Hi folks

I'm a newbie to this forum and looking for some advice. I've suffered from scalp psoriasis for over 30 years and tried almost everything but nothing seems to work. I've tried Dovonex scalp solution in the past and t-gel but it no longer keeps it at bay.

I'm looking to see if anyone knows of a shampoo and conditioner and/or scalp solution that treats psoriasis successfully or have given good results. I don't mind buying online or from a high street shop as long as I can get it in the uk.

Any advice would be much appreciated.

Many thanks

Have not been online..... Greetings

The Saudi Society for Dermatology and Dermatological Surgery (SSDDS) announced the launch of the National Record for Psoriasis Patients at a press conference held at the Jeddah Hilton.

Until now, no reliable studies or statistics in Saudi Arabia that record the prevalence of the disease are available. Current studies have been carried out by individual hospitals and do not reflect the exact spread of the disease in the Kingdom.

According to these studies, the national psoriasis rate ranges from 3 to 5 percent. Patients who suffer from the disease require constant monitoring and continuous assessment in addition to follow up visits to determine the impact of treatments on patients.

The new program mechanism begins with a workshop that explains the registration process. Later, a special booklet will be published and distributed in which instructions are provided on how to use the program. A four-month trial period will then place to judge the accuracy of the information and review the results. The final stage will see the program being implemented in hospitals Kingdomwide. The program aims to raise awareness on the disease, treatment possibilities and study and analyze data on psoriasis patients and publish competitive studies and research in international journals and conferences. It also aims to spread the program in the wider Arab region in cooperation with concerned scientific departments.

The comprehensive record, which is not only the first of its kind in the Kingdom but the entire Middle East region, is being implemented by the SSDDS in cooperation with the pharmaceutical company Pfizer. The record aims to know more about the spread of the disease in the Kingdom, the psychological and social impact on patients and their families and the future planning for medication budgets and related requirements.

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A dermatology researcher at *Case Western Reserve University School of Medicine has secured a five-year, $1.9 million federal grant to explore whether a specific molecule may play a pivotal role in the development and progression of psoriasis.

Nicole Ward, PhD, assistant professor of dermatology, is investigating whether interleukin-17C (IL-17C), a protein key to the regulation of the immune system, may also play a role in the onset and escalation of psoriasis, a chronic, debilitating skin disease that affects an estimated 7.5 million Americans.

The award, from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), part of the National Institutes of Health, is the second Research Project Grant (R01) Ward has received in the last eight months. This grant will allow her to build upon earlier research suggesting a relationship between IL-17C and another protein (called TNF-alpha) in the emergence of psoriasis.

Ward and colleagues published an article in the Journal of Immunology that reported that psoriasis patients have elevated levels of IL-17C in their skin. Following treatment with TNF-alpha inhibitors, a standard therapy, IL-17C levels drop rapidly, even before the skin visibly improves. This development suggests that the presence, or interaction, of IL17-C and TNF-alpha are critical for the pathogenesis of the disease.

Ward and her colleagues also found that mice genetically engineered to overproduce IL-17C in the skin develop spontaneous lesions that resemble human psoriasis, suggesting a potential critical role for this molecule in disease initiation.. She now hopes to identify how IL-17C synergizes with other inflammatory molecules to cause disease—an understanding that may help identify a new target for drug development.

Although psoriasis is among the most common autoimmune diseases in the country, its cause remains unknown. While treatments to alleviate the condition exist, psoriasis has no cure. Patients are also more likely to be diagnosed with inflammatory bowel disease, cardiovascular disease, and depression. Even more troubling, psoriasis patients generally die seven to 10 years earlier than those without the disease.

Research funded by the NIAMS grant will be directed by Ward with collaborators and co-authors of the Journal of Immunology paper, Thomas McCormick, PhD, of Case Western Reserve, and Johann Gudjonsson, MD, PhD, and Andrew Johnston, PhD, of the University of Michigan.

*Case Western Reserve University School of Medicine is the largest medical research institution in Ohio and is among the nation's top medical schools for research funding from the National Institutes of Health. The School of Medicine is recognized throughout the international medical community for outstanding achievements in teaching.

