimuli.

Aim:
To assess the possible role of PENK in the pathogenesis of psoriasis and to assess if it is related to the severity of psoriatic lesions.

Methods:
Serum and tissue PENK levels were estimated in 20 patients with psoriasis vulgaris, and compared with those of 20 healthy controls (HCs).

Results:
PENK levels were found to be significantly increased both in serum and in psoriatic lesions in patients compared with HCs. No significant correlation was found between PENK levels and patient age, disease duration or disease severity (Psoriasis Area and Severity Index).

Conclusion:
Our results support the role of PENK in the aetiopathogenesis of psoriasis, and indicate that giving anti-PENK drugs in addition to current antipsoriatic therapies might be of value in treating this common chronic skin disease.

This study looked at the Minimal disease activity (MDA) in patients with psoriatic arthritis that are being treated with TNFα blockers, MDA is a concept that has been defined by the Outcome Measures in Rheumatology (OMERACT) as a state of disease activity deemed a useful target of treatment by both the patient and physician.

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Objective:
A state of minimal disease activity (MDA) was defined and validated as target for treatment in psoriatic arthritis (PsA). We aimed to identify disease characteristics, outcome, and predictors of MDA in patients treated with tumor necrosis factor α (TNFα) blockers.

Methods:
Patients fulfilling the Classification of Psoriatic Arthritis criteria treated with TNFα blockers were followed every 3–6 months. Patients were considered in MDA when they meet at least 5 of the 7 criteria. Sustained MDA was defined as an MDA state lasting ≥12 months. Patients achieving MDA were compared to non-MDA patients. A proportional odds discrete time survival analysis model was applied, adjusting for sex, age, PsA duration, abnormal erythrocyte sedimentation rate (ESR) and clinically damaged joint count at each visit to identify predictors for MDA.

Results:
Of the 306 patients treated with TNFα blockers identified from our database, 23 patients were in an MDA state when treatment was commenced; 57 were taking TNFα blockers prior to enrollment. Therefore, 226 subjects were in a non-MDA state and constituted the study population. One hundred forty-five patients of 226 patients (64%) achieved MDA within a mean ± SD duration of 1.30 ± 1.68 years. The mean ± SD duration of MDA was 3.46 ± 2.25 years. At total of 17 patients withdrew from therapy and remained in an MDA state. Male sex (odds ratio [OR] 1.65, 95% confidence interval [95% CI] 1.08–2.53; P = 0.02) and normal ESR (OR 2.27, 95% CI 1.22–4.17; P = 0.009) increased the odds for achieving MDA.

Conclusion:
MDA is achieved in 64% of patients treated with TNFα blockers in a clinical setting. Male sex and normal ESR are predictors for MDA. On withdrawal or reduction in treatment, 11.6% of patients maintained MDA state.

Hi everyone,

Its been a while since I posted here,the last time I posted was in 2014 when I was first diagnosed with plaque and scalp psoriasis and I was covered from my scalp to my lower legs. I just wanted to post a quick update.

My second flare up happened in winter (not surprised, I was actually expecting it) December 2014. But this time it was not too bad. It was however more concentrated on my face and inner arms. The derm prescribed Protopic for the face and it stung horribly after 20 min of application. It worked, but for a short time(approx 1 week) and it comes back, although I still have a tube just in case. My mom made a facepack made from cucumbers, oats, yogurt. Miraculously, it cleared all the scales and red bumps on the face after 2 applications per week for a month, the face has been cleared ever since.
Since my first flare up in January 2014, my lower legs and scalp have never been clear.
But recently, a hair stylist suffering from eczema recommended Denorex, a tar based shampoo available at drug stores. This is an amazing shampoo and it has been able to control the flakiness of my scalp.I would recommend this to anyone suffering from scalp psoriasis.

For my legs, I've strictly used Dovobet gel. Which actually clears up my legs within 3-4 applications, but but but but but but....the itch....
I absolutely cannot control the itch. Even after taking prescribed anti histamines, I'm not able to stop scratching. Which ultimately cancels the effect of the Dovobet gel. Does anyone have any suggestions on what to do about this? because to be honest, I really don't want to try anymore sprays, steroids, light therapy which might just worsen the condition.

