This study investigated the risk of cancer in TNFi treated psoriatic arthritis (PsA) patients compared with standardized rates from the general population in Denmark, Finland, Iceland and Sweden.

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Background: Tumour necrosis factor inhibitors (TNFi) effectively reduce inflammation in Psoriatic arthritis (PsA). However, a possible association between treatment with TNFi and an increased cancer risk has previously been suggested.

Objectives: To investigate the risk of cancer in TNFi treated PsA patients compared with standardized rates from the general population in Denmark, Finland, Iceland and Sweden.

Methods: TNFi-treated PsA patients were followed from first registration with TNFi-treatment in ARTIS (Sweden), DANBIO (Denmark), ICEBIO (Iceland) or ROB-FIN (Finland) and linked to the national Cancer Registry in each country. Patients with a cancer history prior to start of follow-up were excluded. We investigated the risk of primary cancer among TNFi-treated PsA patients compared with general population cancer rates standardized to age, sex and calendar period within each country. Standardized incidence ratios (SIRs) were estimated for each country and pooled SIRs were subsequently calculated for both any cancer and site-specific cancers of interest.

Results: A total of 5218, 2039, 270 and 526 patients were registered as ever TNFi-treated in ARTIS, DANBIO, ICEBIO and ROB-FIN, respectively, contributing a total of 44 041 patient years of follow-up across all 4 countries.

For all cancers, the SIRs of TNFi-treated patients from ARTIS, DANBIO, ICEBIO and ROB-FIN were 0.94 (0.80 to 1.10), 0.99 (0.77 to 1.26), 1.71 (0.88 to 2.99) and 1.28 (0.82 to 1.90), respectively. The number of observed and expected cancers and the SIRs of any and selected site-specific cancers are listed in table 1

Table 1
Standardized incidence ratios (SIR) of TNFi-treated patients from 4 Nordic countries compared with the general population.

Observed cancers  Expected cancers SIR (95% confidence interval) All cancers
282                           281.6                      1.00 (0.89 to 1.13)
Colorectal
32                             26.5                        1.21 (0.85 to 1.71)
Hodgkin’s and non-Hodgkin’s lymphoma
21                             11.4                        1.84 (1.20 to 2.82)
Lung
20                             25.4                        0.79 (0.51 to 1.22)
Malignant melanoma
20                             18.6                        1.07 (0.69 to 1.66)
Pancreas
8                               6.6                          1.21 (0.60 to 2.41)
Brain
7                              7.4                           0.95 (0.45 to 1.99)
Female breast
58                            48.4                         1.20 (0.93 to 1.55)
Corpus uteri
6                              9.0                           0.67 (0.30 to 1.49)
Prostate
34                            48.8                         0.70 (0.50 to 0.98)
Only included sites with >5 cancer outcomes.

Conclusion: Our results suggest that the overall cancer risk for TNFi-treated PsA patients is not increased compared to the general population. Further analysis of the risk of malignant lymphomas will inform on whether the increased risk we observed is attributed to the PsA disease or treatment with TNFi.

This study set out to identify possible differences in satisfaction with biological treatment between female and male psoriasis patients.

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Background:
Female sex has been reported as a predictor for treatment discontinuation with biological therapies for psoriasis, although reasons remain unclear. It can be hypothesized that lower satisfaction with biological treatment in women might add to the lower drug survival rates.

Objectives:
To identify possible differences in satisfaction with biological treatment between female and male patients using the Treatment Satisfaction Questionnaire for Medication (TSQM).

Methods:
Data of psoriasis patients treated with biologics were obtained from the prospective, multicentre, daily‐practice BioCAPTURE registry. Longitudinal TSQM data were analyzed by linear mixed models. Relevant patient characteristics were incorporated as possible confounding factors. Post hoc analysis of adverse events was performed in order to investigate differences between sexes.

