Hi I've just joined and wondered if I could pick someone's brains? I've had p for 10 years I've got plaque p 90% covered and nail p I'm not sure how to work out my p score? I'm using dovobet and it's great at clearing it but the minute I stop using it I'm covered again and worse! I've been trying to decide weather to go to tablet treatment but they worry me. I've been offered methotrexate but I'm unsure. I have bowel stomach trouble also so I'm unsure if I'd be prescribed the fumaderm? One more thing (sorry) I think I may have psoriatic arthritis just wondering how you find out if you do? Thankyou and hope someone can advise me on some new treatment x

Eli Lilly have released their phase 3 data for Ixekizumab and stating it is statistically superior to Enbrel (etanercept) and placebo on all skin clearance measures.

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Study design:
In the three UNCOVER studies, patients were assigned to receive either placebo or ixekizumab (80 mg every two or four weeks) for 12 weeks, following a 160 mg starting dose. In the two active comparator studies (UNCOVER-2 and 3), patients could be assigned to receive etanercept 50 mg twice weekly for 12 weeks. In UNCOVER-1, responders to treatment were assigned to continue treatment on either placebo or ixekizumab (80 mg every 4 or 12 weeks) for up to 60 weeks.

Results:
Patients treated with both dosing regimens of ixekizumab had significantly greater levels of skin clearance compared to placebo and to etanercept at the 12-week endpoint. Skin clearance was measured by standard primary endpoints for psoriasis studies: the Psoriasis Area and Severity Index (PASI) and the Static Physician Global Assessment (sPGA).

For patients treated with ixekizumab either every four weeks or every two weeks, between 78 to 90 percent of patients achieved at least a 75 percent reduction in PASI score (PASI 75) at 12 weeks. Additionally, 31 to 41 percent of these patients achieved PASI 100, or clear skin, at week 12. For comparison, between 5 to 7 percent of patients treated with etanercept in the UNCOVER-2 and 3 studies achieved PASI 100.

Statistically significant improvements in skin clearance measures for patients treated with ixekizumab were observed as early as the first week when compared to either placebo or etanercept, and continued through week 12. In the UNCOVER-1 study, high levels of response were maintained through 60 weeks of treatment.

Adverse events were comparable for patients receiving ixekizumab in the 12-week, randomized control portion across all three studies. The overall rates and severities of adverse events observed were comparable to those for etanercept in the two active comparator trials. The most frequently reported events (more than five percent across all three studies) were nasopharyngitis and injection site reaction. Most injection site reactions were mild, and most patients who experienced an injection site reaction continued treatment with ixekizumab.

"Moderate-to-severe plaque psoriasis can have a devastating life impact for patients," Ricks said. "Clear skin is their goal, but many patients are not able to achieve complete resolution using currently-available treatments."

Lilly plans to submit full data from the UNCOVER studies for disclosure at scientific meetings and in peer-reviewed journals in 2015. The company intends to submit ixekizumab to regulatory authorities in the first half of 2015.

"Ixekizumab was discovered and engineered to achieve high affinity and specificity to the IL-17A cytokine by Lilly Research Laboratories scientists, and is the most advanced asset in Lilly's pipeline of biotechnology-based medicines for the treatment of autoimmune diseases," said Tom Bumol, Ph.D., senior vice president of biotech discovery research, Lilly Research Laboratories, and president, Applied Molecular Evolution. "These data appear to confirm our hypothesis -- that IL-17A is a major driver of excess keratinocyte (skin cell) proliferation and activation in psoriasis. We're encouraged that this discovery by Lilly scientists could provide a new treatment option for patients with moderate-to-severe plaque psoriasis."

About the UNCOVER studies:
Patients enrolled in the UNCOVER 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. UNCOVER-1 compared the safety and efficacy of different dosing regimens of ixekizumab to placebo after 12 weeks and 60 weeks of treatment. UNCOVER-2 and 3 evaluated different dosing regimens of ixekizumab compared to either placebo or etanercept for 12 weeks.

