Greetings,

I randomly discovered this forum and decided to join. I was diagnosed with psoriasis in 2012 and it's majorly frustrating how it affects my life! I am hoping to hear stories from others, and learn how others deal with it.

 

Another treatment for psoriasis (Risankizumab) in the pipeline has done well against Stelara and Humira.

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AbbVie today announced positive top-line results from three pivotal Phase 3 clinical trials evaluating risankizumab, an investigational interleukin-23 (IL-23) inhibitor, compared to ustekinumab and adalimumab for the treatment of patients with moderate to severe chronic plaque psoriasis. Results showed that after 16 weeks of treatment, risankizumab (150 mg) met the co-primary endpoints of at least a 90 percent improvement in the Psoriasis Area and Severity Index (PASI 90) and a static Physician Global Assessment (sPGA) score of clear or almost clear (sPGA 0/1) across all three studies versus placebo or adalimumab (based on trial design). Risankizumab is not approved by regulatory authorities and its safety and efficacy have not been established.

"We are encouraged by these positive results for risankizumab. What is particularly exciting is the number of patients who achieved high rates of skin clearance in these three head-to-head clinical trials. Risankizumab has the potential to provide a meaningful new treatment option for people living with psoriasis," said Michael Severino, M.D., executive vice president, research and development and chief scientific officer, AbbVie.

Risankizumab is part of a collaboration with Boehringer Ingelheim, with AbbVie leading future development and commercialization of risankizumab globally.

 Hello everyone! Delighted to find such a friendly and welcoming group! Still getting to grips with 'new technology' so I can only hope I'm in the right place...
I'm looking forward to getting to know the group (and how to access bits etc!). 
Fine day here in N.E. Scotland and I hope life's being kind to you all today.
Regards,
Maggie

The first patient has been dosed in MC2 Therapeutics Phase 3 clinical trial assessing the safety and efficacy of MC2-01 Cream (calcipotriene and betamethasone dipropionate, w/w 0.005%/0.064%)

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MC2 Therapeutics A/S, a clinical-stage dermatology and eye care company today announced that first patient has been dosed in its pivotal Phase 3 clinical trial assessing the safety and efficacy of MC2-01 Cream (calcipotriene and betamethasone dipropionate, w/w 0.005%/0.064%) compared to MC2-01 vehicle and an active comparator for the treatment of plaque psoriasis in adult patients.

“The initiation of the Phase 3 trial of MC2-01 Cream is a significant milestone in the development of MC2-01 Cream across territories and in our efforts to introduce a new standard of topical therapies,” says Jesper J. Lange, President of MC2 Therapeutics. “We are encouraged by the results that we have seen to date with MC2-01, which is based on our proprietary PAD™ Technology – a new class of vehicle. Psoriasis is a chronic condition that affects the daily lives of millions of people. MC2-01 Cream is a new topical treatment designed with 100% focus on the acute and long-term needs of patients. It quickly absorbs into the skin leaving it nicely moisturized allowing patients to move on in daily routines – a life companion for people living with psoriasis.”

About the MC2-01 Phase 3 Trial:
The trial is a Phase 3, randomized, multicenter, investigator-blind, parallel-group trial to evaluate the efficacy and safety of MC2-01 Cream compared to MC2-01 vehicle and active comparator in subjects with psoriasis vulgaris. The trial is expected to enroll approximately 790 patients in about 57 centers across the United States. Subjects will apply trial medication topically once daily for up to 8 weeks.

The primary objective is to show therapeutic non-inferiority of MC2-01 cream to active comparator, as well as to characterize the safety profile of MC2-01 cream in subjects with psoriasis vulgaris. The primary efficacy endpoint is the proportion of subjects in each treatment group with “treatment success” at Week 8, defined as a minimum 2-point decrease from Baseline to Week 8 in PGA score. A variety of secondary endpoints will be assessed including patient acceptability of treatments on a Psoriasis Treatment Convenience Scale

Topline results are expected in Q3 2018 and will constitute the basis for an NDA submission.

