Hi everyone! Hope you are all well 

So I am a 25 year old from London, and for three years ago i came up with a really small patch of psoriasis. At the time I didn't think anything of it. It went away (lived quite a healthy lifestyle etc).


This year i have come up with psoriasis quite badly- at first it was only on my elbows (plaque) and a think patch on my leg and lower back. I started using dovabet, but I also started getting guttate spots all over. Now it has spread to my face, scalp, arms, legs, back and is even on my...well yeah sorry for too much info!!

Currently having photothreapy three times a week but its still coming up so probably going on Cyclosporine  in a couple of months after the photothreapy (which is scary so any experiences would be appreciated!!)

I guess the reason I am posting here is that I am finding it difficult to come to terms with - I know there are so many worse things out there and I should consider myself lucky, but I can't help feeling very UNlucky - i just look around at all my friends, colleague, people on the tube, and wonder how come everyone else is fine and I've got psoriasis - i cant even really cover the scars on my face that well! I haven't always treated myself well, and I have been a smoker for years, so I guess I feel like it is my fault and i deserve it - none of my family have it and i just can't understand how has happened. I feel really sad but I am embarrassed to talk to much about it because I feel like my friends do not understand and think i am just being a self indulgent, vain, narcissist - does anyone else feel like this??

Any tips on how to come to terms with the fact I will be living with this forever, or any treatment suggests/ experience would be really appreciated  

thanks!!

Good news for those in the UK waiting for Taltz The National Institute for Health and Care excellence (NICE) are about to approve it for use on psoriasis patients.

The key dates for this appraisal are:

Closing date for comments: 22 November 2016

Second appraisal committee meeting: 25 January 2017

Until final guidance is issued, NHS organizations should make decisions locally on the funding of specific treatments.

Source: nice.org.uk

Taltz (ixekizumab)

Hi all and thank you for having me. I have suffered from plaque psoriasis for over 10 years now. Glad to find a group to share experiences, hope and treatment options with! I took a year off from my Stelara treatments, and just resumed them. Got my first injection last month at the doctor's office, and my booster today. I can honestly say that NOTHING has worked for me the way the Stelara does. Thank God my insurance pays for it.

This study looked at the difference between early (before 40) and late (after 40) onset of psoriasis and suggests they are different.

Quote:

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Background:
There is accumulating evidence that early-onset psoriasis (EOP; presenting at or before 40 years of age) and late-onset psoriasis (LOP; presenting after 40 years of age) are different diseases.

Objectives:
We aimed to identify potential clinical and immunocytochemical differences between EOP and LOP.

Methods:
We assessed immunocytochemistry in involved (PP) skin and uninvolved skin (n = 31) and demographics, psoriasis phenotype and psychological parameters (n = 340) in a cross-sectional study.

Results:
Immunocytochemistry revealed (17 EOP, 14 LOP) a greater lymphocytic infiltrate in PP skin of EOP compared with LOP (P = 0·03), with a higher epidermal CD4+ : CD8+ ratio in LOP (1·3) compared with EOP (0·5) (P = 0·002). In 340 patients with psoriasis (278 EOP, 62 LOP), we found an association with a positive first or second degree family history of psoriasis [62·0% vs. 35·6%, adjusted odds ratio (OR) 8·32, 95% confidence interval (CI) 1·90–36·52] and a higher likelihood of having parents with EOP (adjusted OR 10·34, 95% CI 1·32–81·83) in the EOP group. Patients with EOP were more likely to have received biological therapy (13·3% EOP vs. 3·5% LOP, P = 0·042), while patients with LOP had a higher likelihood of having type 2 diabetes (adjusted OR 3·43, 95% CI 1·004–11·691) and autoimmune thyroiditis (adjusted OR 5·05, 95% CI 1·62–15·7). Patients with LOP also had greater anxiety than patients with EOP (mean Hospital Anxiety and Depression Scale-A score LOP 8 ± 5, EOP 5 ± 5; P = 0·006).

Conclusions:
Our findings provide further evidence for the difference between EOP and LOP.

