This study constructed the most comprehensive structural variations (SV) map for psoriasis

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Background:
Structural variations (SVs, defined as DNA variants ≥50 bp) have been associated with various complex human diseases. However, research to screen the whole genome for SVs predisposing to psoriasis is still lacking.

Objectives:
This study aimed to investigate the association of SVs and psoriasis.

Methods:
We performed a genome-wide screen on SVs using an imputation method on 5 independent cohorts with 45,386 subjects from the Chinese Han population. Fine mapping analysis, genetic interaction analysis and RNA expression analysis were conducted to explore the mechanism of SVs.

Results:
We obtained 4,535 SVs in total and identified 2 novel deletions (esv3608550, OR=2.73, P<2.00×10-308; esv3608542, OR=0.47, P=7.40×10-28) at 6q21.33 (MHC), 1 novel Alu element insertion (esv3607339, OR=1.22, P=1.18×10-35) at 5q33.3 (IL12B), and confirmed 1 previously reported deletion (esv3587563, OR=1.30, P=9.52×10-60) at 1q21.2 (LCE) for psoriasis. Fine mapping analysis including SNPs and small Insertions/Deletions (InDels) revealed that esv3608550 and esv3608542 were independently associated with psoriasis, and a novel independent SNP (rs9378188, OR=1.65, P=3.46×10-38) was identified at 6q21.33. By genetic interaction analysis and RNA expression analysis, we speculate that the association of 2 deletions at 6q21.33 with psoriasis might relate to their influence on the expression of HLA-C.

Conclusions:
Our study constructed the most comprehensive SV map for psoriasis thus far and enriched the genetic architecture and pathogenesis of psoriasis as well as highlighted the nonnegligible impact of SVs on complex diseases.

NICE the National Institute for Health and Care Excellence UK recommends Xeljanz (tofacitinib) for juvenile psoriatic arthritis.

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NICE has published final draft guidance which recommends tofacitinib (also known as Xeljanz) as an option for treating juvenile psoriatic arthritis in people 2 years and older.

The treatment is available for young people whose arthritis has not responded well enough to disease-modifying antirheumatic drugs (DMARDs) and only if:

• A tumour necrosis factor (TNF)-alpha inhibitor is not suitable or does not control the condition well enough.   
  
• The company provides tofacitinib according to the commercial arrangement.
  

Clinical evidence shows that tofacitinib is effective when compared with a placebo and indirect comparisons suggest it has a similar effect to other treatments for the same indication.

Active polyarticular juvenile arthritis and juvenile psoriatic arthritis are types of juvenile idiopathic arthritis. Juvenile idiopathic arthritis is an inflammation of the joints that begins in people under 16 years of age where the cause or trigger is uncertain or unknown. In total about 3,000 in England have juvenile idiopathic arthritis.

There are more than 1,000 people in England who would be eligible for treatment with tofacitinib.

Does anyone know what happens after we have used our single use syringes and am I doing it right ?

Once I'm finished here is what I do.

1. The swab I use to clean the skin goes in the bathroom waste bin.
   
2. The cardboard box, inner packaging, leaflet and needle cap I put in the recycle bin.
   
3. The syringe goes in my yellow sharps bin.
   

NICE The National Institute for Health and Care Excellence UK have given approval for the use of Cosentyx (secukinumab) in children.

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Recommendations:

1.1 Secukinumab is recommended as an option for treating plaque psoriasis
in children and young people aged 6 to 17 years, only if:

• the disease is severe, as defined by a total Psoriasis Area and Severity
  Index (PASI) of 10 or more and
  
• the disease has not responded to other systemic treatments, including
  ciclosporin, methotrexate and phototherapy, or these options are
  contraindicated or not tolerated and
  
• the company provides the drug according to the commercial
  arrangement.
  

1.2 Stop secukinumab treatment at 12 weeks if the psoriasis has not responded adequately. An adequate response is defined as a 75%  reduction in the PASI score (PASI 75) from when treatment started.

1.3 Choose the least expensive treatment if patients (or their parents or carers) and their clinicians consider secukinumab to be one of a range of suitable treatments. Take into account availability of biosimilar products, administration costs, dosage, price per dose and commercial arrangements.

