The Effects of Chronic Periodontitis and Its Treatment on the Subsequent Risk of Psoriasis

Background: 
Although psoriasis and *chronic periodontitis (CP) may share an underlying immune dysregulation as part of their pathologies, only one small-scaled cross-sectional pilot study has investigated the potential association between CP and psoriasis to date.

Objective: 
This study aimed to investigate the subsequent risk for psoriasis following a diagnosis with CP by utilizing a cohort study design and population-based dataset in Taiwan.

Methods: 
In total, 115,365 patients with CP were included in the study cohort and 115,365 patients without CP were included in the comparison cohort. We individually tracked each patient for a five-year period to identify those who had subsequently received a diagnosis of psoriasis. A Cox proportional hazards regression was performed to compute the five-year risk of subsequent psoriasis following a diagnosis of CP.

Results: 
We found that the incidence rate of psoriasis during the five-year follow-up period was 1.88 (95% CI=1.77-1.99) per 1,000 person-years in patients with CP and 1.22 (95% CI=1.14-1.32) per 1,000 person-years in comparison patients. After censoring those who died during the follow-up period, and adjusting for monthly income and geographic region, compared with comparison patients, the HR of psoriasis for patients with CP was 1.52 (95% CI=1.38-1.70). Furthermore, the study subjects who had undergone a gingivectomy or periodontal flap operation only had a slightly higher adjusted risk of psoriasis than comparison patients (HR=1.26).

Conclusions: 
This study detected an increased risk for psoriasis among patients suffering from CP. Treatment for CP attenuated, but did not nullify, the risk for subsequent psoriasis.

Source: onlinelibrary.wiley.com

*Chronic periodontitis is a common disease of the oral cavity consisting of chronic inflammation of the periodontal tissues.
Symptoms may include: Redness or bleeding of gums while brushing teeth, Gum swelling that recurs, Halitosis, Gingival recession, Deep pockets between the teeth and the gums, Loose teeth.

So I'm currently covered in psoriasis from head to toe it is easier to tell you that I don't have it on 7 out of 10 fingers and 8 out of 10 toes!!! 
Being pregnant means I'm rather limited on what treatments are open to me and most creams come with risks to the baby.

I was in the pharmacy the other day and noticed a product which I toyed with the idea of using before but chose to try forever living aloe products, the kind lady in the pharmacy gave me some trial samples and a leaflet. I checked it's all safe to use while pregnant so on saturday I purchased my first lot, I had to buy more today from the pharmacy where I got given the samples and another lady asked how I was getting on with it a a few people have tried the product and gone back singing it's praises.

Since starting it I do feel more moisturised and far less itchy and my flakey-ness decreased loads, I ran out of the product yesterday so had to use my epaderm moisture cream, itchiness came back and lots of flakes!!

So here's my plan, I'm giving this product 6 weeks hopefully without running out again. I will try and update on here a much as possible, and hopefully with positive results.
If this doesn't work I may bite the bullet and have more UVB.

I'm not naming what I'm using just yet as I want to see results from my own trial first. But if you really want to know PM me as the company is doing sample products that you need to pay £2 p&p for (uk) 

Hello everyone, I'm Keesha!
I'm 22 now, and ive known about my psoriasis since I was 8. I know a lot of you have had it longer than me and a lot of you have a very serious case of it. Run down of my story.... my psoriasis started behind my ears, my mom thought I wasn't washing behind them when I showered. Lol. But when it started to build up, and when my mom would pull my ear forward and the back would split and hurt really bad then bleed she took me to the doctors.. and they sent me to the dermatologist, and that's how I found out. So creams it was, and they worked for years.... actually my breakouts stopped for a while... when I got pregnant they started showing back up, and after I had my baby it got really bad.. I was using a breast pump but then my chest area got covered and I had to stop. I started on humira injections and it was working great.. but the more injections I got, the bigger my injection sites would irritate. So they took me off.. I was back to creams for a while, and some dermal smooth for my scalp. But my back, stomach, chest and scalp started getting bad again... at the point where I couldn't do anything with my hair and I hated going out. See I have very dark hair, and everytime I brush these white flakes go everywhere..
well story already long... I stared stelara in march.. second dose in April, and do for my third injection next week. Its been working good so far, but I went to get my blood work done on Friday and my doctors official called me and said I have to get it done again because my liver levels were high.. what does that mean? They also said if it comes back high again I cant get my third injection... this has me kinda. Dummed

Hi Folks,
I'm on Fumaderm for the first time and got to the Blue tabs, 3 times a day, without any problems, then boom! Omg! Stomach cramps and the runs, has anyone come across anything that alleviates either of these issues?