Another feather in the cap for Cosentyx

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Novartis has been awarded the prestigious 2016 Prix Galien USA Award for Best Biotechnology Product for Cosentyx® (secukinumab), as well as the Prix Galien Foundation "Discovery of the Decade" Award for Best Pharmaceutical Product for the drug Gleevec® (imatinib mesylate). The awards were presented at a ceremony in New York City on October 27.

"We are honored to receive these prestigious awards for Cosentyx and Gleevec, which not only have changed the practice of medicine for certain conditions, but also represent years of hard work by our scientists," said Joseph Jimenez, CEO of Novartis. "These wins underscore our commitment to addressing the unmet medical needs of patients through science-based innovation."

Cosentyx was the first fully human interleukin-17A (IL-17A) antagonist approved by the US Food and Drug Administration (FDA) in 2015 for the treatment of adults with moderate to severe plaque psoriasis1. Psoriasis affects an estimated 7.5 million people in the US2. It is a chronic immune-mediated disease characterized by thick and extensive skin lesions (plaques), which can cause itching, scaling, and pain2. Cosentyx was also approved for the treatment of active ankylosing spondylitis and psoriatic arthritis in 20161.

The discovery of Gleevec marked the first time in the history of cancer treatment that scientists were able to identify a chromosomal abnormality and then develop a drug that would target that specific protein. Gleevec, a molecularly targeted treatment, rapidly became a therapy of choice for Philadelphia chromosome-positive chronic myeloid leukemia (Ph+ CML) and KIT (CD117)-positive gastrointestinal stromal tumors (KIT+ GIST)3. By showing that certain diseases can share a drug-sensitive target with seemingly unrelated ailments, and that molecular targeting can be medically and commercially successful, Gleevec helped establish a new paradigm for drug development.

###

About the Prix Galien Awards

Considered "the pharmaceutical industry's Nobel Prize," the Prix Galien rewards excellence in scientific innovation that improves the state of human health. The award was first established in 1970 by French pharmacist Roland Mehl and was inaugurated in the United States in 2007 to recognize the technical, scientific and clinical research skills necessary to develop innovative medicines. Since 1970, Novartis has received more than 40 national Prix Galien awards in fifteen countries for innovative therapies such as Gleevec® (imatinib mesylate), Rimactane® (rifampin), Parlodel® (bromocriptine mesylate), Sandimmune® (cyclosporine), Sandostatin® (octreotide acetate), Simulect® (basiliximab) and Visudyne® (verteporfin)4.

The "Discovery of the Decade" is a special once-in-10-years recognition for distinguished industry achievement in medical innovation. The awards honor extraordinary human health impact in three categories - Best Pharmaceutical Product, Best Biotechnology Product, and Best Medical Technology. In addition to Gleevec® (imatinib mesylate), two other Novartis products were nominated for "Discovery of the Decade," including Coartem® (artemether/lumefantrine) for Best Pharmaceutical Product and Promacta® (eltrombopag olamine) for Best Biotechnology Product. Gleevec won the Prix Galien International Prize in 2002, and was recognized again in 2009 by the Prix Galien USA committee for "Best Pharmaceutical Product"5.

About Cosentyx and interleukin-17A (IL-17A)

Cosentyx is a fully human monoclonal antibody (mAB) that selectively binds to the interleukin-17A (IL-17A) cytokine and inhibits its interaction with the IL-17 receptor1.

Cosentyx is approved in more than 65 countries for the treatment of moderate to severe plaque psoriasis which includes the European Union countries, Japan, Switzerland, Australia, the U.S. and Canada6. In the U.S., Cosentyx is approved for the treatment of moderate to severe plaque psoriasis in adult patients who are candidates for systemic therapy or phototherapy (light therapy). Cosentyx is also approved in the US for adult patients with active ankylosing spondylitis and active psoriatic arthritis1.

More than 10,000 patients have been treated with Cosentyx in clinical trial settings across multiple indications, and over 50,000 patients have been treated in the post-marketing setting worldwide7.

