This abstract concludes: We need more un‐biased and well‐designed studies to improve our diagnostic procedure in inflammatory skin diseases. In the future, diagnostic decision‐making will most likely be guided by artificial intelligence‐driven image analysis as well as by molecular diagnostics.

Quote:

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Abstract:

Therapeutic developments have profoundly changed our understanding of the pathogenesis of inflammatory skin diseases, and with it our treatment aims. In particular, the newest generation of biologics in psoriasis, namely antibodies targeting either the IL‐17 or the IL‐23 signalling cascade, comes with a good chance to relieve the patient completely from disease symptoms. However, diagnostic tools have not been co‐developed with these therapeutic options, and our disease classification is partially old‐fashioned and cuts off numerous patients from access to these new therapeutic options. Furthermore, it is currently impossible to predict which patients benefit from a given therapy as well as to stratify patients according to their risk to develop aggravating disease and/or comorbidity.

These facts demand progress in the field of inflammatory skin diseases. First, a modern classification of inflammatory skin diseases that is based on molecular events and with it immune response patterns is needed and second, objective biomarkers that improve our diagnostic power have to be identified. Such biomarkers can improve diagnostics, mirror disease severity,4 stratify patients according to the risk of aggravating disease course or developing comorbidities or predict therapeutic response. Numerous efforts are currently undertaken to assess the quantity of target biomarkers in serum or skin. In parallel, the potential of specific genotypes to stratify patients is investigated.

In a landmark paper published in this issue of the JEADV, Vugt and colleagues demonstrated that therapeutic response to IL‐17 inhibitors is not associated with genetic variation in the IL‐17 gene region. Even though reporting negative data, this study underlines how important well‐designed multi‐centre approaches are to prove hypothesized biomarkers. As it is straight forward to investigate the target region itself for the potential to predict therapeutic response, it is also promising. In the field of melanoma and checkpoint inhibitors, levels of PDL‐1 in tissue have been proposed to stratify response to PD‐1 antagonists as they predict overall survival in combination with the quantity of tumour‐infiltrating lymphocytes. Furthermore, while parallel studies confirm there is no association of IL‐17 genetic variants with response to IL‐17 there is also evidence that the genotype predicts therapeutic response in psoriasis. Namely, the PSORT registry recently published that polymorphisms in HLA‐cw6 are associated with therapeutic response to ustekinumab as compared to TNF inhibitors.

The study of Vugt and colleagues also illustrates how difficult it is to identify reliable biomarkers of therapeutic response. Beyond the detection method (nucleic acids or protein in serum or skin versus genotype), choosing the optimal readout is challenging. This refers both to the time point and to the chosen endpoint – is 24 weeks long enough to determine therapeutic response? Is it primary or secondary non‐responders that are more interesting to investigate? Is skin severity/PASI the ideal readout or should it be a patient‐related outcome or rather an indicator of inflammation/comorbidity?

This is why we need more un‐biased and well‐designed studies to improve our diagnostic procedure in inflammatory skin diseases. In the future, diagnostic decision‐making will most likely be guided by artificial intelligence‐driven image analysis as well as by molecular diagnostics. The latter will determine (a combination of) biomarkers ranging from genotype over serum factors to cutaneous determinants. With time, assessment of such objective biomarkers will become more and more easy and minimally invasive. The future starts now, and it will result in true precision medicine in inflammatory skin diseases.

This study evaluated the effects of patient demographic and disease characteristics on Ilumya / Ilumetri (tildrakizumab) efficacy using phase 2b/3 trial data.

Quote:

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Background:
Tildrakizumab is a high‐affinity, anti–interleukin‐23p19 monoclonal antibody approved for treatment of moderate to severe plaque psoriasis.

Objectives:
To evaluate the effects of patient demographic and disease characteristics on tildrakizumab efficacy using phase 2b/3 trial data.

