Hi everyone,

I'm Amy and have had Psoriasis for 2/3 of my life and have just about reached my limit! It started as small patches on my knees and elbows and has gotten worse as I have gotten older. As it stands it covers in excess of 70% of my body and I have finally accepted that steriod cream and moisturiser isnt gonna fix it.

I have had my first consult with a dermatologist and been advised that my options are Methotrexate or Ciclosporin in the first instance and that within the space of a few months my dermatologist is pretty sure i will need to be on biologicals.

I guess im relieved that there is another way and that I do have options but at the same time the possible side effects scare the hell out of me.

My husband is great and has been nothing but supportive but he just heard I can take a pill and it will get better - my next appointment is tomorrow and my head is buzzing with questions.

Augh!!!!

Anyway i figured you guys would understnad where im at right now!

Just though i'd share what I use to combat my scalp psoriasis.

I've developed a routine for my scalp which keeps it in check. I do this most days, or just when I feel like it needs it (I try not to overdo it if I can help it).

1. Take a shower and use Capasal medicated shampoo. It contains Salyic acid and coal tar extracts which has proved very beneficial for me.

2. Make sure I wait for my hair to thoroughly dry before I try applying anything.

3. Apply either E45 cream to keep hydrated or Bio-oil for the same effect (again, I find that alternating treatment can be beneficial).

4. Leave on for as long as I can bear it/ keep applying throughout the day. I say as long as I can bear it as I find that once i've applied something like bio-oil it can make it itchy after a while and it drives me mad

5. Wash hair again with normal shampoo. Personally I use a coconut based shampoo because coconut oil can be good for the skin.. but I have no actual basis for this, I just thought it couldn't hurt

That's pretty much it. It's not complicated, it's more about getting into a routine to keep it under wraps.

Also, I make a real effort and a point of removing plaque when I find it. Letting it build up is never good and it only compounds the situation.

Hope it helps someone!

Sam.

Fred I know we don't have links to other sites, but when I just tried to post a thread with a link already in it said I can't post live links. the link was already live as you had posted it and it was a link to another thread. but i can't post a link to another thread on the forum.

This is a study published by Pediatric Rheumatology. The aim of the study was to determine the long-term outcome and clinical course of patients with juvenile psoriatic arthritis (JPsA) and to define subgroups of JPsA.

Background:
Following the introduction of the ILAR criteria for juvenile idiopathic arthritis, juvenile psoriatic arthritis (JPsA) has become a better recognized category within the inflammatory arthritides of childhood. There are fewer reports describing the characteristics and long-term outcome of patients with JPsA than other subtypes of JIA.

The aim of our study was to determine the long-term outcome and clinical course of patients with juvenile psoriatic arthritis (JPsA) and to define subgroups of JPsA.

Methods:
Clinical records of all patients meeting criteria for JPsA were reviewed and divided into 4 groups depending on their clinical features and onset type. Patient characteristics and clinical features at onset and during follow-up were determined.

Results:
The cohort consisted of 119 patients: 65 with oligoarticular-onset (55%; persistent 44 and extended 21), 34 (29%) with RF(-) and 4 (3%) RF(+) polyarticular and 16 (13%) enthesitis-related arthritis (ERA). At diagnosis patients with ERA were oldest and more commonly male (p=0.001 and =0.01 respectively). Patients with a polyarticular course had more involvement of small joints of the hands and wrist when compared to patients with persistent oligoarticular and ERA (p<0.001) while patients with ERA had more hip and sacroiliac arthritis (p<0.001 for both). Nail changes were seen in 66 patients (57%) and were associated with DIP involvement (p=0.0034).

Outcome:
Time to first inactive disease on, but not off, therapy was significantly longer among patients with polyarticular course when compared to oligoarticular and ERA (p=0.016 and p=0.48 respectively). Patients with polyarticular course more frequently had contractures during follow-up than other groups (p=0.01)

Conclusion:
The long-term outcome of with JPsA was generally good. Patients with JPsA did not appear to form distinct sub-group of patients but rather resembled JIA patients with onset types without psoriasis.

