This study looked at bone erosion in patients with psoriatic arthritis.

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Objective:
Psoriatic arthritis (PsA) has been recognized as a severe erosive disease. However, some patients do not develop erosions. We aimed to determine the prevalence, characteristics, and predictors of erosion-free patients (EFP) as compared with erosion-present patients (EPP) among patients with PsA followed prospectively.

Methods:
This is a retrospective analysis conducted on patients from the Toronto PsA cohort. Patients with at least 10 years of followup and radiographs were analyzed. Radiographs were scored with the modified Steinbrocker method. Baseline (first visit to clinic) characteristics were used to predict the development of erosions with logistic regression models. To examine the effect of time-varying covariates, Cox regression models were fit for the time to development of erosions from baseline.

Results:
Among 290 patients, 12.4% were EFP and 87.6% were EPP over the study period. The mean time to development of erosion in the EPP over the course of followup was 6.8 ± 6.1 years. EFP were diagnosed with psoriasis at a younger age compared with EPP. In both models, actively inflamed joints and clinically damaged joints were predictive of the development of erosion, whereas a longer duration of psoriasis at baseline decreased the odds of developing erosion. EPP had a higher percentage of unemployment as compared with EFP at baseline and followup visits.

Conclusion:
Among patients with PsA followed for at least 10 years, 12.4% never develop erosions. The clinical and radiographic findings can ultimately assist in the stratification of a patient’s prognosis regarding the development of erosions.

This Danish cohort study looked at the risk of Abdominal aortic aneurysm (AAA) in psoriasis patients and suggests that further investigations are needed.

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Objective:
Abdominal aortic aneurysm (AAA) is a complex multifactorial disease associated with a high morbidity and mortality. Increased inflammation including T-helper 17 cell–mediated effects has been implicated in AAA pathogenesis. Psoriasis is considered to be a T-helper 17-driven chronic inflammatory disease and in view of potentially overlapping inflammatory mechanisms, we investigated the risk of AAA in patients with psoriasis in a nationwide cohort.

Approach and Results:
The study comprised all Danish residents aged ≥18 years followed up from January 1, 1997, until diagnosis of AAA, December 31, 2011, migration or death. Information on comorbidity, concomitant medication, and socioeconomic status was identified by individual-level linkage of administrative registers. Incidence rates for AAA were calculated and incidence rate ratios adjusted for age, sex, comorbidity, medications, socioeconomic status, and smoking were estimated in Poisson regression models. A total of 5 495  203 subjects were eligible for analysis. During the study period, we identified 59 423 patients with mild psoriasis and 11 566 patients with severe psoriasis. The overall incidence rates of AAA were 3.72, 7.30, and 9.87 per 10 000 person-years for the reference population (23 696 cases), mild psoriasis (240 cases), and severe psoriasis (50 cases), respectively. The corresponding adjusted incidence rate ratios for AAA were increased in patients with psoriasis with incidence rate ratios of 1.20 (95% confidence interval, 1.03–1.39) and 1.67 (confidence interval, 1.21–2.32) for subjects with mild and severe disease, respectively.

Conclusions:
In a nationwide cohort, psoriasis was associated with a disease severity-dependent increased risk of AAA. The mechanisms and consequences of this novel finding require further investigation.

Hello all,

I have severe PsO on my knees, back and elbow. I'm looking for natural treatments. Can someone advise me?

Regards,

Mike

This is a small abstract from an early view of a discussion that suggests Oestrogen could be a potential therapeutic option for psoriasis.

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Abstract:

Majority of female patients show improvement of psoriasis during pregnancy. This is demonstrated to be correlated with high levels of oestrogen.

Even in male patient, oestrogen level is inversely correlated with the severity of psoriasis. However, a minority of female psoriatic patients still experience worsening during pregnancy.

Oestrogen might improve psoriasis by suppressing the T-cell immune response, reducing the keratinocyte (KC) cytokine and chemokine production, restoring the balance of redox and enhancing the skin barrier. However, it might worsen the disease by stimulating KC proliferation and promoting angiogenesis.