1.4 Take into account how skin colour could affect the PASI score and make any appropriate clinical adjustments.

1.5 These recommendations are not intended to affect treatment with secukinumab that was started in the NHS before this guidance was published. People having treatment outside these recommendations may continue without change to the funding arrangements in place for them before this guidance was published, until they and their NHS clinician consider it appropriate to stop. This decision should be made jointly by the clinician, the child or young person and their parents or carers.

This could be bad news for some of the Janus kinase (JAK) inhibitors for treating psoriasis.

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FDA (U.S. Food and Drug Administration) requires warnings about increased risk of serious heart-related events, cancer, blood clots, and death for JAK inhibitors that treat certain chronic inflammatory conditions.

Based on a completed U.S. Food and Drug Administration (FDA) review of a large randomized safety clinical trial, we have concluded there is an increased risk of serious heart-related events such as heart attack or stroke, cancer, blood clots, and death with the arthritis and ulcerative colitis medicines Xeljanz and Xeljanz XR (tofacitinib). This trial compared Xeljanz with another type of medicine used to treat arthritis called tumor necrosis factor (TNF) blockers in patients with rheumatoid arthritis. The trial’s final results also showed an increased risk of blood clots and death with the lower dose of Xeljanz. A prior DSC based upon earlier results from this trial, reported an increased risk of blood clots and death only seen at the higher dose.

We are requiring new and updated warnings for two other arthritis medicines in the same drug class as Xeljanz, called Janus kinase (JAK) inhibitors, Olumiant (baricitinib) and Rinvoq (upadacitinib). Olumiant and Rinvoq have not been studied in trials similar to the large safety clinical trial with Xeljanz, so the risks have not been adequately evaluated. However, since they share mechanisms of action withXeljanz, FDA considers that these medicines may have similar risks as seen in the Xeljanz safety trial.

Two other JAK inhibitors, Jakafi (ruxolitinib) and Inrebic (fedratinib), are not indicated for the treatment of arthritis and other inflammatory conditions and so are not a part of the updates being required to the prescribing information for Xeljanz, Xeljanz XR, Olumiant, and Rinvoq. Jakafi and Inrebic are used to treat blood disorders and require different updates to their prescribing information. If FDA becomes aware of any additional safety information or data that warrants updates to the prescribing information for these medicines, we may take further action and will alert the public.

Hello!  

Thank you for membership in this forum.  I look forward to getting to know you, to your help, and to learning more about psoriasis.

I saw a dermatologist in April 2021 and had two punch biopsies.  Before the biopsies, the doctor said that it looked like I had Psoriasis.  However, pathologist report said it was possibly a "drug-induced psoriasis or psoriasiform drug eruption."  

The literature for Humira says that a user may develop new or worsening psoriasis. I have been on Humira for Crohn's Disease since 2007.  Humira has given me a wonderful remission from Crohn's, and I have returned to an active lifestyle following many years of illness.  

I am 56-year-old female who developed Crohn's at the age of 21. With this remission, I returned to the love of my teenage years--roller skating--and found the sport of Artistic Roller Skating (think figure skating) was open for all ages.  The rashes are annoying wherever they are on my body, but the part that is most concerning involves my feet since they spend a lot of time in skates.

My dermatologist gave me prescriptions for Augmented Betamethasone ointment (and lotion for scalp) as needed when psoriasis is present.  He said that it could take a few months to see results.  The prescription contains 11 refills for a one-year period.  He also prescribed a Desonide ointment for delicate skin.  I assumed that with so many refills, this medication could be used long-term. 

The rash was originally located in only a couple places on my shins and arms and in my scalp.   Now it is on my legs from hip to toes, a little on my front torso, on my back torso, and lightly on my forehead.  

I developed thin skin and bleeding in my instep, ankle, and on the two fingers I most commonly used to apply the ointments (I always washed hands with soap and water after applying), so I quit using the ointments on August 25, 2021, but resumed the today (August 31) on a few spots that had become extra painful/itchy.  

Through this forum, I am learning that topical steriods are not good long term . . . or maybe not good at all.  I hope to learn more.   Did the use of the ointments possibly cause more rashes?  I have been using Lubriderm lotion or Cetaphil Cream after morning showers and bathing with colloidal oatmeal on most afternoons, hoping that moisturizing will help.

The cost for the office visit with biopsies was nearly $700, with my co-pay being $60.  When I was 21-years-old and met the gastroenterologist who diagnosed Crohn's Disease, the initial consultation cost was only $55.  I don't know how US medicine became so expensive.

