My husband had a kidney function of 9 on Tuesday and is in hospital. They have taken him off the psoriasis treatment which was Accitretin as they thought the Fumaderm was causing the kidney problem, when function dropped from 90-50! Dermo did say Acitretin which had been used before, would not control  the psoriasis but wanted him to take them until they could sort out the injections. However the function dropped even more when he was no longer on Fumaderm!

So we now have Eric coming home today or tomorrow on NO medication for the psoriasis and I think they may have taken him off the allupurinol as well for his gout. He is also not to take painkillers. He has to go back on Wednesday to see the nephro.

He is seeing the Dermotologist on Tuesday but has been told not to take anything until passing it by the Nephro.
Are injections likely to cause kidney problems? I realise that there are several options so this is just a general question.

I do think we specialists taking 'snapshots' and not really seeing the whole patient although I do accept that the kidney function of 9 was the most dangerous and needed to be sorted. They still do not seem sure what caused the sudden drop.......

But psoriasis can cause infections and very low quality of life..He literally could not walk this time last year and his skin was peeling off.
I do not know if anyone has co -morbidities and has been through similar things? I know that the injections are the last resort in the UK.
Thanks for reading. I shall print out the discharge from the unit and get husband to take it with him when he sees the dermo on Tuesday. It is going to be a difficult bank holiday!

Following on from this report Taltz (ixekizumab) gets FDA approval for Psoriasis  Taltz (ixekizumab) has now also been given approval for psoriasis in the EU.

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Lilly is expecting to start rolling out Taltz in EU countries from this summer and through to the end of 2018, taking into account the typical cycle times for reimbursement assessment.

The approved dosing regimen for Taltz is a 160mg subcutaneous injection, followed by an 80mg injection every two weeks for 12 weeks and then a maintenance dose of 80mg each month. In trials, around 90% of patients treated with Lilly's drug had a 75% or more clearance in skin lesions after 12 weeks, with the majority (80%) showing clear or almost clear skin.

While second to market after Cosentyx, some clinicians say the phase III data for the two drugs suggest that Taltz may have some efficacy advantages over Novartis' product - though no head-to-head comparison is available - and could allow it to mount a strong challenge.

This study suggests there is no need for exploration of alitretinoin in palmoplantar pustulosis.

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Background:
Palmoplantar pustulosis (PPP) is an inflammatory, debilitating skin disease. Topical drugs and systemic immunosuppressive agents are often ineffective. Previous uncontrolled studies have suggested that alitretinoin could be a meaningful treatment option for PPP.

Objectives:
The primary objective was to determine response to alitretinoin for the treatment of PPP based on the Palmoplantar Pustulosis Area and Severity Index (PPPASI) after 24 weeks of treatment.

Methods:
A phase II, randomized, double-blind, placebo-controlled, multicentre study. Adult patients with PPP (with or without psoriasis) refractory to topical therapy and standard skin care were randomized 2:1 to alitretinoin 30 mg once daily or placebo for up to 24 weeks. The primary end point was PPPASI at week 24 (or the last visit in case of early withdrawal). Secondary end points included: percentage change from baseline in the modified Psoriasis Area and Severity Index (mPASI); percentage of patients with ≥ 50% or 75% improvement in PPPASI or mPASI scores from baseline; change in pustule count on the palms and soles; change in the Nail Psoriasis Severity Index and safety and tolerability assessments.

Results:
Thirty-three patients were randomized: 24 patients to alitretinoin 30 mg and nine to placebo. Overall, there were no significant differences between alitretinoin 30 mg and placebo for any end point. The safety profile was consistent with that seen in patients with chronic severe hand eczema refractory to potent topical corticosteroids.

Conclusions:
Although the results were unexpected based on previous studies of alitretinoin in the treatment of PPP, this study provided no evidence to support further exploration of alitretinoin in the treatment of severe PPP.

Following on from this thread MALT1 gene could be new target in psoriasis you may also find this interesting.

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Background:
The CARD14 gene encodes a protein that enhances nuclear factor (NF)-κB activation and the upregulation of proinflammatory pathway genes. CARD14 is upregulated in psoriatic vs. normal skin, and rare and common CARD14 variants have been associated with the risk of developing psoriasis. Our hypothesis was that CARD14 variants could also influence the response to antitumour necrosis factor (anti-TNF) therapies among patients with psoriasis.

Objectives:
To determine whether CARD14 gene variants were linked to a significant positive anti-TNF response in patients with psoriasis.

Methods:
DNA from 116 patients with psoriasis was subjected to next-generation sequencing of the CARD14 gene. All of the patients were nonresponders or had contraindications to conventional systemic treatments.

