We have been saying for a long time now that psoriasis is an autoimmune disease, well here's an article ahead of full print that suggests psoriasis is not an autoimmune disease after all.

The basics:

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The concept that psoriasis is an autoimmune disease needs to be questioned. The autoimmune label has been based on molecular mimicry between streptococcal and keratin proteins and the existence of homologous peptides between these proteins. However it is only peripheral blood CD8, and not CD4, T lymphocytes that respond to the homologous peptides.

This ignores the fact that it is CD4 T cells which are necessary to initiate psoriasis. Recent studies on skin bacterial microbiota have found a variety of bacteria in both normal skin and psoriatic lesions. In biopsy specimens the most common phylum was Firmicutes and the most common genus streptococcus in both psoriasis and normal skin.

The innate immune system is activated in psoriasis and recent genetic findings have shown the majority of susceptibility loci are associated with innate immunity. There is a known clinical relationship between both Crohn's disease (CD) and periodontitis, and psoriasis, and psoriasis patients share mutations in some innate immunity genes with individuals with CD. It is now accepted that CD is due to a breakdown of immune tolerance (dysbiosis) to bacteria in the intestine.

These findings suggest that psoriasis is initiated by an abnormal response to bacteria in the skin due to genetic factors.

*This article is protected by copyright. All rights reserved.

More good news from Amgen and AstraZeneca about Brodalumab, after announcing phase 3 results in May about their phase lll AMAGINE-1TM study Brodalumab phase 3 results today they have announced results from AMAGINE-3TM which shows Brodalumab could be set to knock Stelara off it's perch.

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Amgen and AstraZeneca today announced that AMAGINE-3TM, a pivotal, multi-arm Phase 3 trial evaluating two doses of brodalumab in more than 1,800 patients with moderate-to-severe plaque psoriasis, met its primary endpoints when compared with both Stelara® (ustekinumab) and placebo at week 12. Brodalumab was shown to be superior to Stelara on the primary endpoint of achieving total clearance of skin disease, as measured by the Psoriasis Area Severity Index (PASI 100). When compared with placebo, a significantly greater proportion of patients treated with brodalumab achieved at least a 75 percent improvement from baseline in disease severity at week 12, as measured by the Psoriasis Area Severity Index (PASI 75). A significantly greater proportion of patients treated with brodalumab also achieved clear or almost clear skin at week 12 compared with placebo, according to the static Physician Global Assessment (sPGA 0 or 1). All key secondary endpoints comparing brodalumab with Stelara and placebo were also met.

Results showed that 36.7 percent of patients in the brodalumab 210 mg group, 27.0 percent of patients in the brodalumab 140 mg group, 18.5 percent of patients in the Stelara group and 0.3 percent of patients in the placebo group achieved total clearance of skin disease (PASI 100). In addition, 85.1 percent of patients in the brodalumab 210 mg group, 69.2 percent of patients in the brodalumab 140 mg group, 69.3 percent of patients in the Stelara group and 6.0 percent of patients in the placebo group achieved PASI 75.

"Despite a variety of treatment options available for psoriasis, many patients still do not meet skin clearance goals," said Sean E. Harper, M.D., executive vice president of Research and Development at Amgen. "These results are of particular importance as they are the first to demonstrate superiority to Stelara in achieving total skin clearance, and the second positive pivotal Phase 3 study evaluating brodalumab in patients with moderate-to-severe plaque psoriasis."

The most common adverse events that occurred in the brodalumab arms (more than 5 percent of patients in either group) were common cold, joint pain, upper respiratory tract infection and headache. Serious adverse events occurred in 1.4 percent of patients in the 210 mg group and 1.6 percent of patients in the 140 mg group compared with 0.6 percent for Stelara and 1.0 percent for placebo during the placebo-controlled period.

Brodalumab is the only investigational treatment in development that binds to the interleukin-17 (IL-17) receptor and inhibits inflammatory signaling by blocking the binding of several IL-17 cytokines (A, F, A/F and C) to the receptor. The IL-17 receptor and cytokine family play a central role in development and clinical manifestation of plaque psoriasis.

"These results add to the growing body of evidence supporting the potential value that brodalumab may bring to the treatment of psoriasis by targeting the IL-17 receptor," said Briggs W. Morrison, M.D., executive vice president of Global Medicines Development at AstraZeneca. "We look forward to sharing results later this year from AMAGINE-2TM, our remaining head-to-head study evaluating brodalumab versus Stelara."