Source: NO LINKS ALLOWED

Evening all, still new to forum chatting but here goes

I have been prescribed exorex tar lotion and dovobet gel in the past and these haven't really worked for me

My pseriosis come up in round patches which have gradually got larger. It is quite stubborn and it only appeared to clear up a little after spending a week at the Red Sea.
Obviously I don't really want to move to Egypt but I would love to find a gel or lotion which you guys believe really does make a difference

Hi my name is Adam, I have suffered with psoriasis for years now, never been part of a forum/chat group but decided to join this forum in hope of getting some advice from other sufferers. My psoriasis seems to be getting worse in all areas. Look forward to chatting to you guys.

Aloha,

Just searched google to see if there was a forum for Psorisasis so I thought i'd say hello!

I devoped scalp psoriasis about 4 years ago when I was 19. The area was initially about the size of a fingernail and has now spread to the entire back of my head. I didn't know what it was and put off going to the doctor for ages. Once I got it diagnosed it was easier to find treatment and i've managed to calm it down with a variety of lotions and shampoos

It can be embarassing when i'm out as it can flake and make it look like I have bad dandruff. I don't tell anyone about it because I doubt they'd understand. Recently i've been attacking it with medicated shampoo, E45 cream, anti itch E45 cream, Bio-oil and whatever else I can lay my hands on! I'm glad to report that it's calmed down and is the best it's been for years.

It's caused problems with relationships, it's unsighly and basically a royal pain in the arse! I just wanted to find some people that could relate to me really.

All the best,

Sam.

Hi My name is Rohan

Ive suffered for many years with Psoriasis...

My condition was limited to my legs intially and was very bad...in the last 3 years its moved to my upper body although not so bad there.

I have been through ever conventional western treatment the only ones left are lethal drugs such as 'Methotrexate'. The only effective treatment I had was UV but that was a temporary fix.

I found Chinese herbal medicine effective for a few months but the herbal concoctions had to be boiled twice a day and they smelt pretty bad!...drinking them were even harder...but you know what lengths we go to in our quest for relief from this burden we bear!

In the last 3 years I have been going to India for Ayurvedic treatment ...which almost totally clear my condition for periods of up to 6 months. These treatments consist of having your body purified through diet restriction internal medicines and twice daily massages and other external treatments. You have to stay in a clinic for 2 weeks and it can be expensive and torturous. The last time I went was around 14 months ago and I dont have time to go back.

I did have some medicine I was taking which help to control it but its run out now!.

I had almost a year of feeling human again and began to forget the pain and sorrow this illness brings!...recently my legs have got really bad and my upper body is rapidly getting worse...

Ive joined this forum because like anything you have to suffer directly to understand the trauma an illness can cause....and after a year of normality in my life Ive dropped down to earth with a bang!

Will this journey ever end ?....if not I need company to ease the pain!

Hi Everyone
My name is Anthony and this is my first time posting on here, its nice to meet you all.
I have had psoriasis for about 6 years but its been particularly bad this past few months and I thought I would start being active on forums in order to find people who have similar issues as me
I saw a doctor and he reccomended I go on methotrexate but at this time I knew little about it. I did some research on its effects and have decided not to try it until I have tried more natural solutions to see if that will make a difference.
I also thought it would be good to document it so I have started a blog where I am going to post pictures of my progress and can chat to anyone who is struggling from psoriasis too. I dont know anyone personally who has it so I often struggle with having anyone to talk to
I would be very grateful of anyone who wants to follow my blog and if it makes a difference hopefully it can inspire others to try what I am going to try

Thanks all!!

We all know the benefits of sea water for psoriasis, especially the Dead Sea salt and there is lots of information. But what about salt intake via our diet, could salt be bad for psoriasis?