I have suffered with psoriasis for over 20 yrs. first the itching I use Germ x hand sanitizer. I have recently started to use petroleum jelly for the plaque, i had about 30% of my body covered in plaque.

I'm glad to report about a 15 yr reversal in my condition. I no longer have any significant plaque anywhere. This is almost a miracle, well who am I kidding it is a miracle. I could not go out in public, I had to where as much clothing as possible. I felt like a freak I had so much plaque, not anymore. 20 yrs of Dovonex treatments failed.

Then i tried a simple petroleum gel coating to relive the dryness, now after 3 months I'm almost completely free of plaque. No more vacuuming the floor everyday. No more constant scratching and shedding skin. I hope this helps you and others, please tell your friends.

Edwin & Debbie

Now my psoriasis is flaring up again, I was noticing how symmetrical it is.

Symmetrical I have

• Above my left and right ear.
  
• Both armpits.
  
• Both undersides of my lower arms.
  
• Both thumbnails are lifting.
  
• Left and right toenails look the same.
  
• Left and right front lower legs are the worse, and look much the same.
  
• I suppose you could class as symmetrical, my lips and genital area are both flaring up.
  

• One small patch on my right torso.
  
• My right hand outside upper leg.
  
• Right hand toes.
  

Celgene today announced top-line results from the PALACE-1 study, the first of three pivotal phase III, randomized, placebo-controlled studies evaluating the Company’s novel, oral small-molecule inhibitor of phosphodiesterase 4 (PDE4) in patients with psoriatic arthritis who had received an oral disease-modifying antirheumatic drug (DMARD), biologic therapy or had failed on an anti-tumor necrosis factor (TNF) agent. *Apremilast treatment in this study was used alone or in combination with an oral DMARD.

In the study, statistical significance for the primary endpoint of ACR20 was achieved for patients receiving apremilast. Patients in the active treatment arms also maintained significant improvements in arthritis-related endpoints, including ACR50 and ACR70 through week 24. Significant and sustained improvements in various measures of physical function were also observed in apremilast-treated patients.

The overall safety profile was consistent with previous experiences in the phase II program and tolerability was improved. Common side effects for PDE4 inhibitors have been gastrointestinal in nature. In the PALACE-1 study, gastrointestinal adverse events, upper respiratory tract infections, as well as headache, were no more common in apremilast-treated patients than in those receiving placebo.

The PALACE-1 study is ongoing and the study extension remains blinded until all patients complete week 52. Full data from this phase III study will be submitted for presentation at appropriate medical meetings.

Source: celgene.com

*Apremilast is an oral small-molecule inhibitor of phosphodiesterase 4 (PDE4), works intracellularly to modulate a network of pro-inflammatory and anti-inflammatory mediators. PDE4 is a cyclic adenosine monophosphate (cAMP)-specific PDE and the dominant PDE in inflammatory cells. PDE4 inhibition elevates intracellular cAMP levels, which in turn down-regulates the inflammatory response by modulating the expression of TNF-α, IL-23, and other inflammatory cytokines. Elevation of cAMP also increases anti-inflammatory cytokines such as IL-10.

Hello,

First post, suffered with P for 25 years, Im only 29. tuff life as everybody knows. I used to get this stuff skin cap. Cleared my skin in 2 days. It worked great. Now its been banned. Im broken out, no insurance, and have been looking on internet for skin cap and I heard about Psor Val that is supposedly same ingrediant and works better. I want to order this immediately since it worked so well. Has anybody else tried doing that, or have heard of Psor Val, or even if the skin cap on the web still works, it says its by the same corporation. Please let me know if anybody else has tried or heard about these two products. Skin cap was the best and I hope its still the same as a couple years ago before it was banned. Thanx for all your help, and Im glad Im not alone having to deal with this. I wish all of you the best. Thanx for any feed back on my question!!!!