Thank you for reading.

During lockdown here on Exmoor, I was looking online for something and I came across black cherry juice concentrate.

In title, it said something about how good black cherry juice is for arthritis, gout etc etc and I thought to myself; “I wonder if it would work on PSA sufferers ?”

Well, I purchased a couple of bottles and when they arrived on my doorstep, I mixed some with with my Pepsi Max and drank it for around two weeks.
I noticed that the swelling went down in my fingers and the aches & pains had eased right up in my body.

Now, black cherry juice is NOT a cure for psoriatic arthritis, but it does take around 75% of the pain away and to be honest, that’s better than nothing and better than taking pills !

Where to purchase black cherry juice ?

Supermarkets, health food shop’s, online auction sites etc.

For the poor PSA sufferers out there, give black cherry juice a go, you’ve nothing to loose, well, around £13

GB

Caroline passed this on to me and although the abstract doesn't mention psoriasis, is does mention "inflammatory arthritis" so some of you may find it interesting.

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Objectives:
The impact of inflammatory arthritis (IA) on male fertility remains unexplored. Our objective was to evaluate the impact of IA on several male fertility outcomes; fertility rate (number of biological children per man), family planning, childlessness and fertility problems.

Methods:
We performed a multicentre cross-sectional study (iFAME-Fertility). Men with IA 40 years or older who indicated that their family size was complete were invited to participate. Participants completed a questionnaire that included demographic, medical and fertility-related questions. To analyse the impact of IA on fertility rate, patients were divided into groups according to the age at the time of their diagnosis: ≤30 years (before the peak of reproductive age), between 31 and 40 years (during the peak) and ≥41 years (after the peak).

Results:
In total 628 participants diagnosed with IA were included. Men diagnosed ≤30 years had a lower mean number of children (1.32 (SD 1.14)) than men diagnosed between 31 and 40 years (1.60 (SD 1.35)) and men diagnosed ≥41 years (1.88 (SD 1.14)).This was statistically significant (p=0.0004).The percentages of men diagnosed ≤30 and 31–40 years who were involuntary childless (12.03% vs 10.34% vs 3.98%, p=0.001) and who reported having received medical evaluations for fertility problems (20.61%, 20.69% and 11.36%, p=0.027) were statistically significant higher than men diagnosed ≥41 years.

Conclusions:
This is the first study that shows that IA can impair male fertility. Men diagnosed with IA before and during the peak of reproductive age had a lower fertility rate, higher childlessness rate and more fertility problems. Increased awareness and more research into the causes behind this association are urgently needed.

New guy here. I did an intro post with most of my details. Have had PS since somewhere around 2010. Currently on Humira but want to get my diet in order and then come off the Humira.

I have done some research on PS and anti-inflam diets. WOW. Everything I currently eat is a big no no. Well,I guess then its no wonder i have PS lol.

Im trying to comprehend how this will work because we are talking about a huge lifestyle change for me.



Long story short. I DONT COOK.    Well, make that I "DIDNT" cook. I guess I do now.

The main snag I see is that I am a meat eater and I need my proteins. I lift weights. I hate the use the term "bodybuilder" (since i dont look like one lol) but thats the general idea. I see "no red meat" listed. Ok, that sucks but maybe not the end of the world. Then I see proteins listed as Salmon and Trout. lol. ok. Thats it???

What I dont see much guidance on is CHICKEN?!? I see eggs sometimes listed as bad, sometimes not. But I dont see much listed about actual chicken. If I were to dream that I could be on a strict bodybuilder type diet...that would typically be tons of chicken breast. So is chicken ok or is it no good or what??


Any guidance on these foods would be nice:


chicken?

veal?

any other good meat options besides fish?

eggs? I sometimes see them listed as a no no. What about egg whites? what about egg substitutes?


fruits in general. i see "no citrus fruits" and then i see on the "good" side stuff like blueberrys and cherries. lol. ok. Thats it though? What other fruits are ok?


What about green grapes? I see that "sour grapes" may be a no no. Are all green grapes considered sour? I hope not lol



what about protein powders? I am assuming most would have gluten? or would they be considered too "processed"?


The main snag for me (besides the obvious huge lifestyle change) is I dont see how i will get enough protein. Say, 200grams per day or thereabouts.



