I've been playing with a new feature "Random Thread"

It's only available to members that are logged in, and you can find it on the menu at Random Thread and in the footer at Random.

Just click it and you should be taken to a random thread from the forum that you may have missed.

Any problems or questions please let me know.

Biocon India's largest biotechnology company by revenue announced today that it has received Marketing Authorization from the Drugs Controller General of India (DCGI) for its Novel Biologic Itolizumab, anti CD6 molecule, for the treatment of chronic plaque Psoriasis.

Quote:

---

Itolizumab, is a first in class therapy with a unique Mechanism of Action (MOA) and an excellent safety profile as indicated during the 52 week Phase III multi-centric clinical study conducted in India. It is the second Novel Biologic developed by Biocon at Asia’s largest Biotech hub in Bangalore.

This approval paves the way for the launch of Biocon’s Alzumab in India, later during 2013. Alzumab is a differentiated biologic drug with a superior safety profile compared to other approved biologic therapies given its very low opportunistic infection rates. A novel biologic indicated for the treatment of Moderate-to-Severe Psoriasis, Alzumab will be marketed by Biocon’s Immunotherapy Division. Alzumab, will be manufactured and formulated as an infusion drug at Biocon’s Biopharma manufacturing facility at Biocon Park, Bangalore.

Commenting on this development Ms. Kiran Mazumdar-Shaw, Chairman & Managing Director, Biocon said, “We are very excited to receive this marketing authorization for Itolizumab from DCGI which will enable Biocon to introduce this novel, first in class biologic for the treatment of psoriasis patients in India. This is our Second novel biologic that we have developed in India, BioMab EGFR, an anti-cancer monoclonal antibody, being the first. This approval paves the way for us to extend clinical development for other indications like Rheumatoid Arthritis (RA), Multiple Sclerosis (MS) and Vitiligo. We also intend to file a US IND shortly to enable us to embark on a global clinical development plan. This is a defining moment for Biocon as it reaches a significant milestone in its mission of delivering affordable innovation to patients worldwide.”

I have a mild case of scalp psoriasis that is one persistant mofo' and it's recently developed in my ears,i had no idea that could even happen.. and every now and again minor lesions appear on my legs or elbows or even my face and every timethese minor lesions appear itry to apply just som regular cream asmuch as i can because the ointments tend to bleach skin, something i learned the hard way. Any whoo i recently had a baby, and so i have all the creams and lotions and everything of the likes to take care of her beautiful baby skin, and sooo finally to the grain: i started to get a patch of psoriasis on my chin and i tried to put on normalface cream at every hour of the day and nothing helped, when finally...this might sound odd...but i put some diaper rash cream on it during the night, and i woke up and it was gone. So tonight i'm going to try and use the diaper rash cream on more of my skin to see if it can help because i've been living for years with this psoriasis that nothing else can help.
Try it! Baby diaper rash ointment.

I have never been told that I have psoriatic arthritis, but lately I have some swelling around my thumb joint (top of thumb). It doesn't hurt really, but is hot. Is this one of the symptoms to psoriatic arthritis?

Has anyone here had any odd internal problems? I have had chronic Pancreatitus. I just seems odd to me that I have P and PA and also another rare condition the Pancreatitus. My Gastro Dr. claims that there is no connection but I am sceptic. Right now I sit here with my gut jutting out swelled up and half luppy from Oxycotten.

Decision Resources, one of the world's leading research and advisory firms for pharmaceutical and healthcare issues, finds that, in 2011, tumor necrosis factor-alpha (TNF-alpha) inhibitors dominated sales in the psoriatic arthritis (PsA) drug market, contributing to 89 percent of the nearly $1.7 billion PsA market in the United States, France, Germany, Italy, Spain, the United Kingdom and Japan.

The upcoming Pharmacor advisory service entitled Psoriatic Arthritis, which will be published soon, finds that the TNF-alpha inhibitor etanercept (Amgen/Pfizer/Takeda's Enbrel) was the 2011 market leader, leading by a small margin over adalimumab (Abbott/Eisai's Humira). Decision Resources expects Humira to displace Enbrel as the sales leader in 2012, with its patient share surpassing that of Enbrel in 2013.

"Interviewed thought leaders believe that Humira's superior efficacy on skin symptoms over Enbrel, its excellent efficacy on joint symptoms, twice-monthly dosing and years of physician experience for treating PsA will continue to drive its uptake in this market," said Decision Resources Analyst Bingnan Kang, Ph.D.

