This small study looked at plasma osteopontin and MIMT-CCA in psoriasis patients.

Quote:

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Background:
The association between psoriasis and cardiovascular disease is well documented, but the underlying mechanisms remain unknown. The relationship between osteopontin and psoriasis has been studied. High serum levels of osteopontin are reported in psoriasis, with increased cardiovascular risk factors in these patients.

Objectives:
We evaluate the extent of subclinical atherosclerosis by measuring the mean intima–media wall thickness (MIMT) of the common carotid artery (CCA) in patients with psoriasis and assessing its correlation with osteopontin to identify vascular risk factors associated with psoriasis.

Methods:
Intima–media wall thickness of the CCA and plasma osteopontin were determined in 40 patients and 40 age- and sex-matched healthy control subjects.

Results:
Median serum osteopontin was significantly higher in patients with psoriasis than in healthy control subjects. Mean intima–media wall thickness of the CCA was positively associated with plasma osteopontin level (r = 0.47, P < 0.0001), body mass index (r = 0.62, P < 0.0001), age (r = 0.54, P < 0.0001), total cholesterol (r = 0.54, P < 0.0001), and triglycerides (r = 0.65, P < 0.0001).

Conclusions:
This study shows higher levels of plasma osteopontin and MIMT-CCA in psoriasis patients than in healthy controls. This is the first study to show a positive correlation between plasma osteopontin and MIMT-CCA.

Here's some more good news for people with psoriasis. Scientists at Trinity College Dublin have discovered the molecules that convert Interleukin-36 from its harmless form to its destructive one.

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Scientists at Trinity College Dublin have made an important breakthrough in understanding how an ‘immune SOS signal’, the protein Interleukin-36, serves an important role in switching on the immune system. The discovery may pave the way for the development of new therapies for treating psoriasis.

Interleukin-36 functions akin to an intruder alarm in the body, especially in the skin, switching on when injury and infection damages our tissues, and mobilizing all of the forces of the immune system to repair the damage. This process is called inflammation and causes the swelling and redness that we are all familiar with when we sprain our ankles or bump our heads.

Inflammation is generally a good thing as it is how the body heals wounds and shuts down infection. The problem is that some people, those with psoriasis, for example, switch on this alarm protein too readily and experience skin inflammation almost continuously. So, the question has been: How does interleukin-36 get switched on to send out the SOS signal?

Now, Professor Martin and recent Trinity PhD graduate, Dr Conor Henry, have discovered the molecules that convert Interleukin-36 from its harmless form to its destructive one, by removing a small piece of Interleukin-36, rather like pulling the pin out of a grenade.

These molecules, called proteases, are overactive in the skin of people that suffer from psoriasis, which suggests an entirely new way of treating this condition.

Indeed, scientists from the Martin laboratory have also discovered and patented inhibitors of the Interleukin-36 activating proteases, and hope to develop their strategy further in partnership with a Pharma or Skincare company.

Commenting on the findings, Professor Martin said: “This discovery is very exciting and we really hope to develop this approach into a new way of treating psoriasis.”

“We are very grateful for the support of Science Foundation Ireland, who funded this research. This work represents an excellent example of how basic research leads to fundamental breakthroughs in our understanding of how diseases arise. Without such knowledge, it would be very difficult to develop new therapies.”

The work was carried out in Trinity’s Department of Genetics by a team led by Professor Martin, which included Trinity PhD students Conor Henry and Graeme Sullivan. The Trinity team is internationally recognised for its work in the areas of cell death and inflammation.

Does anyone know of a treatment that helps with scalp psoriasis? I'm currently using capasal (I think it's called) and its has not helped in the slightest, it just smells bad. Any suggestions are more than welcome.

Thanks

Claire

The FDA (U.S Food and drug administration) has made changes to the warnings and precautions section of the label for Simponi.