About ixekizumab:
Ixekizumab is a monoclonal antibody with high affinity and specificity that binds to and neutralizes the pro-inflammatory cytokine interleukin-17A (IL-17A). In psoriasis, IL-17A plays a major role in driving excess keratinocyte (skin cell) proliferation and activation. Ixekizumab does not bind to cytokines IL-17B, IL-17C, IL-17D, IL-17E or IL-17F. Ixekizumab is administered via subcutaneous injection (under the skin). Ixekizumab is also in clinical development for the treatment of psoriatic arthritis.

"These data are important for people suffering from moderate-to-severe plaque psoriasis, as up to 41 percent of those treated with ixekizumab were able to achieve clear skin at week 12, with just one injection per dose. These results give us confidence that if approved, ixekizumab could make complete resolution of psoriasis possible for significantly more people," said David Ricks, Lilly senior vice president, and president, Lilly Bio-Medicines.

I have "medicine paranoia". No, I have not been officially diagnosed with that, but I really don't like taking different types of medicine at the same time. Not that anyone does. On a site, I saw where Meloxicam (I'm on a low dose, prescribed by my rheumatologist... I do not have PsA, it's for inflammation in my joints due to osteo arthritis) and a steroid MedPac (which I was just prescribed for a sprained wrist) can have a "moderate" interaction. I did tell the doctor that I was on Meloxicam and he said it was ok. I asked the light therapy nurse if it was ok for me to use the Fluocinolone Acetonide topical (which is a corticosteroid) if I take the steroid MedPac and she said it was fine. So, I asked the pharmacist (told you I was paranoid!) if it was ok to take the MedPac along with the 2 prescriptions I've mentioned plus the other meds I'm on (which I thought it was fine with those) and he said it was fine.

So, why am I hesitant to start the steroid MedPac? I don't see my GP until next month or I'd ask him as I feel he really pays attention to the overall picture. I've also laid off my Vit D supplement until after I meet with him since Acitretin and Light Therapy was added.

This is what the dermatologist diagnosed me with. I'm just learning about psoriasis so have not asked the doctor many questions, mostly just listened.

So, I've read this:

"Once the erythrodermic psoriasis flare passes, the psoriasis usually reverts to the way it looked before the flare".

Does that mean that it is a type of flare up as in I "had" erythrodermic psoriasis but could now have plague psoriasis or is it once diagnosed with erythrodermic, that's your diagnosis? I've had problems with infections (3 rounds of antibiotics but I think that was because it flared pretty bad right as I was getting diagnosed so things had got a bit out of control.) Right now, although still very red, it isn't that bright fiery red that it was.

This study suggests there is a high prevalence of Tinea Pedis (Athletes Foot) in people with psoriasis. Typically Tinea Pedis affects the feet, but may infect or spread to other areas of the body such as the groin and tends to spread to areas of skin that are kept hot and moist, such as with insulation, body heat, and sweat.

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There are discrepancies in the literature regarding the prevalence of tinea pedis in psoriasis. The aim of this investigation was to conduct a cross-sectional study of the prevalence of tinea pedis in psoriasis compared to atopic dermatitis patients and normal controls.

We enrolled 232 psoriatic patients, 190 atopic dermatitis patients and 202 normal controls, between the years 2010 and 2013. The prevalence of tinea pedis was 13.8% in psoriasis patients, not significantly different from that in atopic dermatitis patients 8.4% (P = 0.092)), but significantly higher than in normal controls 7.4% (P = 0.043). Both gender and age affected the prevalence of tinea pedis in psoriasis and normal controls, while only age affected the prevalence of tinea pedis in atopic dermatitis.

Regarding gender, there was higher prevalence of tinea pedis in men: 19.1% (P = 0.019) in psoriasis and 12.1% (P = 0.013) in normal controls. Age affected the prevalence of tinea pedis in normal controls (P < 0.001), psoriasis patients (P = 0.001) and atopic dermatitis patients (P = 0.001), with higher prevalence with increasing age. Trichophyton rubrum was the most common species in psoriasis (71.9%), atopic dermatitis (75.0%) and normal controls (73.3%).