Results:
We included 315 patients with 396 corresponding treatment episodes (137 adalimumab, 90 etanercept, 137 ustekinumab, 24 secukinumab, 8 infliximab). Almost forty percent of the patients were female. Females had significantly lower baseline PASI scores (p=0.01). Longitudinal analyses demonstrated lower TSQM scores for ‘side effects’ (p=0.05) and ‘global satisfaction’ (p=0.01) in female patients compared to male patients over one year of treatment. Females reported more relevant adverse events in the context of biologic treatment compared to males (rate ratio 1.79; p<0.001), with more fungal (rate ratio 2.20; p=0.001) and herpes simplex infections (rate ratio 3.25; p=0.005).

Conclusions:
This study provides a prospective, longitudinal analysis of treatment satisfaction with biologics in female and male patients with psoriasis. Women were slightly less satisfied with treatment regarding side effects and global satisfaction. Differences in treatment satisfaction and side effects might add to the fact that women discontinue biological treatments more often.

This study suggests a picture‐based method is the most advantages in terms of reliability, speed and user‐friendliness for the correct dosage of topical treatments.

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Background:
The accurate determination of the dosage of topical treatments is important given its repercussions on patient adherence and therapeutic efficacy. Up till now, the fingertip unit calculated by the rule of hands is considered the gold standard, although its use is associated with several drawbacks.

Objective:
To compare different methods to estimate the affected body surface area (BSA) and dosage of topical treatments in atopic dermatitis and psoriasis and investigate its reliability, user‐friendliness and timing.

Methods:
In this study, we compared the reliability of 3 different methods: (1) the fingertip unit calculated by the 1% hand rule; (2) a picture‐based tool [termed cutaneous inflammatory disease extent score (CIDES)] and (3) a digital drawing tool. 11 observers scored 40 patients with psoriasis and eczema to assess the inter‐ and intrarater reliability. Timing was automatically recorded and user‐friendliness was investigated by a questionnaire.

Results:
An excellent intraclass correlation (ICC) was found for both inter‐ and intrarater agreement for the picture‐based tool (ICC=0.92 and ICC=0.96, respectively). The ICCs for drawing the area of involvement on a silhouette were 0.89 and 0.93, respectively. Finally, the rule of hands was associated with an increased interrater variability although an excellent intrarater agreement was found (ICC=0.79 and 0.95, respectively). Automated calculation of the amount of topical treatment improved reliability and CIDES was associated with the least variation. CIDES was considered the preferred method by all observers and was fast to perform (median: 30 sec).

Conclusion:
A picture‐based method offered the most advantages (in terms of reliability, speed and user‐friendliness) to estimate the affected BSA and calculate the dosage of topical treatments.

This study looked at circulating plasma claudin‐3 in patients with psoriasis

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Background:
Gut dysbiosis and increased intestinal permeability play a significant role in the pathogenesis of psoriasis and its comorbidities. Claudin‐3 is a key component of tight junctions, which may serve as marker of gut barrier integrity.

Objectives:
The aim of the study was to investigate circulating plasma claudin‐3 in patients with psoriasis and to evaluate clinical and metabolic factors, which determine its concentration.

Methods:
This cross‐sectional study included 60 patients with psoriasis (39 men and 21 women, mean age: 45.6±12.1 years) and 30 healthy controls (18 men and 12 women, mean age: 46.3±15.5 years) age, sex and body mass index‐matched. Plasma claudin‐3 concentration was measured using an enzyme‐linked immunosorbent assay.

Results:
Plasma claudin‐3 concentration was significantly higher in patients with psoriasis in comparison to healthy control [median (interquartile range), 50.7 ng/ml (47.3‐54.2) vs 43.3 ng/ml (42.3‐44.2), p < 0.001]. Patients who achieved ⊗PASI90 response after 16 weeks of treatment showed tendency to decrease in circulating claudin‐3 plasma concentration. Positive correlations between claudin‐3 concentration and the PASI score (r = 0.828; p < 0.001) as well as claudin‐3 and neutrophil‐to‐lymphocyte ratio (r = 0.847; p < 0.001) were found. A multivariable linear regression analysis confirmed association of claudin‐3 with the PASI score (p < 0.001), neutrophil‐to‐lymphocyte ratio (p < 0.01) and active smoking (p < 0.05).

