This might be a stupid question but I see threads where people say they had psoriasis over 70% 80% or 90% of their body.

Now I probably have psoriasis over arms, legs, back, bottom, face, scalp and a little on my torso. 

So that equates to about 60% of my body but as a total of my skin surface area its only a small amount as its lots of patches and I have a lot of skin.

My consultant said that I rated about 3 out of 10 on a "how bad is my psoriasis scale" which is ok, well I don't want to be a 10 out of 10.

So how do I measure my psoriasis. I have seen the scoring methods but then I have to decide whats good bad or indifferent and it varies every few days on how itchy, angry or generally pee'd off I get.

Even more good news for Cosentyx (secukinumab) after it goes head to head against it's main rival Stelara (ustekinumab), and after the 52-week, double-blind study of 676 subjects Cosentyx won the head to head battle.

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Background:
Secukinumab, a fully human anti-interleukin-17A monoclonal antibody, has shown superior efficacy to etanercept with similar safety in moderate to severe plaque psoriasis (FIXTURE study).

Objective:
We sought to directly compare efficacy and safety of secukinumab versus ustekinumab.

Methods:
In this 52-week, double-blind study (NCT02074982), 676 subjects were randomized 1:1 to subcutaneous injection of secukinumab 300 mg or ustekinumab per label. Primary end point was 90% or more improvement from baseline Psoriasis Area and Severity Index (PASI) score (PASI 90) at week 16.

Results:
Secukinumab (79.0%) was superior to ustekinumab (57.6%) as assessed by PASI 90 response at week 16 (P < .0001). The 100% improvement from baseline PASI score at week 16 was also significantly greater with secukinumab (44.3%) than ustekinumab (28.4%) (P < .0001). The 75% or more improvement from baseline PASI score at week 4 was superior for secukinumab (50.0%) versus ustekinumab (20.6%) (P < .0001). Percentage of subjects with the Dermatology Life Quality Index score 0/1 (week 16) was significantly higher with secukinumab (71.9%) than ustekinumab (57.4%) (P < .0001). The safety profile of secukinumab was comparable with ustekinumab and consistent with pivotal phase III secukinumab studies.

Limitations:
The study was not placebo-controlled and of short-term duration.

Conclusions:
Secukinumab is superior to ustekinumab in clearing skin of subjects with moderate to severe psoriasis and improving health-related quality of life with a comparable safety profile over 16 weeks.

Hi , i i just found this place. its great to see that many people are sharing a lot of information .

about me - today was my first STelara injection and i am a bit afraid ....

dont know what to tell you , but i gonna send some post here about how it works with me ...

you are wellcome to ask me , i gonna share my expirience with my dear psoriazis 

Hi. New to this, usually suffer alone drenched in self pity. Had a bout of above disgusting disease in 1993 till 1997 which inexplicably disappeared when my son was born only for it suddenly to return in all its glory last year. Im 58 yrs old, been taking acetretin this time round and its been a miracle drug, at least on the outside, i can walk (though not as far as i could when i didnt have ppp) and use my hands fairly normally. Thats such a blessing, but i still feel like a monster. How i envy those who can take all this in their stride. Side effects are many but mostly light and livable with. Anyone else hate with a vengeance bloody zipzok. So...i dread if i ever have to come off the medication. Hoping for another remission but dont know why it happened in the first place. Anyway this is me. Just wanted to introduce myself xxx

Hey all

Been dealing with psoriasis now for over 10 years, always trying new things, products, diets etc to try to find something that would alter my condition.
At the beginning of this year I started a (not due to psoriasis) low fat diet, which indirectly led me to go full vegan. I kept this up for about 1½-2 months and to my surprise this actually affected my rashes. It took a while for it to be noticeable, but today about 80-90% of all my rashes are gone and it has been pretty bad.
I have noticed that for example, a week or so ago I eat crackers several days in a row that contained milk powder and butter. Not in any large quantities at all, but this was apparently enough to flare up. Initially, when I first started the low fat diet I though it was the fat that was the issue, but after eating cod that only has 1% fat it I am sure it is animal protein that is the problem. Be it eggs, milk, butter, meat or fish, I seem to react the same to them all.

I know that not all psoriasis are the same, but if you are looking for an alternative way to handle your psoriasis and you have not tried this, perhaps going full/strict vegan for a couple of months would be worth giving a shot.

Cheers!