The AMAGINE program is composed of three Phase 3 studies designed to assess the efficacy and safety of brodalumab in patients with moderate-to-severe plaque psoriasis. Top-line results from AMAGINE-1TM, designed to assess the efficacy and safety of brodalumab compared with placebo, were released in May 2014. Detailed results from the AMAGINE-3 study will be submitted to the appropriate scientific forum for presentation and/or publication. Results from AMAGINE-2 are expected by year end.

The DCP (Department of Consumer Protection) is to hold a public hearing on November 26, 2014 08:30 at 165 Capitol Ave, Room 126, Hartford, CT 06106 following a petition for the use of medical marijuana in people with Severe Psoriasis and Psoriatic Arthritis.

Source: NO LINKS ALLOWED

That's all I have and please excuse my ignorance, but I assume this in the USA and not Hartford UK

If anyone knows more please add.

The psoriasis drugs market is set to experience huge growth over the next few years, with Stelara representing nearly 22 percent of total psoriasis sales by 2023.

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Decision Resources, one of the world’s leading research and advisory firms for pharmaceutical and healthcare issues, finds that the psoriasis market will experience robust growth over the next decade as sales increase from $6.6 billion in 2013 to $10.7 billion in 2023 in the United States, France, Germany, Italy, Spain, the United Kingdom and Japan. The continued uptake of Janssen’s interleukin (IL)-12/23 inhibitor Stelara in earlier lines of therapy and the entry of therapies with novel mechanisms of action (notably the IL-17 inhibitors), will drive sales growth. Stelara is forecast to achieve major-market sales of approximately $2.4 billion in 2023, representing nearly 22 percent of total psoriasis sales.

Emerging agents will drive sales: The launches and uptake of several emerging agents—the IL-17 inhibitors (Novartis’s secukinumab, Eli Lilly’s ixekizumab, and Amgen/AstraZeneca/Kyowa Hakko Kirin’s brodalumab), and Pfizer’s Jak inhibitor Xeljanz—will also drive sales over the 2013-2023 forecast period.

Competition from emerging biologics: TNF-alpha inhibitors and Stelara will experience competition from emerging biologics and oral agents with novel mechanisms of action. Although concerns about their long-term safety profiles will restrict uptake initially, the emerging IL-17 inhibitors, Xeljanz, and emerging IL-23 inhibitors (Sun Pharma/Merck’s tildrakizumab and Janssen’s guselkumab), will increase competition within the TNF-alpha-refractory space.

Oral therapies will expand treatment options: Although the perceived lower efficacy of Xeljanz and concerns about the drug’s safety profile will restrict is market potential, Xeljanz will also compete for use in the TNF-alpha-refractory space. Another oral agent, Celgene’s phosphodiesterase-4 inhibitor Otezla, has recently been approved for the treatment of psoriasis (in addition to psoriatic arthritis), and will present an alternative to conventional systemic therapies as an interim step prior to biological therapy.

Thought leaders are particularly interested in the emerging IL-17 inhibitors, which have shown impressive efficacy in late-stage trials, with similar efficacy to the most potent current therapy for psoriasis—Remicade (Janssen/Merck/Mitsubishi Tanabe Pharma). The efficacy and safety of emerging IL-17 inhibitors and IL-23 inhibitors are being evaluated in head-to-head clinical trials with current biologics, which will increase dermatologists’ confidence adopting these new therapies.

Although these agents will initially compete in the TNF-alpha-refractory population and in patients who lose response to Stelara, as their long-term safety profiles become more established, physicians will be comfortable prescribing them earlier—potentially as first-line biologics—in the treatment algorithm.

We've all been through that itch cycle where you just can't seem to get off, some treatments help and some can even make you itch more.
This study suggests that Enbrel (etanercept) can significantly improve the Itch (Pruritus) and Quality of Life (QoL).

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Background:
Pruritus is a clinically important symptom of psoriasis that has a major impact on quality of life (QoL).

Objective:
The objective of this study was to examine pruritus and QoL in patients with moderate-to-severe psoriasis treated with etanercept (ETN) in the PRISTINE clinical trial.

Methods:
Patients were randomized (1 : 1, double-blind) to ETN 50 mg QW or 50 mg BIW for 12 weeks, followed by 50 mg QW for 12 weeks. Pruritus was reported as 0 (no itching) to 5 (severe itching). Associations were examined between pruritus and Psoriasis Area and Severity Index, Dermatology Life Quality Index (DLQI), Hospital Anxiety and Depression Screening (HADS), Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue), Euro-Qol 5D (EQ-5D) and Medical Outcomes Study (MOS) Sleep Index II.