The changes are:

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5.2 Malignancies

In the controlled portions of clinical trials of TNF blockers, including SIMPONI, more cases of lymphoma have been observed among patients receiving anti-TNF treatment compared with patients in the control groups. During the controlled portions of the Phase 2 trials in RA, and the Phase 3 trials in RA, PsA and AS, the incidence of lymphoma per 100 patient-years of follow-up was 0.21 (95% CI: 0.03, 0.77) in the combined SIMPONI group compared with an incidence of 0 (95% CI: 0, 0.96) in the placebo group. In the controlled and uncontrolled portions of these clinical trials in 2347 SIMPONI-treated patients with a median follow-up of 1.4 years, the incidence of lymphoma was 3.8-fold higher than expected in the general U.S. population according to the SEER database (adjusted for age, gender, and race). Through Week 60 of the UC trials, there were no cases of lymphoma with SIMPONI. Patients with RA and other chronic inflammatory diseases, particularly patients with highly active disease and/or chronic exposure to immunosuppressant therapies, may be at higher risk (up to several fold) than the general population for the development of lymphoma, even in the absence of TNF-blocking therapy. Cases of acute and chronic leukemia have been reported with TNF-blocker use, including SIMPONI, in rheumatoid arthritis and other indications. Even in the absence of TNF-blocker therapy, patients with rheumatoid arthritis may be at a higher risk (approximately 2-fold) than the general population for the development of leukemia.
Rare postmarketing cases of hepatosplenic T-cell lymphoma (HSTCL) have been reported in patients treated with TNF-blocking agents. This rare type of T-cell lymphoma has a very aggressive disease course and is usually fatal. Nearly all of the reported TNF blocker associated cases have occurred in patients with Crohn's disease or ulcerative colitis. The majority were in adolescent and young adult males. Almost all these patients had received treatment with azathioprine (AZA) or 6-mercaptopurine (6–MP) concomitantly with a TNF blocker at or prior to diagnosis. The potential risk with the combination of AZA or 6-MP and SIMPONI should be carefully considered. A risk for the development for hepatosplenic T-cell lymphoma in patients treated with TNF blockers cannot be excluded.

5.3 Congestive Heart Failure

Cases of worsening congestive heart failure (CHF) and new onset CHF have been reported with TNF blockers, including SIMPONI. Some cases had a fatal outcome. In several exploratory trials of other TNF blockers in the treatment of CHF, there were greater proportions of TNF-blocker-treated patients who had CHF exacerbations requiring hospitalization or increased mortality. SIMPONI has not been studied in patients with a history of CHF and SIMPONI should be used with caution in patients with CHF. If a decision is made to administer SIMPONI to patients with CHF, these patients should be closely monitored during therapy, and SIMPONI should be discontinued if new or worsening symptoms of CHF appear.

5.5 Autoimmunity

Treatment with TNF blockers, including SIMPONI, may result in the formation of antinuclear antibodies (ANA) and, rarely, in the development of a lupus-like syndrome. If a patient develops symptoms suggestive of a lupus-like syndrome following treatment with SIMPONI, treatment should be discontinued.

Following on from the news that Stelara is available to adolescents in Scotland. Health Canada has approved Stelara (ustekinumab) for the treatment of chronic moderate-to-severe plaque psoriasis in adolescent patients.

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Janssen Inc. announced today that Health Canada has approved STELARA® (ustekinumab) for the treatment of chronic moderate-to-severe plaque psoriasis in adolescent patients (12 to 17 years) who are inadequately controlled by, or are intolerant to, other systemic therapies or phototherapies. Psoriasis is a chronic, inflammatory autoimmune disease, in which skin cells multiply faster than normal. This can result in raised, red, scaly patches that appear on the skin. While psoriasis can present at any age, approximately one-third of people living with the disease develop it before 20 years of age.

"The long-term efficacy and safety of STELARA® is well-documented in adults," says Dr. Ian Landells, MD, FRCPC, Clinical Associate Professor Department of Pediatrics and Medicine, Memorial University of Newfoundland and Clinical Chief of Dermatology, Eastern Health in St. John's, Newfoundland and Labrador. "It's encouraging that adolescents now have this effective treatment option to help manage their psoriasis, and one that has demonstrated good tolerability according to the CADMUS clinical study results."