The findings also reveal that methotrexate (Dava Pharmaceuticals' Rheumatrex, generics) was the patient-share leader in 2011 but comprised only 4 percent of total PsA sales, owing to the availability of inexpensive generics. Other conventional disease-modifying antirheumatic drugs are also highly genericized and represented only a small percentage (less than 6 percent) of market sales in 2011.

Over the next decade, four branded therapies will enter the market and will represent over one-third of the total PsA market in 2021. Of these agents, three emerging therapies offer novel mechanisms of action--the interleukin-12/23 inhibitor ustekinumab (Janssen's Stelara), the selective costimulation inhibitor abatacept (Bristol-Myers Squibb/Ono Pharmaceutical's Orencia) and the phosphadiesterase-4 inhibitor apremilast (Celgene). During this time, the TNF-alpha inhibitor certolizumab pegol (UCB/Astellas's Cimzia) will also enter the PsA market.

Source: NO LINKS ALLOWED

Idera Pharmaceuticals today announced that 48% of patients with moderate-to-severe plaque psoriasis (12 of 25) treated with IMO-3100, a selective antagonist of Toll-like Receptors (TLRs) 7 and 9, demonstrated improvements in Psoriasis Area Severity Index (PASI) scores of 35% to 90% from baseline at the completion of a randomized, double-blind, placebo-controlled Phase 2a clinical trial of two dose levels of IMO-3100 administered for four weeks, with a four-week follow-up period. None of the 12 placebo-treated patients had improvement in this range; this difference was statistically significant (p<0.005). The Company believes the results of this trial provide clinical proof-of-concept for the mechanism of action of selective TLR inhibition in patients with psoriasis and potentially other autoimmune and inflammatory disorders.

“The clinical activity of IMO-3100 demonstrated in patients with moderate-to-severe plaque psoriasis is encouraging, especially given the short duration of treatment in this study that was designed for initial explorations of safety and efficacy,” commented Alexa Kimball, M.D., M.P.H., Vice Chair, Department of Dermatology at Massachusetts General Hospital, Boston, and an investigator in the trial.

“The achievement of statistically significant PASI reductions with only four weeks of treatment in a placebo-controlled double-blind trial directly supports the rationale that the modulation of specific TLRs plays a key role in the treatment of psoriasis and, potentially, other autoimmune and inflammatory disorders,” commented James Krueger, M.D., Ph.D., of The Rockefeller University, New York. “We are excited to see these data, which demonstrate the translation of targeting a novel mechanism of action into clinical activity and support further studies of TLR antagonists for the treatment of psoriasis. Our laboratory is continuing to evaluate the immunological pathways by which TLR antagonists suppress the signaling cascades that underlie psoriasis and have the potential to open up a new approach to disease treatment.”

About the IMO-3100 Phase 2 Trial in Psoriasis:
The Phase 2 trial was a randomized, double-blind, placebo-controlled trial of IMO-3100 in patients with moderate-to-severe plaque psoriasis. In the trial, 44 patients were randomized to receive IMO-3100 monotherapy at 0.16 or 0.32 mg/kg or placebo by subcutaneous injection once weekly for four weeks with four weeks of follow-up. Assessments of safety were performed throughout the treatment and follow-up periods. Multiple parameters were monitored to assess the clinical activity of IMO-3100, including Psoriasis Area Severity Index (PASI), mean focal psoriasis severity and Physician Global Assessment (PGA) scores. In addition to the clinical assessments, biopsies of psoriasis plaques were evaluated for treatment-related changes in epidermal thickness and immune cell infiltrates consistent with the intended mechanism of action. Patients were enrolled at eleven sites in the United States.

Top-line clinical results from this trial include:
Of the 44 enrolled patients, 40 were clinically evaluable at the end of the four-week treatment period and 37 were evaluable following the four-week follow up period.

Treatment at both IMO-3100 dose levels was well tolerated, with no treatment-related discontinuations.
   
Among evaluable patients, the median PASI scores at treatment initiation were 14.9, 16.1, and 12.5 in the 0.16 mg/kg, 0.32 mg/kg, and placebo cohorts, respectively.
   
A treatment effect was demonstrated in measures of clinical efficacy in patients in both IMO-3100 dose cohorts; PASI reductions at both dose levels were sustained throughout the four-week follow-up period.
   