Thanks for any suggestions or ideas.  

Peace, JonJon

JonJon here. Currently 54 years old. Ive had Psoriasis since somewhere around 2010. Maybe even some symptoms as far back as 2008ish? It started on my elbows and I didnt pay much attention to it but you know how that goes.

Some years back I was taking Methotrexate and one thing lead to another and now i am on Humira.

Other than Humira I am not on ANY meds. Even with the Humira I still have plenty of scalp issues and some visible spots including one on my face which has been there a good while.

At this point my plan is to totally change my diet and to come off of Humira entirely. it is what it is.

When I look at "Psoriasis diets" or anti inflam diets, they basically rule out EVERYTHING I eat. Of course that is also a good clue as to why I ended up with Ps in the first place

I am also quite overweight. about 236lbs at 5.8".....which I read is also a contributor to chronic inflammation. Since I have a goal to be around 185lbs anyway, there is no way around a massive diet overhaul.

Stats. 7-29-2021

54 y.o.

5'8" 236lbs (goal 185ish)

taking Humira. Plan to come off of it eventually. Am on no other meds.

Ill be asking some diet and cooking questions im sure! lol

Cheers, JonJon

Interesting article about a woman that had problems with onset of remitting seronegative symmetrical synovitis with pitting oedema and palmoplantar psoriasis flare-up after covid vaccination.

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An 83-year-old woman referred to the dermatology division of our hospital because of recent acute onset of stiffness with limitation in basic activities of daily living and pain, swelling and palmar skin eruption of both hands. All symptoms showed up 48 h after the second administration of BNT162b2 Pfizer/BioNTech® Sars-Cov-2 vaccine.

The patient presented with a history of palmoplantar psoriasis since 1996, in long-standing remission with methotrexate (MTX) 10 mg every 10 days. She took also anti-hypertensive and oral antidiabetic medications. She had no history of rheumatic or allergic diseases.

At physical examination, both hands on palmar side showed psoriasis with erythematous, scaly plaques, while on dorsum and wrist joints, painful oedema was present. Dactylitis was also detected in all fingers associated with severe functional impairment. Musculoskeletal ultrasound (MSUS) revealed tenosynovitis of the digital extensor tendon and the carpal extensor tendon of wrists based on the presence of hypoechoic signals around the tendon sheath with power Doppler signal both in transverse and in longitudinal planes. Acute phase reactants were elevated, rheumatoid factor was negative, and X-rays revealed no joint erosions. The scenario indicated a flare-up of palmar psoriasis associated with the onset of psoriatic arthritis with remitting seronegative symmetrical synovitis with pitting oedema (RS3PE). The patient started oral prednisone (25 mg once daily) and increased MTX dosage (10 mg weekly), with a rapid clinical improvement.

New onset or exacerbation of psoriatic disease following vaccinations, though rare, is reported in literature. To date, the cases of psoriasis flare-up have been described with influenza, pneumococcal polysaccharide, Bacillus Calmette–Guerin (BCG) and tetanus–diphtheria vaccines.

In this case, the close temporal link between Sars-Cov-2 vaccination and the onset of psoriasis flare-up associated with joint involvement suggests a possible causal association between the two events.

It is known that vaccination itself triggers an IFN-gamma and TNF-α release from Th1 cells, which could represent a possible mechanism for vaccination-induced psoriatic disease.

Polyethylene glycol (PEG) – one of the compounds of BNT162b2 – could also have been the cause for the systemic reaction observed, acting as the antigen that activated the immune pathway as reported in other cases.

RS3Pe syndrome is characterized by symmetrical synovitis and swelling of both the upper and lower extremities. RS3PE syndrome may overlap several rheumatic disorders such as polymyalgia rheumatica, rheumatoid or psoriatic arthritis, especially at the onset in the elderly, similar to our case. The aetiology of the disease is still unknown, although some authors have related it to genetic predisposition, infectious diseases or α-TNF released by tumours or a paraneoplastic syndrome when recovery was observed after a complete tumour removal. In literature, two cases of RS3PE following intravesical instillation of BCG8, are reported.

Typical RS3PE treatment includes NSAIDs, hydroxychloroquine and corticoids, and full recovery usually occurs between 3 and 36 months after starting corticoid treatment.