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#1 Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1.
TH17 cells (interleukin-17 (IL-17)-producing helper T cells) are highly proinflammatory cells that are critical for clearing extracellular pathogens and for inducing multiple autoimmune diseases. IL-23 has a critical role in stabilizing and reinforcing the TH17 phenotype by increasing expression of IL-23 receptor (IL-23R) and endowing TH17 cells with pathogenic effector functions. However, the precise molecular mechanism by which IL-23 sustains the TH17 response and induces pathogenic effector functions has not been elucidated. Here we used transcriptional profiling of developing TH17 cells to construct a model of their signalling network and nominate major nodes that regulate TH17 development. We identified serum glucocorticoid kinase 1 (SGK1), a serine/threonine kinase, as an essential node downstream of IL-23 signalling. SGK1 is critical for regulating IL-23R expression and stabilizing the TH17 cell phenotype by deactivation of mouse Foxo1, a direct repressor of IL-23R expression. SGK1 has been shown to govern Na+ transport and salt (NaCl) homeostasis in other cells. We show here that a modest increase in salt concentration induces SGK1 expression, promotes IL-23R expression and enhances TH17 cell differentiation in vitro and in vivo, accelerating the development of autoimmunity. Loss of SGK1 abrogated Na+-mediated TH17 differentiation in an IL-23-dependent manner. These data demonstrate that SGK1 has a critical role in the induction of pathogenic TH17 cells and provide a molecular insight into a mechanism by which an environmental factor such as a high salt diet triggers TH17 development and promotes tissue inflammation.

#2Dynamic regulatory network controlling TH17 cell differentiation.
Despite their importance, the molecular circuits that control the differentiation of naive T cells remain largely unknown. Recent studies that reconstructed regulatory networks in mammalian cells have focused on short-term responses and relied on perturbation-based approaches that cannot be readily applied to primary T cells. Here we combine transcriptional profiling at high temporal resolution, novel computational algorithms, and innovative nanowire-based perturbation tools to systematically derive and experimentally validate a model of the dynamic regulatory network that controls the differentiation of mouse TH17 cells, a proinflammatory T-cell subset that has been implicated in the pathogenesis of multiple autoimmune diseases. The TH17 transcriptional network consists of two self-reinforcing, but mutually antagonistic, modules, with 12 novel regulators, the coupled action of which may be essential for maintaining the balance between TH17 and other CD4+ T-cell subsets. Our study identifies and validates 39 regulatory factors, embeds them within a comprehensive temporal network and reveals its organizational principles; it also highlights novel drug targets for controlling TH17 cell differentiation.

#3Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells.
There has been a marked increase in the incidence of autoimmune diseases in the past half-century. Although the underlying genetic basis of this class of diseases has recently been elucidated, implicating predominantly immune-response genes, changes in environmental factors must ultimately be driving this increase. The newly identified population of interleukin (IL)-17-producing CD4+ helper T cells (TH17 cells) has a pivotal role in autoimmune diseases. Pathogenic IL-23-dependent TH17 cells have been shown to be critical for the development of experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis, and genetic risk factors associated with multiple sclerosis are related to the IL-23–TH17 pathway. However, little is known about the environmental factors that directly influence TH17 cells. Here we show that increased salt (sodium chloride, NaCl) concentrations found locally under physiological conditions in vivo markedly boost the induction of murine and human TH17 cells. High-salt conditions activate the p38/MAPK pathway involving nuclear factor of activated T cells 5 (NFAT5; also called TONEBP) and serum/glucocorticoid-regulated kinase 1 (SGK1) during cytokine-induced TH17 polarization. Gene silencing or chemical inhibition of p38/MAPK, NFAT5 or SGK1 abrogates the high-salt-induced TH17 cell development. The TH17 cells generated under high-salt conditions display a highly pathogenic and stable phenotype characterized by the upregulation of the pro-inflammatory cytokines GM-CSF, TNF-α and IL-2. Moreover, mice fed with a high-salt diet develop a more severe form of EAE, in line with augmented central nervous system infiltrating and peripherally induced antigen-specific TH17 cells. Thus, increased dietary salt intake might represent an environmental risk factor for the development of autoimmune diseases through the induction of pathogenic TH17 cells.