Conclusion:
Claudin‐3, a biomarker for gut permeability, is increased in psoriasis and correlates with disease severity and smoking. Further investigations are needed to determine whether reinforcing intestinal barrier may be a new therapeutic target in psoriasis.

I stumbled across this wonderful forum searching for answers, yet again, sigh!!

2019 marks my 30th year as a psoriasis sufferer, so ill try give a bit of background on what i have tried over all those years

tar baths/cortisone creams
Naturopath - natural concoctions and acupuncture 
Chinese herbalist - yes i drank "soup" made from boiled beetles, among other things   
PUVA - several times
PUVB 
Methotrexate twice - 1st time cleared ok, 2nd time no good and got very sick even with folic acid supplements
Cyclosporin
Stelara since 2010 (last dose 25/3/19)

and 1 week ago started my first loading dose of 
Cosentyx ( 2 pens x 150ml) 

Stelara and i were getting along fine   , however, at the start of 2018 i began to have issues with my knee. Pain, swelling & stiffness.  Did all the imaging and started physio. Dermatologist put me on Celebrex, which helped, but GP said only to take it short term/when needed, so stopped.  After 4 months of physio i decided to stop going, while my knee did get stronger, my symptoms were the same.  Easter time my lower back started hurting without any cause, ignored it.  At my recent Dermatologist appt he switched me to Cosentyx as he believes the knee issue is PsA related. Back on the Celebrex too.

So here I am, feeling quite odd because for 9 years i had a 3 monthly injection and my psoriasis was completely clear,,,,,,,, now i feel like I'm heading into the unknown yet again. Whilst my psoriasis is completely clear, I'm really hoping it stays that way!!!

Nice to be part of such a supportive group

Howdy y'all,

A real quick rundown of my dose of Methotrexate. Also, note that my dermatologist is a man. But I interact more with the resident under him, who is a woman. So if I get gender-confused, that's why haha

My dermatologist had me start a daily regimen of folic acid 2 days before she had me start the MTX (that I skip on the days I take MTX). I was taking the MTX on Tuesday's. But because of the required labs and the clashing with my job, I had to move the dose to Wednesday. 


1. I started a 2-pill dose on April 23. 

• The first labs came back normal. I discovered I am anemic based on my lab results. I didn't know but had an idea that I am. 
  
• I also had serious heartburn. There was also occasional pressure under my sternum like gallstones. I had experienced gallstones 15 years ago after having my son. Never had that issue resolved but the pain stopped after a couple of years. I emailed my dermatologist about this symptom and she says it is not related to the MTX and to contact my primary. 
  
• No change in psoriasis
  

• Labs again were normal. But I've started having issues with my job. I couldn't concentrate. Distractibility was high. 
  
• 2 days after this dose, I had a full-blown gallstone attack that had me down and out for a couple of hours. Then again another attack the next day. No clue what triggered the attack
  
• A small change in psoriasis.
  

• Labs were normal so dr upped the dosage. 
  
• Emailed my dr about the fatigue, distractibility and how it affects my very unique job. 
  
• Inverse psoriasis has begun to clear up.
  

• Fatigue has been kicking my butt. My boss has given me permission to take off early if I can't work with a clear head, providing I have the vacation/sick hours to cover.
  
• Distractability wasn't an issue until today (5 days post-dose). 
  
• I feel like my mind goes blank sometimes. I'll be doing something and stop and just think "what was I doing?" That actually happened while I was creating this thread.
  
• The inverse psoriasis was almost cleared up but seems to be making a come-back.
  
• Plaques/guttate has started clearing up on the larger areas but itches like hell. Anytime I scratch, I bleed all over the place.
  
• Psoriasis had started moving down my legs more but seems to have stopped progressing.
  

Hi all,

I have joined this board in hopes of finding some info on the treatments for psoriasis.

I first experienced psoriasis when I was a teen. At the time, I didn't realize what it was. I just itched a lot on my arms and legs and didn't know why. After a change in detergents, it went away. I've had various short episodes since then. Most of the time my flare-ups are triggered by an allergic reaction to detergents or fabric softeners. That alone has limited me to using only All Free & Clear to wash my clothes.  I have a reaction to ALL box soaps and anything scented. Recently, All released their new Free & Clear softener and I was hoping I could use that since I pretty much live off the detergent. That was a big fat NOPE. It resulted in a flare-up that I'm currently dealing with.

