Background:
Our understanding of the genetic bases of predisposition to psoriasis is increasing exponentially due to the progresses of genetics. However, so far little is known about genetic predisposition in relation to the response to psoriasis treatments. Recent data identified genetic predictors for the clinical outcome of conventional treatments such as methotrexate, acitretin and vitamin D derivatives, but few studies are available on genetic predictors of response to biologics.We hypothesized that genetic variations associated with increased risk of developing psoriasis may also act as predictors for the biologic therapy outcome.

Objectives:
Aim of our study was to analyze the presence of three different psoriasis susceptibility genetic variations (HLA-Cw6; TNFAIP3 rs610604 polymorphism; LCE3B/3C genes deletion) in a cohort of patients affected by moderate to severe psoriasis under ustekinumab treatment. Our primary endpoint was to evaluate the association between PASI 75 response at week 12 and HLA-Cw6 status.

Methods:
Fifty-one patients were genotyped by standard methods and psoriasis severity (PASI score) was evaluated at day 0 and after 4, 12, 24 and 40 weeks of treatment.

Results:
We observed increased response to ustekinumab in Cw6POS patients (PASI75 at week 12 96.4% in Cw6POS vs 65.2% in Cw6NEG patients p=0.008). In addition we show that HLA-Cw6POS patients responded faster to ustekinumab, 89,3% of them reaching PASI 50 at week 4, after a single injection (versus 60,9% of HLACw6NEG patients). Superior response of HLA-Cw6POS patients was maintained throughout the study period, reaching the highest statistical significance for PASI 75 at week 28 (96.35% Cw6POS vs 72.7% Cw6NEG; odds ratio 9.8). Analysis of TNFAIP3 rs610604 polymorphism and LCE3B/3C genes deletion did not show any significant association with response to ustekinumab.

Conclusions:
Our observations underline the role of HLA-Cw6 not only as a psoriasis susceptibility gene, but also as a pharmacogenetic marker of response to ustekinumab in psoriasis.

Source: NO LINKS ALLOWED

Here's a piece of news in it's unedited form ahead of full publication about how psoriasis is due to a breakdown of immune tolerance to the microbiota of the skin.

Quote:

---

There is a known association between psoriasis and Crohn's disease (CD). Patients with CD are five times more likely to develop psoriasis, and, conversely, patients with psoriasis are more likely to develop CD. Many gastroenterologists now accept that CD is due to a breakdown of immune tolerance to the microbiota of the intestine in genetically susceptible individuals.

The microbiota of the skin has recently been investigated in psoriasis. Firmicutes was the commonest phylum, and Streptococcus the commonest genus identified. Beta-haemolytic streptococci have been implicated in both guttate and chronic plaque psoriasis. Furthermore, the innate immune system has been shown to be activated in psoriasis, and many of the genes associated with the disease are concerned with signalling pathways of the innate immune system, notably IL-23 and NFκB. Psoriasis patients also have an increased incidence of periodontitis a disease thought to be due to an abnormal response to normal oral commensals.

Based on the similarities between CD and psoriasis, we propose that psoriasis is due to a breakdown of immune tolerance to the microbiota of the skin. In support of this hypothesis we provide evidence for microbiota in the skin, activation of the innate immune system, and genetic abnormalities involving the innate immune system.

Background: 
Phenotypically diverse autoimmune conditions share common genetic susceptibility loci and underlying molecular pathways.

Objectives: 
By systematically searching for single nucleotide polymorphisms (SNPs) associated with another autoimmune disease, rheumatoid arthritis (RA), we aimed to elucidate novel genetic markers of psoriasis.

Methods: 
We investigated 18 SNPs, previously confirmed as being associated with RA, in a U.K. cohort of 623 patients with early-onset psoriasis (presenting before age 40 years), comparing them with 2662 control subjects.

Results: 
Our findings confirm the association of early-onset psoriasis with REL (rs13031237, P = 0·0027). The minor allele of REL had opposing effects upon susceptibility to disease in patients with psoriasis and RA.