Following on from this post in November 2011 https://psoriasisclub.org/showthread.php?tid=307 Merck have presented findings at the annual meeting of the American Academy of Dermatology (AAD)

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Patients with chronic plaque psoriasis showed significant improvement after 16 weeks of treatment with the humanized monoclonal antibody MK-3222, based on early data from an ongoing randomized, controlled, dose-ranging study of 355 adults. The findings were presented in a late-breaker session at the annual meeting of the American Academy of Dermatology.

The patients were randomized to receive MK-3222 doses of 5 mg, 25 mg, 100 mg, 200 mg, or a placebo, injected subcutaneously at weeks 0 and 4, then every 12 weeks thereafter until week 52. The mean baseline Psoriasis Area and Severity (PASI) index score of the patients was 12, and all patients had greater than 10% body surface area involvement and at least a moderate Physician Global Assessment (PGA) scale score.

Responses at 16 weeks were dose-dependent; PASI 75 responses occurred in 33%, 64%, 66%, 74%, and 4.4% in the 5-mg, 25-mg, 100-mg, 200-mg and placebo groups respectively, said Dr. Kim Papp of Probity Medical Research, Waterloo, Ontario, Canada. PGA responses were 33%, 58%, 62%, 74%, and 2%, respectively. The differences were statistically significant for each dose compared with placebo for both PASI 75 responses and PGA responses.

MK-3222 is a high-affinity humanized anti-IL-23p19 monoclonal antibody that doesn't bind human IL-12 (subunit p40), Dr. Papp said. "We know from results of previous studies that blockade of IL-23 is, in fact, an effective route to treating psoriasis," he said.

Dr. Papp noted that safety signals have been linked with IL-12 blockade, but not with IL-23 blockade, which provides support for further research of this agent.

In this study, MK-3222 was generally safe and well-tolerated, with a low drop-out rate. Adverse events were similar across all treatment groups. Four serious adverse events were reported within the first 16 weeks of treatment, including one case of bacterial arthritis possibly related to treatment, and one death that was unrelated to treatment.

"Those of us who see these patients know that there is an exquisite need for additional therapies," Dr. Papp said. The findings are encouraging, and MK-3222, which is currently in phase III development, "certainly deserves further exploration as a therapy for psoriasis," he said.

Just wanted to share some positive news....

That's me been taking MTX for about 8 -9 months now and I'm still only on 10mg/wk. I've not had to up the dosage any in order to keep my PsA at bay. I had a slight flare a couple of weeks ago but anti-inflammatories and some strong pain killers sorted it out. Apparently the cold had gotten to my joints and caused them to become more inflamed than normal.... One reason to leave frostbitten Scotland for Oz if you ask me.

I've not really been suffering any severe side effects, I have a dry mouth and feel lethargic about a day after taking the MTX but no other nasty surprises. My blood tests are all coming back fine (I'm still having them taken every 4 weeks which is a bit of an inconvenience) and both my GP and Rheumy are very happy.

BUT!!!! Taking the MTX has not done anything or my skin.. in fact it's actually made it worse. I flake a whole lot more and it itches so damned much.... I've never had this problem as I moisturise daily and exfoliate every couple of days....

Thankfully I have been lent a UVB unit from a colleague of my hubby so that I can home treat my skin... Derm don't really want to know now that I am on MTX, they think that it should be treating my skin and only suggest upping the dose (which I am totally against, I'll only increase it when I NEED to for my joints).

I'm hoping to see a difference in my skin soonish.

But, this brought to mind a question I thought of when I first had really bad problems with my PsA. It was just after my skin was cleared with UVB that I started having issues and I wondered if the treatment of the external symptoms had exacerbated the internal ones... Now I am wondering if the reverse could be true... My PsA is being treated so my skin is getting worse..