My eyes have been very dry and itchy for a few weeks now, I have an appointment with my GP on Wednesday about it, but just wondered if it was connected to stelara as a side effect. Anyone ever experienced this?

Hi there sorry but i am new to forums any all thse types of things.

O was just wondering if anybody has used clobaderm and dovobet as i have been prescribed them by the doctor and old to use them together. I have been prescribed many steroid creams to no avail and  he will not refer me to 
A dermotologist

 many thanks in advance

 danny

One for the DMF Gang to have a chinwag about.

Quote:

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Background:
Fumaric acid esters (FAE) have been used for over 30 years in the management of psoriasis. There have been a number of case reports linking the use of FAE with nephrotoxicity, including acute renal injury and Fanconi syndrome. However, one large multicentre retrospective trial showed no evidence of renal dysfunction with FAE.

Objectives/Aims:
The aim of this study was to determine the number of patients in our institution being treated with FAE who developed significant proteinuria or renal dysfunction.

Methods:
This was a single-centre retrospective study assessing all patients on FAE who attended for follow-up during an 18-week period between February and June 2015. Demographics, co-morbidities, duration and dose of treatment with FAE, proteinuria, renal function and other biochemical serum abnormalities were recorded.

Results:
One hundred and twenty seven patients were included in the study. Eighty-two patients had proteinuria detected at some stage during treatment with FAE, and 18 of these had persistent proteinuria (positive in at least 3 consecutive specimens, 12 weeks apart). Six patients (5 female) developed proximal tubular dysfunction (PTD). The risk factors for the development of PTD appear to be lower body weight (p=0.03), higher dose per weight (p=0.03) and longer duration of treatment (p=0.03). Renal dysfunction improved on discontinuation or dose reduction of FAE.

Conclusion:
Fumaric acid esters are frequently associated with transient or persistent proteinuria. Significant renal dysfunction is rare and usually reversible on dose reduction or discontinuation of FAE. This study highlights the importance of screening for proteinuria. Higher doses per weight of treatment and longer duration of FAE therapy are likely risk factors for PTD.

Hi all, new to the forums, and hoping that you may be able to answer some of my questions to help with my anxiety re Acitretin.

I am a 30 yo male who has been suffering with Psoriasis since I was 19. This was mainly plaque psoriasis on my elbows and knees but when I was 25 i developed a major case of guttate following tonsillitus. I went for UVB treatment for this and it cleared all the Psoriasis up. Unfortunately within 6 months the plaque had returned and another strep infection 2 years later caused another bout of guttate. I went for more UVB treatment and the same cycle repeated itself to where I am today.

I went through major depression following my first bout of guttate as it covered me from head to toe. I was much better the 2nd time round as I understood the condition, and it wasn't as severe as the first time. I treat my plague with Dovabet but this this little to the guttate scales. I wouldn't consider my Psoriasis to be having a detrimental effect to my life; it's annoying it's there but I can live with it!

I went to see the Derm today regarding my Psoriasis as the patch on my knee is growing and I have developed two patches in my groin area that I have never had before (ironically one looks like the male 'bits' - Psoriasis is mocking me now?!  ) - I am going on holiday in March and would prefer to have a clear body rather than it be there. Rather than refer for UVB he has asked me to take Acetritin 20mg per day. I was initially game for this but I've since read horror stories about Acetritin and one thing is particularly worrying me - hair loss! Call me vain but I really like having hair and it's something I will try hold onto if I can!

Am I thinking too much into it or is this something I should be worried about? I was thinking about taking Biotin to try and counteract the effects but it's unclear if this will help or if it will have an effect on the Acitretin. 

Any peoples experiences with this would be appreciated. From reading 20mg is a low dose compared to what others have been taking anyway?

Thanks in advance.

I have a home narrow band UVB box and the mfr recommends 14" distance. If I go closer is it really bad or does the 14" distance just allow for proper diffusion?

The unit has a protective cage on the exposure side and I rest my hands on it, so my hands are only a few inches from the UVB bulbs.