Following on from the introduction of Simponi (golimumab) by NICE in April 2011 for England. Scotland has now followed suit, But its use is restricted to patients in whom treatment with at least two other disease-modifying antirheumatic drugs (DMARDs) or NSAIDs has failed to alleviate symptoms. And doses must be restricted to 50mg.

The Scottish Medicines Consortium ruled that the drug can be used alone or in combination with methotrexate. Evidence reviewed by the watchdog found golimumab was cost effective at this dose. A study showed it outperformed placebo at reducing symptoms. Side-effects were similar to placebo and included nasopharyngitis and URTI.

Source: scottishmedicines.org.uk

More on Simponi here: https://psoriasisclub.org/showthread.php...169#pid169

After the past few years of being on the Biological's and having almost totally clear skin, I had forgotten how annoying psoriasis can be.

I've been a lot worse and have had it for years, but the past few years I have been spoiled. I'm going through a bit of a flare up at the moment, mostly on my lower legs but also some on my toes, lips, arm pits, and genital area.

It feels like I have peeled the top layer of my skin off with one of those potato peeler things and then rubbed the wound with stinging nettles and salt.

Must get positive Fred

At 2 weeks after psoriasis patients received their first dose of the investigational interleukin-17 inhibitor ixekizumab, their gene expression pattern resembled that of healthy controls.

At the annual meeting of the Society for Investigative Dermatology, Dr. James G. Krueger presented a translational medicine study aimed at defining the impact that turning off IL-17 signaling has on pathological tissue structures, molecular pathways, and biomarkers.

His conclusion: "I think these data suggest IL-17 is the central cytokine driving pathogenesis in psoriasis," said Dr. Krueger of Rockefeller University in New York.

Eight psoriasis patients received a subcutaneous 150-mg dose of ixekizumab at weeks 0, 2, and 4 and underwent skin biopsies at weeks 0, 2, and 6. He compared their inflammatory gene expression profiles 2 weeks into treatment vs. those obtained from 15 psoriasis patients 2 weeks after beginning treatment with etanercept (at 50 mg twice weekly for 12 weeks).

IL-17 blockade with ixekizumab proved to have a greater impact on the expression of inflammatory genes known to be associated with psoriasis than did tumor necrosis factor inhibition via etanercept. Ixekizumab resulted in greater-than-75% normalization of expression of 643 of these inflammatory genes, compared with 104 with etanercept.

The structural result of IL-17 blockade was reversal by week 6 of the epidermal hyperplasia that is the hallmark of psoriasis, he added.

Two of the eight patients on the ixekizumab 150-mg regimen achieved PASI 75 (that is, a 75% improvement from baseline on the Psoriasis Area and Severity Index) in 2 weeks. That’s remarkably fast improvement, Dr. Krueger noted. By week 6, all eight patients had achieved PASI 75.

Another point in favor of IL-17’s being a central cytokine driving psoriasis is that ixekizumab shut down not only the IL-17A target genes downstream, but also genes controlling the production of key cytokines located upstream, including interferon-gamma and IL-22, he noted.

Phase III trials investigating ixekizumab for psoriasis are underway. The drug is also being investigated for the treatment of rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis.

Source: skinandallergynews.com

Context: 
Based on limited data, the live attenuated herpes zoster (HZ) vaccine is contraindicated in patients taking anti–tumor necrosis factor (anti-TNF) therapies or other biologics commonly used to treat immune-mediated diseases. The safety and effectiveness of the vaccine are unclear for these patients.

Objective: 
To examine the association between HZ vaccination and HZ incidence within and beyond 42 days after vaccination in patients with selected immune-mediated diseases and in relation to biologics and other therapies used to treat these conditions.

Design, Setting, and Patients: 
Retrospective cohort study of 463 541 Medicare beneficiaries 60 years and older with rheumatoid arthritis, psoriasis, psoriatic arthritis, ankylosing spondylitis, or inflammatory bowel disease using Medicare claims data from January 1, 2006, through December 31, 2009.

Main Outcome Measures: 
Herpes zoster incidence rate within 42 days after vaccination (a safety concern) and beyond 42 days; hazard ratios estimated using Cox proportional hazards models for HZ comparing vaccinated vs unvaccinated patients.