Anyone else relate to this?

Krissie

Following on from the PALACE study for Apremilast oral treatment for Psoriatic Arthritis. Celgene announce their results for the ESTEEM study on it's use for Psoriasis.

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Celgene International Sàrl, a subsidiary of Celgene Corporation (NASDAQ: CELG) today presented the results from ESTEEM 1, the Company’s first phase III study in psoriasis, at the American Academy of Dermatology annual meeting in Miami, Florida.

The company previously announced statistical significance for the primary and major secondary endpoint of PASI-75 at Week 16 and the Static Physician Global Assessment for patients receiving apremilast in the ESTEEM 1&2 phase III studies. ESTEEM 1&2 are the phase III registrational randomized, placebo-controlled studies evaluating the Company’s oral small-molecule inhibitor of phosphodiesterase-4 (PDE4) in patients with moderate-to-severe chronic plaque psoriasis.

ESTEEM 1, presented today, evaluated efficacy and safety in a range of patients. Approximately one-third of the study population was systemic and/or phototherapy treatment-naïve. Nearly 30 percent of the overall study population had prior biologic therapy, which included biologic-failures.

In the ESTEEM 1 study, a significantly higher percentage of apremilast-treated patients demonstrated PASI-75 at week 16 than did placebo patients (33.1% vs. 5.3%; P<0.0001). Significantly higher PASI-75 scores at week 16 were demonstrated across all patient segments enrolled in this study, including systemic-naïve and biologic-naïve patients receiving apremilast 30 mg BID compared with placebo (38.7% vs. 7.6%; P<0.0001 and 35.8% vs. 5.9%; P<0.0001 respectively). Apremilast demonstrated maintenance of effect over time, as measured by the Mean Percent Change from Baseline in PASI score over 32 weeks, with apremilast demonstrating a 54.9% reduction at week 16 and a 61.9% reduction at week 32.

Statistical significance at week 16 was also demonstrated in the major secondary endpoint, Static Physician Global Assessment (sPGA) of clear or almost clear (P<0.0001), and other key secondary endpoints (change in BSA, Pruritus VAS, DLQI), as well as in assessments of difficult to treat areas (nail and scalp psoriasis).

“I see this as a prime candidate for future management of psoriasis that allows us to treat a range of patients, including more moderate cases earlier on,” said Kristian Reich, M.D., SCIderm Research Institute and Dermatologikum Hamburg, Germany.

The overall safety and tolerability profile was consistent with results from previously reported phase III psoriatic arthritis trials. No cases of tuberculosis or lymphoma were observed through week 16, and there was no increased risk of cardiovascular events or serious opportunistic infection. Apremilast was generally well tolerated. The most common adverse events (AEs) greater than placebo were diarrhea, nausea and headache. Greater than 96% of patients in the study reported no AEs or mild to moderate AEs. A similar percentage of patients reported both serious AEs and severe AEs in the apremilast 30 mg BID treatment group compared to placebo (2.1% vs. 2.8% and 3.6% vs. 3.2%, respectively).

An NDA submission to the U.S. Food and Drug Administration, based on the combined ESTEEM 1&2 studies for psoriasis, is expected in the second half of 2013. The Company previously announced it expects to file a separate NDA for psoriatic arthritis in the first quarter of 2013. A combined PsA/psoriasis MAA submission in Europe is also planned for the second half of 2013.

Hi Emma, My name is also Emma! I joined a while back, but forgot that this site existed for a while. I also have guttate psoriasis. It just came up for the first time about a year ago and has been a constant battle ever since. I recently had my first outbreak on my face, which was incredibly upsetting. I am currently a student, and it was right during a really stressful week of paper writing etc., which I am sure was part of what set it off. But needless to say, it was incredibly upsetting.
So yeah, just wanted to say hi, and that I understand how much it sucks to have psoriasis on your face.