Methods:
Data from patients who received placebo, or tildrakizumab 100 or 200 mg, in P05495 [NCT01225731], reSURFACE 1 [NCT01722331] and reSURFACE 2 [NCT01729754] were analysed. Patient subgroups were defined by age, sex, race, weight, self‐reported psoriatic arthritis, failure of ≥1 traditional systemic treatment, and prior biologic use. Percentage of Psoriasis Area and Severity Index (PASI) 75 and 90 responders at Week 12 were compared across treatment arms in each subgroup. Absolute PASI at Weeks 0 and 12 were also determined for each subgroup.

Results:
Among patients randomised in P05495 (N = 355), reSURFACE 1 (N = 772) and 2 (N = 1090), percentage of PASI 75 and 90 responders were significantly greater for each tildrakizumab dose vs. placebo (P<0.0001). PASI 75 and 90 responder percentages were numerically greater in patients <65 years of age, body weight ≤90 kg, without psoriatic arthritis, and with no prior biologic exposure (only PASI 90), vs. their counterparts in corresponding subgroups. There were no clear or consistent differences in efficacy between the other subgroups. Absolute PASI scores were generally similar across subgroups.

Conclusions:
Small numerical differences in tildrakizumab efficacy were observed between subgroups defined by patient age and weight, presence of psoriatic arthritis, and prior biologic use. These differences were not clinically meaningful; however, analyses of long‐term data may be of value. Tildrakizumab efficacy did not differ with respect to patient sex or race, or number of prior failed conventional systemic treatments. Overall, these results suggest tildrakizumab may be appropriate for treatment of moderate to severe plaque psoriasis in patients with a range of demographic and disease characteristics.

This study suggests Taltz (Ixekizumab) may help to improve the well-being of patients with genital psoriasis (GenPs)

Quote:

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Background:
Epithelial surface disruption in genital psoriatic lesions may manifest as erosions, fissures and/or ulcers, causing pain and significantly impacting a patient’s sexual health.

Objective:
To evaluate the impact of erosions, fissures and/or ulcers in genital psoriatic lesions on pain and sexual activity in patients with moderate‐to‐severe genital psoriasis (GenPs) and treatment responses to ixekizumab versus placebo until Week 12.

Methods:
This post‐hoc subgroup analysis of patients presenting with and without erosions, fissures and/or ulcers in genital lesions from a phase IIIb multicentre, randomised, double‐blind, placebo‐controlled study (IXORA‐Q; NCT02718898) in 149 adults with moderate‐to‐severe GenPs treated with subcutaneous ixekizumab (80 mg every 2 weeks; n = 75) or placebo (n = 74) evaluated outcomes for clinician‐rated GenPs severity (static Physician’s Global Assessment of Genitalia; sPGA‐G) and patient‐reported genital pain and itch (Genital Psoriasis Symptoms Scale; GPSS) and sexual health (Genital Psoriasis Sexual Frequency Questionnaire; GenPs‐SFQ).

Results:
At baseline, 38% (n = 57) of patients presented with genital erosions, fissures and/or ulcers independent of overall body surface area involvement (<10% or ≥10%). These signs were associated with higher scores for disease severity (sPGA‐G) and pain (GPSS) but not sexual health (GenPs‐SFQ). Complete resolution of these signs was observed in 62% of ixekizumab‐treated patients (25% for placebo) at Week 1 and 83% (21% for placebo) at Week 12. Patients treated with ixekizumab reported significant improvements in pain, itch, disease severity and sexual health over 12 weeks compared to placebo and irrespective of the presence/absence of genital erosions, fissures and/or ulcers at baseline.

Conclusion:
Ixekizumab led to rapid and sustained resolution of erosions, fissures and/or ulcers and significant improvements in GenPs severity, genital pain and sexual health. Ixekizumab may help to improve the well‐being of patients with GenPs.