This complex role of oestrogen in the pathogenesis of psoriasis might explain why the two opposite effects of pregnancy coexist. Data shows that the number of improving patients with psoriasis in pregnancy is double the number of the worsening patients, suggesting that oestrogen may be potentially useful in the treatment of psoriasis.

However, oestrogen is not considered suitable as a long-term treatment subject to negative side-effects. This review discusses current studies on taking selective oestrogen receptor mediators as a novel potential therapeutic option for psoriasis.

Hello everyone! My name is Shane and I am new to this forum. 

I am actually very happy to have found this website, reading through many posts (being the huge researcher that I am), it seems a comforting place when psoriasis can be quite a physiological condition. 

I first had Guttate back in 2012, and it did what it does - appears, stops you from going out much, gets you down, then disappears. However, in about October last year, I started having a couple of patches of dry red skin, then more and more. I was origionally diagnosed with Pityriasis Rosea, another temporary condition. However, after it lasting longer than a few weeks, I paid to see a dermatologist. He diagnosed me with plaque psoriasis. He then told me to google "BAD psoriasis methotrexate" and click on the first link. I am going back to him on May 4th, for blood tests and to start treatment. However, after reading on different websites including this one, it has made me very wary about MTX and I have more questions than answers I can find, so, I would really appreciate some help and advice. 

I am going on two holidays, one with the girlfriend May 17th and one with a group of friends June 24th, these are my main concerns to get it to at least stop looking so angry. I am currently using coal tar, salt baths and moisturiser as this helped with the Guttate. 

•The doctor told me I can drink small amounts of alcohol only. Is this because of it affecting the liver, or low tolerance levels or both?

•How long do they start to take affect?

•Due to being 27, kids are a future thought, what affect have people had stopping after a decent period of time on MTX?  

•I seem to have found more negative stories than good. Can anyone actually recommend MTX or should I push for something else?

As I said earlier, I would really appreciate the help, I want to have a clear plan in my head when I go back to see the doctor in 3 weeks time. Thank you!

This study was To evaluate the efficacy of clazakizumab an interleukin (IL)-6 blocker in patients with psoriatic arthritis.

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Objective:
To evaluate the efficacy of clazakizumab, a monoclonal antibody with high affinity and specificity for the interleukin (IL)-6 cytokine, in psoriatic arthritis (PsA).

Methods:
In this randomized, double-blind, placebo-controlled, dose-ranging study (NCT01490450), patients with active PsA and an inadequate response to non-steroidal anti-inflammatory drugs were randomized (1:1:1:1) to subcutaneous placebo or clazakizumab 25 mg, 100 mg, or 200 mg every 4 weeks, ± methotrexate. The primary endpoint was American College of Rheumatology (ACR) 20 response rate at week 16, with secondary efficacy endpoints at weeks 16 and 24.

Results:
A total of 165 patients were randomized. At week 16, ACR20 response was significantly higher with clazakizumab 100 mg versus placebo (52.4% vs 29.3%; P=0.039). ACR20 responses at week 16 were 46.3% with clazakizumab 25 mg (P=0.101 vs placebo) and 39.0% with clazakizumab 200 mg (P=0.178 vs placebo). ACR50/ACR70 response rates were numerically higher with clazakizumab versus placebo at weeks 16 and 24. Compared with placebo, clazakizumab treatment significantly improved musculoskeletal manifestations (joint signs and symptoms, enthesitis, and dactylitis), with minimal improvements in skin, without clear evidence of a dose response. Clazakizumab was well tolerated.

Conclusions:
This is the first clinical trial of an IL-6-targeted therapy in PsA. Clazakizumab may be an effective treatment option for musculoskeletal aspects of PsA, but further studies are required to confirm the appropriate dose due to the lack of dose response in this study. The safety profile was consistent with the pharmacology of IL-6 blockade and prior clinical experience with this antibody in rheumatoid arthritis.

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I have my little purple booklet and now my consultant tells me that my booklet should go everywhere with me incase I have an accident then medical professionals can know that I have a potentially compromised immune system.