Conclusion: 
Similar exploration of additional autoimmune loci and fine mapping of such regions may provide further insight into the genetics and molecular pathophysiology of psoriasis.

Source: NO LINKS ALLOWED

This is another safety study for Stelara (ustekinumab), this one is 5 year use with moderate-to-severe psoriasis.

Background: 
Long-term safety evaluations of biologics are needed to inform patient management decisions.

Objectives: 
To evaluate the safety of ustekinumab in patients with moderate-to-severe psoriasis treated for up to 5 years.

Methods: 
Safety data were pooled from four studies of ustekinumab for psoriasis. Rates of adverse events (AEs), serious AEs (SAEs) and AEs of interest [infections, nonmelanoma skin cancers (NMSCs), other malignancies and major adverse cardiovascular events (MACE)] per 100 patient-years (PY) of follow-up were analysed by ustekinumab dose (45 or 90 mg) and by year of follow-up (years 1–5) to evaluate the dose response and impact of cumulative exposure. Observed rates of overall mortality and other malignancies were compared with those expected in the general U.S. population.

Results: 
Analyses included 3117 patients (8998 PY) who received one or more doses of ustekinumab, with 1482 patients treated for ≥ 4 years (including 838 patients ≥ 5 years). At year 5, event rates (45 mg, 90 mg, respectively) for overall AEs (242·6, 225·3), SAEs (7·0, 7·2), serious infections (0·98, 1·19), NMSCs (0·64, 0·44), other malignancies (0·59, 0·61) and MACE (0·56, 0·36) were comparable between dose groups. Year-to-year variability was observed, but no increasing trend was evident. Rates of overall mortality and other malignancies were comparable with those expected in the general U.S. population.

Conclusions: 
No dose-related or cumulative toxicity was observed with increasing duration of ustekinumab exposure for up to 5 years. Rates of AEs reported in ustekinumab psoriasis trials are generally comparable with those reported for other biologics approved for the treatment of moderate-to-severe psoriasis.

Source: NO LINKS ALLOWED

Another study for Stelara (ustekinumab), this time focusing on it's use for treating severe refractory palmoplantar pustular psoriasis (PPPP). And the results look good.

Background:
Palmoplantar pustulosis (PPP) is characterized by sterile pustules with hyperkeratosis, erythema, scaling and fissuring on the palms and soles. PPP can present alone, or in association with palmoplantar pustular psoriasis (PPPP).

Objectives:
To examine treatment with ustekinumab in patients with severe refractory PPPP.

Methods:
Five patients (two men and three women, age 30–50 years) with severe refractory PPPP were treated with ustekinumab, according to a pre-established protocol. A 45 mg dose of ustekinumab was administered subcutaneously, followed by a 45 mg dose 4 weeks later and every 12 weeks thereafter. The severity of involvement and the therapeutic outcome were evaluated in every patient before, during and after treatment.

Results:
Positive responses to ustekinumab were initially seen in all of the patients 2–3 weeks after the first dose, and were more remarkable after the second injection. Complete resolution of PPPP was achieved at week 20 and was maintained in all patients.

Conclusions:
Ustekinumab appears to be an effective and safe therapeutic option in PPPP, leading to complete or nearly complete resolution of lesions and a significant improvement in patients’ quality of life.

Source: NO LINKS ALLOWED

This contest study puts three psoriatic arthritis (PsA) detection tools in a head to head test to see which is the best. The tools tested are Psoriatic Arthritis Screening Evaluation (PASE), Psoriasis Epidemiology Screening Tool (PEST), and Toronto Psoriatic Arthritis Screen (ToPAS).

Background: 
Multiple questionnaires to screen for psoriatic arthritis (PsA) have been developed but the optimal screening questionnaire is unknown.

Objectives: 
To compare three PsA screening questionnaires in a head-to-head study using CASPAR (the Classification Criteria for Psoriatic Arthritis) as the gold standard.