To the best of our knowledge, this is the first case of palmoplantar psoriasis flare-up and RS3PE onset after Sars-Cov-2 vaccination. Currently, BNT162b2 Pfizer/BioNTech ® remains a very safe and effective vaccine10 and its use is strongly recommended.

Its been well over a year since I stopped my treatment, due to problems with my eyes. Still have problems but very mild.

Last night, I had my fist injection of ilumetri. See how that goes. Scared it will affect my eyes, if I tell the truth

ANYWAY. 
A few weeks ago I was given oral steroids (prednisone) for inflammation in my nose. Had them a few years ago. Not a problem.
Only a short 5 day treatment but boy did it clear my skin .
After 5 days its pretty amazing. I didnt even know Prednisone was used to clear Psoriasis. Apparently its only short term and works way better in men.
I cant find anything about it on here.

Hi everyone, it's been a while since I last posted.

So I've been trying to dodge covid while slowly getting covered in psoriasis. My derm convinced me to hold off going on to any meds while covid was in full swing and over the last year or so im now at a point where I have no choice. 

I was previously on Fumaderm which was a miracle drug for me where I got full clearance on just 1 full strength tablet. I then got moved to skillerence but I  had very bad stomach pains and ended up stopping them.

So a year later im in need of more meds and for my sins I asked to try skillerence again. I got on so well with Fumaderm I want to give it another go. 

So I'm now on 3 initial tablets a day and although I've had stomach pains im determined to see it through. 

Second time lucky? Fingers crossed.

Galapagos reports positive topline results with selective TYK2 inhibitor GLPG3667 in Phase 1b psoriasis study.

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Galapagos reports positive topline results with tyrosine kinase 2 (TYK2) inhibitor GLPG3667 in a Phase 1b study in psoriasis patients. GLPG3667 was discovered by Galapagos.

Galapagos evaluated GLPG3667, a proprietary selective TYK2 compound, in a randomized, placebo-controlled, double-blind Phase 1b study in 31 patients with diagnosis of moderate to severe plaque psoriasis. Patients were randomized in a 1:1:1 ratio to a daily oral dose of GLPG3667 (low dose or high dose) or placebo, for a total of four weeks. Main objectives were to evaluate the safety and tolerability of GLPG3667 as well as signs of clinical activity at Week 4.

GLPG3667 was well tolerated in this Phase 1b trial. One patient in the low dose group interrupted the study for one day for exacerbation of psoriasis. The majority of treatment related adverse events (AEs) were mild in nature and transient. There were no deaths or serious adverse events (SAEs) in this 4-week study. At Week 4, four out of 10 patients in the high dose group had a PASI1 50 response, defined as at least a 50% improvement in PASI from baseline, compared to one out of 10 subjects on placebo. There were no subjects with a PASI 50 response on the low dose of GLPG3667. The four responders in the high dose group of GLPG3667 achieved a 52%, 65%, 74% and 81% improvement respectively in their PASI scores from baseline, while the subject randomized to placebo improved by 52%. Positive efficacy signals were also observed with the high dose for other endpoints, including affected Body Surface Area and physician and patient global assessment, versus placebo at Week 4.

“We are pleased with the efficacy signal and safety profile observed with GLPG3667 in patients with psoriasis over a 4-week period,” said Dr. Walid Abi-Saab, Chief Medical Officer of Galapagos. “Based on these results, we aim to initiate a global Phase 2b program in psoriasis next year as part of a program to develop our selective oral TYK2 inhibitor GLPG3667 broadly in inflammatory indications.”

“The PASI 50 scores and other efficacy data after only four weeks of treatment, combined with the safety profile observed, are very supportive for moving this compound into a larger trial in psoriasis. People living with psoriasis remain in need of alternative treatments, especially oral ones,” said Prof. Dr. Diamant Thaci, Professor of Medicine at the Comprehensive Center for Inflammation Medicine, University of Lübeck, Germany.

Galapagos intends to submit study outcomes with GLPG3667 for publication at scientific conferences and in peer-reviewed medical journals.

GLPG3667 is an investigational drug and not approved by any regulatory authority. Its efficacy and safety have not been established.

Along with my regular psoriasis I now have sebopsoriasis around my nostrils and down the sides of my nose. It is so sore (obviously not helped by having to wear face masks - but not for much longer!), dry, itchy, unslightly. Dermatologist prescribed protopic but that’s not helped. Does anyone else suffer from this and has any tips on how to manage it? I’m really self conscious of it.