How do I know it was psoriasis you ask? Besides a Dr's diagnosis, my mother is a lifetime psoriasis sufferer as well. We have worked through this fight together to find out what works and what doesn't. I also have an aunt and an uncle on my dad's side who has psoriasis but I don't interact with them very much. 

I have had inverse psoriasis most of my life. I live in Texas and the heat (sweating) makes it worse. Sweating, in general, makes it worse. It makes me miserable, unhappy, and in a lot of pain. So I tend to avoid exercise because sweat = pain. When I say I have had a flare up I'm referring to plaque and guttate psoriasis. The inverse is ever-present in my life and quickly rears it's head if I sweat too much. 

With this new and most recent flare-up, I was finally able to get a real dermatology referral. Past dermatology experiences have had me doing creams only. A few times, I had done light therapy. With my current schedule of kids, being a full-time student, and a full-time job, light therapy isn't an option. So, I am now on methotrexate as the "first step" towards biologics. I feel like I am struggling with this medication and so here I am hoping to find support.

This study suggest that patients over 90 kg could benefit from moving to a two week between shots regime with Cosentyx (secukinumab).

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Background:
Secukinumab is a fully human monoclonal antibody that selectively binds to and neutralises interleukin‐17A.

Objective:
To assess the efficacy and safety of different maintenance‐dosing regimens of secukinumab 300 mg based on PASI response at Week 24 in patients with moderate to severe plaque psoriasis.

Methods:
OPTIMISE was a randomised, open‐label, rater‐blinded Phase 3b study. Subjects (n=1,647) received secukinumab 300 mg at baseline, Weeks 1, 2, 3, and 4, and every 4 weeks (q4w) to Week 24. At Week 24, PASI 90 responders (n=1306) were randomised to secukinumab 300 mg q4w (n=644) or every 6 weeks (q6w, n=662) regimen to Week 52; PASI ≥75 to <90 responders (n= 206) were randomised to secukinumab 300 mg q4w (n=114) or every 2 weeks (q2w, n=92) regimen to Week 52.

Results:
PASI 90 response was maintained at Week 52 by 85.7% subjects with q4w dosing vs 74.9% with q6w dosing; odds ratio 1.91 (95% confidence interval 1.44, 2.55). The primary endpoint, non‐inferiority of q6w vs q4w dosing, was not met. In PASI ≥75 to <90 responders, the proportion of subjects with PASI 90 response at Week 52 was numerically higher in q2w vs. q4w group (56.5% vs. 46.5%, respectively; P=0.1013). Heavier subjects (≥90 kg) demonstrated numerically higher PASI 90 response with q2w (57.1%) vs q4w regimen (39.6%, P=0.1053).

Conclusion:
Standard q4w dosing of secukinumab 300 mg is the optimal dosing regimen to achieve and maintain clear or almost clear skin. Subjects with body weight ≥90 kg not achieving PASI 90 at Week 24 may benefit from the q2w dosing regimen.

Hi All,

I just had my first real experience with arthritis this morning (aside from the ache in my hips). I awoke with my knuckle swollen, hand disfigured and experiencing dull pain. Any remedy aside from the Cosentyx that I am currently taking?

Thanks!
Kevin

I was just reading Kat's post RE: Cosentyx - Kat's journey and it got me thinking.

Are there any of our members using Cosentyx that got completely clear and staying that way ?

For me it started off well, but now I find I still get the occasional flare up and have to resort to using some Diprosone with it. This usually happens if I get wound up about something, but I have also noticed it happens around week three.

What about you, anyone staying clear with just Cosentyx ?

Hi All:

I've been on Cosentyx for about three months now and it is not getting any better. Lesions are all over and more are appearing in inconspicuous locations. Curious if there are best practices concerning administering the shot (i.e. time of day, location, etc.)?

Any help would be appreciated.

Thanks.

Kevin

Hey all, it may be obvious by now that as a new member I am posting my biggest questions here and there.