At the end of the four-week follow-up period, 48% of patients treated with either dose of IMO-3100 (12 of 25) demonstrated improvements of 35% to 90% from baseline PASI scores compared with 0 of 12 in the placebo cohort; this difference was statistically significant (p<0.005)
   
The trial achieved the pre-specified clinical endpoint of reduction in PASI scores at the end of treatment in the 0.16 mg/kg dose cohort with statistical significance (p<0.02) compared to the placebo cohort, but not in the 0.32 mg/kg dose cohort.
   
The 0.16 mg/kg cohort also achieved, with statistical significance (p<0.02), the pre-specified clinical endpoint of improvement in induration, a measure of plaque thickness, at the end of treatment and during the follow-up period.
   
At the end of the four-week follow-up period, 25% (3 of 12) of patients treated with 0.16 mg/kg dose and 31% (4 of 13) with 0.32 mg/kg dose achieved PASI 50 or greater, compared to 0 of 12 placebo patients.

Skin biopsies were collected at baseline and after completion of treatment to investigate changes in epidermal thickness and immune cell infiltrates. Change in epidermal thickness was the primary endpoint for the trial. Placebo treated patients had a median change in epidermal thickness of +7.7% compared to a median change of -6.4% among IMO-3100 treated patients; this difference was not statistically significant. A known limitation of skin biopsies after four weeks of treatment is that psoriatic plaques do not resolve in a uniform fashion, and therefore, biopsies may not provide a representative sampling of lesions (ref: Ann Rheum Dis 2005;64:65-68).

The Company plans to present complete clinical data from this trial at an upcoming medical meeting.

“We believe this trial in patients with moderate-to-severe plaque psoriasis provides clinical proof-of-concept for this first-in-class TLR antagonist, which represents a novel approach to the treatment of autoimmune diseases. We are very pleased to have observed clinical responses after only four weeks of treatment,” stated Sudhir Agrawal, D. Phil., Chief Executive Officer of Idera. “The insights gained from this trial support expansion of our TLR antagonist program for the treatment of autoimmune diseases. In 2013, we plan to advance the clinical development of a selective TLR antagonist for the treatment of moderate-to-severe plaque psoriasis and also for the treatment of lupus.”

Source: iderapharma.com

Previous thread on IMO-3100: Idera announce phase 2 trial of IMO-3100

Actelion announced today that its selective S1P1 modulator, ponesimod, successfully met the primary endpoint - the proportion of patients with at least 75% improvement in Psoriasis Area and Severity Index (PASI) from baseline (PASI75) at week 16 - in a double blind, placebo-controlled study conducted in 326 patients with moderate to severe chronic plaque psoriasis.

Results of the primary endpoint were highly statistically significant with both tested doses. With Ponesimod 20 mg, 46 % of patients improved by at least 75 % at week 16 (p<0.0001 versus placebo). With Ponesimod 40 mg, 48.1% of patients improved by at least 75 % at week 16 (p<0.0001 versus placebo). An improvement by at least 75 % was observed at week 16 in 13.4% of the placebo treated patients. Both doses were administered once daily.

At the end of induction, ponesimod patients improving at least 50% or more in their PASI score at week 16 were re-randomized to either continuation of the same dose of ponesimod, or to placebo.

After the initial 16 week induction phase of the study, further improvement was seen with ponesimod during the 12-week double-blind, placebo-controlled maintenance period. Among patients continuing on ponesimod 20 and 40mg, 71 % and 77 % achieved PASI75 at the end of the study, respectively.

Efficacy was also demonstrated across other endpoints of the study, including Physician Global Assessment (PGA) at week 16.

Guy Braunstein, M.D. and Head of Clinical Development at Actelion commented: "This is the first time that this mechanism has demonstrated efficacy with psoriasis patients. Analysis during the maintenance period of the study showed patients continued to improve beyond the initial 16 week induction phase. Having conducted such a large Phase II study we have the information we need for the design of the pivotal Phase III program."

Safety and tolerability data from the study are consistent with the safety profile of ponesimod observed in previous studies conducted including the Phase II study with multiple sclerosis patients. At initiation of ponesimod treatment, transient reductions in heart rate and less frequently, a transient effect on atrioventricular conduction were observed in the study as expected. The most frequent adverse events (AEs) reported for ponesimod was dose-dependent dyspnea and asymptomatic liver enzyme elevations. Overall, there were no indications of an increased infection rate with ponesimod in the study with the exposure to ponesimod up to 28 weeks. The safety data-base from all studies with ponesimod, now comprises more than 1,100 patients and healthy volunteers with some patients treated for up to 3.3 years.