So, this thread is for everybody who wants to follow my new journey with trying to heal psoriasis through diet and supplements. Also for myself; to follow my progress.
After failing on both Humira ( depression, a much reported side-effect ) and Stelara ( floored for a week per month with heavy flu symptoms, not to mention recuperation time )

on the 22th of july 2019 I began leaving out nightshade foods ( tomato, peppers and potatoes ) and gluten ( grains, pasta ).
But I did eat a lot of ricecakes, nuts and seeds )  
This is the Pagano diet; Healing Psoriasis the natural way. Supplements; slippery elm bark tea and Safflower Petal tea.

Lost weight quickly but the psoriasis didn't subside; it just got worse.

on the 25 of september 2019 I've started doing the AIP Paleo diet. That's like Paleo only stricter. All the known allergens are left out ( tho shellfish is allowed ) 
no seeds
no nuts
( no glory )
no nightshades, grains or oils based on seeds and nuts )
Anyway, you can easily look this up. Heaven knows I did just that bordering obsession   

took a standard probiotic, stopped the Slippery Elm but still continuing the Safflower Petal tea. Slippery Elm is supposed to create a muceous barrier on your intestinal walls. The AIP Paleo diet says no to this. 
Other supplements; some Vitamine D, Fish oil capsules and digestive enzymes.

AIP Paleo is all about not letting food particles ( those on the no list ) not slip into your bloodstream. The idea is that you eliminate those foods as it is said that the intestinal walls of a person with a autoimmune disease are compromised. Or you can call it Leaky Gut, or hightnened permeability of the intestinal walls.

This is all in what is called the 'elimination stage'  after which some foods can be reintroduced slowly and properly monitored. I have no idea how to do that yet, because symptoms are not immediately like in painfull autoimmune diseases like Psoriais Arthritis and such. 
In the USA such diets are already being prescribed, albeit slowly and science is only just taking this more seriously.



Also, alcohol is not allowed in the 'elimination stage'  
This was a hard one for me but I've managed not to drink since the first of January this year. And boy do I looooove my wine and cider.

So basically you could say I've begun this journey in earnest as of the first day of 2020.

I'm now down 9,5 kilo, which is nice.

As of today I'm taking an exta supplement; the probiotic Bacillus Coagulens. I read some interesting scientific reports on 'rheumathoid arthritis and this probiotic, where the results reported where mentioned as "borderline statistically improvement" Apparantly it takes care of harmfull intestinal bacterial growth and because it's spore forming will survive stomach acid and manages to do it's magic in your intestines.

Did I mention I lost weight?   Not that I was much overweight but occurance and severity of psoriasis is higher in overweight people, I've read in my googling.

P scale; not so good yet. Daily showering, steel wire brush and calcipotriol salve to ease the scaliing.

Anyway, this is the first post, let me know if there are any questions and I'll update here when I get a chance.

Hi everyone
My son (who is 16) was diagnosed with psoriasis over a year ago. After finding our way through many doctors we have finally found a dermatologist that has started him on Stelara. First does was on November 16th and his next injection is scheduled for December 14th.
No sign of immediate improvement as of yet. Scalp is flaking very badly and making it difficult for him to attend school. We struggle with the emotional issues that psoriasis can cause, especially when you are a teenager.

Time for another experiment. I have had a plaque on my right knee in some form for at least 25 years. I would treat it with topical and cover it in band aids, but I invariably develop an irritation to the band aid adhesive before the thing heals. After reading a bit of research relating to b vitamins and psoriasis, I thought I'd try a 5mg a day folic acid supplement along with a b complex supplement. This did bugger all, but a little more reading alerted me to a 1963 paper by some British researchers who claimed a 75% positive response (not sure what they mean) to subcutaneous b12 injections directly into plaques.

I don't have b12 for injections, but I do have injectable b12/folic acid (500micrograms/15mg per ml) and sterile insulin syringes suitable for subcutaneous injections. I have been injecting the plaque on my knee daily since Saturday (30/11/2019), initially with 0.075ml, and 0.15ml from Sunday. Below is an image I took of my knee at the start of treatment.



