I recently was prescribed Psoriderm bath additive and found it helped. It is 40% distilled Coal Tar. There is also a cream available. Has anybody else used it as 'Psoriderm' did not find any results in a search.

It is made by Dermal Laboratories in England.

Good afternoon my fellow lepers

Have any of you been prescribed Cocois ?

Because polytar is not available at the moment, i asked my GP for something for my head.

It seems this Cocois has Coal tar 12%, Salicylic acid 2%, Sulphur 4% & coconut oil compound ointment in it's ingredients.

Is it any good ?

Happy scratching

GB

I am pretty certain I have an ear infection. Not trying to self diagnose here, I've just had so many of them over the years and know the symptoms all too well. This is the first time I've had one since being diagnosed with psoriasis, however, and I don't want to do ANYTHING that might cause a flare after being clear on Acitretin 8 months after starting it. I've been tolerating the ear pain, pressure and dizziness for about two weeks now taking only Tylenol and hoping it would clear on its own yet it's getting particularly bothersome when singing - ears are popping. Ugh.

Thoughts?

In the process getting this approved... more later.

I was thinking after Stelara finally giving up on me after almost five years it would be interesting to see if we could find out from our members and guests what has been the longest amount of successful time on one psoriasis treatment, you can vote in the poll above and members can add to this thread if they wish.

For me it's been my latest treatment that has been the most successful, Stelara almost made five years but has let me down a couple of times and now it's failed big time with psoriatic arthritis. So I'm voting 4

Here's some good news about researchers that have found new gene that confirms existence of psoriatic arthritis (PsA). The research has established PsA as a condition in its own right, and it could have major implications in the way that patients are treated and lead to the development of drugs specifically developed for PsA.

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Researchers led by the Arthritis Research UK Centre for Genetics and Genomics at The University of Manchester have identified genetic variants that are associated with psoriatic arthritis (PsA) but not with psoriasis, in the largest study of PsA ever published.

PsA is a common form of inflammatory form of arthritis causing pain and stiffness in joints and tendons that can lead to joint damage. Nearly all patients with PsA also have skin psoriasis and, in many cases, the skin disease is present before the arthritis develops. However, only one third of patients with psoriasis will go on to develop PsA.

The researchers, who are part of a European consortium, say that their work, which took three years to complete and is published in Nature Communications, is a breakthrough because genetic changes have been identified that increase the risk of PsA but not psoriasis.

Until recently opinion was divided as to whether psoriatic arthritis was a disease in its own right, or psoriasis combined with rheumatoid arthritis.

The findings could, in future, lead to the identification of people with psoriasis who are at risk of developing psoriatic arthritis.

Dr John Bowes, who led the analysis of the work, said: “Our study is beginning to reveal key insights into the genetics of PsA that explain fundamental differences between psoriasis and PsA. Our findings also highlight that CD8+ cells are likely to be the key drivers of inflammation in PsA. This will help us to focus on how the genetic changes act in those immune cells to cause disease”.

The gene identified by the research team lies on chromosome 5 and is not the first PsA-specific gene to be identified. Patients who carry the HLA-B27 gene are also more likely to develop PsA.

Professor Anne Barton, a rheumatologist and senior author on the study explained: “By identifying genes that predispose people to PsA but not psoriasis, we hope in the future to be able to test patients with psoriasis to find those at high risk of developing PsA. Excitingly, it raises the possibility of introducing treatments to prevent the development of PsA in those individuals in the future”.

Dr Stephen Simpson, director of research at Arthritis Research UK added: "This is a significant finding. Not only does it help establish PsA as a condition in its own right, but it could have major implications in the way that patients with this condition are treated and lead to the development of drugs specifically developed for PsA, which are greatly needed.”

The research was funded by the National Institute for Health Research Manchester Musculoskeletal Biomedical Research Unit.

Nice to see more and more being put into helping us live with psoriasis, it's been a long time coming but these past few years have been encouraging and today the pipeline is still looking healthy. And today we have another positive phase 1 result from Akall for their APK-11 psoriasis topical treatment.