If anyone has any questions regarding the above described treatments, then please let me know, I will be happy to help. Or even any suggestions that might help me, please let me know.

I do have one question, I'm sure this has been asked a few times, but....will a cure ever be available in the near future? and by cure I don't mean treatments.

Thanks
Karl

Just seen a link on the npf Twitter page showing that obesity and severity of psoriasis are connected and it recommended weight loss. I've never heard this before, and to be honest seems a load of rubbish to me, but would be interested to hear your thoughts on it.

Chugai Pharmaceutical Co has submitted a new drug application for M8010 a topical combination of maxacalcitol (an active vitamin D3 derivative) and corticosteroid betamethasone butyrate propionate for the treatment of psoriasis.

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Chugai Pharmaceutical Co., Ltd. [Head Office: Chuo-ku, Tokyo; Chairman & CEO: Osamu Nagayama] (hereafter “Chugai”) announced today that it has submitted a New Drug Application (NDA) to the Ministry of Health, Labour and Welfare for a combination topical drug preparation of maxacalcitol and betamethasone butyrate propionate (Development Code: M8010). M8010 has been co-developed with Maruho Co., Ltd. [Head Office: Kita-ku, Osaka; President and CEO: Koichi Takagi] (hereafter “Maruho”) for the indication of psoriasis vulgaris.

M8010 is a topical preparation combining maxacalcitol, an active vitamin D3 derivative created by Chugai, and the corticosteroid betamethasone butyrate propionate. Both drugs are indicated for psoriasis vulgaris and are used together to treat the disease in medical practice.

A Japanese phase III clinical study was conducted to evaluate a once-daily topical application of M8010 against maxacalcitol ointment monotherapy (twice daily inunction) and betamethasone butyrate propionate ointment monotherapy (once daily application). The result showed superiority over both monotherapies in terms of primary endpoint (total score of PSI at four weeks), and secondary endpoint (rate of reduction of mPASI at four weeks). As for safety, rhinopharyngitis and reduction of blood cortisol were observed as major adverse events during the study. However, these were mild and no major difference was observed in the rate of occurrence compared with both monotherapies, so safety of M8010 was similar to that of both drugs.

The collaboration between Chugai and Maruho started with the launch of Oxarol® Ointment, a product of maxacalcitol in 2001. Both companies will make efforts to obtain early approval and make sure that M8010 can be delivered to patients and healthcare professionals as soon as possible. Maruho will be responsible for providing information and marketing activities after an approval is obtained, the same responsibilities Maruho has for Oxarol® Ointment and Lotion, which are already on the market.

Brodalumab an investigational IL-17 inhibitor in development for patients with psoriasis and psoriatic arthritis has been dumped by Amgen,  they have commenced termination of its participation in the co-development and commercialization of brodalumab with AstraZeneca.

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Amgen announced the Company has commenced termination of its participation in the co-development and commercialization of brodalumab with AstraZeneca.  Brodalumab, an investigational IL-17 inhibitor, is in development for patients with moderate-to-severe plaque psoriasis, psoriatic arthritis, and axial spondyloarthritis.  The decision was based on events of suicidal ideation and behavior in the brodalumab program, which Amgen believes likely would necessitate restrictive labeling.

"During our preparation process for regulatory submissions, we came to believe that labeling requirements likely would limit the appropriate patient population for brodalumab," said Sean E. Harper, M.D., executive vice president of Research and Development at Amgen.  

After Amgen transitions the program to AstraZeneca, future decisions on the clinical development and submission of marketing applications for brodalumab will be at the sole discretion of AstraZeneca for all territories, except for certain Asian territories, including Japan, where Kyowa Hakko Kirin has rights to brodalumab.

Amgen has decided to focus its efforts and resources on other key molecules that address unmet medical needs and deliver value to patients and shareholders.  The Company continues to make progress against its strategic and financial commitments and does not expect any meaningful impact from this decision on its ability to meet them.