Researches at the Universities of Dundee and Oxford suggest that one day the humble cucumber could help psoriasis and more.

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Research from the Universities of Dundee and Oxford has shown how combining the tetanus vaccine with a viral particle that normally affects cucumbers can be used to treat psoriasis and allergies, and may even protect against Alzheimer’s disease.

Scientists led by Dundee’s Dr John Foerster and Oxford’s Professor Martin Bachmann, were able to take the protein coat of cucumber mosaic virus and incorporate a tetanus vaccine-derived protein structure known to stimulate the immune system in order to create vaccines to treat multiple chronic diseases.

The vaccine showed positive results in models of psoriasis and cat allergy and was shown to raise antibody levels thought to be beneficial in Alzheimer’s disease. These vaccines can be either preventative, which is the hope for Alzheimer’s but also therapeutic, meaning they can cure a disease like psoriasis after it has already been established.

More research is required to test the efficacy of the therapeutic in a clinical setting, but the Dundee-Oxford study raises the possibility of hundreds of thousands of people being spared the ravages of chronic diseases.

Dr Foerster said, “As an academic dermatologist with special interest in the immune system, my specific attention is on vaccines to be developed against chronic skin diseases. The idea is pretty simple – for diseases such as psoriasis or eczema, the newest and most effective medicines on the market are so-called ‘antibodies’, which are what you and I produce against bugs in a common cold.

“For chronic diseases, these antibodies are specially made against one of the body’s own proteins. By blocking that single protein, the disease gets better. To use the example of psoriasis, a protein called Interleukin 17 needs to be active for the disease to progress. By creating a vaccine that stimulates the body to make antibodies against Interleukin 17 itself we can replace the need for frequent and expensive injections and make this type of treatment much more affordable and accessible to patients who could otherwise not afford specially made antibodies.

“Our research shows that this technique works in mice and, importantly, our new vaccine technology shows that it is likely to be a more effective type of vaccine than existing ones in older people. Since many patients with chronic conditions like psoriasis are elderly this technology may work much better to obtain effective vaccines.”

The researchers are now looking to begin clinical testing of the vaccine and have already received regulatory approval to initiate testing in humans. Present antibodies for psoriasis treatment typically need to be injected at least once a month to keep working, and cost around £10,000 per patient annually. A vaccine would offer much more affordable treatment.

Following on from this thread Phase 1 Study of PRX003 for the Treatment of Psoriasis Prothena have announced disappointing results for PRX003 in Patients with Psoriasis.

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Prothena Corporation plc a late-stage clinical biotechnology company focused on the discovery, development and commercialization of novel protein immunotherapies, today announced clinical results of a Phase 1b multiple ascending dose (MAD) study of PRX003 in patients with psoriasis. PRX003 is a monoclonal antibody targeting CD146, also known as melanoma cell adhesion molecule (MCAM), a cell adhesion molecule located on the surface of T helper 17 cells (Th17). While the primary objectives of the study were achieved, advancing PRX003 into mid-stage clinical development required a well-defined relationship between biological activity and meaningful clinical effects, and these prerequisites were not met. In this study, PRX003 administration resulted in dose- and time-dependent occupancy and downregulation of CD146 on Th17 cells, consistent with prior Phase 1a SAD study results. However, the pharmacodynamic effects did not translate into meaningful clinical benefit in patients with psoriasis treated with PRX003, as measured by responses in the Psoriasis Area and Severity Index 75 (PASI 75), a clinical assessment used to evaluate psoriasis severity in patients. Additionally, skin biopsy data demonstrated insufficient reduction in measurements of Th17 cell infiltration and other inflammatory markers required to advance PRX003 into mid-stage clinical development for psoriasis or psoriatic arthritis as previously planned.