Methods: 
This study recruited from 10 U.K. secondary care dermatology clinics. Patients with a diagnosis of psoriasis, not previously diagnosed with PsA, were given all three questionnaires. All patients who were positive on any questionnaire were invited for a rheumatological assessment. Receiver operating characteristic (ROC) curves were used to compare the sensitivity, specificity and area under the curve of the three questionnaires according to CASPAR criteria.

Results: 
In total, 938 patients with psoriasis were invited to participate and 657 (70%) patients returned the questionnaires. One or more questionnaires were positive in 314 patients (48%) and 195 (62%) of these patients attended for assessment. Of these, 47 patients (24%) were diagnosed with PsA according to the CASPAR criteria. The proportion of patients with PsA increased with the number of positive questionnaires (one questionnaire, 19·1%; two, 34·0%; three, 46·8%). Sensitivities and specificities for the three questionnaires, and areas under the ROC curve were, respectively: Psoriatic Arthritis Screening Evaluation (PASE), 74·5%, 38·5%, 0·594; Psoriasis Epidemiology Screening Tool (PEST), 76·6%, 37·2%, 0·610; Toronto Psoriatic Arthritis Screen (ToPAS), 76·6%, 29·7%, 0·554. The majority of patients with a false positive response had degenerative or osteoarthritis.

Conclusion: 
Although the PEST and ToPAS questionnaires performed slightly better than the PASE questionnaire at identifying PsA, there is little difference between these instruments. These screening tools identify many cases of musculoskeletal disease other than PsA.

Source: NO LINKS ALLOWED

This study looks at the use of Remicade (infliximab) and the reduction of Serum levels of chemerin, resistin, visfatin, C-reactive protein (CRP), lipids, glycaemia and liver enzymes.

Background: 
Chronic plaque psoriasis is associated with obesity, which is a metabolic and inflammatory disorder. Adipokines are involved in the pathogenesis of psoriasis and they are biomarkers of obesity-related inflammation.

Objectives: 
To measure serum adipokines in patients with chronic plaque psoriasis treated with infliximab.

Methods: 
Serum levels of chemerin, resistin, visfatin, C-reactive protein (CRP), lipids, glycaemia and liver enzymes were measured in 40 patients with psoriasis and 40 controls matched by age, sex and body mass index (BMI). Adipokines were measured at baseline and after 2–12 months of treatment with infliximab 5 mg kg−1.

Results: 
At baseline, levels of chemerin (195·9 ± 48·5 vs. 145·6 ± 27·1 ng mL−1), resistin (2·03 ± 0·9 vs. 1·4 ± 0·5 ng mL−1) and CRP (5·5 ± 7·3 vs. 1·9 ± 4·4 mg L−1) were higher (P < 0·01) in patients with psoriasis compared with controls. Psoriasis was associated with elevated chemerin level independently of age, sex, BMI and levels of cholesterol and triglycerides. Chemerin was linearly correlated to CRP (r = 0·4, P = 0·01) and resistin (r = 0·3, P = 0·01). Chemerin levels were higher in patients affected by psoriatic arthritis than in patients with psoriasis without arthritis (195·5 ± 49·1 vs. 158·1 ± 37·5 ng mL−1, P = 0·01). After 2 months of infliximab treatment a significant reduction of chemerin, resistin and CRP levels was observed.

Conclusions: 
Patients with psoriasis have higher blood levels of adipokines, which normalize during therapy with infliximab. Whether this reduction is a direct effect of infliximab or secondary to a reduction of inflammation should be further investigated.