Hey everyone ?
So .. I have been taking methotrexate since around the 21st of July and have only gone up by 5mg's ? My Derm is completely useless ! I started on 5mg for around 4 weeks and the for the remainder I have been on 10mg's . Side effects are fine to be fair ?
My problem is it's not working .. not even a little ! In fact if anything it's getting worse . I spoke to my derm as I have an appointment on the 31st of this month and told her I'd took 15mg's last week instead of the 10 they had prescribed me and why .. she wasn't happy ! She said that if they increase they only increase at 2.5mg's a time and appointments to get that are 12 weeks apart !!!  Think where they have kept me on a low dose for so long my body has maybe just got used to it and now a few patches that had started to calm a little have gone back to how they were with extra bits added and my scalp is worse than ever ?
Really not sure what to do .. part of me thinks stuff it and come off .
They won't consider anything apart from acitretin ( already tried that and didn't like it at all )  or ciclosporin ( majority don't seem to clear on that and it's quite harsh at 1st so quite unsure on that one too ) help ?

This snippet suggests γδ T cells and IL-9 as new players in the pathogenesis of psoriatic arthritis.

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Cytokines such as tumour necrosis factor (TNF)-α, interleukin (IL)-12, interferon (IFN)-γ, IL-23 and, more recently, IL-9, have been implicated in the initiation/maintenance of inflammation in psoriasis and psoriatic arthritis (PsA). In the present study we aimed to characterize the role of γδ T cells in peripheral blood and synovial fluid of PsA patients and to investigate their response to in-vitro stimulation with antigen or cytokines (IL-9 and IL-23). γδ T cells isolated from peripheral blood mononuclear cells and synovial fluid were analysed by flow cytometry to evaluate the phenotype and cytokine production. IL-23R and IL-9R gene expression were also evaluated by reverse transcription–polymerase chain reaction (RT–PCR). Peripheral blood mononuclear cells (PBMC), sorted γδ T cells and γδ cell lines were also stimulated in vitro with isopentenyl pyrophosphate (IPP), recombinant IL-9 or recombinant IL-23. Our results show an expansion of γδ T cells with a predominant effector memory phenotype in peripheral blood and synovium of untreated PsA patients, which reverses significantly after treatment with anti-TNF-α or anti-IL-12/IL-23R monoclonal antibodies (mAbs). Moreover, in PsA patients γδ T cells activation is driven prevalently by IL-9/IL-9R interaction, and not only by IL-23/IL-23R. Together these findings indicate γδ T cells and IL-9 as new players in the pathogenesis of PsA.

This study evaluated myocardial scintigraphy as a screening method in patients with psoriasis.

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Background:
In recent years, cardiac comorbidities in psoriasis patients have increasingly moved into the focus of clinical research. The objective of the present study was to evaluate myocardial scintigraphy as a screening method in patients with psoriasis.

Patients and methods:
Assessment of various comorbidities in 50 psoriasis patients without clinical symptoms of cardiac disease. Myocardial scintigraphy was employed to detect cardiac risk/exercise-induced ischemia.

Results:
Twenty-eight patients (56 %) had pathological findings on myocardial scintigraphy. Fourteen individuals showed evidence of small-vessel disease (cardiac syndrome X). Other comorbidities included obesity, arterial hypertension, nicotine and alcohol abuse, as well as elevated CRP levels. Frequencies largely corresponded to those reported in the recent literature. There was no significant correlation between the severity of psoriasis or any comorbidities and pathological findings on myocardial scintigraphy.

Conclusions:
Myocardial scintigraphy seems to be a very sensitive, noninvasive method for the early detection of cardiac comorbidities in psoriasis patients. However, determining its true diagnostic value will require larger studies with control subjects and control methods such as coronary angiography.

