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.

Quote:

---

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.

Brave statements made by Leo Pharma and 4SC Discovery in their joint press release for an oral psoriasis treatment.

Quote:

---

Leo Pharma a global pharmaceutical company specialising in dermatology, has entered into an exclusive research and license agreement with the German biotech company 4SC Discovery GmbH with the primary aim of jointly researching, developing and commercialising an oral treatment for inflammatory skin diseases such as psoriasis.

The collaboration has the potential to result in a novel and convenient break-through therapy for chronic skin conditions. The innovative compound, currently in the early development state, has already been proven in preclinical models to significantly reduce if not entirely eradicate symptoms of psoriasis.

Under the agreement, LEO Pharma will issue an upfront payment of EUR 1 million to 4SC Discovery and additional funding for research and development. LEO Pharma will receive an exclusive option to license the worldwide marketing and commercialisation rights of the compound for use in inflammatory skin diseases, including psoriasis and other therapeutic areas. Upon LEO Pharma exercising the option, 4SC Discovery will be eligible for a milestone payment of up to EUR 3 million and further payments upon achieving specific development milestones of up to EUR 92 million as well as up to double-digit royalties.

The deal marks the latest milestone in LEO Pharma’s ambitious growth strategy, which involves actively seeking new opportunities to expand the company pipeline for the benefit of patients.

Kim Kjoeller, Senior Vice President, Global Development, LEO Pharma, said: ”LEO Pharma is excited about the agreement with 4SC and the possibilities it offers patients. The compound has the potential to completely eradicate symptoms of psoriasis, liberating people from the burden of this chronic skin disease. LEO Pharma strives to constantly expand and improve treatment options for patients and this latest deal is the perfect example of our commitment to meeting patient needs with breakthrough novel therapies.”

For 4SC Discovery, the deal marks a key early-stage partnering deal with one of the company’s compounds from its research engine.

Dr. Daniel Vitt, Managing Director of 4SC Discovery GmbH and Chief Scientific Officer at 4SC AG, commented: “We are delighted to have won LEO Pharma, a global leader in skin diseases, as an ideal research and license partner for our highly innovative compound, which is based on the modulation of cytokines. Our goal is now to speed up and jointly develop a novel breakthrough therapy addressing the high medical need in chronic inflammatory skin diseases such as psoriasis. This partnership again demonstrates the great expertise and scientific potential of 4SC in the fields of autoimmune and inflammatory diseases.”

Following on from this thread I started last August: Pig parasite could help psoriasis

Coronado a biopharmaceutical company focused on the development of novel immunotherapy biologic agents for the treatment of autoimmune diseases and cancer, announced today the initiation of an Investigator-Initiated Study (IIS) evaluating TSO (Trichuris suis ova or CNDO-201) for the treatment of psoriasis. The first site initiated in the multicenter study is the Icahn School of Medicine at Mount Sinai (ISMMS). Dr. Mark G. Lebwohl, Sol and Clara Kest Professor and Chairman of the Department of Dermatology, is the Principal Investigator of the trial at ISMMS.

"We are excited to be working with Mount Sinai and Professor Lebwohl, a renowned thought leader, in our pursuit of potential treatments of diseases for our lead program, TSO, where the hygiene hypothesis and immunology are important for their basic epidemiology," said Dr. Karin Hehenberger, Executive Vice President & Chief Medical Officer of Coronado. "Psoriasis is one of these diseases with critical medical need and we believe the objective nature of the assessment of progression or worsening of this disease lends itself well to this type of pilot trial."

This trial is an open-label study designed to enroll 20 patients with moderate to severe plaque psoriasis. ISMMS is the first of three sites which the company anticipates being involved in this study. Participants will receive eight doses of either TSO 2500 or TSO 7500 orally every other week over a 16-week treatment period. The trial will evaluate the effect of TSO on clinical response of psoriasis. The primary endpoint will be the average improvement in Psoriasis Area and Severity Index (PASI) from baseline at week 16. The goal of the pilot study is to test for early safety and efficacy of TSO at two different doses.

Source: coronadobiosciences.com

*TSO (Trichuris suis ova or CNDO-201), the microscopic eggs of the porcine whipworm, is a novel, orally administered, natural immunomodulator that regulates T-Cells and pro-inflammatory cytokines. The use of TSO as a therapeutic is based on the "hygiene hypothesis" and numerous animal and human studies. TSO was chosen as the biological agent of choice because it is not a human pathogen, and is spontaneously eliminated from the body within several weeks after dosing.