Our study found a relatively high prevalence of tinea pedis among psoriasis patients.

I have an appt with one on weds. Curious to see what they will say about my skin. Was just wondering if anyone else here had tried this type of medical route.

Hello all
My name is Tom and I am looking forward to participating in the club forum.


TOM

Hello! I'm really happy to be here as this is all new to me.

A bit about myself... My name is Kathy (Kat for short) and I live in the U.S. in the state of Georgia. A bit over a year ago, my ears started to get red, itchy, scaly and I had no clue as to why so I just moisturized (which didn't help much.) After a couple of months, I had a visit with a doctor for a test and showed the nurse my ears and she recommended an over the counter cream... which as you can probably figure, didn't help either. A few months after that, I had a visit with my regular doctor and told him what was going on and also that I had a spot on my upper back and on my neck and he gave me a prescription cream..... which of course didn't help either. So on my follow up visit, 4 months later, he sent me to a dermatologist. By then it had started on my scalp and the doc took one look and said psoriasis. Initially, I was simply thinking, good, now maybe someone can fix it! So when he explained that psoriasis is "no cure" I thought... WHAT? I had heard of psoriasis, but thought it was such that you'd apply a cream and it would be gone. But, ok, so they have treatments, that won't be so bad, right? /sigh I had no understanding at all. Anyway, my first dermatologist visit was about 4 months ago and he prescribed a topical - Fluocinolone Acetonide Scalp Oil. Along with an antibiotic because I had a staph infection. So, I start using the messy oil. Over the past months, the psoriasis has came out on my face, neck, ears, back, elbows, knees and stomach. The oil helped somewhat with the itchiness but oh my, the scalp psoriasis is just horrible. I want to scratch myself to death and I leave a trail behind due to the scaling. So, back to the dermatologist I went and he put me on Acitretin (took the first one today as the pharmacy had to order it) and UVB light therapy (did the first session of 20 seconds on Friday, with three scheduled this next week and to continue at 3 per week until....they say everyone is different so no clue how many I'll need) so hopefully something helps.

So as you can see, I probably don't have a lot of helpful stuff to share on what has worked for me, but hopefully that changes with these treatments I've just started. I'm looking forward to reading through the forums and learning more as well as just chatting with people who understand.

Hi,

I am a father to a 4 months old beautiful daughter. My mother has psoriasis and We are from Sri Lanka. There is no any organization directly related to psoriasis to talk to. Therefore I need your help and advises. Will my baby get psoriasis genetically from her grandmother? What tests we can have to know whether she is vulnerable to the psoriasis?
My mother has had it heavily at her younger age around 20 years old and now she is 57 with almost no visibility of psoriasis. But my daughter is showing no symptoms for now and I need to know whether it is possible to do certain tests. Thanks a lot in advance.

Nishan

Hello all,

A little ( not that little in truth ) introduction about myself. I have had Gout since my early 20's, which tied in nicely with developing Psoriasis, which was almost overnight in covering my scalp ( these were triggered I believe by the passing of both parents within a year of each other) was a good few years before I got that under control ( which is a slight understatement *wry smile*)

I was on the radar for Psoriatic Arthritis at least 6 years ago when my Rheumatologist mentioned it in a letter to my GP ( fortunately I have GP And specialist that send me a copy of all correspondence) No follow up... Until last year when it was followed up and diagnosed.

Diagnosed in September and treatment was Methotrexate, I did not take this until January this year.. this was just so I could research and get myself in the frame of mind to take this drug, highest dose was 17.5, and I was not going any higher, stopped in mid July to losing hair and frankly it not working. ( personally had a awful time on the drug) Because one has to fit a specific criteria for a biologic ( at my Rheumatologists in Kent) I have now been put on Sulphasalazine, which I have informed the Rheumatologist that this will be started at the end of this month.