Hi Everyone,

Hope life is treating you all kind.. I am a male in my mid thirties and had been suffering now for a few years... I have been put on Acitretin since yesterday and feeling very depressed as heard a lot of bad things about it. I have tried every thing from  moisturisers  to oral steroids and light therapy but nothing seems to working and now Acitretin..I would appreciate if  any one can share their  experience with Acitretin. Currently I am on a 25 mg tab..

Thanks

Hi Everyone! 

Thrilled I found this forum!  Looks fantastic!       Can't wait till I have time to sit and browse through it!   I have plaque psoriasis and started it in about 2007.  Have done at home phototherapy and most prescription topicals.  Sick of it all!   Start Cosentyx next week and can't wait.   Have health care coverage through my company, but of course this new drug is EXCLUDED!   Has me a little worried to say the least.....    Most of my psoriasis is located on my legs, arms, but now developing on my eyelids and lips.  Very painful and not pretty!  Glad to be part of a support group, finally!!  Take care!

I have been having a weird feeling that there's a piece of sticky tape stuck to my big toe, especially when walking. I looked it up (as you do!) and to my surprise I'm not alone in this. I keep coming across the word 'neuropathy' which sounds basically to do with nerves.

Do you guys think it could be connected with my pa (as yet confined to carpal tunnel, plantar fasciitis and Achilles tendinitis) as I'm seeing the derm on Friday and I'm wondering whether to bring it up or if it's something to mention to the GP (not that she'll do anything..)

So if some of you were following my aloe vera and vitamins thread, you will know I decided to go back onto medication and tomorrow was when I'm due to talk to them about it. I have now been off medication for about 8 weeks, and my psoriasis has now..calmed down significantly I have had no new pustules appearing on my feet for a good while, my psoriasis on my stomach has cleared and the legs are clearing up as well, and I've only been using double base and some other creams now and again on my feet.

I'm now considering just getting some more creams tomorrow and continuing with them to see if I still stay clear as my crohns and arthritis is doing ok at the moment, so I don't need any medication for them. I'm guessing all the different medications that has been pushed around my body over the past few years were just making everything worse!

More good news for Cosentyx and psoriatic arthritis patients as Novartis announce one year results from the pivotal Phase III FUTURE 2 study, it shows improvements were sustained over one year of treatment in the majority of patients.

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Novartis announced today that new one year results from the pivotal Phase III FUTURE 2 study of secukinumab in psoriatic arthritis (PsA) were published in The Lancet following fast-track review. Secukinumab is the first interleukin-17A (IL-17A) inhibitor to demonstrate efficacy in a Phase III study in adult patients with active PsA. PsA is a long-term, debilitating, inflammatory disease associated with joint pain and stiffness, skin and nail psoriasis, swollen toes and fingers, persistent painful tendonitis and irreversible joint damage.

The new study results published in The Lancet show improvements observed with subcutaneous secukinumab 300 mg and 150 mg were sustained over one year of treatment in the majority of patients (64% for both doses), as measured by the American College of Rheumatology response criteria (ACR 20). Moreover, ACR 50 response rates were also sustained to one year in secukinumab 300 mg and 150 mg (44% and 39% respectively). Secukinumab met the primary endpoint of the study, which was ACR 20 at Week 24 with response rates significantly higher in the secukinumab 300 mg (54%; p<0.0001) and 150 mg (51%; p<0.0001) groups versus placebo (15%), with clinical improvements observed as early as Week 3. ACR 20 and 50 are standard tools used to assess improvement of PsA signs and symptoms, and represent a 20% and 50% improvement from baseline, respectively.

"Secukinumab is the first IL-17A inhibitor to show consistent efficacy through one year in Psoriatic Arthritis, Psoriasis, and Ankylosing spondylitis" said Vasant Narasimhan, Global Head of Development, Novartis Pharmaceuticals. "Novartis has recently filed global regulatory submissions for secukinumab in both psoriatic arthritis and ankylosing spondylitis and will continue to work to bring this important advance to patients with these debilitating diseases."

Secukinumab 300 mg and 150 mg also significantly improved a key secondary endpoint which was improvement in psoriasis symptoms, as measured by 90% improvements in Psoriasis Area and Severity Index score (PASI 90). Achieving PASI 90 means that patients can attain clear to almost clear skin. This is important as the majority of people living with PsA have a history of, or concomitant, psoriasis, another long-term condition which is characterized by thick and extensive skin lesions, called plaques, known to cause itching, scaling and pain.