The Health Canada approval of STELARA® for adolescents with psoriasis is based on data from the Phase 3 CADMUS study, designed to evaluate the efficacy and safety of STELARA® in patients aged 12 to 17 years with moderate-to-severe plaque psoriasis. The primary endpoint of the study was the proportion of patients achieving a Physician's Global Assessment of cleared/minimal (PGA 0/1) at week 12. This psoriasis assessment tool demonstrated that 69.4 per cent of patients who received standard dosing of STELARA® achieved PGA 0/1 at week 12.6

"The emotional and social impact of psoriasis can affect many aspects of day-to-day life," says Andrew Gosse, President, Canadian Psoriasis Network, who lives with psoriasis. "For adolescents living with the disease, this can be particularly devastating as they are in a pivotal time of life, when self-esteem and confidence can be fragile."

STELARA® blocks the action of two naturally occurring proteins called interleukin 12 (IL-12) and interleukin 23 (IL-23) that are believed to play a role in inflammatory conditions such as psoriasis and psoriatic arthritis. STELARA® received approval in Canada in 2008 for the treatment of adults living with psoriasis.

The Scottish Medicines Consortium (SMC) has completed its assessment of Stelara and advises NHS Boards and Area Drug and Therapeutic Committees (ADTCs) on its use in NHS Scotland in adolescent patients.

The advice is summarised as follows:

Quote:

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Following an abbreviated submission ustekinumab (Stelara) is accepted for restricted use within NHS Scotland.

Indication under review: Treatment of moderate to severe plaque psoriasis in adolescent
patients from the age of 12 years and older, who are inadequately controlled by, or are intolerant
to, other systemic therapies or phototherapies.

SMC restriction: continued treatment should be restricted to patients who achieve at least 75%
improvement in their Psoriasis Area and Severity Index (PASI 75) within 16 weeks.

started in March 2002 ended in September 2015 I did have a 2 year break after 9 or 10 years.
to cut a long story short the hospital did a different blood test than normal (it has a name but I have
forgotten it ) and they found my white blood cells were so low that I was in great danger of
becoming very ill.

Phil

India has picked up another biosimilar for the treatment of psoriasis. This one is a biosimilar of Humira (adalimumab) and will be known as Adfrar.

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Ahmedabad based Torrent Pharma enters New Year 2016 by announcing the launch of biosimilar Adalimumab in India under the brand name ‘Adfrar’.

Adalimumab is the most preferred therapy for the treatment of auto immune disorders and has wide applications like Rheumatoid Arthritis, Ankylosing Spondylitis, Psoriatic Arthritis, Ulcerative Colitis and Plaque Psoriasis. Adalimumab is the largest selling drug across the globe (innovator brand Humira has sales of 15 billion USD). Torrent’s brand ‘Adfrar’ will be the second biosimilar Adalimumab in the world.

Autoimmune disorders are growing ailments and Monoclonal Antibodies (MAb’s) are becoming mainstay of treatment, therefore launch of ‘Adfrar’ is a significant step towards fortifying its presence in MAb market.

Biosimilar Rituximab - ‘Toritz RA’ is already launched in Rheumatology segment and now with launch of biosimilar Adalimumab - ‘Adfrar’, Torrent presence in this segment will get a major fillip, making it a significant player in this super speciality.

‘Adfrar’ will be available as Pre Filled Syringe of 40mg. Torrent will promote this biosimilar to Rheumatologists, Gastroenterologists and Dermatologists pan India, for which three separate super specialty task force have been introduced. Around 100 highly trained professionals are employed in these Greenfield divisions.

This super speciality team, besides promoting biosimilar Adalimumab – ‘Adfrar IB’ to Gastroenterologists, will also cater to the advanced therapy needs in Hepatology. Torrent has launched new generation Hep C Antiviral Sofosbuvir – ‘Sofocruz’, a combination of Sofosbuvir + Ledipasvir - ‘Sofocruz LP’ and Daclatasvir – ‘Daclacruz’. Moreover, the company has also launched Hep B Antiviral Tenofovir – ‘Tenocruz’.

Torrent is already marketing biosimilar Rituximab ‘Toritz’ in Oncology segment, while a super specialty division for Nephrology launched in 2014 is marketing biosimilar Darbepoetin alpha - ‘Darbatitor’.