First thing is, do I need to take it everywhere?

How "compromised" is my immune system?

This thread was going to be titled whats purple and in my pants and goes everywhere with me but!

So this is my first thread. I started it in pingu's "Starting MTX" and now I'm moving it here:

Hi guys,

First of all, a BIG thanks to pingu for this user guide, I just finished reading it 

I started mtx last Thursday, 15 mg/week (5 mg/2 pills every 8 hours). On Friday I felt like a zombie, I had a terrible headache, and I threw up several times. Now, everything is good, and I look forward for the next Thursday. Tomorrow I will have my first set of blood tests 
I am covered with P about 3-4%, I hope to see big improvements soon. 
I will keep you updated.

M

I'm posting this thread here, I hope I have it in the right place. If not, please let me know.

For anyone who has read my journal, you'll know I was recently diagnosed with IGA nephropathy. (For those who don't know what this is, it's basically a build up of protein on my kidneys that could possibly affect their function down the line)

While talking to the nephrologist, he mentioned that there was link between psoriasis and IGA N, that psoriasis can trigger protein changes in the urine. Has anyone else ever heard of this? Is there anyone else who has had protein abnormalities in their urine samples?

I would like to say firstly that this is my personal experience and may or may not be indicative of other peoples experiences.

I have had psoriasis for about 35 to 40 years I am now 49 so most of my life. Admittedly in that time the treatments and the efficacy of those treatments has changed. However I want to comment on how to deal with your GP and or consultant.

When I first got psoriasis I was referred to a consultant and went through many different creams. My parents had psoriasis so it was not new but as a child really difficult.

I went through all sort of creams but was never prescribed UVA treatment.

When we discovered a cream that was reasonably effective I was left on that for a very many years. Basically I was a statistic now. A psoriasis sufferer. A sufferer of a chronic illness without a cure. Simply a cost. I received repeat prescriptions at the drop of a hat. At the end of the day I was a patient on my GPs register and he kept me "reasonably content" with repeat prescriptions.

This was not one GP but several as you can imagine in 35 years I moved a few times and every single one was the same. register get a prescription and never see them with reference to my psoriasis again

I discovered sunlight helped so sometimes went on sunbeds and whenever we had sun got some respite there. I was alone. There was no help. OK there were secret remedies guaranteed to cure me on the internet and special diets of knitted oats cooked with the tears of baby unicorns sprinkled with moon dust but they were expensive and dare I say probably not worth it.

In all that time my GP was quite content to have me on steroid creams long term, never calling me in for a consult to see how it was going, offering other therapies or a referral.

It was only when I investigated a little as my psoriasis was getting a little worse and I discovered many new treatments were available.

Now here is the point.

Do not take what your GP or consultant say as gospel, at the end of the day YOU are a CUSTOMER and deserve certain things. Make sure they understand you and your expectations and understand if they are firstly realistic and secondly achievable.

NO that does not mean you always get your own way but certainly I discovered my GP actually knew very little about what was available and I had to request a referral. So first thing is get your referral. Then work with your consultant. You have a lifestyle so some treatments may not be right for you. Some may disagree with you. You also need to give the treatment time.

Bare in mind that this is cost driven, the NHS is a business and somewhere someone has to pay even if its through insurance. If you were paying for your own therapy you wouldn't necessarily go out and get the most expensive when something at a tenth of the cost was effective. Well certainly that's how the NHS works, it works well most of the time. To a degree I feel it is keep the masses at bay with lotions and creams at their GPs. Its only when you ask that you get something a little better. Knowing WHAT to ask is also key.

Educate yourself but be reasonable. You can't expect to go on the very latest high cost treatments if you have not tried the lower cost alternatives. Stick to your guns about getting the right treatment that works for you and your lifestyle, educate yourself and ask questions of your consultant and in here.

It's your life and your skin, work with your consultant. I certainly have been treated a lot better following the little knowledge I have gained through more research. After 4 weeks on MTX I was pretty clear. I was delighted but felt I was a little cheated as I could have been offered the treatment sooner. I had to aks for it though because I would still be on repeat prescriptions if I hadn't.