Results: 
Median duration of follow-up was 2.0 years (interquartile range, 0.8-3.0); 4.0% of patients received HZ vaccine. The overall crude HZ incidence rate was 7.8 cases per 1000 person-years (95% CI, 3.7-16.5) within 42 days after vaccination. The rate among the unvaccinated was 11.6 cases per 1000 person-years (95% CI, 11.4-11.9). Among 633 patients exposed to biologics at the time of vaccination or within the subsequent 42 days, no case of HZ or varicella occurred. After multivariable adjustment, HZ vaccination was associated with a hazard ratio of 0.61 (95% CI, 0.52-0.71) for HZ risk after 42 days.

Conclusions: 
Receipt of HZ vaccine was not associated with a short-term increase in HZ incidence among Medicare beneficiaries with selected immune-mediated diseases, including those exposed to biologics. The vaccine was associated with a lower HZ incidence over a median of 2 years of follow-up.

Herpes zoster (HZ), caused by the reactivation of latent varicella-zoster virus (VZV), manifests as an acute, painful vesicular rash and is often accompanied by chronic pain or postherpetic neuralgia. In the United States, the incidence rate of HZ in the unvaccinated general population 50 years or older is estimated to be 7.0 cases per 1000 person-years. A live attenuated vaccine reduces HZ risk by 70% and 51% among immunocompetent individuals 50 to 59 years and 60 years and older in 2 randomized blinded trials, respectively. The Advisory Committee on Immunization Practices (ACIP) recommends a single dose of the zoster vaccine for all people 60 years or older.

The risk of HZ is elevated by 1.5 to 2 times in patients with rheumatic and immune-mediated diseases such as rheumatoid arthritis (RA) and Crohn disease. This increase has been attributed to both the underlying disease process and treatments for these conditions. Currently, the Food and Drug Administration (FDA), the ACIP, and the American College of Rheumatology consider the live HZ vaccine to be contraindicated in patients receiving some immunosuppressive medications commonly used to treat these conditions, including all immune-modulating biologic agents; some nonbiologic immunosuppressive medications, such as methotrexate at doses of greater than 0.4 mg per kg per week; and glucocorticoids at prednisone-equivalent doses of 20 mg or more per day. The safety concern is that these individuals may develop varicella infection from the vaccine virus strain. Based on the VZV incubation period, the first 42 days following vaccination was chosen as the primary safety risk window in the Shingles Prevention Study, a randomized blinded trial that preceded the FDA approval of the vaccine.

In light of the uncertainties regarding the safety and effectiveness of zoster vaccine in patients with immune-mediated diseases, we used administrative claims from US Medicare beneficiaries diagnosed with these diseases to evaluate the association between receipt of zoster vaccine and HZ risk within the first 42 days and up to 3.5 years following vaccination.


Source: jamanetwork.com

I am 57 and I've lived with guttate psoriasis since age 22. I used light therapy and ointments off and on for the first 4 or 5 years but have just lived with it for the past 30 or so years for the most part. I have never been completely clear but other than the occasional flareup it hasn't been too bad. Until just recently, I haven't seen a dermatologist since 1996. In 96' Me and my son both had a bad experience with bad food at a local restaurant and that triggered one of the worse psoriasis flareups I've ever had and I made one of my rare doctor appointments to have it looked at. At the time, as well as most of my adult life, I had no health insurance. Thats another thing we learned to live quite well without, but it also helped us to learn to take better care of ourselves and to make the most of home remedies. The prescription I got for my flareup in 96' cost me about $80 US for each refill. Kind of expensive but not terribly so. Just recently, I had another flareup that wound up covering a large area of my body. I have a weak left knee and I injured that knee not long ago and the injury to that knee that must have triggered my psoriasis flareup as I can't think of anything else and the area covered worse by my psoriasis was on my left leg including for the first time below the knee and on the back of my knee. The itching this time was also the worse I've ever experienced. Reluctantly, I finally made an appointment with a dermatologist a couple of weeks ago and was prescribed Clobex spray and Vectical ointment. I've been using them for a week and a half and they have been pretty effective so far, but certainly no more effective than the ointment I used in 1996. . The thing that shocked me was the price of these drugs. At the Walmart pharmacy, 2oz of Clobex was almost $700 US and the tube of Vectical was over $300 - the two together was over $1000 and that is every time I refill them. I believe this is complete medical insanity. Have things really changed THIS much since 1996 ? Here in the US we have just recently had socialized medicine imposed upon us and I can't help but think that this is at-least partially responsible for the ludicrous cost of these two prescriptions. Fortunately for me I am currently employed on a job that provides health insurance and my co-pay part of these drugs cost me a mere $10 but that is not the point. If the insurance I have was not provided and paid for by my employer I could not afford to pay for it myself and would not have any. The new US insurance law also prohibits me from seeing a doctor and paying for the visit myself unless I can prove I have insurance, so I wouldn't have even been able to make the appointment. Now I have found out that even if I could see a doctor and get a prescription, without insurance, the cost of the medication would prohibit me from having it filled. I shudder not for myself, but for everyone that can't afford to buy insurance and there are lot of people that can't. Something has gone terribly wrong. I can't imagine where this will wind up years down the road but no one will ever convince me that anything good will come from this.