This study investigated whether selected clinical/serum biomarkers were associated with remission duration, and psoriasis clearance at the end of phototherapy.

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Background:
Remission duration and treatment response following phototherapy for psoriasis are highly variable and factors influencing these are poorly understood.

Objectives:
Our primary outcome was to investigate whether selected clinical/serum biomarkers were associated with remission duration, and secondly with psoriasis clearance at the end of phototherapy. In addition, we looked at whether early trajectory of UVB clearance was associated with final clearance outcome.

Methods:
We performed a prospective cohort study of 100 psoriasis patients, routinely prescribed Narrowband UVB and measured selected clinical and biochemical biomarkers, including weekly PASI (psoriasis-area-and-severity-index) scores. Patients were followed up for 18-months.

Results:
The median time to relapse was 6-months (95% CI 5-18) if PASI90 was achieved, and 4-months (95% CI 3-9) if less than PASI90 was achieved. Achieving PASI100 did not result in prolonged remission.
On UVB completion, the median final PASI (n=96) was 1.0 (IQR 0.5, 1.6) with 78 (81%) achieving PASI75 and 39 (41%) achieving PASI90. Improved PASI90 response was significantly associated with lower BMI, higher baseline PASI, non-smoking status and lower cumulative NbUVB. Serum levels of C reactive protein (CRP) and vitamin D were not associated with clearance or remission duration.
Early treatment response from weeks 2-3 was predictive of final outcome. For example, achieving PASI30 at week 3 was significantly associated with PASI90 at the end of the course (36/77 (51%) versus 2/24 (8%), p < 0.001).

Conclusions:
Raised BMI and positive smoking-status predicted poorer phototherapy response. For the first time, we have shown that PASI clearance trajectory over the first 2-3 weeks of UVB, can predict psoriasis clearance. This is an important new step towards developing psoriasis personalised prescribing, which can now be formally tested in clinical trials. These simple clinical measures can be used to inform patient treatment expectations; allowing treatment modifications and/or switching to alternative therapies.

This cohort study looked at the effect of methotrexate and targeted immunosuppression on humoral and cellular immune responses to the COVID-19 vaccine BNT162b2

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Background:
Patients on therapeutic immunosuppressants for immune-mediated inflammatory diseases were excluded from COVID-19 vaccine trials. We therefore aimed to evaluate humoral and cellular immune responses to COVID-19 vaccine BNT162b2 (Pfizer-BioNTech) in patients taking methotrexate and commonly used targeted biological therapies, compared with healthy controls. Given the roll-out of extended interval vaccination programmes to maximise population coverage, we present findings after the first dose.

Methods:
In this cohort study, we recruited consecutive patients with a dermatologist-confirmed diagnosis of psoriasis who were receiving methotrexate or targeted biological monotherapy (tumour necrosis factor [TNF] inhibitors, interleukin [IL]-17 inhibitors, or IL-23 inhibitors) from a specialist psoriasis centre serving London and South East England. Consecutive volunteers without psoriasis and not receiving systemic immunosuppression who presented for vaccination at Guy's and St Thomas' NHS Foundation Trust (London, UK) were included as the healthy control cohort. All participants had to be eligible to receive the BNT162b2 vaccine. Immunogenicity was evaluated immediately before and on day 28 (±2 days) after vaccination. The primary outcomes were humoral immunity to the SARS-CoV-2 spike glycoprotein, defined as neutralising antibody responses to wild-type SARS-CoV-2, and spike-specific T-cell responses (including interferon-γ, IL-2, and IL-21) 28 days after vaccination.

Findings:
Between Jan 14 and April 4, 2021, 84 patients with psoriasis (17 on methotrexate, 27 on TNF inhibitors, 15 on IL-17 inhibitors, and 25 on IL-23 inhibitors) and 17 healthy controls were included. The study population had a median age of 43 years (IQR 31–52), with 56 (55%) males, 45 (45%) females, and 85 (84%) participants of White ethnicity. Seroconversion rates were lower in patients receiving immunosuppressants (60 [78%; 95% CI 67–87] of 77) than in controls (17 [100%; 80–100] of 17), with the lowest rate in those receiving methotrexate (seven [47%; 21–73] of 15). Neutralising activity against wild-type SARS-CoV-2 was significantly lower in patients receiving methotrexate (median 50% inhibitory dilution 129 [IQR 40–236]) than in controls (317 [213–487], p=0·0032), but was preserved in those receiving targeted biologics (269 [141–418]). Neutralising titres against the B.1.1.7 variant were similarly low in all participants. Cellular immune responses were induced in all groups, and were not attenuated in patients receiving methotrexate or targeted biologics compared with controls.