For this thread my question is if anyone has tips about the best way to dry long (no idea if length is relevant) hair after a shower with scalp psoriasis. I typically let my hair air dry or towel dry but sometimes I blow dry for expediency. I was wondering if anyone knew if there was a "best" way to keep my scalp healthier. Is the heat from a blowdryer bad? is a cool setting better? is towel drying best? what are your thoughts?

and one more question: I love hot showers! They are the most relaxing thing to me, especially after a long day, is that bad for my scalp psoriasis? I don't think I can give up hot showers even if it is, but I think I should know for reference.

Hello, new member here who was just put on otezla by my dermatologist.

The doctor put me on a tapered dose to start and I just started taking twice a day pills at 10mg each yesterday, I will slowly be working up to the twice a day 30mg pills (6omg total).

I have been concerned about the side affects specifically nausea and migraines hurting my ability to study and carry on with life stuff so I wanted to ask peeps here how they have done/are doing on otezla? And specifically, when did you experience side affects? Immediately, or did it take longer (and/or until you were up to the full 60mg)? and how long did the side affects last for you?

I know everyone is different and my experience may not be the same, but I am just looking for some kind of reference of what I might be able to expect.

Hi, I have just recently in the past week, been diagnosed with psoriasis and found this group while searching for a community that I could feel safe discussing this condition with. I am 30, female.

I mainly have scalp psoriasis but also have it on other parts of my body. Before my dermatologist's appointment I had no idea what this was and thought it was just a rash or fungal infection! I was so embarrassed because my scalp started shedding and I am a student and an intern studying to be a teacher and it just has been hammered into me that I need to professional all the time in everything! I am a bit relieved to know the cause because I was trying to treat it on my own and nothing was working!! But I am still a little concerned about scalp shedding in my chosen profession. I am worried my supervisor or a principal or mentor will think it is unprofessional and I have been contemplating telling my professors about my condition before someone says something, but it is a bit private and I'm not sure I should say anything. I have mostly been hiding it now by always braiding my hair.

Anyway, I finally went to a dermatologist and was given a month's supply of otezla (which I am not sure I will qualify for the free service in the future, but my doctor wants me to try). As well as some prescription topicals. She also suggested I use tgel shampoo.

I am now on a tapered dose of otezla and started with one ten mg dose in the morning and moving up to 20 taken in two 10mg pills twice a day today, and slowly building to the 30mg twice a day. I haven't noticed any side affects so far, but maybe it takes until you are on a higher dose?

I don't know much about psoriasis treatment, medications or anything, so any tips for a beginner would be nice.

The Food and Drug Administration (FDA) has approved Skyrizi (risankizumab-rzaa), an interleukin-23 (IL-23) inhibitor, for the treatment of moderate to severe plaque psoriasis in adults.

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AbbVie today announced that the U.S. Food and Drug Administration (FDA) approved SKYRIZI™ (risankizumab-rzaa), an interleukin-23 (IL-23) inhibitor, for the treatment of moderate to severe plaque psoriasis in adults who are candidates for systemic therapy or phototherapy.3 In clinical trials, SKYRIZI produced high rates of durable skin clearance – most people (82 and 81 percent) treated with SKYRIZI achieved 90 percent skin clearance (PASI 90) at one year, with the majority (56 and 60 percent) achieving complete skin clearance (PASI 100).

"The complex nature of psoriasis and the variability or loss of treatment response over time can prevent some patients from achieving their treatment goals," said Kenneth B. Gordon, M.D., a principal investigator for the ultIMMa-1 pivotal trial and professor and chair of dermatology at the Medical College of Wisconsin. "In clinical trials, risankizumab demonstrated high levels of skin clearance that persisted through one year. I'm pleased the dermatology community now has a new option that can help patients achieve and maintain a high level of treatment response."

The recommended dose for SKYRIZI is 150mg – administered by two subcutaneous injections every 12 weeks following two initiation doses at week 0 and 4. SKYRIZI can be administered in-office or by self-injection after training.

