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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Good Afternoon All,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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   .