I was pointed to this article. Maybe weird... but.. logical.
In Germany they are working on a kind of vaccination treatment for psoriasis, in a way that your own body takes care of the bacteriological cause of psoriasis.

Cell-wall-deficient bacteria: a major etiological factor for psoriasis?

Background Psoriasis is a common inflammatory skin disease, yet knowledge of the factors that may induce, trigger, or exacerbate psoriasis is not fully delineated. Recent advances have improved our understanding of the link between psoriasis and cell-wall-deficient bacteria (CWDB) infections. In the present study we assessed the prevalence of CWDB infection in patients with psoriasis.
Methods The carriage rate of CWDB in the tonsil or pharynx of psoriasis patients, chronic tonsillitis patients and controls were investigated using hypertonic medium. Psoriasis patients with CWDB were randomly assigned to two groups and respectively treated with antibiotics or systemic therapy without antibiotic. Human peripheral blood mononuclear cells (PBMC) from psoriasis patients, chronic tonsillitis patients and control subjects were stimulated with bacteria antigens and extra-cellular levels of interferon-γ (IFN-γ) and interleukin (IL)-10 were measured in the supernatants using the ELISA technique, in vitro. Meanwhile, the proliferation ability of PBMC to respond to bacteria antigens was detected by MTT assay.
Results CWDB were isolated from 74.2% of psoriasis patients, 23.5% of chronic tonsillitis patients and only 6.3% of controls. Antibiotic therapy was appropriate for approximately 80% of psoriasis patients with CWDB infection, and in only 8.9% psoriasis patients CWDB infection was detected after antibiotic therapy. Meanwhile, our study showed that CWDB and wide-type bacteria did remarkably enhance the production of IFN-γ, in vitro, and PBMC proliferation.
Conclusion CWDB infection may be a virtual triggering factor in psoriasis by regulating T-cell activation.

Chinese Medical Journal 2009;122(24):3011-3016

I have always found that in the winter my skin always behaves more than in the summer, I think this is because the cold keeps my skin cool and the sun isn't strong enough to burn me!
Most people find that the summer months are when they see the most improvement, I'm curious to know of others experience with the seasons

Hanna x

UCB announced today two new regulatory filings with the US Food and Drug Administration (FDA) and with the European Medicines Agency (EMA) to extend the marketing authorization for Cimzia® (certolizumab pegol) for the treatment of adult patients with active psoriatic arthritis (PsA) and for adult patients with active axial spondyloarthritis (axSpA). The regulatory filings for two new indications for certolizumab pegol are now under review by the US FDA and EMA.

"We are committed to providing treatments for patients with severe diseases such as PsA and axSpA which can affect adults at a very productive and active time of their lives. These new regulatory filings bring us one step closer to supporting more people living with immunological conditions and to building UCB’s immunology franchise,” said Professor Dr. Iris Loew-Friedrich, Chief Medical Officer and Executive Vice President UCB. “The clinical study supporting the axSpA filing represents the first Phase 3 study with an anti-TNF to include axSpA patients with and without definitive radiographic evidence of structural damage to the spine. Similarly the study supporting the PsA filing was the first randomized, controlled study of an anti-TNF in PsA to include patients with and without prior anti-TNF exposure.”

Certolizumab pegol is a Fc-free, PEGylated anti-TNF. In the US, certolizumab pegol is approved for the treatment of adults with moderately to severely active rheumatoid arthritis. It is also approved for reducing signs and symptoms of Crohn's disease and maintaining clinical response in adult patients with moderately to severely active disease who have had an inadequate response to conventional therapy. Certolizumab pegol is marketed under the trade name Cimzia®.

In the EU, certolizumab pegol in combination with methotrexate (MTX) is approved for the treatment of moderate to severe active rheumatoid arthritis in adult patients inadequately responsive to disease-modifying anti-rheumatic drugs including MTX. Certolizumab pegol can be given as monotherapy in case of intolerance to MTX or when continued treatment with MTX is inappropriate.

Source: NO LINKS ALLOWED

Other posts about Cimzia:
UCB's Cimzia for psoriatic arthritis Phase 3 results
Certolizumab Pegol and Psoriatic Arhtritis study results

Catechol-O-methyltransferase (COMT) is one of several enzymes that degrade catecholamines such as dopamine, epinephrine, and norepinephrine. And the regulation of catecholamines is impaired in a number of medical conditions. This study ahead of print suggests that COMT is higher in patients with psoriasis, but can be reduced with Narrowband UVB treatment.