"The approval of SKYRIZI is an important advance in the treatment of adults with plaque psoriasis who are seeking high levels of durable skin clearance that can be maintained over time," said Michael Severino, M.D., vice chairman and president, AbbVie. "SKYRIZI builds on AbbVie's legacy in immunology, expanding our portfolio to help meet the evolving needs in psoriatic disease and reinforcing our continued pursuit of innovations that improve care for people living with immune-mediated conditions."

Affecting 7.5 million Americans, psoriasis is the most prevalent autoimmune disease in the U.S.4 It is characterized by over activation of the immune system and widespread inflammation that causes painful, itchy plaques anywhere on the skin.5 People with psoriasis also experience a significant emotional, psychological and social burden that can negatively impact their quality of life.

"People living with plaque psoriasis can be profoundly impacted by their disease both physically and emotionally," said Stacie Bell, Ph.D., vice president of research and medical affairs, National Psoriasis Foundation. "The approval of a new therapy represents an important step forward in the treatment of psoriasis, offering dermatologists another option to help patients achieve their treatment goals."

The approval of SKYRIZI is supported by results from AbbVie's global Phase 3 psoriasis program, which assessed the safety and efficacy of SKYRIZI in adults with moderate to severe plaque psoriasis across four randomized, placebo and/or active-controlled pivotal studies: ultIMMa-1, ultIMMa-2, IMMhance and IMMvent. The co-primary endpoints of these studies were Psoriasis Area and Severity Index (PASI 90) and static Physician Global Assessment [sPGA] score of clear or almost clear [sPGA 0/1] at 16 weeks versus placebo.

This study suggests immunogenicity incidence over 5 years of treatment was consistently below 1% in psoriasis patients treated with Cosentyx (secukinumab)

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Background:
Secukinumab is a fully human monoclonal antibody that selectively neutralizes IL‐17A, a key cytokine involved in psoriasis (PsO) and psoriatic arthritis (PsA) development, and has shown rapid and long lasting efficacy and safety in the complete spectrum of psoriasis manifestations. Monoclonal antibody therapies may be associated with the production of treatment‐emergent anti‐drug antibodies (TE‐ADA) that can affect drug pharmacokinetics, diminish clinical responses via inhibition of target binding, or cause hypersensitivity reactions. Secukinumab exhibited minimal immunogenicity up to 52 weeks in patients with moderate‐to‐severe plaque psoriasis, as evidenced by TE‐ADA in <1% patients.

Objective:
To investigate the immunogenicity of secukinumab treatment up to 5 years in two phase 3 extension studies (NCT01640951 and NCT01365455) in patients with moderate‐to‐severe plaque psoriasis.

Methods:
Immunogenicity was evaluated up to Week 268 (5 years). TE‐ADA were defined as positive anti‐drug antibody (ADA) signals detected in post‐treatment samples from patients with negative baseline signals. Confirmed positive samples were further analysed for their neutralizing potential.

Results:
In total, 1821 patients entered the extension studies. Among patients receiving secukinumab and evaluated for ADAs (n = 1636), 32 developed TE‐ADA, which resulted in an incidence of new TE‐ADA cases below 1% per year. Neutralizing antibodies were detected in 9/32 (28%) patients with TE‐ADA. Half of ADA‐positive cases were transient. Among pharmacokinetic samples measured at the times of immunogenicity determination (n = 9992), 544 (5.4%) had secukinumab concentrations higher than the drug tolerance level of 53.8 μg/mL. There was no effect of TE‐ADA, including neutralizing antibodies, on efficacy, safety, or pharmacokinetics of secukinumab.

Conclusion:
The yearly secukinumab immunogenicity incidence over 5 years of treatment was consistently below 1% in patients with moderate‐to‐severe plaque psoriasis. Any TE‐ADA, including neutralizing antibodies, were not associated with loss of secukinumab efficacy or with clinical concerns.

This study suggests that Mental Health Inventory (MHI‐5) is a reliable and valid instrument that can be used to effectively capture psychological distress in psoriasis patients.

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Background:
Patients with psoriasis are at risk of a comorbid diagnosis of depression and/or anxiety. It is therefore essential for dermatologists to have valid and effective instruments that can screen and monitor depression and anxiety symptoms in psoriasis patients.