Jean-Paul Clozel, M.D. and Chief Executive Officer commented: "We are excited to now know that ponesimod, originating from Actelion's discovery effort, has the potential to become an important treatment option in immune-mediated disorders in addition to multiple sclerosis. Actelion will rapidly move forward with the preparation of the pivotal program and discussions with health authorities for the psoriasis indication."

Once full data analysis has been concluded, Actelion will discuss the details of the upcoming Phase III program with health authorities. Actelion will present the results of this dose-finding study through scientific presentations and publications.

Source: NO LINKS ALLOWED

Background:
Symptoms of psoriasis can be embarrassing and distressing, and may increase risk of developing psychiatric disorders in young people.

Objective:
We sought to compare incidences of psychiatric disorders between pediatric patients with psoriasis and psoriasis-free control subjects.

Methods:
Patients (<18 years) with continuous health plan enrollment 6 months before and after first psoriasis diagnosis (index date) were selected (Thomson Reuters MarketScan database, 2000-2006 [Thomson Reuters, New York, NY]). Patients with psoriasis (N = 7404) were matched 1:5 on age and sex to psoriasis-free control subjects (N = 37,020). Patients were followed from index date to first diagnosis of a psychiatric disorder (ie, alcohol/drug abuse, depression, anxiety disorder, bipolar disorder, suicidal ideation, eating disorder), end of data availability, or disenrollment. Patients with psychiatric diagnoses or psychotropic medication use before the index date were excluded. Cox proportional hazard models controlling for age, sex, and comorbidities were used to estimate the effect of psoriasis on risks of developing psychiatric disorders.

Results:
Patients with psoriasis were significantly more at risk of developing psychiatric disorders versus control subjects (5.13% vs 4.07%; P = .0001; hazard ratio = 1.25; P = .0001), especially depression (3.01% vs 2.42%; P = .0036; hazard ratio = 1.25; P = .0053) and anxiety (1.81% vs 1.35%; P = .0048; hazard ratio = 1.32; P = .0045).

Limitations:
Retrospective, observational studies of medical claims data are typically limited by overall quality and completeness of data and accuracy of coding for diagnoses and procedures.

Conclusions:
Pediatric patients with psoriasis had an increased risk of developing psychiatric disorders, including depression and anxiety, compared with psoriasis-free control subjects.

Source: jaad.org

This is the cure for psoriasis.

Get the affected area wet, then pack baking soda on the surface.

You're redness will go away. I guarantee it.

This cure does burn however. If you have psoriasis and you don't feel entirely safe using baking soda on it, you can take baking soda baths and see whether or not it improves. Taking baking soda baths does not burn. What you can also do is apply it to a less important psoriasis effected area such as your arm, back, or leg.

Just a quick Hi from a newcomer.. thank you sooo much for this forum... I have found a lot of useful information.

A couple of questions please...

Is there a way to search by thread content?

I am looking for information on links with melasma and psoriasis - any ideas?

At Fred's request I'll start a new thread on this subject, by pasting what I've written elsewhere on this board.

In a nutshell, in the mid-1990s I had extremely bad psoriatic spondylitis, & was headed for crippledom according to my rheumatologist. I changed my diet & lifestyle fairly radically, & in a year or so I was free of all symptoms & my ESR (blood inflammation) readings had dropped from 43 to 1.

Here is the post:


My arthritis cure:

The first thing I did was get blood tests for inflammation (the ESR at the time - a good basic test still in use), so I could keep objective track of progress. My ESR reading went from 43 down to 19 down to 6, then finally down to 1 - the lowest possible reading. (Normal range for middle-aged people is 1-15; 1-10 if young.) That took less than a year. All symptoms disappeared for good. I haven't had a problem since - tho the rheumatologist at the time said I'd end up a cripple.

From the notes of my 1997 visit to the rheumatplogist:

Q: What is the inflammation? And what causes it?

A: A pathological chain of events within tissues. White cells moving into tissues. For me, mainly characterised by the presence of macrophages and lymphocytes (from the immune response). No-one knows what causes it.

So I take it this was autoimmune.

These days I do get the occasional twinge in a finger if I eat a lot of fruit or drink a lot of beer. (I.e. too many sugars.) So I just stop doing that for a day & it goes.

I was in agony from head to foot: 20 digits swollen like sausages; spine fusing up; even breastbone extremely painful; couldn't turn over in bed at night. So it was a big turnaround.