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(Akaal Pharma), an Australian clinical-stage biopharmaceutical company focused on developing new small molecule drugs for the treatment of inflammatory and autoimmune diseases, today announced the positive results from a randomized, double-blind, placebocontrolled Phase-1 clinical trial of AKP-11, a novel and First-in-Class topical Sphingosine 1- Phosphate receptor-1 (S1P1) modulator for the treatment of mild-to-moderate plaque psoriasis.

In this study, the topical application of AKP-11 to psoriasis patients for 28 days was found to be safe, well tolerated and resulted in a significant reduction in plaque severity. No detectable plasma levels of AKP-11 were found in the pharmacokinetic analysis, which is
attributable to the large therapeutic index of AKP-11.

Although a variety of therapies are available for treating psoriasis, there exists an underserved need for safer and effective topical treatments for long-term use. The Phase 1 clinical data for AKP-11, a topical First-in-Class S1P1 modulator, is very encouraging and
strongly supports our Phase 2 clinical trial in a larger number of patients said Dale Dhanoa, Ph.D., CEO of Akaal Pharma.

Study Details:
The Phase 1 clinical trial was a randomized, double-blind, and placebo-controlled study that involved 16 subjects. This study was conducted in 2 parts, Phase 1A and Phase 1B. AKP-11 or placebo were administered as an ointment to 4 healthy subjects in PART A and extended to 12 psoriasis patients in PART B. The patients were treated once daily with a topical application of AKP-11 for 28 consecutive days. AKP-11 reduced the local psoriasis severity index (LPSI) and demonstrated significant efficacy when compared to baseline (p=0.0016). The placebo group did not show efficacy. No clinically significant local or systemic adverse events were observed in the study.

About AKP-11
AKP-11 is a novel, potent and highly selective sphingosine 1-phosphate receptor subtype-1 (S1P1) modulator undergoing clinical development for topical treatment of psoriasis and other skin diseases. AKP-11, a novel small molecule, has also shown excellent preclinical pharmacokinetic and pharmacodynamics profile as a potential Best-in-Class oral treatment for autoimmune indications. AKP-11 acts via multimodal actions and significantly reduces the overexpression of pro-inflammatory cytokines and factors including the permeability factor VEGF.

Good afternoon,

My insurance company has approved me for Cosentyx. Ive been on everything and cant wait to try it. I'll be on 300mg Sensoready shots. Now I am looking for a specialty pharmacy that has it available to order. Does anyone know who might have it yet?

Following on from the report here Pfizer Results For Phase 3 OPT retreatment study of Tofacitinib Pfizer Announces FDA Acceptance For Review of Oral XELJANZ® (tofacitinib citrate) For Adult Patients With Moderate To Severe Chronic Plaque Psoriasis.

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Pfizer Inc. Announced today that the U.S. Food and Drug Administration (FDA) has accepted for review the supplemental New Drug Application (sNDA) for XELJANZ® (tofacitinib citrate) 5 mg and 10 mg tablets, a Janus kinase (JAK) inhibitor, the first in a new class of oral medicines being investigated for the treatment of adult patients with moderate to severe chronic plaque psoriasis who are candidates for systemic therapy or phototherapy. The FDA has provided an anticipated Prescription Drug User Fee Act (PDUFA) action date in October 2015 for the sNDA.

The submission to the FDA is based on data from the Phase 3 Oral treatment Psoriasis Trials (OPT) Program, a global, multi-study, comprehensive clinical development program that consisted of five studies (including an ongoing long-term extension study), designed to evaluate oral XELJANZ 5 mg and 10 mg twice daily in patients with moderate to severe chronic plaque psoriasis. With more than 3,600 adult psoriasis patients enrolled across 36 countries, the OPT program has yielded one of the largest databases for a potential psoriasis indication at the time of registration.

XELJANZ is a small molecule that targets the JAK pathway, a signaling pathway inside the cells, thought to play a role in chronic inflammatory responses.

“This regulatory milestone demonstrates our commitment to the research of chronic inflammatory diseases with the goal of developing therapies, such as XELJANZ, that can help address unmet medical needs for patients,” said Steve Romano, MD, SVP and Head, Global Medicines Development for the Pfizer Global Innovative Pharmaceutical business. “We continue to play a leadership role in the evaluation of JAK inhibition across chronic inflammatory diseases, such as psoriasis.”