The response has been positive and quite rapid. I will post an updated pic tomorrow as I want to use natural light.

Cheers

Saw a lovely Dermatologist today. Managed to see him privately though he told he I need to get into the NHS system for dermatology at my local hospital. Anyway he was talking about different ways of trying to manage my psoriasis - topical, injections and oral. He said injections wouldn’t help and then said oral would but comes with a lot of side affects. To be honest, I’m not bothered about the side affects at the moment. Just wondering what oral medication anyone is taking and if it’s been successful or if the side affects have been awful - I’m happy to have good and/or bad stories!  My psoriasis gets so sore due to friction from my clothes plus I have them in all the crevices in the body! I’ve got to wait for a letter from him, then I need to go and see my GP to get referred into the system and I go back and see the chap I saw today on 27/1/20 with my research done and ideas of how I want to move on. After 15 years of suffering today has been the first day where I’ve felt someone may be able to give me help and hope!

hi andrews from india

Hello All .... fellow psoriasis sufferer here … have had it since a teenager – now late forties and it has decided to go crazy  ……..got pityriasis rosea in April which really assisted in kicking things south …

went to a dermatologist who is proposing Skilarence – but not too sure I’ll be up for the side effects ive read so doing the usual and trying every other thing else ...
 
ie this month I’m off wheat / taking iodine drops and Astaxanthin ……………………you have to do something ---
Hello .

Hi everyone,

I've posted before on using fumeric acid esters(fumaderm and skilarence) before. I've had great success with these over the last number of years, however they have stopped working 

Seen my derm last week and I've been put on stelera. Nurse is due to call today to help me with my first dose. I'll try to keep this post updated so you can follow the effects 

Let's hope it's as successful as fumaderm was to begin 

Hello everyone I hope you are all well as can be and had a lovely summertime.   Today at dermatology appointment I was told my treatment is changing because the cosentyx has stopped being as effective after almost three years.   I am due to start stelara in a month or so.  I was told a nurse will come to my home to administer my injection every time! With cosentyx this only happened on the first occasion so I’m a little confused at this.   Anyway I’m looking forward to possibility of having clear skin once more.  I also thought stelara was an older biologic but I guess the dr has good reason for making that choice.   I would be interested to hear how others have done with the same switch in treatment too, along with side effects.  I’m concerned about any potential weight gain as I’m no lightweight but I did lose weight when I started cosentyx.  This is important to me because I have reduced mobility and find exercise more difficult.    Other news is we moved house a few months ago into a bungalow and it was very stressful so I think it probably had an effect on my psoriasis.   Thanks for reading !

I started Amgevita (Adalimumab) 4 weeks ago. All the tablet treatments upset my tummy. No side effects as yet other than feeling a little lightheaded on a very few occasions (lasts seconds)
They are free filled injection pens. Brilliant. I feel nothing. It says to nip the injection site skin together, or stretch out. Now when I had to give my wife injections, I was told not to nip the skin. She said it stressed the skin or something, causing bruising.  So I looked up why they nip skin and its to it absorbs in the fat slower. Stretching the skin does the opposite, so I don't get it.
It also says to inject the belly or top of legs. WHY. Yes, the belly is full of fat but not the upper legs?

Hello everybody ,

Today , friday 8th November i have received the first shot ( 45 mg ) of Stelara.
All made in hospital where a kind nurse showed me how to do the injection ( made on the belly ).
More easy than i expected.
My derm explained me all about that Bio drug including possible side effects.
After some hours all ok.
Let's hope that everything will be ok.

Fingers crossed !!

Hi everybody,

Joined the group several years ago. Talked about some of my problems but that is still hard to do. But the website means a lot to me although I m not responding a lot. I hope you will understand.

I have had DMF, light therapy and MTX the past few years and am now progressing to the biologicals. I read Maryam's journal and discovered that people favour humira to stelara? Or is it the other way around. What should I consider? My intake is at November 18 at the AMC Amsterdam.