Hi, I have had PsA for a few years now, and have progressed through a number of treatments such as Mtx (oral and injection), sulfalazine, Enbrel, symponi and now Stelera. I have had bad reactions to these, and I seem to be allergic to most of them.

Over the last 6 months I have developed painful eyes, with eye lids which are swollen, lack of peripheral vision and sensitivity to light.

I have seen an ophthalmologist who has says I either have iritis or euvitis. I have had an MRI today on my eyes, and will see the specialist again soon..

When I saw the ophthalmologist he informed me that a number of people with auto immune diseases, including PsA are prone to these problems.

I was wondering if any other forum members have had similar problems, and how the symptoms have progressed.

Paul

Hi , I was diagnosed October 2015. I am waiting to see a specialist Dermatologist In May.
I am currently using Dobovet Gel and Dermovate cream and Ointment. Would welcome any tips or advice. I have not had definitive diagnosis but due to my symptoms suspect I have Pustular  as only on my palms, soles and scalp. It itches like crazy and is painful.

This study looked at GSK2586184 a JAK1 inhibitor for the treatment of psoriasis.

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Background:
GSK2586184 is a selective oral Janus kinase (JAK)1 inhibitor being evaluated as a treatment for moderate-to-severe plaque-type psoriasis.

Objectives:
To assess the relationship between dose of GSK2586184 and clinical response, primarily by the Psoriasis Area Severity Index (PASI).

Methods:
Sixty patients with moderate-to-severe plaque psoriasis were randomized to cohort A: 100 mg, 200 mg or 400 mg GSK2586184 twice daily or placebo; and eight were randomized to open-label cohort B, a small exploratory cohort treated with 400 mg GSK2586184 twice daily, to explore differential gene expression.

Results:
At week 12, a 75% reduction in PASI (PASI 75) response rates in the intent-to-treat population were 0% in the placebo group compared with 13%, 25% and 57% in the 100 mg, 200 mg and 400 mg GSK2586184 twice-daily groups, respectively. Increases in the proportion of PASI 75 responses were seen across all dose levels by week 4. Improvement in itch and quality of life were observed at all doses relative to placebo with the greatest improvement seen in the 400-mg dose group. Overall, the incidence of adverse events (AEs) was similar across treatment groups, and no relationship between frequency of AE and GSK2586184 dose was identified. Differential gene expression was observed in involved and uninvolved skin at baseline and in involved skin after 2 weeks of treatment with GSK2586184.

Conclusions:
Our study demonstrates that 12 weeks of treatment with GSK2586184 resulted in clinical improvement and was generally well tolerated in patients with moderate-to-severe plaque-type psoriasis.

This study looked at the relationship between the serum total bilirubin and inflammation in patients with psoriasis.

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Background:
Psoriasis is a chronic and recurrent inflammatory skin disease. Previous studies have shown that bilirubin has anti-inflammation and antioxidant effects. However, the various roles of bilirubin in psoriasis patients are still unclear.

Objective:
To investigate the serum total bilirubin (TB) level in the individuals with psoriasis vulgaris and further evaluate the relationship between serum TB concentration and C-reactive protein (CRP) to clarify the effect of bilirubin on inflammation.

Methods:
A total of 214 patients with psoriasis vulgaris and 165 age- and gender-matched healthy control subjects were recruited. The peripheral leukocyte count (white blood cell, WBC) and differential, serum biochemical and immunologic indexes including serum TB, immunoglobulin (Ig) G, IgA, IgM, complement C3 and C4, as well as serum CRP concentrations were measured.

Results:
Results showed that the serum TB level decreased significantly and peripheral WBC, neutrophil, and serum CRP concentrations increased significantly in patients with psoriasis vulgaris. Meanwhile, the serum CRP was negatively correlated with serum TB levels but positively correlated with peripheral WBC and the Psoriasis Area and Severity Index (PASI). Logistic regression analysis showed that the serum TB was a protective factor for psoriasis vulgaris.