XELJANZ is approved in 37 countries around the world for the treatment of moderate to severe rheumatoid arthritis (RA). In the United States, XELJANZ 5 mg tablets are approved for the treatment of adults with moderate to severe RA who have had an inadequate response or intolerance to methotrexate (MTX). The benefit:risk profile of XELJANZ in RA has been characterized through the study of 6,192 RA patients representing 16,800 patient years of exposure in the global clinical development program for XELJANZ in moderate to severe RA.

Hello all, I've, got Graves' disease, which has given me plaque psoriasis, and when I'm over active, I need help keeping my psoriasis under control by the use of acitretin, but I dont like the same de affects, also it doesn't clear my scalp, so I was looking for any advise, on what to use on my scalp, thank you

hello I am Deena. I'm 45 years, female, and a mommy of a son and a daughter. i have been diagnosted of artritis psoriatica when I was 16 years. Sinds September 2014 I use Psorinovo and reishi/ganoderma capsules. sinds december 2014 I'm clean of psoriasis. thanks to the psorinovo. ohw I am from Holland and I came to this forum, because in Dutch there are not much forums abouth psoriasis who are up to date, and the one there is you have to become a paying member, and that one is also not much in use. I hope there are more confersations going on here. and I hope to share experiences here.

Hi all. I've been dealing with this flipping rash for about five years now. First person to see it declared it ringworm (one lesion was a classic ring shape). Second person called it eczema. Five years, five doctors and two herbalists later, and I'm told it's psoriasis. This was a couple of weeks ago.

Hoo boy. Talk about a club I never wanted to join.

I just woke up one morning covered in it (including my special, tinder sittin' down place), but it quickly resolved itself to two symmetrical bands around my ankles. Not too awful, except when it flares up...then my shoes cut into it and walking is painful.

So my first priority is learning what triggers flare-ups, so I can stop doing...whatever it is. That's the problem; I really haven't a clue.

I'll do a lot of reading and hope there's stuff here already to give me ideas. But my name will be hovering around, so I thought I should introduce myself.

So, hello from the sunny South coast of England. Where it's snowing a little.

This small study ahead of publication suggests granulysin may be a potential target for immunomodulatory therapy for psoriasis.

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Background:
Psoriasis is an erythematosquamous dermatosis, which has strong expression of antimicrobial peptides (AMPs), imparting a high resistance to lesional skin infection. Granulysin is a proinflammatory AMP that has been found in some infection-resistant dermatoses.

Aim:
To assess granulysin expression in psoriasis.

Methods:
Immunohistochemical expression of granulysin was assessed in lesional skin biopsies taken from 30 patients with psoriasis and 10 normal skin specimens from healthy controls (HCs) matched for age, gender and skin site. Granulysin expression was found to be high in 11 patients (36.7%), moderate in 10 (33.3%) and low in 9 (30%). A highly significant (P = 0.001) difference in granulysin expression between patients with psoriasis and HCs was found. There were also significant differences in granulysin expression between patients with low Psoriasis Area and Severity Index (PASI) (≤ 10) and those with high PASI (> 10) (P = 0.001), and between patients with early-onset (< 40 years of age) and those with late-onset (> 40 years of age) disease (P < 0.04). There was a significant (P = 0.001) positive correlation between granulysin expression and PASI (r = 0.84) and a significant (P = 0.02) negative correlation with age of onset (r = −0.38). Patients with psoriasis hadhigh granulysin expression, which increased with increased clinical severity of the disease.

Conclusions:
These findings suggest a role for granulysin in psoriasis pathogenesis, and may explain the triggering effect of skin infection in psoriasis. If the pathogenic role of granulysin is substantiated by further studies, granulysin may be a potential target for immunomodulatory therapy for psoriasis.

This is an early view of a descriptive study that the authors hope may serve to inspire a more mechanistic approach exploring not only Wnt5a, but other inflammatory pathways in between the skin and the fat.

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Substantial epidemiological evidence indicates that psoriasis associates with a predisposition to develop metabolic dysregulation leading to obesity and insulin resistance. However, the nature of this association and the potential underlying mechanisms remain unclear.