Results:
At baseline, patients (n = 270) had a mean pruritus level of 3.6. Itching (level ≥1) was reported by 96% of patients, 62% of whom had severe itching (level ≥4) and 26% had the highest level of itching. DLQI, HADS-Anxiety, HADS-Depression, FACIT-Fatigue, EQ-5D visual analog scale, and MOS Sleep Index II were significantly associated with itch. At week 12, mean pruritus improvement in the ETN BIW/QW group was greater than in the QW/QW group (2.4 vs. 1.6, P < 0.001), but not at week 24 (2.2 vs. 2.0, P = 0.180). Patients with the most severe itching at baseline (score of 5) had a mean score of 1.7 at week 24. Overall, patients with clinically meaningful pruritus improvement at week 24 reported greater improvement in QoL measures than other patients.

Conclusion:
Most patients with moderate-to-severe psoriasis in this study (96%) reported pruritus. Pruritus improved significantly with ETN therapy and was strongly associated with improvements in QoL. These data support the clinical relevance of pruritus as an important symptom of patients with moderate/severe psoriasis.

Ever wondered how many people like you there are around the world living with psoriasis? well this report suggests the figure will be well over 40 Million by 2022.

It makes interesting reading, and it was first released in 2013 for use by businesses shaping and driving the global psoriasis market.

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Psoriasis has a complex collection of risk factors, such as genetics, lifestyle choices, and exposure to certain environmental conditions, states a new report from research and consulting firm GlobalData.

According to the report, there were approximately 36.5 million prevalent cases of psoriasis across all the US, France, Germany, Italy, Spain, UK, Japan, China, and India in 2012. By 2022, GlobalData epidemiologists forecast that this figure will reach approximately 40.93 million prevalent cases, following a 12.1% increase based on projected population growth - prevalence proportions are expected to remain constant.

Psoriasis is an immune-mediated chronic dermatological disorder characterized by redness and irritation. The condition affects individuals of both sexes and all ethnicities and ages, although there is a higher prevalence of psoriasis in the colder, northern regions of the world.

The age-standardized prevalence of psoriasis varies among different countries, from as low as 0.03% in Japan to as high as 1.84% in Germany. These regional differences may be attributable to variations in environmental factors such as the weather, as well as genetic factors, and differences in data collection across different countries.

The prevalence of psoriasis in the central region of Italy is 2.8 times greater than the prevalence in southern Italy, and similar regional differences have been reported in Spain, with psoriasis more common among the residents of central Spain, who experience colder and drier weather than individuals in the northern and southern regions.

Ethnicity may also play a part - studies have shown that Caucasians have a higher prevalence of psoriasis compared with African-Americans, but African-Americans in the US tend to suffer from a more severe form of the disease.

Psoriasis is an autoimmune disorder, so family history plays an important role in the development of the disease. Approximately 40% of psoriasis patients have first-degree relatives with the disease. Since psoriasis is categorized as an immune-mediated inflammatory disorder (IMFD), sufferers are also at an increased risk of developing other, more severe IMFDs, such as rheumatoid arthritis and Crohn’s disease. Psoriasis patients are also at risk of developing psoriatic arthritis, which is a progressive, deforming, and debilitating disease and the most common comorbidity associated with psoriasis.

However, lifestyle choices, and certain diseases and medications can affect the condition. Smoking increases the risk of developing psoriasis, and increases the severity of the disease. In addition, it has been noted that psoriasis is a common disease among obese patients, although the relationship between the two disorders remains unclear. Obesity also predisposes individuals to inverse or flexural psoriasis, which occurs in the folds of the skin. Various medications, such as lithium, anti-malarial agents, beta-blocking agents, and non-steroidal anti-inflammatory drugs (NSAIDs), are also considered as possible risk factors, though there is insubstantial evidence to prove this as yet.

The disease can be controlled with medication, but a cure has not yet been found. Psoriasis is often associated with unsightly lesions, scales, and inflammation, which can affect an individual’s self-esteem, leading nearly half of all psoriasis patients to report elevated stress levels, depression, and thoughts of suicide. Stress can trigger pathological processes, exacerbating many dermatological conditions, particularly psoriasis. Psoriasis patients suffering from these anxieties can also limit their social interactions and abuse alcohol and tobacco, further worsening their condition.