Conclusion:
The present study suggests that lower serum TB is associated with the enhancement of the inflammatory response in psoriasis vulgaris. Therefore, lower serum TB has a prognostic significance for worsening psoriasis vulgaris. Bilirubin may play a crucial role in inflammation by contributing to the inhibition of the inflammatory response.

I've had Psoriasis and psoriatic arthritis for several years. I was on Humira for the last two years, and recently switched to Stelara. The symptom I am having has been consistent with both medications. It could be really common, I just don't know. That's why I'm here    My knees are 100% clear. However, if I kneel down, or if the skin rubs on the lower part of the kneecap in a certain way, it feels like I'm rubbing an open wound. It is super painful. It's not a "sore" feeling, but more like a burning. Its like I have a sore under my clear skin. I really hope somebody knows what in talking about, and if there's any known way to get relief. 

Thanks!

Hi Members 
I have  just  gone  through a relapse  ( first  time  ) .My  first  year  of  it  .Im 67  Things were  going good  my back all cleared  , arms  . Just  some old  stuff  on my  legs  , then  pow  bumps  rash  on  lower  back and  buttocks  .Keep thinking  what  brought this  on ? .Food ,red wine  , a few  shrimp ?
I'm stumped  its  my  first  year /Any  thoughts appreciated  .Is this  a  typical  .....

Inflectra a biosimilar of Remicade has been given FDA approval for psoriasis and psoriatic arthritis.

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The U.S. Food and Drug Administration today approved Inflectra (infliximab-dyyb) for multiple indications. Inflectra is administered by intravenous infusion. Inflectra is biosimilar to Janssen Biotech, Inc.’s Remicade (infliximab), which was originally licensed in 1998.

The FDA’s approval of Inflectra is based on review of evidence that included structural and functional characterization, animal study data, human pharmacokinetic and pharmacodynamics data, clinical immunogenicity data and other clinical safety and effectiveness data that demonstrates Inflectra is biosimilar to Remicade. Inflectra has been approved as biosimilar, not as an interchangeable product.

The most common expected side effects of Inflectra include respiratory infections, such as sinus infections and sore throat, headache, coughing and stomach pain. Infusion reactions can happen up to two hours after an infusion. Symptoms of infusion reactions may include fever, chills, chest pain, low blood pressure or high blood pressure, shortness of breath, rash and itching.  

Inflectra contains a Boxed Warning to alert health care professionals and patients about an increased risk of serious infections leading to hospitalization or death, including tuberculosis, bacterial sepsis, invasive fungal infections (such as histoplasmosis) and others. The Boxed Warning also notes that lymphoma and other malignancies, some fatal, have been reported in children and adolescent patients treated with tumor necrosis factor blockers, including infliximab products such as Inflectra. Other serious side effects may include liver injury, blood problems, lupus-like syndrome, psoriasis, and in rare cases nervous system disorders. The drug must be dispensed with a patient Medication Guide that describes important information about its uses and risks.

Inflectra is manufactured by Celltrion, Inc, based in Yeonsu-gu, Incheon, Republic of Korea, for Hospira, of Lake Forest, Illinois.

Just been reading about tests that went on a few years back where they injected bee venom into plaques with good results, has anyone else heard of this?!

This study of Baricitinib is a randomized phase 2b trial for psoriasis.

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Background:
Plaque psoriasis is a chronic and often debilitating skin disorder and proinflammatory cytokines are known to play a key role in the disease process.

Objectives:
To evaluate the safety and efficacy of baricitinib, an oral Janus kinase (JAK) 1/JAK2 inhibitor, in patients with moderate-to-severe psoriasis in a randomized, double-blind, placebo-controlled, dose-ranging phase 2b study.

Methods:
Patients were randomized (n = 271) to receive placebo or oral baricitinib at 2, 4, 8 or 10 mg once daily for 12 weeks (Part A). Dose adjustment for 12 additional weeks was based on percentage improvement in the Psoriasis Area and Severity Index (PASI) score. The primary end point was Psoriasis Area and Severity Index (PASI) 75% (PASI-75) at 12 weeks for North American patients (n = 238); secondary end points were safety and efficacy measures in the entire population.