Hi,

Sorry for being out of touch there for a while. Had a lot going on with my new business and took me all over the country on a weekly basis.
History so far:

Been put on Acitretin (25mg/day) since July 2015. First 8 months, significantly flared up to a point where I wanted to stop. (No real side effects apart from the fact that I started to look like a lizard )

Derm advised after 9 months to increase to 75mg. All my psoriasis cleared after a couple weeks but, then all my other problems started:
Dry lips - I had never used any lip balm in my life as I did not believe in them. Suddenly my lips were so cracked and sore, I had to start using them. To a point where I would use a tube of 15mg in a couple days time.
Insomnia - Not sure if that is a side effect but during the time I was on 75mg - my sleep pattern was severely disrupted. (Coincidence?)
Hair Loss - lost about 70% of my hair on my head, including my eybrows and beard. Lost 100% of hair on my legs and arms. Looked like I was shaving them.
Sore finger tips - This is the one thing that is really getting me down. Feels like I have ingrown fingernails all the time. (Nails are kept short and tidy). Some days it's a real struggle just to put my wristwatch on. The thing is, I work with my hands - tried gloves but that just makes me bump my fingers even more. At this point I just push through the pain and work. (being self employed does that to a person   )
Peeling on palm and feet - yeah, painful is all I can say about that.

Three months ago, I told the Derm that I am changing my dose to 50mg a day. Still have sore fingertips. Hair has started to grow back. Some patches have come back on my arms (I can live with that - Long sleeves!). Lips still very dry but manageable. Peeling of feet and palms are now minimal.

Feeling better about myself but I still think that there are better stuff out there. Acitretin is poison!

Derm has cancelled my latest appointment now three times and still do not have a rescheduled date for another appointment . Going to phone them on Monday to find out what is going on? I need to change my medication.

Sorry for the negativity but this is just what my experience was/is.

Hello all, 

I just joined the forum because I'm hoping to find some help and support for dealing with this frustrating condition.  I'm currently breast-feeding so I'm very limited on what I can take. For a while it seemed to get better, but I started getting a period again after giving birth and it seems that every time I get my period the psoriasis get way worse. I don't know if anyone else experiences this. If so I don't know if there's anything I can do to help. Also, does anyone know of any natural treatments I can use while breast-feeding that will not harm the baby?  Why is it that the condition seems to get worse when I get my period?  How can I prevent it from happening?   Any and all suggestions are welcome.  Thank you in advance.

This snippet from Clinical and Experimental Dermatology may make you think again about the use of topical vitamin D3 analogue calcitriol.

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A 55-year-old man with severe plaque psoriasis presented with a 2-week history of feeling generally unwell with lethargy and thirst. His symptoms had developed 6 weeks after commencement of the topical vitamin D3 analogue calcitriol. Investigations revealed hypercalcaemia and acute-on-chronic kidney injury, probably directly induced by systemic absorption of vitamin D3 following extensive topical use. Topical calcitriol had been started as a steroid-sparing agent to reduce the patient's liberal potent corticosteroid usage during anti-tumour necrosis factor-alfa therapy. Topical vitamin D analogues are commonly prescribed in dermatological and general practice, with hypercalcaemia being a rare but potentially serious adverse effect. This case serves to outline key factors that may predispose to hypercalcaemia, such as disease extent, quantity of drug applied, comorbidities and concurrent medications, and it highlights the importance of considering these factors when prescribing topical therapies.

Hi everyone, just found your group whilst trawling around the internet checking up on the headlines in the press today about 'miracle cure' - otezela , its been interesting reading some of the posts regarding otezela  and for me I'll wait and see before I charge down to the doctors to see if its available and suitable for me. 

As a long term sufferer you can guess I have tried most potions and lotions but now I tend to just put up with it and make the most of the sunshine to ease it back.

Whilst I have some hefty patches on my legs, arms and strangely on my butt (difficult to get the sunshine there without being arrested) , for me the biggest problems are when my scalp flares up and when it comes up under my nails.  Its like having bamboo slivers driven in, not nice at all.

Consultant recommended  Dovobet for both which seems to help but as ever it always comes back and usually a little worse.  When its really bad over the winter periods I get out to dermalight that I had had for years

I'll keep an eye on posts and hopefully I will pick up a few ideas that may help in the future

cheers everyone

If you use methotrexate for psoriasis and drink beetroot juice you may be interested in this snippet from an early view in Clinical and Experimental Dermatology.