Hi everyone

Im new to the forum. Just joined last night. I was on twitter and someone suggested the Psoriasis club to me.

I have had psoriasis almost 33 years, since I was a baby. I have been hospitalized many times with it. I can be in hospital anything from 3 weeks to 2 months at a time. I have just been informed by my dermatologist that I need to be hospitalized again before end of july. I have a young daughter so I am worried about leaving her this time as the last time I was in hospital was in 2007 before she was born.

My flare ups are getting worse and affecting my worklife, home life and self esteem. I never buy tops with short sleeves or short trousers as my limbs are particularly bad. I was put on Methotrexate last November and had serious side effects to it so am no longer on it. For the time being I am using Liquid parafin 50:50 and tar pomade to try and control it until I go back into hospital.

Even though I have had psoriasis for so long I have never come to terms with it. I just hope some day doctors find a cure to help people living with it.

If anyone can give me advice on new treatments, nutrition etc I will be very grateful. Many thanks [/color]

Background:
Tumor necrosis factor inhibitory agents are currently considered to be contraindicated in psoriatic patients with *hepatitis B.

Objective:
We aim to provide guidance to dermatologists on the use of tumor necrosis factor inhibitor therapy in these patients.

Methods:
The current literature was reviewed regarding the use of tumor necrosis factor-alpha inhibitory agents Atanercept (Enbrel), Adalimumab (Humire), and Infliximab (Remicade) in psoriatic patients with particular reference to hepatitis B infection.

Results:
Tumor necrosis factor-alpha inhibitor therapy may result in reactivated hepatitis B in hepatitis B surface antigen-positive patients with psoriasis. This also occurs, although less frequently in patients with an isolated positive hepatitis B core antibody. Thus, all psoriasis patients should be screened for hepatitis B surface antigen plus hepatitis B core antibody prior to the initiation of tumor necrosis factor-alpha inhibitor therapy. Infliximab (Remicade) has been associated with more reactivation cases than the other 2 agents and fatalities have been reported with this agent. Evidence is presented that the risk of reactivation can be greatly minimized or eliminated by early or pre-emptive antiviral therapy.

Limitations:
The data is largely based on small case series that are retrospective in nature.

Conclusions:
Hepatitis B screening is essential prior to the initiation of tumor necrosis factor-alpha inhibitor therapy. Psoriatic patients found to be hepatitis B surface antigen or hepatitis B core antibody-positive should be referred to an appropriate specialist for evaluation and therapy. This would allow for the safe use of tumor necrosis factor-alpha inhibitors in psoriatic patients despite recently published guidelines to the contrary.

Source: eblue.org

*Hepatitis B is an infectious inflammatory illness of the liver and causes liver inflammation, vomiting, jaundice and, rarely, death.

Profiles of *Dental Caries and *Periodontal Disease in Individuals With or Without Psoriasis

Background: Studies of oral health in psoriasis patients are limited. The aim was to assess the experience and risk of caries and periodontal disease in psoriatics and non-psoriatics.

Material and Methods: The material consisted of 89 individuals with mild to moderate chronic plaque psoriasis and 54 non-psoriatics, recruited at the University Hospital in Gothenburg. Psoriasis arthritis was diagnosed in 25 of the psoriatics. All participants answered questionnaires and were subjected to saliva sampling and oral radiological and clinical examinations. Two computer applications were used for illustration of oral disease risk profiles.