Results:
At week 12, more North American patients in the 8-mg (43%) and 10-mg (54%) baricitinib groups than in placebo group (17%; P < 0·05) achieved PASI-75. All baricitinib-treated groups had greater mean changes from baseline in their PASI scores (P < 0·05) at 12 weeks and (except 2 mg) had higher rates of PASI-50 than the placebo group; statistically significant PASI-90 responses were achieved in the 8-mg and 10-mg groups at 8 and 12 weeks. More than 81% of PASI-75 responders maintained their scores through 24 weeks. During Part A, study discontinuations due to adverse events (AEs) were 0%, 0%, 2·8%, 6·3% and 5·8% and treatment-emergent AE rates were 44%, 50%, 47%, 58% and 64% for placebo and 2-, 4-, 8- and 10-mg baricitinib groups, respectively. No opportunistic infections were observed in any treatment group. Dose-dependent changes in laboratory values were observed.

Conclusions:
Patients with moderate-to-severe psoriasis treated with baricitinib for 12 weeks achieved significant improvements in PASI-75.

Pfizer have announced top-line results from its first Phase 3 study investigating tofacitinib for the treatment of psoriatic arthritis.

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Pfizer Inc. announced today top-line results from its first Phase 3 study investigating tofacitinib for the treatment of psoriatic arthritis, Oral Psoriatic Arthritis triaL (OPAL) Broaden. This study evaluated the efficacy and safety of tofacitinib 5 mg and 10 mg twice daily (BID) in adult patients with active psoriatic arthritis (PsA) who had an inadequate response to at least one conventional synthetic disease-modifying antirheumatic drug (csDMARD) and who were tumor necrosis factor inhibitor (TNFi)-naïve. OPAL Broaden met its primary efficacy endpoints demonstrating that both tofacitinib 5 mg BID and 10 mg BID were superior to treatment with placebo at 3 months as measured by American College of Rheumatology 20 (ACR20) response and Health Assessment Questionnaire Disability Index (HAQ-DI) score.

“As a chronic inflammatory disease, psoriatic arthritis can have a significant impact on a person’s daily life. Despite available therapies, including biologic and oral treatments, there remains an unmet need for additional options,” said Michael Corbo, Category Development Lead, Inflammation & Immunology, Pfizer Global Innovative Pharmaceuticals Business. “The results seen in the OPAL Broaden study are encouraging as they suggest that tofacitinib may have the potential to offer an additional effective oral option for patients living with psoriatic arthritis. We look forward to sharing detailed results at a future scientific meeting.”

OPAL Broaden is a Phase 3 placebo-controlled study that investigated the efficacy and safety of tofacitinib 5 mg and 10 mg BID in treating the signs and symptoms of PsA, and improvement in physical function in patients with active PsA who had an inadequate response to at least one csDMARD due to lack of efficacy or adverse event, and who were TNFi-naive. Patients enrolled in the study were required to be on one csDMARD as background therapy and continue that dose for the duration of the study. The study also included adalimumab 40 mg subcutaneously administered every 2 weeks (q2 wk) as an active control arm. However, this study was not powered for non-inferiority or superiority comparisons between tofacitinib and adalimumab. A total of 422 patients were randomized in a 2:2:2:1:1 ratio to the following treatment arms: tofacitinib 5 mg BID, tofacitinib 10 mg BID, adalimumab 40 mg q2 wk, placebo to tofacitinib 5 mg BID and placebo to tofacitinib 10 mg BID treatment sequences.

Overall safety findings in this study were consistent with those observed in the broader rheumatology clinical development program for tofacitinib. All treatment groups had similar rates of treatment-emergent adverse events, serious adverse events, and discontinuations due to adverse events over the 12-month duration of the study. Serious adverse events observed were similar to those seen in other clinical development programs for tofacitinib.