Although the secukinumab benefits seen in FUTURE 2 were generally higher in patients without previous treatment with standard of care anti-TNF therapy, clinical benefits were observed in both anti-TNF-naïve patients and those with an inadequate response to anti-TNFs. This is important as many patients do not respond to, or tolerate these therapies and approximately 40% of people are dissatisfied with current treatments. There is therefore, a high unmet need for patients with PsA.

Secukinumab was well tolerated in FUTURE 2, with a safety profile consistent with that observed in the psoriasis clinical trial program involving nearly 5,000 patients. The most common adverse events (AEs) were upper respiratory tract infections and the common cold.

OK so I am new here and decided to come along as my psoriasis has been very hit and miss since they stopped making Dovobet cream and I had to use the gel.

Just had my first dermatology consult in about 20 years and given a choice of MTX and something else. Decided to try MTX even though I know its tea total and there are portential side effects. Hopefully it will work.

I had my consult last Wednesday and bloods taken Friday. I get the blood results tomorrow and hopefully start MTX on Wednesday. 5mg first week then 10 and upto 15 with fortnightly bloods. It may not be right for me as I am traveling a lot at present but getting really fed up with the daily ritual of creams and hoovering, well Mrs Pingu does the hoovering!

I know already what Fred will say! But I think its a process, eliminate certain tried and tested drugs before we get to the new expensive ones! It might work and I have no ill effects. I may be sick as a dog.

I have read peoples experiences, the good, the bad and the ugly but one question is how soon should I start to notice any effect, besides throwing up the morning after I take them?

I was going to say "Hi, my names Pete I'm an alcoholic" but a) its getting old b) its the wrong club.

I am a 48 year old male who has had psoriasis for about 35-40 years. Thoroughly fed up with it and as my last year has been massively stressful with work it has got a little worse. Probably the worst it has been for a long tiime but I could if I had to live with it but decided to see whats out there.

I am self employed and my partner (GF) has 4 children all grown up and she keeps me sane. Two dogs live in the north west and travel extensively with work. Cirrently spending far to much time away from home.

Hi

Had psoriasis since I was 24 I'm 39 now. I firmly believe in the theory (well for me anyway) it's a stress based illness, as when I am happy it slowly goes away on it's own. I have however tried a couple of creams.. Dovonex was excellent! one application lasted 6 months at one time another 8 months, while Dovobet is a hard slog for me.. it works..kinda, takes ages and many many applications, I can finish a tube in under a week if i'm not careful (my psoriasis is quite extreme, covering I'd guess 16th of my body). I asked the doctor for Dovonex again a few years ago..but he said the NHS don't prescribe it anymore because it's too expensive. He offered me Dovobet.. I tried to insist but no. Then in 2011 I got confused between them and asked for Dovobet.. I was so surprised when he agreed! Using it.. ahh it reduces my plaque but I need to keep using it but then I have to go back.. pay for a taxi..you get the idea. I have sleep apnoea also (which is stress related) so my memory is junk, and im not awake at the same time + remember to get to the doctors. They get quite annoyed if you miss appointments ..not so much with me, but i wouldn't like to let anyone down. 

I bought Dithrocream online to give it a go.. my fiancee is always telling me to look after myself and im starting to think she's right. I just wish I could get that Dovonex again.. that was brilliant for me!

feel free to chat and share experience and info

Dava

Hi guys

New here, thought i'd say hi.

trying to find some info..but ill make a proper post.

thanks

Dava

An interesting one for the DMF gang, this study looked at the effectiveness of Dimethyl Fumarate (DMF) in modulating the Th17, Th1 and Th2 helper cells. We have a lot of members using DMF in it's various forms (Fumaderm, Psorinovo, and even Bill using it raw) so I thought you may find this interesting.

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Background:
Fumaric acid esters such as dimethyl fumarate (DMF) have proven to be effective in the treatment of psoriasis.

Objectives:
In view of the role of Th17 in the pathogenesis of psoriasis, the present study was conducted to investigate the effects of DMF on Th1, Th2, and Th17 responses in patients.

Methods:
Peripheral blood mononuclear cells (PBMCs) were isolated from psoriasis patients and healthy individuals and were cultured in the presence or absence of phytohemagglutinin and DMF. The cell supernatants were removed to measure cytokine secretion, and the lymphocytes were used for real-time polymerase chain reaction to establish gene expression.