Results: Psoriatics had lower salivary pH, fewer remaining teeth, fewer sites with probing pocket depth ≤4 mm and a lower radiographic alveolar bone level than non-psoriatics (p<0.05). Most of the differences remained significant after controlling for confounders. Differences in alveolar bone levels were no longer significant, particularly after introducing “gender” into the regression model. Similar numbers of decayed and filled teeth, sites with deep pockets, sites that bled on probing and risk profiles were observed. Individuals with psoriasis arthritis exhibited a lower stimulated salivary secretion rate than non-psoriatics (p<0.05).

Conclusions: There were no differences in profiles of caries and periodontal disease experience and risk between individuals with and without psoriasis. Fewer remaining teeth were observed in psoriatics. However, the exact reason for tooth loss could not be identified. Meanwhile, the reduced salivary pH in psoriatics and salivary secretion in psoriasis arthritis individuals, may pose a risk for future caries.



*Dental caries, also known as tooth decay or a cavity, is an infection, usually bacterial in origin, that causes demineralization of the hard tissues (enamel, dentin and cementum) and destruction of the organic matter of the tooth.

*Periodontal disease is a type of disease that affects one or more of the periodontal tissues that both surround and support the teeth.

Hybrigenics bio-pharmaceutical company, with a focus on research and development of new treatments against proliferative diseases, announces the first results of the placebo-controlled double-blind clinical Phase II efficacy study of oral inecalcitol at the single dose of 4 mg per day in moderate to severe psoriasis.

Of the total 60 enrolled patients, 57 (20 placebo and 37 inecalcitol) have completed their treatment for at least 10 weeks and up to 16 weeks. One early study withdrawal was due to grade 3 hypercalcemia caused by inecalcitol within the first week of treatment. Of the 37 patients treated with oral inecalcitol, 24 patients (65%) showed a PASI 50 response and, among them, 10 patients (27%) had a PASI 75 clinical improvement. However, these results were not statistically different from the placebo group, in which women had an unexpectedly strong improvement of their disease with a PASI 75 rate of 63% vs. 17% observed in placebo-treated men, which is more in line with usual values from the literature on psoriasis studies of similar duration.

Blood levels of inflammatory biomarkers such as IL-4, IL-10, IL-12, IL-17, interferongamma (IFN-γ) and tumor necrosis factor alpha (TNF-α) are currently being assayed in samples from all patients, as well as the levels of vitamin D receptor in white blood cells. Biopsies of skin lesions have been taken in subsets of patients and their histopathological examination is also ongoing.

This additional data will be available in the coming weeks and may shed some light on the reasons for the strong placebo effect observed in women, and why there weren’t more PASI 50 responders progressing to PASI 75 clinical improvement.

During the entire treatment period (16 weeks) and still one month later, after the follow-up period, the PTH levels of each of the 20 patients on placebo changed by less than 50% from their initial value and remained within the normal range. By contrast, the PTH levels of each of the 37 patients receiving inecalcitol decreased by more than 50% during the treatment.

PTH levels were decreased below the normal range in 34 inecalcitol-treated patients (92%) and below LoQ in 24 of them (65%). This PTH lowering effect was highly statistically significant as compared with placebo at all times during treatment (p< 0.001), even as soon as week 4, the earliest time point measured. This pharmacological effect of inecalcitol was totally and rapidly reversible because all PTH levels were back within the normal range after the one-month followup period.

“Two-thirds of inecalcitol-treated psoriasis patients showed some degree of response (PASI 50) but only one fourth had a clinically-relevant improvement (PASI 75) at week 12 or at week 16. A hypothesis could be that a longer duration of treatment might be necessary for inecalcitol to fully improve all the responders”, commented Dr Jean- François Dufour-Lamartinie, Hybrigenics’ Head of clinical R&D. He added: “the confirmation of inhibition of normal PTH secretion by inecalcitol, a fast, strong and straightforward effect observed in all treated patients, without any placebo effect, deserves further clinical investigation in chronic kidney disease patients who suffer from pathologically elevated PTH levels”.

Source: hybrigenics.com

An international team of scientists led by principal investigator Richard L. Gallo, M.D., Ph.D., professor of medicine and chief of UC San Diego’s Division of Dermatology, analyzed skin biopsies of patients with and without psoriasis, as well as the skin of mice with psoriasis and with wounds on their backs. They discovered that a molecule called regenerating islet-derived protein 3-alpha (REG3A) is highly expressed in skin cells during psoriasis and wound-healing, but not under normal skin conditions.