"While we observed occupancy and downregulation of CD146 following administration of PRX003 consistent with our previous Phase 1a SAD study, the clinical results in this study did not meet our pre-specified criteria for evidence of a well-defined relationship between biological activity and meaningful clinical effects required to advance PRX003 into mid-stage clinical development for psoriasis or psoriatic arthritis as previously planned," said Sarah Noonberg, MD, PhD, Chief Medical Officer of Prothena. "Moreover, these results indicate the need for a deeper understanding of CD146 modulation in the treatment of complex disease states. We want to thank the patients, clinicians and site coordinators who have helped us execute this thorough study."

The Phase 1b double-blind, placebo-controlled, MAD study enrolled 33 patients with psoriasis and was designed to assess the safety, tolerability, and pharmacokinetics of PRX003. Further effects of PRX003 were evaluated through multiple exploratory endpoints of pharmacodynamic activity, including measures of CD146 occupancy and downregulation, efficacy evaluations of psoriasis severity as measured by PASI 75 response rates, and histopathologic and RNA transcript assessment of skin biopsies to measure changes in cytokines that are known markers of inflammation. All patients enrolled were randomized 3:1 to receive PRX003 at 1 mg/kg (n=7), 3 mg/kg (n=6), 10 mg/kg (n=6), or 30 mg/kg (n=6) or placebo (n=8) every 28 days for three months and were then observed for an additional three months. The study results demonstrated, in PRX003 treated-patients, near-complete (>99 percent) occupancy of CD146 with a dose- and time-dependent effect. Occupancy led to a statistically significant (p<0.0001) dose- and time-dependent downregulation of CD146 on Th17 cells at saturating drug exposures. These results were consistent with pharmacodynamic effects observed in the previous Phase 1a SAD study in healthy volunteers. Across all PRX003 dose levels in the Phase 1b MAD study, no clinically relevant or statistically significant benefit on PASI 75 response was observed. At week 12, 29 percent of PRX003-treated patients (2 out of 7) in the 1 mg/kg dose cohort achieved a PASI 75 response  (p=0.2 relative to placebo), and no patients in the 3 mg/kg, 10 mg/kg or 30 mg/kg dose cohorts achieved a PASI 75 response. Evaluation of Th17 cell migration revealed insufficient decreases in Th17 cell infiltration into tissue. Additionally, as measured from skin biopsies there were no clinically meaningful or dose-dependent changes in RNA transcript levels of genes associated with Th17-mediated inflammation, including IL-17A, IL-17F, IL-6, TNFα, and IFNγ. Despite modest evidence of a clinical effect on PASI 75 response at the lowest dose level, there was no relationship between dose levels, RNA transcript levels or other markers of inflammatory activity that provided evidence of a meaningful therapeutic effect. Collectively, these data demonstrated that near-complete downregulation of CD146 is insufficient to inhibit Th17 cell infiltration and associated inflammation to the degree necessary to achieve meaningful clinical benefit in patients with psoriasis.

PRX003 was shown to be generally safe and well tolerated up to and including the highest dose level tested at 30 mg/kg. There were no serious adverse events in PRX003-treated patients and two patients discontinued study drug due to adverse events. Treatment-emergent adverse events reported in ≥2 PRX003-treated patients, regardless of relationship to study drug, were arthralgia, fatigue, gamma-glutamyl transferase increases, presyncope, and upper respiratory tract infection.

"As an organization guided by science and data-driven decision-making, we will only advance programs into mid- or late-stage clinical development that have the potential to offer clear and differentiated clinical benefits to patients," stated Gene Kinney, PhD, President and Chief Executive Officer of Prothena. "While we are disappointed that these data do not support moving PRX003 into mid-stage development at this time, we continue to focus on advancing NEOD001 (Phase 2b and Phase 3), PRX002 (Phase 2) and PRX004 (expected to enter Phase 1 by mid-2018), as well as our active discovery programs for new clinical candidates."