Source: NO LINKS ALLOWED

Hi,
My name is Angela and I live in NSW, Australia.
I was misdiagnosed (we think) many years ago with Ankylosing Spondillitis and it is now being re-diagnosed with psoriatic Arthritis.
I'm also being put onto Methotrexate which I've been avoiding for a couple of decades now. That's showing my age.
I'm terrified of the Methotrexate. I'm currently taking 10grams of fish oil per day instead of anti-inflammatories and they help a lot more with much less side effects than the anti-inflammatory medications too.
Being early autumn here I'm probably at my best health wise right now. Psoriatic Arthritis is just one of many health issues I have.
I'm looking for like minded people to talk to about these problems especially treatments.

Background:
There is limited research examining the association between psoriasis, dietary intake and nutritional status in the general U.S. population.

Objective:
This study aimed to compare levels of vitamins and carotenoids as well as intake of protein, fats, sugar, carbohydrates and total calories between individuals with and without psoriasis.

Methods:
We used data from the 2003–2006 National Health and Nutrition Examination Survey (NHANES) in the U.S. Demographic information, physical examination, serum laboratory values and questionnaires on past medical history and dietary intake were used to determine the relationship between psoriasis and nutritional status and diet.

Results:
The cohort consisted of 6260 participants who provided responses to their psoriasis status. Prior psoriasis diagnosis was reported in 156 (2.49%) of the respondents. Based on multivariate regression analysis, psoriasis was significantly associated with increased vitamin A level (OR: 1.01; CI: 1.00–1.02; P = 0.03), increased α-carotene level (OR: 1.02; CI: 1.01–1.04; P = 0.01), lower sugar intake (OR: 0.998; CI: 0.996–1; P = 0.04), increased body mass index (OR: 1.04; 95% CI: 1.02–1.07; P = 0.0003) and arthritis (OR: 2.31; CI: 1.37–3.90; P = 0.002). Non-Hispanic black (OR: 0.56; CI: 0.34–0.96; P = 0.03) and Hispanic race (OR: 0.37; CI: 0.19–0.75; P = 0.005) were inversely associated with a diagnosis of psoriasis compared with non-Hispanic white race.

Conclusion:
Psoriasis is significantly associated with elevated serum levels of vitamin A and α-carotene and reduced intake of sugar. Longitudinal monitoring of nutritional status in psoriasis patients is necessary to determine the effect of nutrition on psoriasis progression and the modifying role of treatments.

Source: NO LINKS ALLOWED

hi just been prescribed prochlorperazine for nausea (suspected vertigo) and googled it, some references to pustular psoriasis as a side effect but not a lot on it, has anyone any info please as im now not sure wether to take tablets but had 3 weeks of nausea
did ask gp and he said he didnt think so

thanx

This pilot study concluded Fibromyalgia Syndrome (FMS) associated pain and fatigue are significantly more frequent in patients with Psoriatic Arthritis (PsA)

Background:
Widespread pain from fibromyalgia syndrome (FMS) is observed in patients with psoriatic arthritis (PsA). We hypothesized that there is increased frequency of FMS in patients with PsA that contributes to fatigue and pain.

Method:
We prospectively enrolled patients with PsA based on the Classification criteria for Psoriatic Arthritis and healthy subjects were used as controls. The frequency of FMS was determined using London Fibromyalgia Epidemiologic Study Screening Questionnaire (LFESSQ) and Symptoms Intensity scale (SIs).

Results:
34 PsA patients and 44 controls fulfilled the inclusion criteria. Median age of PsA patients was 52 years with 53.33% females. Median age of controls was 50.5 years with 59% females. FMS was present in 53.33% of PsA patients compared to 4.54% of the controls (P < 0.001), based on LFESSQ. 37.50% of PsA had FMS compared to 6.66% of controls (P < 0.001) based on SIs. There was a significant correlation between LFESSQ and SIs in the psoriatic group (P = 0.00243). 76.66% of PsA patients complained of fatigue compared to 40.90% of controls, but the mean fatigue score between the two groups was comparable (5.03 versus 5.18).

Conclusion:
FMS-associated pain and fatigue are significantly more frequent in patients with PsA compared to controls.