In tests on mice, researchers found that inhibiting REG3A slowed wound-healing but cleared up psoriasis, which is commonly characterized by patches of inflammation and white, scaly skin.

The scientists also noted that REG3A acts in concert with interleukin-17 (IL-17), an immune system protein involved in the signaling cascade which prompts skin cells to multiply in excess numbers. “IL-17 binds to receptors on skin cells and causes REG3A to be expressed, which then binds to another protein inside the cells that promotes cell growth,” said first author Yuping Lai, Ph.D., professor of microbiology and immunity at East China Normal University in Shanghai.

Gallo said the discovery of REG3A’s dual roles provides a new target for different therapies.

“A drug that inhibits the expression of REG3A could represent a more targeted way to treat psoriasis without the systemic immunosuppression problems of current treatments. Conversely, a drug that stimulates or mimics REG3A could boost cell growth and improve wound healing.”

Source: universityofcalifornia.edu

The Medical College of Wisconsin received a two-year, $200,000 grant from the National Psoriasis Foundation to study the pathogenesis of psoriasis and to identify new drugs that may benefit patients.

Sam Hwang, MD, PhD, and Thomas J. Russell Family/Milwaukee Community Dermatologists Chair and professor of dermatology, is the principal investigator for the grant.

Approximately 7.5 million Americans are living with psoriasis, an autoimmune disease in which dead skin cells accumulate and cause irritation that appears as itchy scales or dry patches. Symptoms can be treated, but there is no cure, and the severity of the disease ranges from mild discomfort to complete disability. Complications include arthritis, ischemic heart disease, and depression. Dr. Hwang’s lab identified two proteins (a chemokine receptor called CCR6 and it binding protein) in prior studies of psoriasis development that appear to have significant involvement in the disease.  In this study, Dr. Hwang will investigate these proteins further to better understand how they impact the pathogenesis of psoriasis.  Dr. Hwang will also use computer modeling to discover drugs that may block the actions of these proteins and thus, potentially, improve therapy for patients with this disease.

This study may verify a pathway for psoriasis and provide new information about its cause. The project may also identify new treatments for psoriasis and other diseases influenced by the proteins Dr. Hwang is investigating.

This special award is called the Lutto Translational Grant in honour of Seymour and Rebecca Lutto, who made this research possible with a gift to the National Psoriasis Foundation. They sought to memorialise their son Lawrence Lutto by advancing scientific knowledge regarding the cause and treatment of psoriasis.

Source: mcw.edu

Objective: 
To assess the risk of incident diabetes mellitus (DM) in patients with psoriasis and to evaluate DM treatment patterns among patients with psoriasis and incident DM.

Design: 
Population-based cohort study.

Setting: 
United Kingdom–based electronic medical records.

Patients: 
We matched 108 132 patients with psoriasis aged 18 to 90 years with 430 716 unexposed patients based on practice and time of visit. For our nested study, only patients who developed incident DM during our study time were included.

Main Outcome Measures: 
Incident DM and adjusted risk of pharmacotherapy among those with incident DM.

Results: 
The fully adjusted hazard ratios (95% CIs) for incident DM were 1.14 (95% CI, 1.10-1.18), 1.11 (95% CI, 1.07-1.15), and 1.46 (95% CI, 1.30-1.65) in the overall, mild, and severe psoriasis groups, respectively. Among those with incident DM and severe psoriasis, the adjusted risk for receiving DM pharmacotherapy was 1.55 (95% CI, 1.15-2.10).

Conclusions:
Our results suggest that psoriasis is an independent risk factor for the development of type *2 DM in a dose-dependent manner, and that patients with severe psoriasis who develop DM are more likely to receive systemic diabetic therapies in comparison with patients with DM but without psoriasis.

Source: archderm.jamanetwork.com

* Diabetes mellitus type 2 is a metabolic disorder that is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency. This is in contrast to diabetes mellitus type 1 in which there is an absolute insulin deficiency due to destruction of islet cells in the pancreas. The classic symptoms are excess thirst, frequent urination, and constant hunger. Type 2 diabetes is initially managed by increasing exercise and dietary modification. If blood glucose levels are not adequately lowered by these measures, medications such as metformin or insulin may be needed.