My Psoriasis did not begin to show until I turned 17 (1983). I was prescribed Oxoralen and it worked, my Psoriasis went dormant for almost a decade. I tried to get it prescribed again about 10 years ago and my Dr. said it causes cancer.

Is this true?

With the Psoriasis Area and Severity Index (PASI) first introduced in 1978, and the Dermatology Life Quality Index (DLQI) developed in 1994 is now time to move on to a newer measure for patients with psoriasis? I made the Psoriasis Score a few years ago because I never felt the PASI was easy to follow, now there is a study that is suggesting it could be time for a change.

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Abstract:
In a non-life-threatening disease such as psoriasis, treatment goals should be referred to the improvement in severity and extent of the disease and their impact on patients’ perceived health-related quality of life (HRQoL), usually measured by the Dermatology Life Quality Index (DLQI).

The ultimate goal of therapy is blanching, and an improvement of 90% or better (PASI90 response) with respect to baseline Psoriasis Area and Severity Index (PASI) is considered as treatment success by the European Medicines Agency. PASI75 response has become accepted as a less stringent reasonable therapeutic goal, but absolute PASI values might provide a better benchmark, irrespective of baseline PASI.

Anyway, objective measures of psoriasis involvement are clinically meaningful only if they correlate with significant improvements in DLQI, and especially with the achievement of a DLQI = 0–1 status, corresponding to lack of effect of the disease on patient's HRQoL. Even though PASI75 response meets therapeutic expectations in most patients, PASI90 response or better has a significantly higher impact on DLQI improvement and is associated with significantly higher DLQI = 0–1 response rates.

The introduction of anti-IL17 drugs in clinical practice bears the promise of achieving PASI90 response or better in the majority of patients, and initial data suggest that the PASI90 benchmark provides better discriminatory value as regards achievement of DLQI = 0–1 response.

Further research is required to confirm the value of absolute PASI cut-offs as a measure of therapeutic success independent of baseline and duration of treatment, and to develop newer, more practical and more accurate measures of psoriasis severity.

For those of you with psoriatic arthritis the results will come as no surprise to you, but it's an interesting little study that set out determine the effects of psoriatic arthritis (PsA) on sleep quality.

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Aim:
The purpose of this study was to determine the effects of psoriatic arthritis (PsA) on sleep quality and investigate the association between sleep quality and clinical parameters of PsA, quality of life and psychological state in patients with PsA.

Method:
Forty-one patients with PsA and 38 healthy volunteers were included in this study. In both patients and healthy controls, sleep quality was assessed by means of the Pittsburgh Sleep Quality Index (PSQI) and anxiety and depression were assessed by means of the Hospital Anxiety and Depression Scale (HADS). In addition, PsA Quality of Life (PsAQoL) Index and Psoriasis Area and Severity Index (PASI) were used on patients. Generalized pain was assessed by means of a visual analogue scale (VAS).

Results:
Subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbance, daytime dysfunction and total PSQI scores were significantly higher in patients with PsA compared to healthy controls. Total PSQI scores significantly correlated with anxiety, generalized pain, PsAQoL scores, enthesitis and levels of C-reactive protein (CPR) and erythrocyte sedimentation rate (ESR) (P < 0.05). Also, multiple regression analysis indicated that ESR level was independently associated with total PSQI score (P <0.05, R2 = 0.325).

Conclusion:
Sleep quality is diminished in patients with PsA. Sleep disturbance is particularly associated with generalized pain, anxiety, enthesitis and levels of CRP and ESR in patients carrying the diagnosis of PsA.

Glycerine is in the skin layers. I use it as a moisturizer especially in winter. My Paloplanter and on hands and feet seem to always be seasonal.i STAY AWAY FROM WATER THAT IS NOT FILTERED. Wash with glycerine soap no itch after bath then moisturize.

I use it in many of my home made mixtures. Non alcohol watch hazel AND GLYCERINE.

SINCE using these my hands and feet P. R in remission for 4 years now. Also a spa with paraffin wax . I use at night night then add glycerine and occlusion over night. Really gets down thru the deep layers of my P. Skin.

JUST having to try DEMARDS To treat PSA. Were also talking about a new bio...

The DEMARDS really help the pain but make me too sick. I also have severe OA 2 THR. My hips r always cold . I'm probably worth more with all that metal in my hips and shoulders.

Some days during this time of year I really need the Tin Man's oil can...