Source: NO LINKS ALLOWED

*Fibromyalgia (FM or FMS) is characterised by chronic widespread pain and allodynia (a heightened and painful response to pressure). Its exact cause is unknown but is believed to involve psychological, genetic, neurobiological and environmental factors. Fibromyalgia symptoms are not restricted to pain, leading to the use of the alternative term fibromyalgia syndrome for the condition. Other symptoms include debilitating fatigue, sleep disturbance, and joint stiffness. Some patients also report difficulty with swallowing, bowel and bladder abnormalities, numbness and tingling, and cognitive dysfunction. Fibromyalgia is frequently comorbid with psychiatric conditions such as depression and anxiety and stress-related disorders such as posttraumatic stress disorder. Not all fibromyalgia patients experience all associated symptoms. Fibromyalgia is estimated to affect 2–4% of the population.

I have recently started to get psoriasis in my ears which is mega itchy. I have been fiddling about with Dovobet gel on the end of a cotton bud
Has anyone got any better/other ideas?

Hi everyone,

I'm Amy and have had Psoriasis for 2/3 of my life and have just about reached my limit! It started as small patches on my knees and elbows and has gotten worse as I have gotten older. As it stands it covers in excess of 70% of my body and I have finally accepted that steriod cream and moisturiser isnt gonna fix it.

I have had my first consult with a dermatologist and been advised that my options are Methotrexate or Ciclosporin in the first instance and that within the space of a few months my dermatologist is pretty sure i will need to be on biologicals.

I guess im relieved that there is another way and that I do have options but at the same time the possible side effects scare the hell out of me.

My husband is great and has been nothing but supportive but he just heard I can take a pill and it will get better - my next appointment is tomorrow and my head is buzzing with questions.

Augh!!!!

Anyway i figured you guys would understnad where im at right now!

Just though i'd share what I use to combat my scalp psoriasis.

I've developed a routine for my scalp which keeps it in check. I do this most days, or just when I feel like it needs it (I try not to overdo it if I can help it).

1. Take a shower and use Capasal medicated shampoo. It contains Salyic acid and coal tar extracts which has proved very beneficial for me.

2. Make sure I wait for my hair to thoroughly dry before I try applying anything.

3. Apply either E45 cream to keep hydrated or Bio-oil for the same effect (again, I find that alternating treatment can be beneficial).

4. Leave on for as long as I can bear it/ keep applying throughout the day. I say as long as I can bear it as I find that once i've applied something like bio-oil it can make it itchy after a while and it drives me mad

5. Wash hair again with normal shampoo. Personally I use a coconut based shampoo because coconut oil can be good for the skin.. but I have no actual basis for this, I just thought it couldn't hurt

That's pretty much it. It's not complicated, it's more about getting into a routine to keep it under wraps.

Also, I make a real effort and a point of removing plaque when I find it. Letting it build up is never good and it only compounds the situation.

Hope it helps someone!

Sam.

Fred I know we don't have links to other sites, but when I just tried to post a thread with a link already in it said I can't post live links. the link was already live as you had posted it and it was a link to another thread. but i can't post a link to another thread on the forum.

This is a study published by Pediatric Rheumatology. The aim of the study was to determine the long-term outcome and clinical course of patients with juvenile psoriatic arthritis (JPsA) and to define subgroups of JPsA.

Background:
Following the introduction of the ILAR criteria for juvenile idiopathic arthritis, juvenile psoriatic arthritis (JPsA) has become a better recognized category within the inflammatory arthritides of childhood. There are fewer reports describing the characteristics and long-term outcome of patients with JPsA than other subtypes of JIA.

The aim of our study was to determine the long-term outcome and clinical course of patients with juvenile psoriatic arthritis (JPsA) and to define subgroups of JPsA.

Methods:
Clinical records of all patients meeting criteria for JPsA were reviewed and divided into 4 groups depending on their clinical features and onset type. Patient characteristics and clinical features at onset and during follow-up were determined.