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I found last year when I went on holiday, I had to take a course of Malaria tablets.
When I told the pharmacist I had Psoriasis, they had to order some in specifically for me.
I stopped the MTX before going on holiday, and when I returned, commenced with my weekly 10mg dose.
Suddenly everything started going wrong and treatment was immediately stopped.
It took a while to pinpoint, but the problem was the 7 week course of Malaria tablets.
This treatment played havoc with my Creatine levels in my Liver, with the high count being around 60, mine was over 1800 !!!!!
So please be aware if you are going on holiday, anywhere you have to take a Malaria course, if you are on MTX, stop the MTX treatment for 2 weeks before you start and don't start again until 3 weeks after the Malaria course finishes.
Regards to all
Micky

This study published in Arthritis & Rheumatism looks at response rates and drug survivals of switching TNFi (tumor-necrosis-factor-alpha inhibitor) in psoriatic arthritis patients.

Objective:
To describe switch frequencies and outcomes among patients with psoriatic arthritis switching tumor-necrosis-factor-alpha inhibitor (TNFi) treatment in routine care.

Methods:
Observational cohort study based on the Danish nationwide DANBIO registry. Treatment outcomes were evaluated by ACR20/50/70-responses, EULAR-good-response and 28-joint Disease Activity Score (DAS28)-remission. Kaplan-Meier and regression analyses were used for drug survival analyses and to identify predictors of outcome after switching.

Results:
Of 1,422 patients starting TNFi, 548 patients (39%) switched to a second biological drug during up to 10 years' follow-up. Median follow-up was 2.3 years (interquartile-range, IQR 1.0-4.3 years). Switchers were more frequently women (56%/45%), had shorter disease duration (3 years/4 years), higher Health Assessment Questionnaire (HAQ) (1.1(0.6-1.6)/0.9(0.5-1.4) (median(IQR))), DAS28 (4.8(4.0-5.7)/4.4(3.6-5.2)), visual-analogue-scale (VAS) pain (65(46-77)/62(40-75)mm) and fatigue scores (67(50-83)/64(42-80)mm) (all p<0.05 at start of first TNFi). During the first and second treatment HAQ, DAS28, CRP and VAS-scores had decreased after 6 months' (all p<0.05), median drug survivals were 2.2 vs. 1.3 years (p<0.001). Lower fatigue score increased survival of the second TNFi. After switching, the proportions of patients achieving sustained ACR20/ACR50/ACR70/EULAR-good-response/DAS28-remission after 3-6 months were 22% (number-needed-to-treat, NNT 4.5)/13%(7.9)/5%(20)/19%(5.3)/34%(2.9) respectively. Response rates were lower during the second treatment (compared to first TNFi, all p<0.01). At the 2-year visit, 47% of switchers had achieved ACR20 response. No differences between drug-drug combinations were found.

Conclusion:
39% of psoriatic arthritis patients switched TNFi. Response rates and drug survivals were lower after switching, however, half of switchers had ACR20 response 2 years after starting the first TNFi.

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Just as I thought things where going well, yesterday and today I was in agony. My PsA felt a bit bad a couple of days ago and yesterday whilst working in the garden I suddenly got a huge pain in my left lower back and top of my leg.

I have never experienced anything like it before and it felt like my leg muscles had exploded! couldn't move all day, no sleep even taking loads of pain killers. And this morning had to get Mrs Fred to help me out of bed. No problem there I thought as she has helped me in the past, but as she helped me stand the pain was like someone ripping the nerves from my body.

Anyway went to A&E and explained I had the problem in December where they thought I'd had a kidney stone which had been passed. So more tests, bloods, urine, x-rays, and another scan, and they have said my nerve is trapped in my spine do to my psoriatic arthritis. I've been on a painkiller drip most of the day, and although they wanted to keep me in I'm now back home with loads of painkillers.

Just wondered if anyone else has experienced this?

I'm pretty sure this will sound like a total overreaction but I've taken my Ierston does of methotrexate and not know myself after less HM a week. The day I took it I was manic, day after tearful and tonight I've just screamed at my cat for no reason to the point here she is hiding. I am disgusted ar myself and don't really know where all that rage came from.

Is this normal?

If it is I'd rather be as I was before regardless of how flakey i am. It's not like me to be like this, not even when my periods are due. I'm not rational.

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.

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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:

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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*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?