Edit by Fred: This thread was split from here: Complete newbie! (Forums of any sort scare me!)

Background:
A substantial proportion of patients with psoriasis do not respond or lose initial response to tumour necrosis factor antagonists. This may partly be attributable to development of an immunogenic antibody response which causes subtherapeutic drug levels because of the clearance of drug-antidrug complexes. The aim of this study was to investigate the association between serum drug adalimumab (Humira) and etanercept (Enbrel) levels, antidrug antibodies, and clinical response in a cohort of psoriasis patients.

Methods:
In a single-centre cohort of 56 adults with psoriasis initiated on adalimumab or etanercept between 2009 and 2011, drug and antidrug antibody levels were measured with a commercially available ELISA at the patients’ routine clinic reviews (4, 12, and 24 weeks of treatment and the last available observation). Responders were defined as having a 75% reduction in psoriasis area and severity index from baseline (PASI 75) within 6 months of treatment, or physician's global score of clear or nearly clear. Non-responders were defined as not achieving a 50% reduction in PASI from baseline (PASI 50) within 6 months or having a loss of PASI 50 treatment response.

Findings:
After 4 weeks of therapy, adalimumab levels were significantly higher in responders than in non-responders (median 5·00 μg/mL [IQR 4·30—5·00] vs 0·12 μg/mL [0·10—1·79], p=0·003) and these higher levels were sustained at 12 and 24 weeks. Anti-adalimumab antibodies were detected in 25% of non-responders (2/8 patients, mean follow-up 22·5 weeks) and not in any responders (n=23, mean follow-up 26·1 weeks). There was no significant association between etanercept levels and clinical response at 4 weeks (median 2·94 μg/mL [IQR 0·78—3·68] vs 1·40 [0·82—2·12], p=0·317), and no anti-etanercept antibodies were detected.

Interpretation:
Adalimumab drug level monitoring at 4 weeks may be useful in predicting treatment response, in contrast to etanercept drug levels. The majority of adalimumab non-responders did not have antidrug antibodies; however, lack of serum trough levels and assay limitations may have underestimated their prevalence. Larger studies are required to investigate other factors contributing to low drug levels and to assess the usefulness of these drug and antidrug assays in personalising therapy in psoriasis.

Source: NO LINKS ALLOWED

Had to Google that. Basically the adipose tissue is what I would call my layer of Fat, so Adiposity is a politicly correct Medical term for being to Fat (Me).

Oops sorry back to the study.

Background: 
Adiposity is a known risk factor for psoriasis. Genome-wide association studies (GWAS) have identified a number of genes associated with risk of psoriasis while the evidence on gene–environment interactions in psoriasis is very sparse.

Objectives: 
To investigate the effect modification by adiposity measures on the association between single-nucleotide polymorphisms (SNPs) from published GWAS and risk of psoriasis.

Methods: 
Our psoriasis GWAS dataset comprised 9194 participants, including 337 individuals with psoriasis and 8857 controls from six GWAS, nested within the Nurses’ Health Study (NHS), NHS II, and Health Professionals’ Follow-up Study. Clinician-diagnosed psoriasis was ascertained with high validity. For stratified analyses, body mass index (BMI) was dichotomized at 25, and waist circumference was dichotomized at 30 (women) and 36 inches (men), while waist–hip ratio (WHR) was dichotomized at 0·8 (women) and 1·0 (men).

Results: 
Forty-one out of 44 previously reported psoriasis-related SNPs were included in our GWAS datasets. After excluding those with high linkage disequilibrium, 33 remained in the analysis. There were significant interactions between BMI and two SNPs in the IL12B (rs3212227) and IL23R (rs7530511) genes. Further analysis of these two SNPs indicated interactions between rs3212227 and waist circumference or WHR [P for interaction (Pint) < 0·05], but not for rs7530511. These observations were confirmed among participants without type 2 diabetes or coronary heart disease. The interactions remained after simultaneously adjusting for BMI as a continuous variable. In addition, we did not observe a significant main effect for rs7530511.