This study looked at the efficacy and impact on quality of life and work productivity of Otezla (apremilast) for the treatment of palmoplantar psoriasis.

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Background:
Palmoplantar psoriasis is a variant of psoriasis vulgaris which can severely impair quality of life.

Objectives:
The main objectives of this double-blind, placebo-controlled, randomized study were to assess the efficacy and impact on quality of life and work productivity of apremilast for the treatment of moderate to severe palmoplantar psoriasis.

Methods:
A total of 100 patients with moderate to severe palmoplantar psoriasis were randomized to either apremilast 30mg bid or placebo for 16 weeks. At Week 16, all patients received apremilast 30mg bid until Week 32. The primary endpoint was the proportion of patients who achieved a Palmoplantar Psoriasis Physician Global Assessment (PPPGA) of 0/1 at Week 16.

Results:
There was no significant difference in the proportion of patients who achieved a PPPGA of 0/1 at Week 16 between patients randomized to apremilast (14%) and placebo (4%; p=0.1595). After 32 weeks of treatment with apremilast, 24% of patients achieved a PPGA of 0/1. In addition, apremilast was superior to placebo in achieving Palmoplantar Psoriasis Area Severity Index (PPPASI) 75 (apremilast: 22%; placebo: 8%; p=0.0499), in improving PPPASI (apremilast: -7.4±7.1; placebo: -3.6±5.9; p=0.0167), Dermatology Life Quality Index score (apremilast: -4.3±5.1; placebo: -0.8±4.5; p=0.0004), and in reducing activity impairment (apremilast: -11.0±22.3; placebo: 2.5±25.5; p=0.0063).

Conclusion:
Despite the absence of a significant difference between apremilast and placebo in proportion of patients achieving a PPPGA of 0/1, the presence of significant differences observed for several secondary endpoints suggest that apremilast may have a role in the treatment of moderate to severe palmoplantar psoriasis.

Not to be confused with Simponi which is injected under the skin Simponi Aria is given intravenously and has received FDA approval for use in psoriatic arthritis.

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Janssen Biotech, Inc., announced today that the U.S. Food and Drug Administration (FDA) has approved SIMPONI ARIA® (golimumab), the only fully-human anti-tumor necrosis factor (TNF)-alpha therapy administered via a 30-minute infusion, for the treatment of adults with active psoriatic arthritis (PsA) or active ankylosing spondylitis (AS). Today’s approvals follow the first FDA approval of SIMPONI ARIA® in 2013 for the treatment of moderately to severely active rheumatoid arthritis (RA). The PsA and AS approvals are supported by comprehensive clinical development programs that demonstrated the significant efficacy of SIMPONI ARIA® over placebo, while offering a consistent safety profile across all indications. In the study for the treatment of active PsA, patients experienced improvement in joint symptoms and inhibition of structural damage. In the study for treatment of active AS, results showed improvement in measures of disease activity.

“There is a need for new treatment options for patients with psoriatic arthritis. The results of the Phase 3 study of intravenous (IV) golimumab in patients with psoriatic arthritis demonstrated significant and clinically important efficacy across various domains including the inhibition of structural damage,” said Arthur Kavanaugh, M.D., Professor of Medicine, University of California San Diego, and Chair of the GO-VIBRANT steering committee. “The approval of IV golimumab for the treatment of active psoriatic arthritis brings an important new treatment option to patients, especially those who prefer IV administration, and offers one with a 30-minute infusion time.”