Background:
Narrowband ultraviolet B (nbUVB) phototherapy is widely used in psoriasis treatment. UVB irradiation decreases catechol-O-methyltransferase (COMT) activity in human keratinocytes and melanoma cells. COMT activity is higher in psoriatic lesions than in normal skin but the effect of nbUVB on COMT activity in psoriasis patients is unknown.

Objectives:
To evaluate COMT activity in patients with psoriasis and determine whether nbUVB modifies this activity.

Methods:
An open observational study was conducted with 20 psoriasis patients and 15 healthy volunteers. Patients were treated with nbUVB thrice weekly during six weeks and evaluated at baseline, three and six weeks after phototherapy and four weeks after stopping. In each evaluation body mass index (BMI), Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index (DLQI) were calculated and blood samples for erythrocytes soluble (S-) COMT activity assessment were taken.

Results:
Before phototherapy (baseline), using a single concentration of substrate adreneline (1,000 μM), S-COMT activity levels (pmol/mg protein/h) were significantly higher in psoriasis patients than in controls. After nbUVB treatment, S-COMT activity significantly decreased. This decrease correlated positively with baseline activity. Four weeks after stopping phototherapy, S-COMT activity returned to baseline levels. After phototherapy, PASI score improved significantly but no correlation to baseline S-COMT values or decrease in S-COMT activity was found.

Conclusions:
This study shows that baseline S-COMT activity is higher in psoriasis patients than in controls and that this activity is significantly decreased by nbUVB treatment for psoriasis. This decrease is more evident in patients with higher baseline S-COMT activity.

Source: NO LINKS ALLOWED

mTOR (mammalian target of rapamycin) also known as mechanistic target of rapamycin or FK506 binding protein 12-rapamycin associated protein 1 (FRAP1) is a protein which in humans is encoded by the FRAP1 gene. mTOR is a serine/threonine protein kinase that regulates cell growth, cell proliferation, cell motility, cell survival, protein synthesis, and transcription. mTOR belongs to the phosphatidylinositol 3-kinase-related kinase protein family.

This study published in the British Journal of Dermatology suggests that mTOR inhibition might be a mode of action suitable to be explored for a new psoriasis treatment.

Background:
mTOR (mammalian target of rapamycin) signalling integrates signals leading to cellular growth, proliferation and differentiation. Disturbance of this tightly regulated interplay leads to malignancies, as reflected by altered mTOR signalling in epidermal tumours. As psoriatic keratinocytes also show features of perturbed cell growth and differentiation, the question arises whether mTOR signalling also plays a role in the pathogenesis of psoriasis.

Objectives:
Investigation of the activation status of mTOR signalling components in psoriasis

Methods:
Biopsies from lesional and non-lesional skin of psoriasis patients (n=10) as well as samples from healthy donors (n=3) were analysed by immunohistochemistry and Western blot, utilizing antibodies detecting phosphorylated mTOR (P-mTOR), P-S6K and P-S6 ribosomal protein.

Results:
We found mTOR and its downstream signalling molecule, the ribosomal protein S6 to be activated in lesional psoriatic skin. While mTOR is activated throughout the whole epidermis, with particularly strong activation in the basal layer, S6 is rather active in suprabasal layers of differentiating keratinocytes.

Conclusions:
Altogether these results suggest a role for mTOR signalling in the epidermal changes leading to the psoriatic phenotype. mTOR inhibition might be a mode of action suitable to be explored for innovative anti-psoriatic drugs.

Source: NO LINKS ALLOWED

This study published in the British Journal of Dermatology looks at efficacy, safety and tolerability of different topical treatments used in plaque psoriasis. It suggests that Corticosteroids are highly effective, and Coal tar and retinoids are of limited benefit. (Topical Treatments are applied directly to the skin)

Background:
The majority of people with psoriasis have localised disease, where topical therapy forms the cornerstone of treatment.

Objective:
To summarise evidence on relative efficacy, safety and tolerability of different topical treatments used in plaque psoriasis

Methods:
Systematic review and meta-analyses of randomised trial data of UK-licensed topical therapies. The primary outcome was clear or nearly clear status stratified for (i) trunk and limbs and (ii) scalp. Network meta-analyses allowed ranking of treatment efficacy.