So it's always trial and error. Some of us have different outcomes with meds than others.

As most of us p.with know it can be so tricky. Does anyone use a dehumidifier in damp areas of the country for PSA.?
I've read it helps with cold weather to control the moisture in the air in homes.

New drug BI 655066 moves on to phase 11 trial after showing psoriasis clearance for 66 months after one single dose Dr. James G. Krueger reported at the annual congress of the European Academy of Dermatology and Venereology. Yes you heard it right 66 months that's 5.5 Years.

Quicky version:

Key clinical point: Up to 66 months after receiving a single subcutaneous injection of a biologic agent that selectively blocks interleukin-23, six patients with moderate to severe chronic plaque psoriasis at baseline remained PASI 100 responders with clear skin.

Major finding: The PASI 75 response rate 12 weeks after receiving a single dose of the investigational agent BI 655066 was 87%, and the PASI 90 rate was 58%.

Data source: This was a first-in-humans, proof-of-concept study involving 39 psoriasis patients.


Longer version:

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“For me, this is one of the most interesting features of this proof-of-concept study,” he added. “If this kind of activity is confirmed in the ongoing phase IIb trial, I think this represents the potential for very long-term disease modification. This could become an important agent in the future to treat psoriasis.”

BI 655066 is a monoclonal antibody that specifically targets the p19 subunit of interleukin (IL)-23. Unlike ustekinumab (Stelara), which blocks both IL-23 and IL-12, BI 655066 selectively blocks only IL-23, which Dr. Krueger believes is the central driving force in activating and sustaining the T-cell subsets responsible for the hyperproliferative and inflammatory reactions that define psoriasis.
“This study is all about testing for the specific pathogenic contribution of IL-23 to psoriasis in a first-in-humans study.

Our findings really emphasize the importance of IL-23 in driving the key pathways of psoriasis,” observed Dr. Krueger, professor of investigative dermatology and director of the Milstein Medical Research Program at Rockefeller University, New York.
The study included 39 patients with moderate to severe plaque psoriasis. Their baseline PASI was 18, and they averaged more than a 20-year history of psoriasis. Twenty-four patients were randomized 3:1 to a single intravenous injection of BI 655066 at various doses ranging from 0.01 mg/kg to 5 mg/kg or to placebo in order to get an initial sense of the agent’s safety and tolerability.
In the second part of the study, 15 other participants received a single subcutaneous injection: two got placebo and the rest were randomized to BI 655066 at either 0.25 mg/kg or 1.0 mg/kg. Safety and efficacy were assessed at weeks 0, 2, 4, 12, and 24. In addition, skin biopsies were obtained at weeks 0 and 8 for immunohistochemistry studies and RNA sequencing analysis.

By week 12, the PASI 75 response rate in subcutaneous BI 655066 recipients was 87% and the PASI 90 rate was 58%. At week 24, nine patients elected to continue structured prospective follow-up while remaining off treatment, including six PASI 100 responders. Those six PASI 100 responders remained PASI 100 at ongoing follow-up 48-66 weeks after receiving their single dose of the agent.

Biopsy specimens obtained at week 8 showed normalization of the epidermal psoriasiform hyperplasia which had been present at baseline. A normal-looking granular layer had been reestablished. “This looks essentially like the pattern of normal or nonlesional skin,” according to the dermatologist.

RNA sequencing analysis and gene profiling showed normalized production of the IL-23/IL-17-induced proteins that had been strongly overexpressed at baseline, including lipocalin, beta-defensin, and psoriasin.

“The immune axis is turned down. The number of immune cells is way down, although they’re not completely eliminated. With placebo, you still see a psoriasislike pattern of the disease. With blockade of IL-23, most cases have a gene profile like nonlesional skin. This represents a profound cellular and disease modulation,” Dr. Krueger said.

Among all 39 participants, the only serious adverse event deemed possibly treatment related was a 5-minute transient ischemic attack (TIA) episode in a patient on BI 655066. This caught Dr. Krueger’s attention as a possible red flag; however, he noted that more than 200 patients have since received the biologic agent in the ongoing phase IIb trial, with no reported major adverse cardiovascular events.

“I think that TIA may just be bad luck with small numbers,” he added.

Asked what he thinks might explain the remarkably lengthy disease remission seen following a single dose of the biologic, Dr. Krueger offered two possibilities.