Objective:
The aim of this study was to validate the Mental Health Inventory (MHI‐5) as a brief measure that can be used to evaluate psychological distress related to anxiety and depression in psoriasis patients.

Methods:
The sample included 76 adult dermatological outpatients diagnosed with psoriasis. Participants completed the MHI‐5, the Hospital Anxiety and Depression Scale (HADS), and six subscales of the Self Compassion Scale (SCS). Confirmatory Factor Analysis (CFA) was applied to examine the factor structure of MHI‐5. Convergent validity was examined by applying correlations among all measures. Discriminant validity was examined by applying hierarchical regression models. Reliability was examined by calculating the Cronbach's alpha coefficient.

Results:
CFA showed that the proposed one‐factor model has a good fit to the data. The MHI‐5 demonstrated satisfactory convergent validity by yielding significant moderate to strong correlations with the HADS and with the positive and negative subscales of the SCS. Discriminant validity was also evident with being at risk for anxiety predicting MHI‐5 scores above and beyond the effect of gender and age. Hierarchical regressions were not performed because a very small number of participants (n = 3) were classified at risk for depression. The MHI‐5 showed high internal consistency (α = 0.84)

Conclusion:
This investigation provided evidence that MHI‐5 is a reliable and valid instrument that can be used to effectively capture psychological distress in psoriasis patients.

This study suggests there is an increased vascular risk in psoriasis patients with depression.

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Background:
Psoriasis is known to confer a higher risk of cardiovascular and cerebrovascular diseases. However, very few studies have investigated whether the development of depression in psoriasis patients may further increase this vascular risk.

Objective:
We investigated the risk of ischaemic heart disease and cerebrovascular disease in Taiwanese psoriasis patients with and without depression.

Methods:
A nationwide population‐based retrospective cohort study was performed using the National Health Insurance Research Database. We included 604 psoriasis patients with depression, who were matched to 2,416 psoriasis patients without depression (1:4 ratio). Relative risks (RR) with 95% confidence intervals (CI) were determined using the Cox proportional hazards regression model, with adjustment for demographic characteristics and comorbidities.

Results:
Compared with psoriasis patients without depression, psoriasis patients with depression had greater risk of developing incident ischaemic heart disease (19.5% versus 8.3%, adjusted RR 1.98, 95% CI 1.57‐2.49), cerebrovascular disease (15.6% versus 5.9%, adjusted RR 2.29, 95% CI 1.76‐2.98), and either ischaemic heart disease or cerebrovascular disease (28.3% versus 12.5%, adjusted RR 1.94, 95% CI 1.60‐2.35). Subgroup analysis showed that in psoriasis patients with depression, a higher risk of incident ischaemic heart disease or cerebrovascular disease was present in age groups 30‐100 years, in both males and females, and in both lower and higher income categories.

Conclusion:
Depression is an independent risk factor for incident ischaemic heart disease and cerebrovascular disease in patients with psoriasis. Therefore, clinicians need to be vigilant for the increased vascular risk in psoriasis patients with depression.

Right, so as i posted in my main thread, i was sick last week and ended up on Antibiotics, so couldn't take my dose of Stelara last thursday like I was supposed to.

Now, i'm going to take it this Thursday, but what i want to know is, should i take my next dose, in 12 weeks, or 11? should i stay on the same schedule, but just take last weeks dose a week late, or should i start a whole new 12 week cycle from this Thursday?

Used Otezla for 5 weeks now. No bad side effects. Had them all very mild and all cleared.
I now have started with a bad rash. Mainly at the top of my legs. I also have it behind my knees, behind my elbows, under arms. Every where my skin folds ( other than top of legs). Didnt bother me at first. Slight itch. Its now a tad irritating, at times. Sometimes its like when you get burnt in the sun. Other times I forget I have it. Had it for about 2 weeks now. Telephoned Hospital and she said to continue if I can. It was the nurse I spoke to.
Today I feel a bit bad. Like mild sun stroke. Then it clears. I can cope with it if I know it will clear. Its listed as a side effect but what I want to know is, Has anyone here had a rash that has cleared?
If my body gets used to it and clears, that's fine. If its a allergic reaction, then not