The approvals of SIMPONI ARIA® for PsA and AS are based on two large-scale, pivotal Phase 3 studies involving more than 600 patients. In both studies, the primary endpoints were met, with a higher proportion of patients demonstrating significant improvement in the signs and symptoms of PsA and AS in the groups receiving treatment with SIMPONI ARIA® compared with those receiving placebo. In the GO-VIBRANT (PsA) study, 75 percent of patients receiving SIMPONI ARIA®, compared with 22 percent of patients receiving placebo (P < 0.001), achieved at least a 20 percent improvement in the American College of Rheumatology (ACR20) response at week 14. Treatment with SIMPONI ARIA® resulted in the inhibition of the progression of structural joint damage and improvement in physical function associated with PsA at week 24. In the GO-ALIVE (AS) study, 73 percent of patients receiving SIMPONI ARIA®, compared with 26 percent of patients receiving placebo (P < 0.001), achieved at least a 20 percent improvement in the Assessment of Spondyloarthritis International Society criteria (ASAS20) at week 16. ACR20 and ASAS20 are standard measures used to assess clinical improvement in PsA and AS, respectively.

Results from a Taltz V Stelara head to head study.

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Background:
It has been shown that the interleukin (IL)-23/IL-17 axis is critical in the pathogenesis of psoriasis.

Objectives:
To present the primary end point (week 12) and safety and efficacy data up to week 24 from a head-to-head trial (IXORA-S) of the IL-17A inhibitor ixekizumab (IXE) vs. the IL-12/23 inhibitor ustekinumab (UST).

Methods:
Randomized patients received IXE (160-mg starting dose, then 80 mg every 2 weeks for 12 weeks, then 80 mg every 4 weeks, n = 136) or UST (45 mg or 90 mg weight-based dosing per label, n = 166). The primary end point was the proportion of patients reaching ≥ 90% Psoriasis Area and Severity Index improvement (PASI 90). Hommel-adjusted key secondary end points at week 12 included PASI 75, PASI 100, static Physician's Global Assessment (sPGA) score of 0 or 1, sPGA score of 0, Dermatology Life Quality Index (DLQI) score of 0 or 1, ≥ 4-point reduction on the itch numerical rating scale (NRS) and changes in itch NRS and skin pain visual analogue scale.

Results:
At week 12, IXE (n = 99, 72·8%) was superior to UST (n = 70, 42·2%) in PASI 90 response (response difference 32·1%, 97·5% confidence interval 19·8−44·5%, P < 0·001). Response rates for PASI 75, PASI 100 and sPGA (0,1) were significantly higher for IXE than for UST (adjusted P < 0·05). At week 24, IXE-treated patients had significantly higher response rates than UST-treated patients for PASI, sPGA and DLQI (unadjusted P < 0·05). No deaths were reported, and the treatments did not differ with regard to overall incidences of adverse events (P = 0·299).

Conclusions:
The superior efficacy of IXE demonstrated at week 12 persisted up to week 24. The safety profiles were consistent with those previously reported for both treatments.

This study looked at sleep quality in psoriasis patients.

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Background:
Research suggests that sleep disturbance is common in psoriasis. While several sleep investigations have been conducted in psoriasis populations, many have methodological shortcomings, and no study has examined multiple dimensions of sleep–wake functioning. Moreover, research has yet to be performed comprehensively examining the range of physical and psychological factors that may affect sleep in people with psoriasis.

Objectives:
To characterize sleep disturbance using validated measures and to identify physical and psychological predictors of sleep quality in people with psoriasis.

Methods:
An online survey was conducted (186 respondents; mean age 39·2 years) comprising validated measures assessing sleep [Pittsburgh Sleep; Quality Index (PSQI), Berlin Questionnaire, Pre-Sleep Arousal Scale]; chronotype (Morningness–Eveningness Questionnaire); mood (Hospital Anxiety and Depression Scale); itch (5-D Itch Scale); and psoriasis severity (Simplified Psoriasis Index). Group comparisons and regression analyses were used to examine predictors of poor sleep.

Results:
The mean PSQI score was 9·2 ± 4·3, with 76·3% scoring above the threshold for poor sleep (≥ 6 on the PSQI) and 32·5% scoring ‘positive’ for probable obstructive sleep apnoea (OSA). Poor sleep and high likelihood of OSA were associated with more severe psoriasis (P < 0·05; η = 0·07; η2 = 0·005). Cognitive arousal (β = 0·26, P = 0·001), itch (β = 0·26, P < 0·001) and depression (β = 0·24, P = 0·001) were the most robust predictors of poor sleep quality, which, together with somatic arousal (β = 0·17, P = 0·022), accounted for 43% of variance in PSQI scores.