Conclusions: 
The association between a polymorphism in IL12B and psoriasis risk may be modified by measures of overall and central adiposity.

Source: NO LINKS ALLOWED

Background: 
Both the safety and efficacy of biologic therapy may be affected in the presence of highly prevalent chronic viral hepatitis.

Objectives: 
To evaluate the safety and effectiveness of ustekinumab (Stelara) and antitumour necrosis factor therapy in patients with psoriasis and concomitant chronic viral hepatitis.

Methods: 
This was a retrospective, multicentre study. Twenty-five patients with psoriasis and concurrent hepatitis C virus (HCV) (20 patients) or hepatitis B virus (HBV) (five patients) infection who had received at least one biologic agent (etanercept (Enbrel), 21 treatments; adalimumab (Humira), four; ustekinumab (Stelara), four; infliximab (Remicade), two) were included. Clinical, imaging and laboratory data were recorded.

Results: 
In the case of HCV infection, the majority of the patients did not exhibit increases in their viral load or serum liver tests. Aspartate aminotransferase, alanine aminotransferase and gamma glutamyl transpeptidase were doubled from the baseline measurement in only one patient treated with etanercept. Two other cases exhibited viral load increases during the follow-up period. In total, 18 of the 26 treatments achieved a 75% improvement in their Psoriasis Area and Severity Index (PASI 75) score during the follow-up period. Two patients treated with etanercept were diagnosed with hepatocellular carcinoma. In the case of HBV infection, all of the patients were being treated with antiviral therapy, and none presented significant variations in viral load or serum liver enzymes. All patients achieved a PASI 75 during follow-up.

Conclusions: 
Biologic therapy was effective and safe for the majority of our patients with HCV and HBV infection, although there may be a risk of reactivation or aggravation. We describe the first cases to receive ustekinumab. The use of biologics should be limited to those cases in which the risk–benefit ratio is justified.

Source: NO LINKS ALLOWED

We have all been told there is a link with psoriasis and our family genes, this study of families in Tunisia sheds a bit more light on it.

Background: 
Psoriasis is a relapsing chronic inflammatory skin disease affecting all population groups, with a peak prevalence of 3% in northern European and Scandinavian caucasians. Epidemiological studies have implicated a genetic component to psoriasis. In the past 12 years multiple genome-wide linkage analyses have identified putative susceptibility loci on several chromosomes, with a major locus in the major histocompatibility complex region.

Objectives: 
To investigate the genetic basis of familial psoriasis in the Tunisian population using a genome-wide linkage scan in seven multiplex psoriatic families from Tunisia.

Methods: 
Following single nucleotide polymorphism (SNP) genotyping on the Affymetrix 10K SNP array, we performed nonparametric linkage (NPL) multipoint analyses to identify genotypes and obtain evidence for linkage with psoriasis across the genome.

Results: 
No chromosomal region gave consistent evidence for linkage, providing evidence for genetic heterogeneity in Tunisian psoriasis families. Significant evidence for linkage of psoriasis to chromosome 2p12 was seen in one family. We also identified several regions of tentative psoriasis linkage on chromosomes 2q, 4q, 6p, 11q, 12q, 9q and 13q. One family exhibiting suggestive evidence for linkage to 17q25 (PSORS2) was identified and all affected members harboured a p.Gly117Ser mutation in CARD14 (caspase recruitment domain family, member 14), recently reported to lead to psoriasis in a large family from the U.S.A.

Conclusions: 
Our results support the genetic heterogeneity of psoriasis in the Tunisian population, provide confirmatory evidence for a novel psoriasis locus at chromosome 2p12 and reveal a psoriasis family with a mutation at PSORS2.

Source: NO LINKS ALLOWED

Dyslipidemia is an abnormal amount of lipids (e.g. cholesterol and/or fat) in the blood. This systematic review aims to synthesize evidence for the association between psoriasis and dyslipidaemia.