Results:
The cohort consisted of 119 patients: 65 with oligoarticular-onset (55%; persistent 44 and extended 21), 34 (29%) with RF(-) and 4 (3%) RF(+) polyarticular and 16 (13%) enthesitis-related arthritis (ERA). At diagnosis patients with ERA were oldest and more commonly male (p=0.001 and =0.01 respectively). Patients with a polyarticular course had more involvement of small joints of the hands and wrist when compared to patients with persistent oligoarticular and ERA (p<0.001) while patients with ERA had more hip and sacroiliac arthritis (p<0.001 for both). Nail changes were seen in 66 patients (57%) and were associated with DIP involvement (p=0.0034).

Outcome:
Time to first inactive disease on, but not off, therapy was significantly longer among patients with polyarticular course when compared to oligoarticular and ERA (p=0.016 and p=0.48 respectively). Patients with polyarticular course more frequently had contractures during follow-up than other groups (p=0.01)

Conclusion:
The long-term outcome of with JPsA was generally good. Patients with JPsA did not appear to form distinct sub-group of patients but rather resembled JIA patients with onset types without psoriasis.

Source: NO LINKS ALLOWED

Evening all, still new to forum chatting but here goes

I have been prescribed exorex tar lotion and dovobet gel in the past and these haven't really worked for me

My pseriosis come up in round patches which have gradually got larger. It is quite stubborn and it only appeared to clear up a little after spending a week at the Red Sea.
Obviously I don't really want to move to Egypt but I would love to find a gel or lotion which you guys believe really does make a difference

Hi my name is Adam, I have suffered with psoriasis for years now, never been part of a forum/chat group but decided to join this forum in hope of getting some advice from other sufferers. My psoriasis seems to be getting worse in all areas. Look forward to chatting to you guys.

Aloha,

Just searched google to see if there was a forum for Psorisasis so I thought i'd say hello!

I devoped scalp psoriasis about 4 years ago when I was 19. The area was initially about the size of a fingernail and has now spread to the entire back of my head. I didn't know what it was and put off going to the doctor for ages. Once I got it diagnosed it was easier to find treatment and i've managed to calm it down with a variety of lotions and shampoos

It can be embarassing when i'm out as it can flake and make it look like I have bad dandruff. I don't tell anyone about it because I doubt they'd understand. Recently i've been attacking it with medicated shampoo, E45 cream, anti itch E45 cream, Bio-oil and whatever else I can lay my hands on! I'm glad to report that it's calmed down and is the best it's been for years.

It's caused problems with relationships, it's unsighly and basically a royal pain in the arse! I just wanted to find some people that could relate to me really.

All the best,

Sam.

Hi My name is Rohan

Ive suffered for many years with Psoriasis...

My condition was limited to my legs intially and was very bad...in the last 3 years its moved to my upper body although not so bad there.

I have been through ever conventional western treatment the only ones left are lethal drugs such as 'Methotrexate'. The only effective treatment I had was UV but that was a temporary fix.

I found Chinese herbal medicine effective for a few months but the herbal concoctions had to be boiled twice a day and they smelt pretty bad!...drinking them were even harder...but you know what lengths we go to in our quest for relief from this burden we bear!

In the last 3 years I have been going to India for Ayurvedic treatment ...which almost totally clear my condition for periods of up to 6 months. These treatments consist of having your body purified through diet restriction internal medicines and twice daily massages and other external treatments. You have to stay in a clinic for 2 weeks and it can be expensive and torturous. The last time I went was around 14 months ago and I dont have time to go back.

I did have some medicine I was taking which help to control it but its run out now!.

I had almost a year of feeling human again and began to forget the pain and sorrow this illness brings!...recently my legs have got really bad and my upper body is rapidly getting worse...

Ive joined this forum because like anything you have to suffer directly to understand the trauma an illness can cause....and after a year of normality in my life Ive dropped down to earth with a bang!

Will this journey ever end ?....if not I need company to ease the pain!