Conclusions:
Poor sleep is common in psoriasis and associated with psychological and physical factors. Rates of probable OSA are also high. Given the importance of restorative sleep for health, sleep complaints should receive greater clinical attention in the management of psoriasis.

Here's one that will get the DMF Gang talking. Coesntyx demonstrated superior efficacy to FAEs in patients with psoriasis over a 24 week period.

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Background:
Secukinumab is a fully human antibody that neutralizes interleukin-17A. It has significant efficacy and a favourable safety profile in moderate-to-severe plaque psoriasis and psoriatic arthritis.

Objectives:
To compare secukinumab with fumaric acid esters (FAEs) in a randomized controlled trial.

Methods:
In this 24-week, randomized, open-label, multicentre study with blinded assessment, patients with moderate-to-severe plaque psoriasis, naive to systemic treatments, were randomized to receive secukinumab 300 mg subcutaneously or oral FAEs. The primary end point was ≥ 75% improvement from baseline Psoriasis Area and Severity Index score (PASI 75 response) at week 24, and missing patients were considered responders if they were responders at the time of dropout.

Results:
In total 202 patients were randomized and 200 were treated with at least one dose. Outcomes at week 24 were available for 147 and imputed for 53 patients. Discontinuations were mostly due to adverse events, which occurred more frequently in the FAE group (1·9% vs. 33·0%). At week 24, significantly more patients receiving secukinumab compared with FAEs achieved PASI 75 response (89·5% vs. 33·7%, P < 0·001), PASI 90 response (81·0% vs. 28·4%, P < 0·001) and Dermatology Life Quality Index 0 or 1 response (71·4% vs. 25·3%, P < 0·001).

Conclusions:
Secukinumab demonstrated superior efficacy to FAEs in patients with psoriasis over a 24-week period.

There has been a recent study looking at the effects of E-Cigarettes and the results are suggesting they could make psoriasis worse.

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Rationale:
E-cigarettes have become increasingly popular and little is known about their potential adverse health effects.  

Objective:
To determine the effects of e-cigarette use on the airways.

Methods:
Induced sputum samples from cigarette smokers, e-cigarette users, and non-smokers, were analyzed by quantitative proteomics, and the total and individual concentrations of mucins MUC5AC  and  MUC5B  were  determined  by  light  scattering/refractometry  and  labeled  mass  spectrometry,  respectively. Neutrophil  extracellular  trap  (NET)  formation  rates  were  also  determined forthe same groups.

Measurements and Main Results:
E-cigarette users exhibited significant increases in aldehyde-detoxification and oxidative stress related proteins associated withcigarette smoke comparing to non-smokers. The levels of innate defense proteins associated with Chronic obstructive pulmonary disease (COPD), such as elastase and matrix metalloproteinase- 9, were significantly elevated in e-cigarette users as well. E-cigarette users’ sputum also uniquely exhibited significant increases in neutrophil granulocyte - and NET- related proteins, such as myeloperoxidase, azurocidin, and protein-arginine deiminase 4, despite no significant elevation in neutrophil cell counts. Peripheral neutrophils from e-cigarette users showed increased sensitivity to PMA - induced NETosis. Finally, a compositional change in the gel-forming building blocks of airway mucus, i.e., an elevated concentration of mucin MUC5AC, was observed in both cigarette smokers and e-cigarette users.

Conclusions:
Together, our results indicate that e-cigarette use alters the profile of innate defense proteins in airway secretions, inducing both similar and unique changes relative to cigarette smoking. These data challenge the concept that e-cigarettes are a healthier alternative to cigarettes.