Interpretation:
Functional humoral immunity to a single dose of BNT162b2 is impaired by methotrexate but not by targeted biologics, whereas cellular responses are preserved. Seroconversion alone might not adequately reflect vaccine immunogenicity in individuals with immune-mediated inflammatory diseases receiving therapeutic immunosuppression. Real-world pharmacovigilance studies will determine how these findings reflect clinical effectiveness.

Hi all. I have a question for those who are familiar and have personal experience with TALTZ. I got on TALTZ because I have inverse psoriasis in the under carriage area. My face (though it’s flared in the past) had been clear for about 6 months before getting on TALTZ. I have had 2 injections. My face is now flaring pretty bad. Is that a temporary side affect? Should I press on? Or quit immediately?

As I reported in my introduction topic, I would talk to my rheumatologist about starting Mtx. His assistant nurse had called me a few weeks back, about de Mri results, and she had said that they would start with Mtx and if that didn't help they would switch to Humira.

But why start with Mtx if you're not sure what it does for PsA? I also told in my introduction topic, that I had found a video on Youtube in which my rheumatologist himself indicates that it is unknown whether Mtx actually works for PsA. 
Given the many negative reports, but also positive reports about Mtx, I myself had a hesitant attitude towards it. Why start with Mtx if you, as a rheumatologist, don't support it yourself? And why not immediately start on the Humira?

So last Tuesday I went for a consultation with my rheumatologist and told him what my reluctance was towards starting Mtx. 
Of course he indicated that it is an insurance policy thing and also the guidelines within the Netherlands, so Mtx is the first choice of treatment, blabla bla bla...

To which I indicated: Yes that's a good story, but not enough for me, because I read that several studies indicate that Mtx does not do much for PsA, that they do not know what it does anyway. And besides, there is a video of you on Youtube in which you indicate that you also do not know whether it really works. So how do you substantiate the choice to start with Mtx?

He looked at me in surprise 
I said: I told you that I have Autism and that I am not a patient like others, I research everything in advance, down to the semicolon, so substantiate your story  

He started laughing really hard and he said “shit, I'm getting caught on my own words here, very good!.
 
He didn't mind at all that I confronted him about the research end video and was impressed that I had sorted out so much information.
He said, “As a rheumatologist I can bound the rules, my assitent nurse is not allowed to do that. I understand that she stated to start with Mtx. But I can deviate from the rules. Obviously is by Mri and also diagnosed, you have axial PsA, and if you don't want to use Mtx, I immediately will let you start with Humira, which I also think is the best option for you.
So I said: that's what I want, no Mtx, but the Humira.

And today I will start with the Humira. I have to pick up the injections at the pharmacy of the hospital later this day. Than go to the rheumatism nurse for a injection instruction and my first injection of Humira will be immediately made.

I'm glad I got into the discussion with my rheumatologist and he went along with it. I'm realy glad I chose him as my rheumatologist. When I told him that the pain is sometimes unbearable, my quality of life is really F.ckedup , that I sometimes couldn't stand it anymore, he also indicated that he understood that very well. (sometime it's very nice to be heard).

If the Humira does not help me, the pain in my neck remains unbearable, he has promised to send me to the pain clinic. So at least he won't let me down and won't send me away like all the other rheumatologists in the past nine years who send me away to the psychologist 

I am curious, I hope the Humira will work for me, that I will hardly get any side effects and that I will finally be freed from stiffness and pain after more than 9 years, I hope so! The most important thing for me is that my quality of life gets better than it is now, that's what I'm going for! 

Y’all, I’m scared!!   

I’m about to do my first auto injection of Taltz and I here it hurts like a mother. I had a regular injection of the stuff at my derm’s office 2 weeks ago and THAT even hurt more than a regular shot. Autoinjecter is supposed to be much worse.

So my questions: 

Which site on the body is best??
Any tips for making it less painful?? 

Thanks all!