This study suggests Cosentyx (secukinumab) could help multiple sclerosis in patients with psoriasis.

Quote:

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Background:
According to the literature, a significant association between multiple sclerosis and psoriasis has been reported. Among the various drugs used to treat psoriasis, tumor necrosis factor (TNF)‐α inhibitors seemed to increase the incidence of demyelinating diseases while IL‐17A inhibitors seemed to reduce the activity of multiple sclerosis.

Objectives:
The aim of this study is to find out if the use of Secukinumab in patients with psoriasis and multiple sclerosis would be both beneficial and safe.

Methods:
A 45‐years‐old woman affected by psoriasis and psoriatic arthritis was diagnosed with multiple sclerosis during the treatment for psoriasis. She performed follow‐up visits at the Dermo‐Rheuma Center of Spedali Civili Hospital in Brescia and, after several different therapies, was finally treated with Secukinumab. Outpatient follow‐up visits were performed every two months valuating PASI, joint involvement with CASPAR and DAPSA score and the neurological state with a clinical evaluation and magnetic resonance imaging.

Results:
A significant improvement of both psoriasis and psoriatic arthritis was observed with Secukinumab 300 mg administered monthly. PASI 75 was reached at 4 weeks of therapy, PASI 90 at 6 weeks and PASI 100 at 12 weeks. At 24 months of treatment PASI 100 was still maintained, no neurological symptoms were reported and multiple sclerosis remained stable over time.

Conclusions:
The blockade of IL‐17A with Secukinumab could be a safe and very promising therapeutic option for patients with psoriasis and multiple sclerosis.

Hi hoping to find likeminded people how understand what it like to suffer with psoriasis and the day to day humdrum that’s involved so to all hope to chat soon ?

This cohort study looked at cardiovascular events in patients with psoriasis.

Quote:

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Background:
The cardiovascular safety profile of biologic therapies used for psoriasis is unclear.

Objectives:
To compare the risk of major cardiovascular events (CVEs; acute coronary syndrome, unstable angina, myocardial infarction and stroke) in patients with chronic plaque psoriasis treated with adalimumab, etanercept or ustekinumab in a large prospective cohort.

Methods:
Prospective cohort study examining the comparative risk of major CVEs was conducted using the British Association of Dermatologists Biologics and Immunomodulators Register (BADBIR). The main analysis compared adults with chronic plaque psoriasis receiving ustekinumab with tumour necrosis‐α inhibitors (TNFi: etanercept and adalimumab) while the secondary analyses compared ustekinumab, etanercept, or methotrexate against adalimumab. Hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated using overlap weights by propensity score to balance baseline covariates among comparison groups.

Results:
We included 5,468 biologic‐naïve patients subsequently exposed (951 ustekinumab; 1,313 etanercept; and 3,204 adalimumab) in the main analysis. The secondary analyses also included 2,189 patients receiving methotrexate. The median (p25 – p75) follow up times for patients using ustekinumab, TNFi, adalimumab, etanercept and methotrexate were: 2.01 (1.16 – 3.21), 1.93 (1.05 – 3.34), 1.94 (1.09 – 3.32), 1.92 (0.93 – 3.45) and 1.43 (0.84 – 2.53) years, respectively. Ustekinumab, TNFi, adalimumab, etanercept and methotrexate groups had 7, 29, 23, 6 and 9 patients experiencing major CVEs, respectively. No differences in the risk of major CVEs were observed between biologic therapies (adjusted HR for ustekinumab vs TNFi: 0.96 [95%CI 0.41 – 2.22]; ustekinumab vs adalimumab: 0.81 [0.30 – 2.17]; etanercept vs adalimumab: 0.81 [0.28 – 2.30]) and methotrexate against adalimumab (1.05 [0.34 – 3.28]).