My Introduction is now over and tea is much needed , Looking forward to contributing to the discussions on here . Kellie

"cl""cmy name is glenda and i have had psoriasis and psoriatic arthritis.I have had the psoriasis for about 15 yrs and didn't know i had it.Thought i had dandriff and dry skin on my ears.Then 9yrs ago my knees started swelling i was sent to a Rhemmy Dr he diagnosed me as having psoriatic arthritis.Tried so many medications none worked.So i was put on Remicade and had some adverse effects.So i am now waiting on a new drug Simponi Aura.The place where i got my infusion has not gotten back to my Dr.I am so miserable i am covered in plaques or scales.I went to see my Dermotologist and she suggested Stelara.I am going to have to get some help somewhere.I also have scalp psoriasis.No matter what i use nothing helps.

Hey Guys, I'm new to this forum so hopefully I'm doing this the right way

I have had Psoriasis (covered head to toe in it) since I was a child, I tried EVERYTHING (creams, diets, UV light etc) which didn't work, and then I found Fumaderm

I have been on fumaderm for over 2 years now and I am down to 1 tablet and I am pretty much clear, except for the tiniest bit on my scalp. I can bare the side effects such as the flushing, but I am constantly tired which I believe is down to the Fumaderm. I will be seeing my dermatologist in September but before I speak to him I wanted to see if anyone has any experiences of coming off fumaderm and what happened.? I feel its time to come off it but I really don't know if its a good idea.
Any help would be very much appreciated, Ruth

Anakinra (Kineret) is an interleukin-1 (IL-1) receptor antagonist used to treat rheumatoid arthritis, here it was tested on two patients with with severe palmoplantar pustular psoriasis.

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Background:
Palmoplantar pustular psoriasis is a clinical psoriasis variant characterised by a high impact on quality of life and poor response to biologics approved for plaque type psoriasis.The recombinant interleukin-1 (IL-1) receptor antagonist anakinra has been recently used for the treatment of isolated refractory cases of generalised pustular psoriasis with contrasted results.

Objectives:
To report the clinical response in two patients treated with anakinra as salvage therapy in two patients with severe palmoplantar pustular psoriasis refractory to currently available antipsoriatic systemic therapies.

Methods:
Anakinra was given subcutaneously at the daily dose of 100 mg, and clinical response was evaluated using the palmoplantar psoriasis area and severity index (PPPASI).

Results:
Only partial and transient responses were observed in both patients, who had to stop anakinra due to lack of efficacy and to side effects.

Conclusion:
Anakinra appears to provide only partial clinical improvement in refractory palmoplantar pustular psoriasis. Prospective clinical studies on larger populations are warranted to investigate more accurately both efficacy and safety of IL-1-inhibiting strategies in pustular psoriasis.

This study from The Journal of Dermatology suggests male predominance in psoriasis may occur in Japan.

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Psoriasis is thought to be a multifactorial disease triggered by both genetic and environmental factors. The HLA-C locus on chromosome 6p21.33 remains the strongest susceptibility candidate locus in psoriasis.

The strong association between psoriasis and the HLA-Cw6 allele has been well documented in various races. It is known that psoriatic patients with early onset are more likely to be familial and associated with HLA-Cw6. Familial occurrence of Japanese psoriasis is smaller than other populations. Furthermore, males are predominant over females in Japanese psoriasis.

We investigated the relation between HLA-C alleles and age of onset, and in each gender for Japanese psoriasis, and discuss male predominance in the incidence of psoriasis in Japan. Four hundred forty six unrelated Japanese patients with psoriasis vulgaris and 557 sex- and age-matched unrelated Japanese healthy controls were investigated by genotyping.

We confirmed the association between early-onset type of psoriasis with HLA-C*06:02 allele in Japanese. In addition, we detected the association between the late-onset type of psoriasis and the HLA-C*12:02 allele in Japanese. No significant differences in allele frequency were observed between females and males.

Our results suggest that there is no genetic factor effect on male predominance in Japanese. In contract, the effect of environmental risk factors on the onset of Japanese psoriatic patients is stronger in males than in females. As a result, male predominant in psoriasis may occur in Japan.

This study in The Journal of Dermatology showed that biologic therapy ameliorates clinical symptoms and controls the immune response in patients with psoriasis.