“It may be that IL-23 is necessary to sustain pathogenic clones of memory cells in the skin, and as we get rid of it those clones most likely apoptose. And if you’ve sufficiently removed the clones, then you don’t get the expansion. That’s guess one. Guess two would be that we’ve renormalized tolerance mechanisms in some way. Both of these hypotheses can be tested,” according to Dr. Krueger.

I started Humira on October 9. Ever since then I have been having some discomfort in my chest and a cough. I am suppose to take another shot on Thursday October 30. I am going to hold off till I talk to my dermatologist. Her office is closed on Thursday so I am going to call her Friday.

Has anyone on here that is on or have taken Humira have any side effects?

This study set out to determine for the first time whether the anti-TNF-α monoclonal antibody Humira (adalimumab) may improve insulin sensitivity in non-diabetic patients with psoriasis.

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Objective:
Psoriasis is a chronic inflammatory disease associated with increased risk of cardiovascular death. Several studies have shown a beneficial effect of anti-TNF-α therapy on the mechanisms associated with accelerated atherogenesis in patients with inflammatory arthritis, including an improvement of insulin sensitivity. In this study, we aimed to determine for the first time whether the anti-TNF-α monoclonal antibody adalimumab may improve insulin sensitivity in non-diabetic patients with psoriasis.

Methods:
Prospective study on a series of consecutive non-diabetic patients with moderate to severe psoriasis seen at the Dermatology Division of Hospital Universitario Marques de Valdecilla (Northern Spain) who completed 6 months of therapy with adalimumab (80 mg at week 0 followed by 40 mg every other week, starting 1 week after the initial dose). Patients with chronic kidney disease, hypertension or body mass index ≥ 35 kg/m[sup]2[/sup] were excluded. Metabolic and clinical evaluation including assessment of insulin sensitivity using the Quantitative Insulin Sensitivity Check Index (QUICKI) was performed at the onset of the treatment (time 0) and at month 6.

Results:
Twenty-nine patients (52% women; 38.6 ± 10.7 years) with moderate to severe psoriasis [body surface area (BSA) 37.9 ± 16.3%], Psoriasis Area and Severity Index [(PASI) 18.9 ± 7.8] were assessed. Statistically significant improvement (P=0.008) of insulin sensitivity was observed after 6 months of adalimumab therapy (QUICKI at time 0: 0.35 ± 0.04 vs. 0.37 ± 0.04 at month 6). Significant improvement of erythrocyte sedimentation rate, ultrasensitive C-reactive protein, BSA, PASI, Nail Psoriasis Severity Index, physician global assessment and psoriatic arthritis screening and evaluation questionnaire was also observed at month 6 (P < 0.05 for each variable).

Conclusion:
Our results support a beneficial effect of the anti-TNF-α blockade on the mechanisms associated with accelerated atherogenesis in patients with psoriasis.

It's been known for a long time there are other disorders (or diseases) co-occurring with psoriasis and psoriatic arthritis, this retrospective study was obtained from the Clinical Practice Research Datalink (CRPD) between 2006 and 2010.

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Background:
Previous studies have demonstrated that patients with psoriasis have higher rates of comorbidities compared to the general population. Despite the clinical and economic burden of psoriatic disease, there have been few large-scale observational studies focused on this condition.

Objective:
To assess rates of cardiovascular, autoimmune, infectious and other conditions in patients with psoriasis or psoriatic arthritis (PSA).

Methods:
The data for this retrospective study were obtained from the Clinical Practice Research Datalink (CRPD). Cohorts of patients with psoriasis (n = 27 672; mild, n = 22 174, severe, n = 5498) and PSA (n = 1952) were generated based on the diagnosis made by general practitioner or specialist recorded in CPRD between 2006 and 2010. Frequencies of comorbidities at baseline and incidence rate ratios (IRR) of medical conditions occurring during follow-up were calculated and compared between groups. Cox proportional hazard models were employed to compare hazard ratios (HR) of comorbidities across the same subpopulations previously described.

Results:
Significant differences in the unadjusted risk of cardiovascular disease, hyperlipidaemia, diabetes, skin cancer and autoimmune diseases were observed between patients with differing severity of psoriasis or between PSA and psoriasis patients. The adjusted HR analyses confirmed patients with severe psoriasis had significantly higher rates of several conditions including diabetes (1.23; 95% CI: 1.01–1.51) and rheumatoid arthritis (2.88; 95% CI: 2.25–3.67) compared to patients with mild psoriasis. Patients with PSA had significantly higher adjusted rates of hypertension (1.30; 95% CI: 1.01–1.68), rheumatoid arthritis (6.93; 95% CI: 5.45–8.80) and ankylosing spondylitis (6.98; 95% CI: 2.37–20.58) compared to those with severe psoriasis.