Results:
A reduction of at least 75% in Psoriasis Area and Severity Index (PASI 75) at week 24 was considered a positive response to treatment. In total 116 patients (79 responders and 37 nonresponders) were next-generation sequenced, and we identified five nucleotide variants that would result in missense amino acid changes. These variants were determined in all of the patients, and allele and genotype frequencies were compared between the two groups. We found a significantly higher frequency of rs11652075 CC (p.Arg820Trp) among the group with a positive response (P = 0.01, odds ratio 3.71, 95% confidence interval 1.30–10.51). Furthermore, among responders, six patients were heterozygous carriers of the rare p.Glu422Lys variant, and two patients were heterozygous for p.Arg682Trp (P = 0.04).

Conclusions:
The common CARD14 p.Arg820Trp variant might have a significant effect on the response to anti-TNF therapies among patients with psoriasis. In addition, rare CARD14 missense variants could also predispose to a better response.

This study suggests the MALT1 gene could be a possible new target to help those with psoriasis.

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Mutations in CARD14 have recently been linked to psoriasis susceptibility. CARD14 is an epidermal regulator of NF-κB activation. However, the ability of CARD14 to activate other signaling pathways as well as the biochemical mechanisms that mediate and regulate its function remain to be determined.

Here, we report that in addition to NF-κB signaling, CARD14 activates p38 and JNK MAP kinase pathways, all of which are dependent on the paracaspase MALT1. Mechanistically, we demonstrate that CARD14 physically interacts with paracaspase MALT1 and activates MALT1 proteolytic activity and inflammatory gene expression, which are enhanced by psoriasis-associated CARD14 mutations.

Moreover, we show that MALT1 deficiency or pharmacological inhibition of MALT1 catalytic activity inhibits pathogenic mutant CARD14-induced cytokine and chemokine expression in human primary keratinocytes.

Collectively, our findings demonstrate a novel role for MALT1 in CARD14-induced signaling and indicate MALT1 as a valuable therapeutic target in psoriasis.

This study shows that the paracaspase MALT1 is indispensable for CARD14-induced NF-κB and MAP kinase signaling. Pharmacological inhibition of MALT1 prevents pro-inflammatory gene expression in primary keratinocytes induced by psoriasis-associated mutation of CARD14.

Read this in the monthly paper of Sanquin.


Sanquin, Dutch blood institute, participates in a British consortium, PSORT, Psoriasis Stratification to Optimize Relevant Therapy. Dermatologists, researchers, pharmaceutical organisations but also patients are here in United to try to Optimize the therapy with biologicals. The consortium received 5 million pounds in 2013 from the English medical research council and another 2 million of the industrial partners.

People with serious forms of psoriasis benefit from the treatment with biologicals. This new class of medication is very expensive, estimated costs 15.000 per patient per year. Unfortunately part of the patients does not respond well. Possible reasons are genetic background, too low medication levels because of metabolic variations of the forming of antibodies against the medication. PSORT strives for personalised treatment, that holds this and other factors into account.
This results in optimal clinical results, but also in insight in other less common immune diseases as well as a cost reduction in health care.

With the division research, dr. Karien Bloem and dr. Theo Rispens are involved with PSORT. And From diagnostics dr. Annick de Vries with her biologicals lab. Direct corporation in Great Britain is going via doctor-researchers from the Kings College in London and from the university of Manchester. "We are very happy that we found a lab that is able to measure medication as well as anti-drug antibodies combined with the expertise of Sanquin Research on the area of immunogenicity. Together with other parameter that we study with the consortium these tests are an easy and cheap way to support personalised medication". Sanquin is busy developing a blood-spot technique for PSORT so patients can take their blood at home and inform their consultant for adjusting the personalised treatment.

I am currently taking Methotrexate (MTX) and its shortcomings are well documented. Having to take bloods regularly, reducing alcohol intake etc etc. Fortunately I have not had any side effects apart from perhaps being slightly more susceptible to catching a cold and struggling to shake it off. Currently struggling to get rid of a cough after a chest infection.

The reason I believe MTX is the drug of choice for starting with psoriasis sufferers is that it is cheap and generally effective. I believe there are several drugs that could be used for the first round with differing degrees of effectiveness. I recal three but can't remember the names but MTX was said to work 80% of the time with the next closest only 50% effective.

I am aware of other drugs like humira, stelara, fumaderm etc but how do they all fit into the cost benefit model and which have the easiest administration and least side effects. Obviously there may be some very expensive drug with no side effects that you only take once a month but you would be unlikely to get that prescribed as a first choice.

Ideally I think a list of treatments, pros and cons, cost might be helpful. Obviously different treatments may cause different side effects in different people but from and ease of use I am thinking which has least impact on lifestyle, ie allows you to drink and not require blood tests etc.