Results:
An increase in gene expression of interferon-γ (IFN-γ), as a marker for Th1 activity, and interleukin-17 (IL-17), granulocyte macrophage colony-stimulating factor (GM-CSF) and IL-22 representing the Th17 subset in the PBMCs of patients in comparison with those of control subjects was observed. Culture of PBMCs from psoriasis patients and controls in the presence of DMF decreased IFN-γ and increased IL-4 gene expression in both groups. Treatment with DMF could significantly decrease IL-17, GM-CSF, and IL-22 mRNA levels in the PBMCs of patients. Decreased release of IFN-γ and GM-CSF cytokine secretion after DMF treatment was also observed in PBMC cultures of patients and controls.

Conclusions:
These data show the effectiveness of DMF in modulating Th17 cells in addition to Th1/Th2 cells and reflect one of the underlying mechanisms of action of DMF in psoriasis. These findings may also support the possible benefits of using fumarate in the treatment of other autoimmune diseases in the pathogeneses of which Th1 and Th17 cells play major roles.

This small Japanese study set out to evaluate the efficacy of Humira (adalimumab) in treating joint disease in patients with PsA, using the PsA magnetic resonance imaging scoring system (PsAMRIS)

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Psoriatic arthritis (PsA), a seronegative arthropathy, may often result in progressive joint damage without treatment, leading to disability and impaired quality of life. Early therapeutic intervention of PsA is therefore crucial before the development of irreversible joint damage.

Because psoriatic skin lesions generally precede the onset of PsA, dermatologists occupy an important position in treating patients with early PsA.

This study aimed to evaluate the efficacy of adalimumab in treating joint disease in patients with PsA, using the PsA magnetic resonance imaging scoring system (PsAMRIS). Five adult Japanese male patients with active PsA were treated with adalimumab. Magnetic resonance imaging was obtained at baseline and 8–32 weeks with 2–3 time points following adalimumab treatment and assessed using PsAMRIS. Adalimumab treatment markedly improved clinical symptoms and disease activities of joint disease, which was confirmed by the reduction of PsAMRIS scores in all patients. Bone marrow edema and periarticular inflammation, reflecting the presence of enthesitis, were dramatically improved at week 8, while improvement of synovitis and flexor tenosynovitis was observed later, at week 24 or 32. However, bone erosion was not improved by adalimumab treatment during the follow-up period.

These results indicate that adalimumab treatment is associated with dramatic improvement of enthesitis in patients with PsA, whereas bone erosion may be resistant to such treatment. PsAMRIS appears to be useful for the evaluation of treatment efficacy in PsA.

I'm just wondering what shampoos and treatments that all you guys use. I'm having a nightmare at the minute with mine it's the first place my psoriasis has flared after coming off cyclosporine :( the shampoo the dermo has given me had just caused it to irritate and flake way more than it previously has. Didn't know if you guys can recommend anything? I've booked an earlier appointment with the dermo to try and get something

Any help would be appreciated

Are we the psoriasis patient expecting to much from our treatments? how soon do we expect them to work, how long do we expect them to work, etc. This study evaluated psoriasis patients subjective future expectations regarding health-related quality of life (HRQOL) and life expectancy, and to explore clinical features associated with under- or overestimating behaviour.

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Background:
Unrealistic expectations regarding treatments and clinical outcomes may lead to disappointment about therapy and sub-optimal compliance; nonetheless, these expectations have not been studied in psoriasis patients yet.

Objective:
To evaluate psoriasis patients' subjective future expectations regarding health-related quality of life (HRQOL) and life expectancy, and to explore clinical features associated with under- or overestimating behaviour.

Methods:
A cross-sectional questionnaire survey of consecutive adult patients with moderate to severe psoriasis was conducted. HRQOL expectations were recorded by applying the EQ-5D descriptive system for 6 months ahead and for future ages of 60, 70, 80 and 90 respectively.

Results:
In total, 167 patients (71% males) were included in the analysis with mean age of 50.4 ± 12.4 years and mean EQ-5D score of 0.71 ± 0.30. Overall 65% had chronic plaque psoriasis, 35% nail psoriasis, 35% scalp involvement, 29% psoriatic arthritis, 9% inverse psoriasis and 5% palmoplantar psoriasis respectively (combinations occurred). Participants expected 0.1 ± 0.23 mean improvement in EQ-5D within 6 months (P < 0.001) that achieves the minimum clinically important difference. Overall 37% expected improvement and 13% decline; however, 49% expected no changes in any of the five dimensions of EQ-5D within 6 months. Female gender, inverse or palmoplantar involvement and more severe psoriasis were likely associated with higher expectations. Patients at the initiation of their first biological at the time of the survey expected 0.18 ± 0.24 increase that seems to be realistic compared to the EQ-5D utility gain achieved in randomized controlled trials. Males expected by 2.7 ± 11.1 more, while females expected by 5.2 ± 9.3 less life years compared to the average statistical gender- and age-matched life expectancy (P < 0.05). Patients who expected to be alive at ages of 60, 70, 80 and 90 scored their future EQ-5D at ages of 60 to 90: 0.59 ± 0.46, 0.48 ± 0.41, 0.42 ± 0.41 and 0.22 ± 0.47 respectively.