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Therapy with monoclonal antibodies to tumor necrosis factor (TNF)-α and the interleukin (IL)-12/23 p40 subunit has significantly improved the clinical outcome of patients with psoriasis. These antibodies inhibit the effects of the target cytokines and thus the major concern during their use is the induction of excessive immunosuppression.

Recent studies evaluating the long-term efficacy and safety of biologic therapy in psoriasis have shown no significant appearance of serious adverse effects including infections and malignancies. However, the immunological consequence and the mechanism by which the blockade of a single cytokine by biologics can successfully control the activity of psoriasis remain unclear.

In the current study, we investigated the effect of biologic therapy on cytokine production of various lymphocytes and on the activity of monocytes and neutrophils in psoriatic patients. Neutrophils, monocytes and T cells were purified from heparinized peripheral venous blood by Ficoll density gradient centrifugation, and γ-interferon, TNF-α and IL-17 production from lymphocytes was measured by flow cytometer. The activation maker of neutrophils and the activated subsets of monocytes were also analyzed.

Biologic therapy induced no significant changes in the cytokine production by lymphocytes from the skin and gut-homing T cells. However, neutrophil activity and the ratio of activated monocyte population increased in severely psoriatic patients were normalized in psoriatic patients receiving biologic therapy.

The present study showed that biologic therapy ameliorates clinical symptoms and controls the immune response in patients with psoriasis.

This is a retrospective, single-centre study assessing all patients commenced on FAEs between October 2003 and July 2012.

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Background:
Fumaric acid esters (FAEs) have been used for over 30 years in the management of psoriasis.

Objectives:
To determine drug survival of FAEs in patients with psoriasis, treatment-limiting adverse drug events and the range of effective drug doses.

Methods:
A retrospective, single-centre study assessing all patients commenced on FAEs between October 2003 and July 2012. Demographic data, length of treatment, reasons for discontinuation of FAEs, side-effects and range of doses were recorded.

Results:
Two hundred and forty-nine patients [160 (64%) male] were included. The mean age at which FAEs were commenced was 44·5 years (range 17–82 years). The mean length of treatment was 28 months (range 1 week to 106 months). In patients who were commenced on FAEs ≥ 4 years before inclusion in this study, the 4-year drug survival was 60% (64/107). FAEs were discontinued in 146/249 patients (59%); this was due to lack of efficacy in 59/146 (40%) and gastrointestinal upset in 39/146 (27%). A very low dose of FAEs (< 240 mg daily) was successful in maintaining control of psoriasis in 26 (10%) patients. The mean treatment duration of these patients was 64 months (range 32–106 months).

Conclusions:
Fumaric acid esters have a 4-year drug survival rate of 60%, which compares favourably with reported 4-year survival rates of 40% for etanercept and adalimumab and 70% for infliximab. Longer drug survival is more likely in the significant subgroup of patients in whom a very low dose of FAEs is sufficient to control disease. The reasons for this are unclear.

Not one for me as I'm a professional couch potato, but some may find this piece interesting.

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Background:
Psoriasis is a common chronic multifactorial disease which can result in restrictions to social and recreational activities. Psoriasis subjects are at high risk to develop metabolic and cardiovascular diseases. Physical activity, a vital component in prevention and management of these diseases, is reported to be potentially associated in a negative way with psoriasis.

Objective:
To investigate the relationship between psoriasis and physical activity.

Materials and methods:
Anamnestic and physical examination as well as a specific doctor-administered questionnaire was performed to a group of 416 consecutive sportive subjects and 489 sex and age-matched controls. Moreover, similar investigations were executed on 400 consecutive psoriatic patients without psoriatic arthritis.