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The interesting part is not in the abstract but the full study goes on to say:

The enhanced NET formation in peripheral blood neutrophils from e-cigarette users also suggests the potential for systemic harm beyond the lung. Given that increased NET formation is closely associated with epithelial and endothelial cell death and subsequent pathogenesis, aberrant NET formation in peripheral blood neutrophils from e-cigarette users should be examined in the context  of  the  pathogenesis  of  systemic  diseases, such  as  systemic  lupus  erythematosus, vasculitis, and psoriasis.

Hi everyone, While I dont have Psoriasis I do suffer from another form of rheumatoid arthritis.  So while our diseases are very different we do share a lot of the same medications.  I really hope no one minds me posting as Im really just searching for some answers.  For whatever reason I have had a difficult time finding some answers concerning my meds on other forums and just general searching.  It does seem like the psoriasis community has a significant amount more of experience with these medications which has led me to post.  Long story short I've now tried Humira and cosentyx.
Humira was somewhat effective however just left me with a sense of malaise that just made using that option not worth it.  I am now on Cosentyx and while for the most part I feel so much better on it.  However, I have this strange pressure sensation in both my thighs.  Its literally deep like almost pressure in my femurs.  Its not pain, but its damn uncomfortable. I do have a follow up next week, but just seeing if anyone that has used cosentyx has had a similar side effect or explanation why this is happening.  I am on the loading phase, so I am doing my best to see this through, but hopefully some one hear can elaborate for me.
Many thanks in advance.

Hi everyone! I am new here. Just diagnosed by accident with inverse psoriasis that is morphing into a more plaquey type. I know this isn't really natural, but that cream, (you know, the one with vitamin A and vitamin D in it?) well, it really works for me. We used it on our babies when they had diaper rash, and by golly it works for me too! Thank you for new ideas.

I have recently had a bad flare-up on my shins and had got to the stage where it felt like someone had peeled my skin off and rubbed salt over it. I was also subconsciously scratching my legs to hell in my sleep, walking had also become difficult as every movement was splitting the skin on my shins so something had to be done and quick.

So I grabbed the bottle of Calamine Lotion that was lurking at the back of the medicine cabinet and dabbed a little on one small patch that was itching the worst. It was so nice and cool and I could feel it soothing almost instantly so I decided to leave it a few hours to see what would happen and I'm pleased to say nothing went wrong and it felt sooooooooooooooooooo nice.

Then I tried one leg and there was a huge difference. No more burning, no more itching and no more bleeding. I thought although this isn't going to get rid of the flare-up it looks like it is going to calm it down so I slapped it on both legs and got a great nights sleep.  

The next morning I found it wasn't easy to wash off, but as I started gently washing it away and got ready for the sting to return from the water. It didn't sting however anywhere as much as it had been even though a few flakes came off. So I re-covered the psoriasis in Calamine Lotion and again it was soothing and stopped the itching which got me through the day and another comfortable nights sleep.

Today I repeated the process and it is definitely calming the flare-up. I'm going to continue doing it over the weekend and will see how it is on Monday.

I doubt it will help the psoriasis much as a long term treatment but I just thought I would share this if anyone ever wants a quick relief from the dreaded flare-up.

*I would recommend if you do try it to do a test first on a small piece just to make sure it's for you. And I don't know how long you can continue using it, but I seem to remember using it for over a week when I had chickenpox in my 20s.

Caroline had a problem not long ago with a quote getting stuck. I have just had the same problem, and whilst I was trying to find how I told how to fix it I found another way. So I thought I will add the solutions to try should you ever get the problem or get asked by another member.

The problem usually happens after you use "multiquote" it will sometimes carry the quote over into a new post elsewhere or in the same thread. I have found two ways of fixing it, but the person with the problem has to do it as there is nothing I can do from my end.

Option #1 Go to the test board and start a new thread. If you see this you need to click "Deselect this post"


*It won't always work in the thread you are having the problem, hence the reason to start a new thread.