Conclusions:
In this large prospective cohort study, we found no significant differences in the risk of major CVEs between three different biologic therapies and methotrexate. Additional studies, with longer term follow‐up, are needed to investigate the potential effects of biologic therapies on incidence of major CVEs.

I started having psoriasis in my 20s (around 1997)   Wasn't surprised and knew what it was since my mom had it.  It got progressively worse as the years went by and I believe it was due to stress (work related).

2006:  Finally decided to do something about it and went to see a dermatologist.   

She was batshit crazy.

1. she made me strip naked
2. put on gloves and was grabbing my limbs with the tips of her fingers
3. then told me I had psoriasis .... (no shit sherlock)
4. told me to take a bath only twice a week but slap on the greasiest cream I could find twice a day and gave me a prescription for Dovobet and something for my scalp

Let's just say I never went back.  I'd rather live with the psoriasis and shower every day!

Winter 2008: I wake up one morning and feel like I got run over by a train.  

Try everything I can put my hands on but after about three weeks, decide to go see a doctor as it is to a point where I'm having trouble driving cause I can't move my neck!

result:  acute arthritis attack

Medication: Celebrex for about 3 weeks

2008 to 2013:  Arthritis is getting worse and psoriasis also

2013:  Got referred to a new dermatologist.  She was excellent.

1. Just looked at me and touched the plaques with no gloves 
2. Gave me a book to read about psoriasis and possible treatments so we could discuss which way to go at the next appointment

Medication:  Metothrexate

2014:  No side effects. Psoriasis is all gone but it doesn't work for the arthritis

My dermatologist wants to send me for a liver biopsy because I've been on MTX for a year even if my blood work tests are ok.

Therefore, I stop MTX as I don't want to do a biopsy

Of course, the psoriasis all came back with a vengeance

2015: Tired of being in pain so back to the doctor who refers me to a rheumatologist

Medication: MTX for about 6 months, psoriasis went away but does nothing for the arthritis.  No side effects.

2016: The guinea pig experiments begin!

Medication:

1. Leflunomide:  again works well for the psoriasis but does nothing for the arthritis

2. Humira: took it for about two months but my face swelled up.  

Result: stop Humira and on prednisone for about a month to reduce the swelling.  Psoriasis starts to come back

2017: Stelara:  Psoriasis goes away
2018: Stelara is not helping with the arthritis.  Stop Stelara and get a prescription for Cosentyx

End of may: in between Stelara and Cosentyx, start to experience chest pains on the left side.  I don't have a cold or anything else however my boss was away from work due to a weird virus.  Wait three weeks (until I am crying because of the pain and can't sleep) before going to the doctor.  

Appointment at the doc in the morning: walk out with a prescription for prednisone and dilaudid plus a paper to go for a chest Xray.  Go for the chest Xray and then to work

late afternoon (4h30):  Get a panicked call from my hubby saying I have to go the the clinic to pick up a piece of paper and head straight to the ER.....result from Xray: possible pulmonary embolism

Spend over 12 hours at the ER (all night)....they passed a woman (in her 30s) with an ear ache before me because she kept comlaining to the nurse.  I was sitting patiently and waiting for my turn      Lesson learned:  Complaining, crying and making a scene will get you seen by a doctor faster.

Did a heart test and a CT scan at about 5 am the next day and got sent home with a promise from the doctor that I will get a phone call with the result.

result:  inflammation and liquid around the left side of the heart and left lung.

On prednisone for about two months and a paper to do a second CT scan three months later

Cosentyx is put on hold

August:  Rheumatologist says that since the internal organs are affected, I have lupus (still don't believe this), put on azathioprine 100 mg.