Conclusion:
Patients with mild psoriasis are less affected by comorbid conditions than those with severe psoriasis, and patients with psoriasis are less affected by comorbidities than those with PSA. Given the differences observed across severities of psoriasis and between psoriasis and PSA, each patient subgroup should be taken into consideration in clinical practice and future research.

This study looked at different patterns of bone spur formation in psoriatic arthritis (PsA) and hand osteoarthritis (OA), using high-resolution peripheral quantitative computed tomography (QCT).

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Methods:
The study group comprised 70 subjects (25 patients with PsA, 25 patients with hand OA, and 20 healthy controls). The 2 patient groups were similar with regard to age and sex distribution and clinical involvement of the metacarpophalangeal (MCP) joints. All patients underwent high-resolution peripheral QCT scanning of the second, third, and fourth MCP joints of the dominantly affected hand. Demographic and disease-specific data were recorded, and the number, size, and distribution of bone spurs were assessed and compared between patients with PsA and patients with hand OA.

Results:
The overall number and size of bone spurs were similar in patients with PsA and patients with hand OA. However, localization of lesions within individual joints was substantially different between patients with PsA and those with hand OA. In PsA, bone spurs dominated the radial sides of the joints (for the metacarpal head of the second joint, P < 0.001 versus hand OA; for the base of the second phalangeal joint, P < 0.001 versus hand OA), whereas the palmar and dorsal quadrants were the predilection sites in hand OA. Detailed anatomic analysis showed that bone spurs in the entheseal regions were prominent in patients with PsA but rare in patients with hand OA, and that bone spurs in patients with hand OA typically emerged at the cartilage–bone interphase and the joint margins.

Conclusion:
Our findings show that the overall number and size of bone spurs are similar in patients with PsA and patients with hand OA. Nonetheless, the anatomic sites of bone proliferation are different between these 2 groups of patients.

It's been known for a long time that our nails play an important part in the detection of psoriatic arthritis (PsA) and this study looks like it confirms that.

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Background:
Patients with psoriatic arthritis (PsA) suffer from increased burden of disease and impairments in quality of life. Early detection and treatment of PsA could contribute to the prevention of clinical and radiological progression.

Objectives:
To analyse the predictive value of clinical and patient-reported outcomes for concomitant PsA in a population-based cohort of patients with psoriasis.

Methods:
We performed a retrospective analysis of data from three independent national cross-sectional studies on health care in psoriasis and PsA, conducted in Germany in the years 2005, 2007 and 2008. Patients with psoriasis were included in the study by dermatologists (n = 3520) and via the German patient advocacy group for psoriasis (n = 2449). In all studies, psoriasis history, clinical findings, PsA, nail involvement, health care and patient-reported outcomes were collected with standardized questionnaires.

Results:
In the regression model on 4146 patients the strongest predictors for concomitant PsA were nail involvement [odds ratio (OR) 2·93, 95% confidence interval (CI) 2·51–3·42, P < 0·001] and inpatient hospital treatment (OR 1·63, 95% CI 1·38–1·93, P < 0·001). By contrast, scalp involvement was not a significant predictor.

Conclusions:
Patients with psoriasis seen by dermatologists and those in patient advocacy groups show clinical indicators of PsA, the most predictive being nail disease. In practice, a comprehensive assessment of clinical findings associated with PsA is needed.

The University of California, Irvine may have found a new way of tackling psoriasis by discovering that a gene called grainyhead, known to be important in epidermal development and wound healing triggers a repair pathway for psoriasis lesions.

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A UC Irvine-led study has revealed the underlying genetic factors that help repair skin lesions caused by psoriasis, which could engender new methods of controlling the lingering condition.


Dr. Bogi Andersen, professor of biological chemistry and endocrinology at UCI, and colleagues discovered that a gene called grainyhead – known to be important in epidermal development and wound healing – triggers a repair pathway for psoriasis lesions. Conversely, they found that deletion of this gene increased the severity and longevity of the disfiguring patches.

“Our research suggests that targeting this mechanism of healing may lead to pharmaceutical products that limit the itchy, painful lesions all psoriasis sufferers must endure,” Andersen said.