Conclusion:
Our findings highlight the importance of exploring expectations that might help to increase patients' compliance.

A new assessment called PSOCUBE has been proposed which may be employed by practising dermatologists to perform standardized assessment procedures on psoriatic patients raising the chances of early recognition of patients at risk for comorbidities.

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Background:
There is increasing awareness of the clinical relevance of psoriasis comorbidities and of the importance of timely and effective screening for such comorbidities in the management of psoriatic patients. Previous works have focused on assessing evidence for prevalence of comorbidities and on the best available evidence for sensitivity in diagnosing suspected comorbidities. No algorithms are available, which have been tested on large numbers of physicians concerning the acceptance of such algorithms both by practicing clinical dermatologists and by their consulting specialists from other fields.

Objective:
To propose a multidimensional assessment algorithm for psoriasis comorbidities which may prove at the same time enough sensitive and practically sustainable in daily clinical practice.

Methods:
After an exhaustive literature search, we performed a Delphi procedure involving 50 dedicated dermatological centres to obtain a standardized assessment algorithm, which would meet requirements of sustainability and acceptability both from the point of view of Evidence-Based Medicine as well as from the point of view of practical and clinical feasibility: to meet both requirements, results from the Delphi procedure were elaborated and modified by a restricted panel of experts.

Results:
The procedure has yielded PSOCUBE, a three-dimensional table comprising 14 clinical examination and history taking items, 32 screening laboratory and instrumental exams and 11 clinimetric scores.

Conclusion:
PSOCUBE, a simple algorithm, may be employed by practising dermatologists to perform standardized assessment procedures on psoriatic patients raising the chances of early recognition of patients at risk for comorbidities, thus fostering more effective prevention; PSOCUBE may therefore contribute to reduce the overall impact of this chronic, widespread disease.

This Egyptian cohort study set out to determine whether inter-ethnic differences exist in the genetic susceptibility to psoriasis, it genotyped single-nucleotide polymorphism variations in the vicinity of candidate genes in 132 Egyptian patients and 175 healthy controls.

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Background:
Psoriasis vulgaris is a common chronic inflammatory skin disease. Development of early onset psoriasis is, to some extent, genetically determined and a strong association with the major histocompatibility complex HLA-Cw6 has been demonstrated. The use of genome-wide association studies has highlighted novel genes associated with the development of psoriasis as IL12B, IL23R, TNFAIP3 and IL13 for instance. The majority of these studies were performed on cohorts of European descent.

Objective:
To determine whether inter-ethnic differences exist in the genetic susceptibility to psoriasis, we genotyped single-nucleotide polymorphism variations in the vicinity of candidate genes in 132 Egyptian patients and 175 healthy controls.

Methods:
Blood samples of patients and controls were screened for nucleotide polymorphisms in four candidate genes by TaqMan single-nucleotide polymorphisms Genotyping Assays.

Results:
We found a significant association between psoriasis and the single-nucleotide polymorphism rs610604, within the TNFAIP3 gene. The TNFAIP3 gene is involved in the TNF-α signalling cascade (P-value: 0.004952), a key step in the pathogenesis of psoriasis. Although there was no significant association found between rs610604 (IL12B) and rs11209026 (IL23R) in this population, the interaction of these two genes showed a significant association with psoriasis (P-value: 0.025). Moreover, when selecting the patients with early disease onset (less than 30 years), we also found that the association of IL12B and psoriasis was highly significant (P-value 1.14 × 10−12). No association between rs20541 (IL13) and psoriasis was observed in our Egyptian cohort.

Conclusion:
Replicating the association of single-nucleotide polymorphisms in the TNFAIP3, IL12B and IL23R genes with psoriasis vulgaris, in subjects from different ethnic backgrounds, underlines their importance in the pathogenesis of the disease. In contrast, the lack of any association between rs20541 (IL13) and psoriasis in our Egyptian cohort suggests the existence of important inter-ethnic genetic differences in psoriasis susceptibility.