Beginning of October:  Second scan done.   All is good
November: Rheumatologist gives the ok to start Cosentyx 150 mg but reduces the azathioprine to 50 mg. 
December: Sick as a dog, take a pause from Cosentyx until I feel better

2019: Start Cosentyx in February

August: Rheumatologist increases the Cosentyx dose to 300 mg as 150 is not doing anything for the arthritis

September: After my second dose of 300 mg, get sick as a dog and sound like a rattlesnake

Medication: 
Prednisone
Antibiotics
2 inhalors

October: got the all clear to continue Cosentyx and a referral for a pulmonary capacity test (appointment in January 2020).  Therefore, took my 3rd dose of 300 mg

Hi,

Are you experiencing Raynaud`s disease/phenomenon and if so, what did your doctor recommend or prescribe?

What is Raynaud's

Raynaud's disease causes some areas of your body — such as your fingers and toes — to feel numb and cold in response to cold temperatures or stress. In Raynaud's disease, smaller arteries that supply blood to your skin narrow, limiting blood circulation to affected areas.

Symptoms can include:

• Cold fingers or toes
  
  
• Color changes in your skin in response to cold or stress
  
  
• Numb, prickly feeling or stinging pain upon warming or stress relief
  

• Connective tissue diseases. Most people who have a rare disease that leads to hardening and scarring of the skin (scleroderma) have Raynaud's.
  
  
• Other diseases that increase the risk of Raynaud's include lupus and arthritis.
  
  
• Diseases of the arteries. These include a buildup of plaques in blood vessels that feed the heart (atherosclerosis), a disorder in which the blood vessels of the hands and feet become inflamed (Buerger's disease), and a type of high blood pressure that affects the arteries of the lungs (primary pulmonary hypertension).
  
  
• Carpal tunnel syndrome. This condition involves pressure on a major nerve to your hand, producing numbness and pain in the hand that can make the hand more susceptible to cold temperatures.
  
  
• Repetitive action or vibration. Typing, playing piano or doing similar movements for long periods and operating vibrating tools, such as jackhammers, can lead to overuse injuries.
  
  
• Smoking. Smoking constricts blood vessels.
  
  
• Injuries to the hands or feet
  

This study suggests neutral to favourable long term trends in metabolic and liver parameters under Cosentyx (secukinumab) treatment.

Quote:

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Background:
Psoriasis is associated with metabolic, liver and cardiovascular comorbidity. Secukinumab, a fully human monoclonal antibody that selectively neutralizes interleukin‐17A (IL‐17A), has shown significant and sustained efficacy in the treatment of moderate to severe psoriasis.

Objectives:
This was an exploratory post hoc analysis of pooled data from three phase 3 studies in plaque psoriasis patient populations. The objective was to show the course of metabolic and liver parameters under secukinumab, etanercept, or placebo treatment over time. A further objective was to assess the impact of selected comorbidities and metabolic characteristics on high‐sensitivity C‐reactive protein (hs‐CRP), as a surrogate marker of systemic inflammation.

Methods:
Data from the phase 3 randomised controlled trials (FIXTURE [NCT01358578], ERASURE [NCT01365455], and SCULPTURE [NCT01406938]; n=3010) were included in this analysis. Patients were treated with secukinumab 150 mg or 300 mg, placebo or etanercept 50 mg (FIXTURE only) as active comparator. A set of metabolic and liver parameters was longitudinally assessed over 52 weeks. Multivariate regression analyses assessed the impact of selected comorbidities and metabolic characteristics on hs‐CRP levels at baseline and under treatment.

Results:

Secukinumab treatment reduced hs‐CRP levels. Body weight and uric acid levels tended to decrease over 52 weeks with secukinumab. Secukinumab showed a neutral effect on fasting plasma glucose, lipid parameters and liver enzymes. Psoriatic arthritis, metabolic syndrome, obesity, impaired glucose metabolism, and hyperuricemia were each associated with increased hs‐CRP levels at baseline. Concomitant obesity attenuated the decline in hs‐CRP under treatment.

Conclusions:
These analyses suggest neutral to favourable long term trends in metabolic and liver parameters under secukinumab treatment. Metabolic comorbidities were associated with increased hs‐CRP levels, reflecting the role of systemic inflammatory processes in their pathophysiology.