Regarding the expected business from these biosimilars, Executive Director - Marketing of Torrent Pharma Mr.Ruchir Modi said that since inception, its focus was never with business intent alone, rather it is a by product. Its purpose has always been to launch specialty niche products to address unmet medical needs arising from major life threatening diseases and reach out to maximum number of patients to offer cost effective treatment with latest quality drugs. He further added that with introduction of these new super specialty divisions, Torrent Pharma now covers most of the specialties and in near future plans to enter Urology and Opthalmology segments to cover the therapy gaps with strategic fit products.

Hi, My name is Stephen.

    I came across your site looking for information about NICE and what you think may happen to the drug Otezla.

I visited my specialist on Friday after being on the drug for the past 3 months only to find out that, even though I can stay on it for the next 9 months because it was a free 12 month trial, it may be denied funds.

Has anybody else been on this drug ?

Thank you.

This study looked at the prevalence of metabolic syndrome (MBS) in Lebanese patients with psoriasis.

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Background:
Psoriasis is a chronic inflammatory disease that affects not only the skin but also other organs as well. Genetic factors play an important role in individual predisposition. Lately, a positive association has been confirmed between psoriasis and metabolic syndrome (MBS), in western as well as in Middle Eastern countries.

Aim:
Assess the prevalence of MBS in Lebanese patients with psoriasis and the differential effect according to types and disease severity.

Methods:
This was a case-control study including 150 psoriasis patients and 150 age- and gender-matched controls admitted to the dermatology clinics at the American University of Beirut-Medical Center, a tertiary care center in Beirut. Psoriasis severity was assessed by the Psoriasis Area Severity Index (PASI). Blood samples were collected from fasting subjects and tested for glucose, HDL cholesterol, triglycerides, and C-reactive protein (CRP). Multivariate binary logistic regression models were built to assess the relationship between MBS and psoriasis, after adjustment for smoking as a possible confounding variable.

Results:
Patients with psoriasis were two times more likely to have MBS as compared to controls (35.3% vs 18.0%, P < 0.001) with an odds ratio (OR) of 2.4. All components of MBS were more prevalent in psoriasis patients than in controls. PASI score was greater in patients with MBS than those without MBS (10.5 ± 11.5 vs. 7.0 ± 8.1, P = 0.05). MBS prevalence tended to be higher in the inverse type than in others (52.2% versus 32.3%; P = 0.06) and in patients with nail pitting versus those without (45.3% vs. 28.2%; P = 0.03).

Conclusions:
This was the first study to assess the prevalence of MBS in Lebanese subjects with psoriasis and, to our knowledge, the first study that showed a higher likelihood of MBS in patients with inverse psoriasis and with nail pitting.

Here is a small study that looked at anti-angiogenesis for the treatment of psoriasis. (Anti angiogenic drugs are treatments that stop tumours from growing their own blood vessels)

Quote:

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Background:
Recent experimental studies revealed that angiogenesis and lymphangiogenesis are closely related to psoriasis. Our microarray analysis suggested that the pro-angiogenic genes platelet endothelial cell adhesion molecule-1 (PECAM1), facio-genital dysplasia-5 (FGD5), prostaglandin-endoperoxide synthase-1 (PTGS1), melanoma cell adhesion molecule (MCAM), vasohibin-2 (VASH2), and stabilin-1 (STAB1) are differentially expressed in dermal mesenchymal stem cells in psoriasis.

Objectives:
The aim of this study was to investigate the mRNA and protein expression of PECAM1, FGD5, PTGS1, MCAM, VASH2, and STAB1 for angiogenesis and the possible mechanisms in psoriasis.

Methods:
We studied 12 patients with plaque psoriasis and 14 healthy controls matched for age and sex. Dermal mesenchymal stem cells were expanded, passaged, and identified by cellular morphology, immunophenotyping, and multipotential differentiation. The mRNA and protein expression of the above-mentioned six genes were confirmed by quantitative real-time reverse transcription–polymerase chain reaction and Western blotting.

Results:
The significantly decreased expression of PECAM1, PTGS1, FGD5, and MCAM at both mRNA and protein level (except VASH2 and STAB1) were demonstrated in mesenchymal stem cells from psoriatic skin lesions compared with non-lesional from healthy controls.