Hello all,


I'm new to this 'sharing my Psoriasis pains with the world' concept, so please bare with me.

I'm a 39 year old retired Firefighter that was only diagnosed with Plaque Psoriasis after being burned in a structure fire in 2002. I also have Lupus Nephritis.  
It has been one of the biggest challenges of my life. Today, I have roughly 80% of my body covered, not so flaky, but red.
I have tried Embrel and Otezla without success. I am currently undergoing UVB light treatment once a week. This coming week I will begin using Cosentyx. 
Based on some of the responses within the group, I am feeling more confident about this treatment.

I will post my experiences as I progress with the treatment.

Thank you all.

Ric

Hi everyone, 

new to the site so first of all just wanted to introduce myself. 

I am 30 and have suffered with severe psoriasis for about 16 years now... I've pretty much got it everywhere.
Up until a couple of years ago i had managed to control it with light treatment after spending a small fortune on a aramid B (i think) sunbed, unfortunately the treatment slowly stopped working and now doesnt work at all. 

Since my psoriasis came back it has affected everything i do, can't sleep, can't shower at work, can't play football anymore because of the pain, its awful, its basically ruining my life at the moment. My doctor has been prescribing me all sorts of steroid ointments and creams that have been having no affect whatsoever..... I'm running out of patience, i want to try something stronger and have been reading about biologics and systemic treatments but my doctor for some reason seems reluctant to prescribe me anything.

So the reason I've signed up is to find out if anyone has had any joy getting any of these kind of treatments through private healthcare??? I am insured through work with axa private healthcare and am contemplating giving it a go..... i can't take anymore ruined clothes/bedsheets from the ointments anymore with 0 results!!

Anyway... any shared experiences would be much appreciated 

Cheers

Jamie

That's very interesting and a bit disturbing, but not surprising, thank you for posting that, it will give users something to ponder  

Now don't get too excited. This is not one of my short stories.
In a serious vein, I've been thinking about the future. Whilst I'm not in a position yet to start thinking about dating (much too early after the break up) I do realise that one day I will be.
But the thought of attempting a new relationship whilst managing psoriasis seems like an insurmountable obstacle.
My relapses, inability to work and general appearance are going to seriously limit my eligibility. Or am I making mountains out of molehills here?
Anyone got any experiences/ advice to share?

This study set out to analyse serum total IgE levels in addition to the presence and distribution of IgE and FcεRI in psoriatic lesions, and to investigate alteration of IgE and FcεRI after successful systemic treatment.

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Background:
Although elevated serum IgE levels have been reported in psoriasis, the role of IgE in psoriasis still needs to be clarified.

Objectives:
To analyse serum total IgE levels in addition to the presence and distribution of IgE and FcεRI in psoriatic lesions, and to investigate alteration of IgE and FcεRI after successful systemic treatment.

Methods:
Total serum IgE levels were determined using enzyme-linked immunosorbent assay. The expression and localization of IgE and FcεRI was investigated using immunohistochemistry and double immunofluorescence.

Results:
Elevated total serum IgE levels were found in 39% of patients with psoriasis. The levels of total serum IgE were significantly higher in male patients compared with female patients. Furthermore, total serum IgE levels decreased after successful systemic treatment. A positive correlation between IgE+ and FcεRI+ cells and a significant increase of these cells was found in psoriatic lesions when compared with normal skin. Interestingly, IgE+ and FcεRI+ cells decreased significantly after successful therapy with ustekinumab. IgE and FcεRI were coexpressed on mast cells, epidermal Langerhans cells, dermal dendritic cells, macrophages and a small number of neutrophils.

Conclusions:
IgE might participate in the development of psoriasis by activating FcεRI-bearing cells.

Hi I am new to this! 
I've suffered with pustular psoriasis on my hands and feet for nearly 3 yrs now. I've tried every cream, light therapy but still no relief so I was put on Methotrexate which gave me horrendous side effects which is why I was given Humira which I've been on for about 4 wks so far. In that 4 wk period my psoriasis has gone from almost clear to out of control and spreading everywhere else so I have had to start taking the methotrexate again along side it in the hope it stops it spreading further. Back to square one. I have tried a few natural products and detox which I think helped in the past so will be trying that again.
I'm still new to psoriasis and how it can affect you, would really appreciate any advice especially from someone with pustular psoriasis, comments appreciated.
Sam

I would never have said that I was the brainiest person, but PHEW, trying to get onto this forum is a job of its own.

Hello Folks, Just wanted to say hi, this is the first time I have come across a psoriasis forum, really pleased.

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

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

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

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

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

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

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

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

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

Hello all,

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

Regards,

Mike

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

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Abstract:

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

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

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

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

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

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

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

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

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

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

•How long do they start to take affect?

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

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

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