Results:
48 studies were available for trunk and limb psoriasis and 17 for scalp psoriasis (n=22,028); the majority included people with at least moderate psoriasis severity. Strategies containing potent corticosteroids (alone or in combination with a vitamin D analogue) or very potent corticosteroids, dominated the treatment hierarchy at both sites (trunk and limbs, scalp); coal tar and retinoids were no better than placebo. No significant differences in achievement of clear/nearly clear status were observed between twice and once daily application of the same intervention or between any of the following: combined vitamin D analogue and potent corticosteroid (applied separately or in a single product), very potent corticosteroids, or potent corticosteroids (applied twice daily). Investigator and patient assessment of response differed significantly for some interventions (response rate to very potent corticosteroids 78% and 39% respectively). No significant differences were noted for tolerability or steroid atrophy, but data were limited.

Conclusions:
Corticosteroids are highly effective and safe in psoriasis when used continuously for up to 8 weeks and intermittently for up to 52 weeks. Coal tar and retinoids are of limited benefit. There is a lack of long-term efficacy and safety data available on topical interventions used for psoriasis.

Source: onlinelibrary.wiley.com

Oral Thrush (oral candidiasis) is a common yeast infection of the Candida species on the mucous membranes of the mouth, this study suggests that the presence of oral thrush is higher in patients with psoriasis



Background:
Infections are known to trigger and exacerbate psoriasis. Although oral candidiasis is often clinically diagnosed, it is not always confirmed by laboratory tests such as oral cytopathology.

Objectives:
The aims of this study were to determine the prevalence of oral candidiasis in patients with psoriasis through clinical and cytopathological diagnosis and to investigate the association between oral candidiasis and psoriasis with regards to the severity of the clinical presentation and the type of treatment for psoriasis.

Methods:
A total of 140 patients with psoriasis and 140 healthy control subjects received an oral examination. Scrapings of the tongue were also obtained for a cytopathological examination.

Results:
The oral examination and the results of the cytopathological smear revealed 37 (26%) cases of candidiasis in the patients with psoriasis and no cases of candidiasis in the healthy control subjects. There was no correlation between the type of psoriasis treatment and the presence of oral candidiasis (P = .616). There was a statistically significant association (P = .033) between the clinical severity of psoriasis and the presence of Candida.

Limitations:
This study was limited by the small number of subjects and the lack of follow-up to determine the development of psoriasis after treatment for oral candidiasis.

Conclusions:
The presence of oral candidiasis is higher in patients with psoriasis and it is associated with disease severity. This increased presence of oral candidiasis was apparent despite any type of treatment for the psoriasis. Cytopathology to rule out oral candidiasis should be used in the routine medical workup of patients with psoriasis.

Source: NO LINKS ALLOWED

Other relevant posts.
Gum disease linked to psoriasis
Psoriasis and oral health
Your Tongue can say a lot

Hello,
I am new to P as I have had it only for about 6 monts. Now my joints in my fingers and toes are clearly affected. What will happen when I go to the doctor. Do I have to go to a specialist, do I have to have many x-rays or other tests et.c.

The Adacolumn is a Japanese adsorptive type extracorporeal leukocyte apheresis device that selectively adsorbs granulocytes, monocytes/macrophages by Fcγ and complement receptor bindings.

Approximately 65% of granulocytes and 55% of monocytes from the blood that passes
through the column are adsorbed. However the total number of blood cells remains constant as the removed cells are rapidly replaced by mobilisation of inactive, CD-10 negative leukocytes.



Background:
Generalized pustular psoriasis (GPP) is a chronic autoimmune disease characterized by fever, erythema, and neutrophilic pustules over large areas of the skin. GPP does not respond well to pharmacologic intervention.

Objective:
We sought to assess efficacy of selectively depleting the myeloid lineage leukocytes in patients with GPP.

Methods:
Fifteen patients with persistent moderate to severe GPP despite conventional therapy were included. Eligible patients had more than 10% of their skin area covered by pustules. Treatment with oral etretinate, cyclosporine, methotrexate, prednisolone, and topical prednisolone/vitamin D3 was continued if had been initiated well in advance of study entry.
Five sessions of adsorptive granulocyte and monocyte apheresis (GMA) with the Adacolumn (JIMRO Co Ltd, Takasaki, Japan) were administered (1 session/wk over 5 weeks) to selectively deplete Fcγ receptor and complement receptor bearing leukocytes. Efficacy was assessed by measuring the skin areas covered by pustules at baseline and 2 weeks after the last GMA session.

Results:
One patient did not complete the first GMA session. Based on the GPP severity scores relative to entry, the overall scores improved (n = 14, P = .0027), and the area of erythroderma (P = .0042), pustules (P = .0031), and edema (P = .0014) decreased. Likewise, Dermatology Life Quality Index improved (P = .0016), reflecting better daily function and quality of life. Twelve patients were judged as responders (85.7%), and 10 patients maintained the clinical response for 10 weeks after the last GMA session without any change in medication.