Conclusions:
We provide the first report that pro-angiogenic genes PECAM1, PTGS1, FGD5, and MCAM rather than VASH2 and STAB1 may be play a vital role in pathological dermal angiogenesis disorders of psoriasis. Therefore, anti-angiogenesis is attractive and offers future potential for application in patients with psoriasis.

Curious about anyone's experience with Leflunomide (Arava) as a solo treatment.

My Rheumatologist has me on 20 mg a day for PSA at the same time as I'm on Enbrel (2 injections/week). 
Enbrel costs $21,000 CDA here in Ontario and without insurance - its a ton of money...
Appreciate people's feedback.
With thanks
(itching and scratching less now than before)

Just looking to see if anybody can help. I had an outbreak of psoriasis in 1995 and was given dithro cream (I think it was) and within a few weeks it was all gone. In October last year I was in a car crash which brought on another outbreak but this one is much worse. Every day I wake up to new plaques. The Dr keeps giving me steroid creams which are useless and will not prescribe anything else. I am going back on Friday and was wondering if I can insist that either the Dr prescribes the cream I ask for or if he can refer me to a dermatologist?

I decided to write something positive here also. My psoriasis spots are fading and I have almost no left. My arthritis in my fingers is gone. I feel almost like a "normal" person   I pray that God will let this continue.

Hi guys! I'm Sarah and I'm 29. Let me just say that I have been looking for a support group like this for a long time!!! I was diagnosed 11 years ago. It runs in my family, but not with my immediate family.... Is that weird? My Gma, aunt, and cousin have it, but they all have plaque, and I have guttate. None of them have tried the drugs that I have. They use topical creams and like to take a more natural approach, as some drugs nowadays have quite the list of side effects. I started with topical, tanning, then enbrel, methotrexate... Both of which didn't work and methotrexate gave me really bad stomach pains. My dermatologist then sent me to a psoriasis specialist. He's amazing! He's one of the lead speakers at the psoriasis association (or something like that) lol But anyways, he put me on humira, which worked, but was a really painful shot. I dreaded it. But, my co pay card eventually ran out, so I stopped taking it... Thinking it was already healed, why would it come back? Boy, was I wrong. It was back and the worst it's ever been. I didn't even want to go to the pool because I was always asked if I had poison ivy. Then, he started me on cosentyx about 4 months ago. It's injection as well. I'm wondering if anyone is on it yet? It's incredible. Everything cleared up within weeks, and the shot is so much less painful. The only problem I have with injections is every couple months, my skin gets flushed. My hands, feet, and legs will feel really hot to the touch and my hands and feet feel really swollen. But it goes away the next day. I was wondering if anyone else had this problem? Anyways, I know I'm rambling. But, any extra information I can gain from everyone, or if there's anything I might be able to help with, I'm here. I Am really happy I stumbled upon this website. Thanks for listening.

Here's some good news for psoriasis patients that don't get on with taking pills but would be happy to try Ciclosporine.

Immune Pharmaceuticals Inc. (Immune), a clinical-stage biopharmaceutical company, announced it has entered into an exclusive worldwide licensing and development agreement with BioNanoSim Ltd (BioNanoSim), an Israeli nanotechnology drug delivery company, for a novel topical nano-capsule formulation of cyclosporine.

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Monica Luchi, M.D., Chief Medical Officer of Immune, commented: "Oral cyclosporine, a potent immunosuppressive drug, known to reduce the activity of the immune system by interfering with T-cells, has revolutionized transplantation medicine. Its use in dermatology has been limited to severe cases of psoriasis and atopic dermatitis, because of significant systemic toxicity. In a validated human skin model of atopic dermatitis, a novel topical nano-capsule formulation of cyclosporine A demonstrated comparable efficacy to a high potency topical corticosteroid. We believe that this product candidate could provide an important therapeutic alternative for millions of patients with chronic inflammatory skin disorders such as moderate atopic dermatitis and psoriasis. We intend to accelerate the development of this product candidate under the abbreviated 505(b)(2) drug development pathway permitted by the U.S. Food and Drug Administration."