In a recent report, Gerdes et al. explored the hypothesis that wingless-type MMTV integration site, Wnt5a, which has been linked to aberrant fat cell metabolism, may be driving this process. In this study, the authors compare circulating serum levels of Wnt5a in individuals with psoriasis and compare with healthy controls matched for age, gender and BMI.

The bottom-line results show higher levels of Wnt5a in psoriasis patients irrespective of BMI compared to the matched non-psoriatic controls, indicating that psoriasis per se may result in increased secretion of Wnt5a into the circulation. In addition, there was a significant difference among patients with higher levels of Wnt5a in the obese psoriasis population.

The study, even though being purely descriptive, may serve to inspire a more mechanistic approach exploring not only Wnt5a, but other inflammatory pathways in between the skin and the fat.

This article looked at the digital phototherapy device Skintrek and concluded it is as effective as conventional cream and bath PUVA, as well as NB-UVB, while simultaneously sparing the healthy adjacent skin.

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Background:
8-Methoxypsoralen–UVA (PUVA) and narrowband ultraviolet B (NB-UVB) are well-established treatments for chronic plaque-type psoriasis vulgaris. However, long-term risks of PUVA therapy include premature skin ageing and squamous cell carcinoma.

Objectives:
To develop a device for targeted UV therapy of psoriatic plaques with protection of the healthy adjacent skin to reduce the risk for premature skin ageing and squamous cell carcinoma.

Methods:
In total 28 patients with exacerbated psoriasis vulgaris were treated with the digital phototherapy device skintrek® [cream PUVA (n = 8), bath PUVA (n = 11) and UVB (n = 9)] or with conventional bath PUVA (n = 9) or NB-UVB (n = 4).

Results:
The local Psoriasis Area and Severity Index (PASI) score was significantly reduced from a mean of 6·25 at baseline to 2·75 at the end of therapy in the skintrek cream PUVA group, from 6·4 to 3·0 in the skintrek bath PUVA group and from 5·5 to 2·0 in the skintrek UVB group. Treatment with skintrek cream PUVA reduced the mean local PASI by 54%, while skintrek bath PUVA did so by 51% and skintrek UVB by 63%. Targeted skintrek PUVA and skintrek UVB of inflamed psoriatic skin avoided skin pigmentation and were not inferior to conventional bath PUVA and NB-UVB therapy regimens.

Conclusions:
Targeted UV therapy of psoriatic plaques with the digital phototherapy device skintrek is as effective as conventional cream and bath PUVA, as well as NB-UVB, while simultaneously sparing the healthy adjacent skin. It therefore potentially reduces the carcinogenic risk, reduces premature skin ageing and avoids tanning of healthy surrounding skin.

This is an early view of a 10 patients study in the use of combination psoriasis treatments Cyclosporine and anti-TNF α.

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Combination therapy has become important in treating psoriasis, using synergism between different mechanisms to maximize efficacy and minimize toxicity. Little has been published on the combination of cyclosporine and anti-tumor necrosis factor (TNF) α agents.

In this study, a retrospective chart review was made of the effects of this combination therapy in 10 patients with recalcitrant psoriasis.

Treatment included a conditioning phase with cyclosporine, 3.14 ± 0.37 mg/kg for 4.6 ± 2 weeks, and a combination phase during which etanercept/adalimumab were initiated and cyclosporine was tapered over 10.2 ± 3.7 weeks.

Treatment success, evaluated after each phase, was classified as complete recovery (CR, more than 75% improvement), partial response (PR, 25–75% improvement), and no response (NR, less than 25% improvement). All patients reached CR at the end of the combination therapy. Two were still on combination therapy after 12 and 20 weeks. Adverse event occurred in three cases, all in the conditioning phase.

We conclude that combination therapy with cyclosporine and anti-TNF α appears to offer an effective and safe approach to treatment of psoriasis.

This study looked at the cost efficacy of systemic psoriasis treatments approved for use by the US Food and Drug Administration (FDA).

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Background:
Newer psoriasis treatments tout higher efficacy but are generally more expensive.

Objective:
We sought to estimate the cost efficacy of systemic psoriasis treatments that have been approved by the US Food and Drug Administration (FDA).