Option #2 Clear the Psoriasis Club Cookies. There are different ways of doing this depending on what browser you use.
*If using this way remind people not to clear their saved passwords at the same time if they store their passwords on the browser.

At the moment there is not other fix I can find.

Hello I'm Tilly  and have had Psoriasis for about 40 years  But this year i have psoriatic arthritis and having treatment now  Would like to know if anyone has had IV injections straight into the vein of steroids as this is what the hospital is  suggesting   as the single injection was not strong enough  So would appreciate from anyone who has had this  Thanks

Hi,
This is my first post here. I decided to join this forum to get in touch with other people who have psoriasis. I'm more concerned about some other non-skin related inflammatory effects of psoriasis, e.g. the link between psoriasis and diabetes, fatty liver, high cholesterol, etc. (what is also called the metabolic syndrome). I'm starting to have these symptoms (pre-diabetes and high cholesterol in my case although I'm only slightly overweight) and I believe they are connected with my psoriasis. I've had psoriasis since childhood (for about 35 years now) and I know its external effects are one problem but the other (and potentially much more serious) problem are the internal autoimmune effects of psoriasis. I even read recently (in a German medical journal) that the average lifespan of a person whose psoriasis was diagnosed during childhood is only 59 years which does sound pretty scary...

Ok so brief background, I've suffered with guttate (mainly on my back, legs and arms) for around 5 years and have been on various creams and had UVB twice. UVB has worked for me in the past however it just isn't feasible to take time off work 3 times a week to get the treatment. Also, I found that my P comes back within the matter of months once I've finished. 

So after speaking with my derm and reading a few posts on here I decided to give Acitretin a go. I started the treatment on 1 August but was only on 10mg to start and was working my way up to 35mg daily (so 10mg for 2 weeks, 25 mg 2 weeks then 35mg). I have now been on 35mg daily for 5 weeks and whilst the side effects have been minimal I have noticed little to no change in my P. On my 6 week check-up with my dorm he said to give it another 12 weeks to see if there is any change. 

I understand that Acitretin is a bit of a slow burner but apart from one patch on my leg I really haven't seen any difference, in fact, this week I think I am noticing a few new patches spring up. So I'm wandering at what point do I call it quits and say this isnt working for my P because surely I would have seen some results by now? 

If anyone has an experience of Acitretin taking this long (2 months) to show any signs of working it would be appreciated. 

Also, if I do move off Acitretin what's the logical next step? MTX is not an option for me to be fair, I'm 25 and the idea of not being able to drink just doesn't fit. I'm open to the idea of injections however, I don't think my P is severe enough to be able to get them through the NHS.

A small pilot study of a wearable device by Thync Global on psoriasis patients has encouraged them to to generate clinical data through collaborations with leading institutions.

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Thync Global, which markets wearables that help users sleep better or relax, reported the first effective use of bioelectronics to treat psoriasis in a pilot study. The noninvasive therapy “significantly” reduced psoriasis symptoms and could fill a gap in psoriasis treatment.

The pilot study involved 28 patients; 18 were treated with Thync’s device, while the remaining 10 received a placebo device. The patients used the device 10 minutes a day for four weeks.

Of the 18 patients in the treatment group, 15 (83%) reported at least a 50% reduction in redness, scaling and itchiness, compared to two patients in the control group, the company said. One-third of the treated patients reported at least a 75% reduction in symptoms, compared to none in the control group, said Sumon Pal, Thync chief scientific officer.

Worn on the neck, Thync’s device uses proprietary algorithms to deliver electrical stimulation to targeted nerves in the cervical and thoracic spine, the company said in a statement. It exploits the link between the sympathetic nervous system and the immune response.

“The nervous system plays a powerful role in modulating the immune response,” Pal said in the statement. “By creating a technology that can noninvasively manipulate the neurogenic pathways that regulate the immune system, we can provide a drug and side-effect free therapy for psoriasis.”