This topical nano-capsule formulation of cyclosporine incorporates a patented technology invented by Professor Simon Benita, the former Director of the Institute for Drug Research and Head of the School of Pharmacy at the Hebrew University of Jerusalem. Professor Benita has pioneered a nano-drug delivery platform for improving the absorption of poorly absorbed drugs. He recently succeeded in incorporating cyclosporine into a nano-capsule formulation that can be absorbed through the skin.  In validated preclinical animal and human skin models, this new topical formulation was shown to deliver therapeutic levels of cyclosporine to targeted skin layers and to limit systemic absorption. "We believe that this collaboration with Immune will leverage our nanotechnology expertise and advance this novel product candidate into the clinic," said Professor Benita.

LI'm 
Hi this is my first time on a forum looking for a miracle lol.
I gave up smoking 2 years ago 3 months after stopping I got my first small plaque ps today I have huge patches on my knees legs elbows nothing I try seems to stop a new patch apering next test is glycerine mite try smoking again next Lol hopfully a cure will be found for this and an in expensive one at that

Hi.I am Acitretin & very good for my Skin problem but i have a side effect i need to visit the toilets
to urinate often is this normal with this drug.
Richie Beaven.

Here's a study that looked into cold atmospheric plasma (CAP) as a potential therapeutic option for psoriasis.

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Background:

Cold atmospheric plasma (CAP) has shown promise for wound healing, although little is understood of the underpinning mechanisms. Little has been reported so far of its potential use in the treatment of immune-mediated diseases such as psoriasis.

Objectives:
To study CAP-induced cell death and cytokine release in human keratinocytes as a first assessment of possible CAP use for psoriasis.

Methods:
Using a CAP generator free of energetic ions, we observed its effects on keratinocytes in terms of morphology, cell viability and apoptosis, intracellular and mitochondrial reactive oxygen species (ROS), lysosomal integrity and mitochondrial membrane potential; and on secretion and expression of eight cytokines at protein and gene levels.

Results:
CAP-induced reduced cell viability, apoptotic death and production of intracellular and mitochondrial ROS in dose-dependent manner. Mitochondrial dysfunction and lysosomal leakage were found in CAP-treated cells. It also induced release of interleukin (IL)-6, IL-8, tumour necrosis factor (TNF)-α and vascular endothelial growth factor (VEGF), and enhanced the mRNA expression of IL-1β, IL-6, IL-8, IL-10, TNF-α, interferon-γ and VEGF. By contrast, IL-12 declined monotonically.

Conclusions:
The results suggest that with appropriate control of its dose, physical plasma could induce cell death via apoptotic pathways and enable simultaneous reduction in IL-12. These effects may be used to suppress keratinocyte hyperproliferation and to target T-cell activation to control amplification of inflammation. This provides an initial basis for further studies of CAP as a potential therapeutic option for inflammatory and immune-related diseases in dermatology, including psoriasis.

This is an ongoing study from Germany looking at Fumaric acid esters in children with psoriasis.

Quote:

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Background:
Given that there is no standard systemic treatment for children and adolescents with plaque psoriasis, this non-interventional, multicenter, retrospective study collected data on the efficacy and safety of long-term treatment with fumaric acid esters (FAEs) in this particular patient group.

Patients and methods:
In patients younger than 18 years of age at the start of FAE treatment, data on efficacy and safety was retrospectively collected for at least 36 months.

Results:
Data from 127 patients (aged 6–17 years) was collected for treatment durations of up to 60 months. Physician's Global Assessment, Psoriasis Area and Severity Index, and Body Surface Area showed marked improvement in the first six months. After 36 months, these parameters had, on average, improved by up to two-thirds of baseline values. Thirty-seven patients experienced at least one adverse event (AE), which was FAE-related in 36 individuals. Three AEs (proteinuria (one case), flushing (two cases)) persisted during the observation period while on treatment. Fifteen AEs led to the discontinuation of therapy; nearly all of these cases were related to gastrointestinal disorders.

Conclusions:
The KIDS FUTURE study – for the first time – included a larger population of children and adolescents with psoriasis who were treated with FAEs. The data obtained suggests that long-term FAE therapy in this patient group may be effective and safe. The results are currently being verified in an ongoing clinical study.