The researchers learned that in psoriasis a compound called grainyhead-like 3 – which binds to DNA to control the rate of transcription of genetic information from DNA to messenger RNA – orchestrates the activation of an epidermal repair pathway. (The grainyhead gene was initially discovered in fruit flies, where it’s important for wound healing.)

They also found it easier to induce psoriasis-like lesions in mice lacking the GRHL3 gene. Furthermore, these lesions did not resolve properly and persisted even in the face of active immune suppression treatments currently being studied for the disease.

“Our study indicates that an evolutionarily ancient epidermal repair pathway is activated in psoriasis lesions and that this pathway suppresses disease severity and helps heal the lesions,” Andersen said. “We speculate that abnormalities in this pathway might contribute to disease severity and that in the future this mechanism could be targeted to help treat psoriasis.”

My new dermatologist recommend I start with Stelara treatments. I have it a patch around my bellybutton, behind, scalp and a starting with a small spot on my face. I am concerned with the health risks. I am a 20 year old male college student. Very self conscious about my looks. Not sure what to do. Scared of the side effects. Any advice would be great.

This study looked at the efficacy and safety of Stelara (ustekinumab) (UST) treatment in elderly patients with psoriasis, and suggests it is the preferable agent for the elderly.

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The ratio of the elderly among psoriasis patients has been increasing. However, satisfactory long-term management of psoriasis for the elderly is challenging because of the more frequent presence of comorbidities, and the higher risk of adverse events from systemic therapeutic agents than younger patients.

The use of ustekinumab (UST) appears to be an appropriate systemic treatment because it is considered less likely to cause adverse events than other systemic treatments, as well as necessitating fewer hospital visits.

Our retrospective study aimed to evaluate the efficacy and safety profile of UST in elderly patients with psoriasis. The study included 24 patients aged over 65 years (range, 65–88 years; mean, 73.1 years) with moderate to severe plaque psoriasis with impaired quality of life.

Efficacy and safety were assessed over a 1-year period using the Psoriasis Area and Severity Index (PASI) and the Dermatology Live Quality Index (DLQI).

The efficacy was evaluated by the proportion of subjects who achieved ≥75% reduction in PASI score (PASI 75). PASI 75 responses were 56.5% at week 16, 59.1% at week 28, and 60.0% at week 52.

None of the patients developed any serious infection during the 1-year treatment. The mean DLQI score at weeks 0, 16, 28, and 52 was 7.8 ± 6.0, 2.5 ± 3.4, 1.4 ± 1.7, and 1.2 ± 1.7, respectively.

UST showed sufficient efficacy for elderly patients with psoriasis without any serious infection over the 1-year treatment. Our results suggest that UST is the preferable agent for the treatment of elderly patients with psoriasis.

None of us like visiting our doctor but getting early diagnoses can pay off in the long run, this study looked at psoriasis patients getting a diagnoses of psoriatic arthritis (PsA) it suggests it may not be a good idea to put off a proper diagnoses longer than 6 months.

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Objectives:
To investigate the demographic and clinical characteristics contributing to the delay from symptom onset to the first visit to a rheumatologist; to compare clinical, radiographic and patient-reported outcome measures of those who saw a rheumatologist early in their disease course with those who were diagnosed later.

Methods:
All psoriatic arthritis (PsA) patients, fulfilling CASPAR criteria, with an average disease duration of >10 years were invited for detailed clinical evaluation. The total lag time from symptom onset to their first rheumatological encounter was studied. The data were extracted from the referral letters and medical records. Patients were classified as early consulters or late consulters depending on whether they were seen by a rheumatologist within or beyond 6 months of symptom onset.

Results:
283 PsA patients were studied. Median lag time from the disease onset to the first rheumatological assessment of the cohort was 1.00 years (IQR 0.5–2). 30% (n=86), 53% (n=149) and 71% (n=202) of the cohort were seen by a rheumatologist within 6 months, 1 and 2 years of symptom onset, respectively. PsA patients with low education status (OR 2.09, p=0.02) and Body Mass Index (OR 0.92, p=0.01) were significantly more likely to have a diagnostic delay of >2 years. On multiple stepwise regression analysis, the model predicted significant association of late consulters with the development of peripheral joint erosions (OR 4.25, p=0.001) and worse Health Assessment Questionnaire scores (OR 2.2, p=0.004).

Conclusions:
Even a 6-month delay from symptom onset to the first visit with a rheumatologist contributes to the development of peripheral joint erosions and worse long-term physical function.