Methods:
A literature review of systemic psoriasis treatments that have been approved by the FDA was performed for the primary end point of a 75% reduction in the Psoriasis Area and Severity Index score (PASI 75). Medication cost was referenced by wholesale acquisition cost (WAC), laboratory fees were obtained from the American Medical Association, and office visit fees are standard at our university. Total expenses were standardized by calculating cost per month of treatment considering the number needed to treat (NNT) to achieve PASI 75.

Results:
Methotrexate ($794.05-1502.51) and cyclosporine ($1410.14-1843.55) had the lowest monthly costs per NNT to achieve PASI 75. The most costly therapies were infliximab ($8704.68-15,235.52) and ustekinumab 90 mg ($12,505.26-14,256.75). Monthly costs per NNT to achieve PASI 75 for other therapies were as follows: narrowband ultraviolet B light phototherapy ($2924.73), adalimumab ($3974.61-7678.78), acitretin ($4137.71-14,148.53), ustekinumab 45 mg ($7177.89-7263.99), psoralen plus ultraviolet A light phototherapy ($7499.46-8834.98), and etanercept ($8284.71-10,674.89).

Limitations:
Drug rebates and incentives, potential adverse effects, comorbidity risk reduction, ambassador programs, and combination therapies were excluded.

Conclusion:
Our study provides meaningful cost efficacy data that may influence psoriasis treatment selection.

Hi everyone, newbie to the board. Im 31 had psoriasis since age 10 recently dx with ms...clearly this complicates things. My neurologist wants me to start tecfidera, im from US btw. I an hoping it will help my p. I have googled and googled and cant find anything. I called biogen and asked them if tecfidera has helped pts with p and they said no studies have shown that. In any event i am starting and hopeful the main ingredient dmf will help my p as well as ms. What is the clearing like. From what i understand it takes a while? Thoughts and comments woyld be appreciated thank you so much. Also, could you be on another drug like stelara and tecfidera? Jw with incidence of pml.

Lot's of Biosimilars coming through lately for well known psoriasis treatments, and today Samsung Bioepis announced that their Enbrel (etanercept) biosimilar candidate, SB4 has been validated and accepted for review by European Medicines Agency (EMA)

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Samsung Bioepis Co., Ltd., today announced that the Marketing Authorization Application (MAA) for its Enbrel (etanercept) biosimilar candidate, SB4 has been validated and accepted for review by European Medicines Agency (EMA). The acceptance of the MAA marks the first Enbrel biosimilar to advance into regulatory review in the European Union (EU). The MAA is based on results from a Phase III clinical trial in patients with moderate-to-severe rheumatoid arthritis (RA).

In Europe, Enbrel is indicated for the treatment of a number of rheumatic diseases, including moderate to severe RA, certain forms of juvenile idiopathic arthritis, psoriatic arthritis, ankylosing spondylitis and plaque psoriasis. If authorized by the EMA, SB4 could be available for use in all of the same indications as Enbrel.

"This MAA validation represents a significant milestone for Samsung Bioepis in our work to develop and manufacture world-class biosimilars. More significantly, it offers an opportunity to provide high-quality and effective therapies for broadening access to patients in Europe" said Christopher Hansung Ko, chief executive officer of Samsung Bioepis.

If authorized by the EMA, SB4 will be commercialized in Europe by Biogen Idec. It will also be produced at the company’s manufacturing facility in Hillerød, Denmark which is one of the largest biologic manufacturing facilities in the world.

In addition to the European filings, Samsung Bioepis intends to move forward with additional applications for regulatory approvals in other territories worldwide.

About the SB4
Samsung Bioepis previously conducted SB4 Phase 1 and Phase 3 clinical studies. The MAA for the etanercept biosimilar was based on data from a Phase 3, controlled, randomized, multicenter study in Europe where SB4 demonstrated its comparability to Enbrel®. The primary and secondary endpoints of the study were assessed and met the qualification standard for the MAA submission. Full data from the study will be available later this year.

Hi all, just joined the forum! Have been reading some of the posts and just have a question I hope ye can help me with. Just started fumaderm this month. My dermatologist has only given me a one month prescription and has then requested for me to see him again one month in. Can anyone tell me if I need to see him every month for a check up and my prescription or will I eventually get to start seeing him less?? Thanks