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Methotrexate is extensively used in the treatment of psoriasis. Although safe and effective, its use may inadvertently lead to intoxication. We report a 50-year-old woman being treated with methotrexate for psoriasis who developed methotrexate intoxication after drinking beetroot juice as a herbal remedy. Patients should be warned about the potential adverse effects of herbal therapies during methotrexate treatment.

This study suggests that the -2518 A/G MCP-1 and -403 G/A RANTES promoter gene polymorphisms may be risk factors for psoriasis and may influence its clinical presentation.

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Background:
Polymorphic variants of the genes encoding monocyte chemoattractant protein-1 (MCP-1/CCL2) and regulated upon activation normal T-cell expressed and secreted (RANTES/CCL5) and their protein serum levels have not been widely explored in psoriasis.

Aim:
To clarify the effect of the MCP-1 (-2518 A/G) and RANTES (-403 G/A) promoter gene polymorphisms on the risk and clinical manifestation of psoriasis.

Methods:
We enrolled 160 unrelated patients with psoriasis vulgaris and 160 healthy, unrelated, age- and sex-matched volunteers. The promoter gene polymorphisms were analysed using amplification refractory mutation system (ARMS)-PCR and single specific primer (SSP)-PCR. Serum levels of cytokines were measured using ELISA.

Results:
The presence of the MCP-1–2518 GG genotype was statistically more frequent in patients and it was associated with an increased risk of psoriasis (OR = 1.94; P = 0.04). In patients with late-onset (≥ 40 years) psoriasis, the presence of the RANTES -403 AA genotype was statistically more frequent (OR = 3.65; P < 0.01) while -403 GG was less frequent (OR = 0.44; P < 0.01). Moreover, the A allele (AA or AG) in the -403 RANTES polymorphism was associated with an increased risk of developing severe psoriasis (OR = 2.02; P = 0.03). Serum levels of both chemokines were elevated. RANTES serum concentration was significantly higher in patients with Psoriasis Area and Severity Index > 15.

Conclusions:
The results of our analysis suggest that the -2518 A/G MCP-1 and -403 G/A RANTES promoter gene polymorphisms may be risk factors for psoriasis and may influence its clinical presentation.

This study suggests immune cells from patients with psoriasis have a defect in upregulating Indoleamine 2,3-dioxygenase (IDO) in response to inflammation associated with the severity of psoriasis.

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Background:
Indoleamine 2,3-dioxygenase (IDO) is an inducible enzyme that suppresses the immune response. The role of IDO as a negative regulator of inflammatory responses has been documented in several experimental autoimmune diseases.

Objectives:
To explore the regulation of IDO by immune cells in psoriasis and its relation with disease severity.

Methods:
The expression and activity of IDO were assessed by reverse-transcriptase polymerase chain reaction, flow cytometry and high-performance liquid chromatography in peripheral blood of patients with moderate-to-severe plaque-type psoriasis. The ability of immune cells to express IDO in response to inflammatory stimuli was studied. The functional role of IDO expression was evaluated in a regulatory T cell (Treg) differentiation assay, using cocultures of immature monocyte-derived dendritic cells with autologous peripheral CD4+ T cells.

Results:
Analysis of the kynurenine-to-tryptophan ratio in serum samples indicated higher IDO activity in patients with psoriasis than in healthy controls. However, correlation studies showed lower IDO activity in those patients with higher Psoriasis Area and Severity Index (PASI). Although myeloid dendritic cells from patients with psoriasis expressed higher levels of IDO than those from healthy controls, these cells did not upregulate IDO in response to a combination of tumour necrosis factor-α, interleukin (IL)-1β and IL-6 cytokines. The defective expression of IDO correlated with PASI. Immature monocyte-derived dendritic cells from patients with psoriasis also expressed low levels of IDO and induced CD4+ Treg differentiation poorly.

Conclusions:
Immune cells from patients with psoriasis have a defect in upregulating IDO in response to inflammation associated with the severity of psoriasis.