Psoriasis may be associated with dyslipidaemia, a known risk factor for cardiovascular disease. This systematic review aims to synthesize evidence for the association between psoriasis and dyslipidaemia.

Through a systematic search using MEDLINE, Embase and the Cochrane Central Register, from 1 January 1980 to 1 January 2012, we identified 25 observational studies that met the inclusion criteria. These 25 studies included over 2·4 million participants, among whom 265 512 were patients with psoriasis.

Twenty studies (80%) reported that psoriasis was significantly associated with dyslipidaemia, with odds ratios (ORs) for dyslipidaemia ranging from 1·04 to 5·55 in 238 385 patients with psoriasis, from a population of 2 340 605 participants. Specifically, four studies defining dyslipidaemia as triglyceride levels ≥ 150 mg dL−1 reported significantly increased ORs of 1·20–4·98 for hypertriglyceridaemia in psoriasis. Three studies found that patients with psoriasis presented with significantly increased ORs (1·36–1·77) for high-density lipoprotein cholesterol levels < 40 mg dL−1, and two studies found hyperlipoproteinaemia to be significantly elevated in patients with psoriasis (ORs 1·55 and 2·09). One cohort study found a significantly higher incidence of hyperlipidaemia among patients with psoriasis (hazard ratio 1·17; 95% confidence interval 1·11–1·23). Among studies that assessed the severity of psoriasis, in 2662 patients with mild psoriasis and 810 patients with severe psoriasis, higher odds of dyslipidaemia were seen in patients with severe psoriasis. Five of the 25 studies (20%) in our review did not show any significant relationship between psoriasis and dyslipidaemia.

This systematic review found that psoriasis was significantly associated with greater odds and incidence of dyslipidaemia. Greater psoriasis severity appeared to be associated with higher prevalence of dyslipidaemia.

Source: NO LINKS ALLOWED

Teva Pharmaceutical Industries LTD and the Ben-Gurion University of Israel have engineered a natural immune system receptor into a promising drug candidate for the treatment of Psoriasis.

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Researchers from the Department of Life Sciences and the National Institute for Biotechnology in the Negev at BGU in collaboration with Teva Pharmaceutical Industries LTD. have engineered a natural immune system receptor into a promising drug candidate for the treatment of Psoriasis.

Psoriasis is an autoimmune disease that affects millions of people, causes great suffering, and costs billions to health care systems worldwide. The main reason for the outbreak of Psoriasis is the disturbance of the natural balance between pro-inflammatory signals and signals that inhibit inflammation. In Psoriasis the outcome of this imbalance is inflammation and unregulated division of the skin cells.

One of the key signals involved in the progression of Psoriasis is the immune system protein Interleukin 17 (IL-17). Dr. Marianna Zaretsky and Prof. Amir Aharoni from BGU together with Dr. Liora Sklair-Tavron, Dr. Joel Kaye and Revital Etzyoni from Teva developed a method to inhibit IL-17 pro-inflammatory signals. The team engineered the extra-cellular soluble domain of IL-17 receptor to bind with high affinity to the natural IL-17 protein. The engineered IL-17R was developed by a directed evolution approach, in which an ensemble of mutants is screened for improved properties.

The resulting engineered IL-17R had a much better binding affinity and possessed more stability relative to the natural IL-17R receptor, making it a promising drug candidate. The team showed that this engineered IL-17R is highly effective in reducing IL-17 induced inflammatory signals in mice models. Moreover, injection of the engineered IL-17 receptor into a mouse model with acute human Psoriasis led to the abolishment of the symptoms, essentially curing the disease.

“Using directed evolution to improve the properties of the IL-17 receptor we have created engineered mutants that might prove there is a viable treatment for patients with severe Psoriasis that do not respond to current drugs.

“Since the directed evolution method can be applied to other receptors involved in autoimmune diseases and cancer, I believe that we are just starting to unravel the potential of this approach” Aharoni added.