Results:
Psoriasis was significantly more common in controls respect to sportive group (n = 27, 5.4% vs. n = 7, 1.7%, P < 0.01) whereas a positive familial history of psoriasis was observed in similar percentages in both groups (n = 51, 10.2% vs. n = 40, 9.6%). The number of subjects performing sports activities was significantly lower in psoriasis group compared to controls (n = 44, 11% vs. n = 106, 21.3%; P < 0.001). Of these psoriatic patients, 35/44 referred that sporting activities showed a positive influence on the natural course of their disease, whereas the remaining 11 patients did not highlight positive or negative influences on their illness. Interestingly, 23.75% of psoriatic patients (n = 95) related that they had regularly carried out sporting activities before the onset of the dermatosis referring that psoriasis represented a huge obstacle to continue practicing physical activities.

Conclusion:
Our survey showed that regular physical activity may lower the risk of psoriasis and have a beneficial effect on the natural course of the disease, positively influencing not only the severity as well as the incidence of metabolic comorbidities, but also, through possible epigenomic, metabolic, anti-inflammatory and psycho-emotional effects, the onset of the dermatosis. However, larger birth cohort studies are needed to confirm these results.

Could be interesting for consulting a dermatologist,so copy under here.

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How to use teledermatology for psoriasis
Not everyone with psoriasis lives near a dermatologist. Sometimes work or family responsibilities can get in the way of maintaining regular appointments.
That's one place where the power of technology can help.
Teledermatology, the practice of consulting with a dermatologist online, continues to expand and is especially important for those with chronic conditions like psoriasis that require ongoing treatment, said Dr. April Armstrong, vice chair of clinical research and director of the psoriasis program at the University of Colorado School of Medicine in Denver.
How does teledermatology work?
There are two main ways that people can use teledermatology, said Armstrong – either by sharing photos (a practice called "store-and-forward") or "live interactive," which is more like a virtual appointment.
"In our practice, we've done both, and I find that most patients prefer live interactive," she said. "They can really talk with the doctor, and the doctor can pick up on non-verbal clues. If a patient has a question, they can ask right then."
To make the most of a teledermatology appointment, Armstrong also offers the following tips:
You must have Internet access and a camera.
If using "store-and-forward," be sure to send the best possible images. In some cases, a primary care physician may even work with you in their office to help you get the best photos.
Write down questions ahead of time.
Be open to technology. Telemedicine providers have to abide by the same legal privacy regulations as a doctor in an office.
How do I find a teledermatologist?
In 2012, there were 38 teledermatology offices in the U.S., according to the U.S. Teledermatology Survey. The trend is growing.
If you are interested in using teledermatology, but do not work with a dermatologist who uses this service, ask for a referral from your primary care provider, Armstrong said. The insurance reimbursement varies for teledermatology from state to state. Be sure both you and your provider’s office check with your state’s reimbursement policies.
There are also online sites where users can send photos to a board-certified dermatologist, such as AccessDerm. Armstrong cautions that if using an online site, visitors should check out the doctors' profiles to be sure they are working with a qualified provider.
In a paper published in March of 2014 in the Journal of the American Medical Association Dermatology, Dr. Carrie Kovarik writes that the Affordable Care Act could mean an increase in people using teledermatology appointments.
Already, patients often have to wait a month for dermatology appointments, writes Kovarik, associate professor of dermatology at the Hospital of the University of Pennsylvania and assistant professor of medicine. She goes on to explain that within the next two years, as more people receive access to health insurance, providers could be flooded with a whole new group of patients.

ok i know i'm supposed to say oh it's so easy to ditch the caffeine, sugar, alcohol and gluten but I am about ready to kill for some sugar right now - or a martini, or both.

Just. Say. NO.

Saw my Derm today. He wanted to do light box but copayments are cost prohibitive for me. He prescribed Soriatane and wants to see me in a month. Told me to continue with Topicals.
Just wondering if anyone here has tried this treatment and had success ?
Oh and the Derm had no comment when I asked him if he felt diet played a role in repairing immune system. But he doesn't make any $ if this clears up with improved diet ;-)

He confirmed I have a severe case of plaque and guttate psoriasis. I left his office content w his diagnosis and more determined than ever to completely eliminate all sugar, gluten, caffeine and alcohol for 90 days.

You are what you eat and toxins are permeating my intestinal wall and being absorbed by my blood (cropping up on my skin) instead of being eliminated by my body.

Just my opinion.