Limitations:
This study was unblinded and without a placebo arm.

Conclusion:
GMA in this clinical setting was safe and effective, suggested a major role for granulocytes/monocytes in the immunopathogenesis of GPP.

Source: jaad.org

Tofacitinib is a drug being investigated by Pfizer for the treatment of rheumatoid arthritis, psoriasis, inflammatory bowel disease, and other immunological diseases, as well as for the prevention of organ transplant rejection.

In November 2012 the U.S. Food and Drug Administration (FDA) approved it for treatment of rheumatoid arthritis. Tofacitinib is an inhibitor of the enzyme Janus kinase 3. More on that here: RE: I need more Psoriasis

Background:
Tofacitinib (CP-690,550) is a novel Janus kinase inhibitor in development as an oral formulation for the treatment of several inflammatory diseases including psoriasis.

Objectives:
This Phase 2a study aimed to assess the efficacy, systemic safety, local tolerability and systemic pharmacokinetics of topical tofacitinib in mild-to-moderate plaque psoriasis.

Methods:
Two tofacitinib ointment formulations were evaluated in this multicentre, double-blind, vehicle–controlled trial (NCT01246583). Seventy-one patients were randomised 2:1:2:1 to 2% tofacitinib Ointment 1, Vehicle 1, 2% tofacitinib Ointment 2 and Vehicle 2, each administered twice daily for 4 weeks to a single fixed 300 cm2 treatment area containing a target plaque +/- one or more non-target plaques and normal skin.

Results:
The primary endpoint of percent change from baseline in Target Plaque Severity Score at Week 4 demonstrated statistically significant improvement for Ointment 1 (least squares mean [LSM] –54.4%) vs Vehicle 1 (LSM –41.5%), but not Ointment 2 (LSM –24.2%) vs Vehicle 2 (LSM –17.2%). Secondary endpoints (Target Plaque Area and Itch Severity Item) improved similarly for tofacitinib ointment vs corresponding vehicle. Adverse event (AE) occurrence was similar across treatment groups. All AEs were mild or moderate and none were serious or led to subject discontinuation. One application site AE (erythema) was reported. Tofacitinib mean systemic exposure was minimal and was greater for Ointment 1 than for Ointment 2.

Conclusions:
Tofacitinib Ointment 1 was well tolerated and efficacious compared with vehicle for the treatment of plaque psoriasis. Further study of topical tofacitinib for psoriasis treatment is warranted.

Source: onlinelibrary.wiley.com

Hello!! I have been "living" with psoriasis since May 26, 1995. I remember it because i had my 16th bday on the 4th..then i had my first baby on the 19th and i remember i had a skirt i was so excited about wearing since i had lost enough baby weight to fit into it...i was also going to look at a apartment with a friend of mine i had known since public school (kindergarten) ...i can remember it like it was this morning...

i got the skirt out and laid it on my bed..went into the bathroom to take a shower and thats when it happened...i noticed there was a long line of "spots" down my shin, i freaked out...went directly to my papa and asked him what it was, he thought it was hayfever and gave me a bunch of benedryl and sent me on my way. A few days later it covered my legs completely, most of my stomach and chest, also my arms were covered, the palms of my hands and face were just red and itchy.
psoriasis had taken over my body.

bless papa's heart he tried so hard to rid me of this horrible skin condition, taking me to any doctor he could find. My friends treated me like i had something contagious and left me to myself, the boyfriend was no help and my parents had no clue...

no one in my family has psoriasis (my father took off when i was born so i have no idea about his family...which is probably where it is from but like i say i have never had contact with them)

I have tried EVERYTHING available to me from creams, tar, UV lights, tanning beds, diet, methotrexate oral and injection and now i am at the max dose for the methotrexate injection but it makes me so unbelievably nauseas that i cannot handle it any longer, now my 10yr old has it on her scalp and face, she is mortified and rightfully so, the biggest problem i am having is she is autistic and feels pain differently then we do and she scratches the spots until she bleeds. i have not sent her to school as kids are extremely cruel and i cannot stand to subject her to that.

i need some help!
i have a dermatologist appointment for her on the 22snd of feb and hope the doc can help her...i refuse to treat mine until i can relieve her of hers.

i hope i have done my introduction properly and look forward to many conversations with the great members of this club!!

thank you for inviting me!

cheers! tammie