To do this I went off acidic food - was eating a lot of tomato paste at the time; and off gluten grains; and off alcohol and cigarettes & pot. And cut way back on the sugars, including fruit. And no dairy.

The regime varied from time to time. Sometimes I found that animal protein was making symptoms worse, and making my tears stingy & acidic. So I went off all animal protein - & those symptoms went away. Other times I just cut down to chicken or fish every second day. That's something to experiment with. (I eat a ton of meat now - no ill-effects: but when one is in a critical state, trying to subdue the autoimmune response, one needs extra measures. Therapeutic diets can be different from maintenance diets.)

I took anti-arthritis herbs, & got mobility exercises from a physiotherapist.

My fastest rate of cure came when I went to live on a quiet beach for a few months, & exercised & swam every day.

Some of my ideas came from an English herbalist named Rowland. I didn't follow every item - excessive fastidiousness is counter-productive, as it causes you to rebel at some point. I also don't agree with him allowing bread and coffee. Other people's laundry lists are for picking the eyes out of, not following fanatically.

My hunch is that for me lowering the intake of sugars was the biggest factor. Cutting out/back on bad fats, gluten (& much grain of any sort) & red meat were also curative I think.

Modern fruit is not the low-sugar, fibrous fruit we evolved on, so there's a good rationale to being careful with even natural sugars.

Fish oil! There's even some science on it for arthritis. MAX-EPA absorption is improved by replacing polyunsaturated fats in the diet with monos.

n-6 fatty acids tend to be pro-inflammatory, a scientist told me at the time.

I also took quite a few supps, tho can't recall which ones. There'd be websites on this now. If you can't take any supps that shouldn't be a barrier to getting well, if her diet is in order.

It's of tremendous practical & psychological benefit to keep track of your ESR - get it measured regularly. Seeing those numbers fall is a real boost.

Going off anything that I reacted to for a while (until the allergic response settled down) was helpful. Some people find rotation diets useful, tho I didn't need one. I tried an elimination diet once, which picked up a couple of things (e.g. more pain after eating chickpeas).

Some writers say going off nightshades is very important: I never had any problem with them (except the acidity of the tomatoes) - but I didn't eat a ton of potatoes either, to keep starches/sugars down.

General points:

1. Medicos will be useless. This is not their field.

2. Pain is your friend, as it tells you you are sick & (when reducing) shows you that what you are doing is working. So I never took painkillers or anti-inflammatories. It's a good spur to try hard.

3. Acting early is a good idea, because the calcifcation caused by the arthritis isn't reversible.

4. If progress is slow, gene testing & fixing methylation is worth exploring. But this is a whole 'nother ballgame, & shouldn't be needed.

5. Most sick people don't want to get well. It's about 1 in 100 IMO. Only very few will follow through with what needs to be done. You would be a rare bird if you made the kind of effort implied in the above.

6. Following my regime exactly may not be optimal: you'll need to experiment a bit. But the broad guidelines should be useful.

I purchased a kilogram of 98% DMF from a chemical supplier in Shanghai at a cost of 160 USD delivered. Customs opened and sampled the package, but were unable to seize it as it is not a registered therapeutic nor is it subject to importation bans in Australia (or maybe they just stuffed up).

A word of caution though: It is a very strong drug with the potential for unpleasant side effects. And dont take it with bananas. I had a headache for 14 hours the last time I did that, and there wont be a next time.

Good luck,

Bill

Hi, I am John.

Had psoriasis since 1974. Has been worse: I keep it with reasonably good diet & lots of supps such as fishoil.

Now want to try dimethyl fumarate - which is why I joined here.

Had psoriatic arthritis very badly in the 1990s (rheumatologist said I'd be a cripple), but cured it with diet & lifestyle changes. ESR went from 43 to 1 (the lowest possible score) & symptoms (agonising pain, 20 digits swollen like sausages) vanished.

Now it's time to get rid of the psoriasis: I am confident there's a way, I just have to find it.

*NOTE:
This thread is made up from posts on a Fumaderm thread, and it was decided it would be better to have it's own thread. You can find the original Fumaderm thread here: Fumaderm

You may also be interested in Caroline's thread about Dimethylfumarates here: Dimethylfumarates and Psoriasis

The first post in this thread is the one below from Johnmac, members are welcome to start another thread about Fumaderm if they wish.

(Fri-25-11-2011, 19:57 PM)Caroline Wrote: Oww....
Can't help it, so must react to Paul and Snookams (what a name)..
I am not on Fumaderm but on an alternative called Psorinovo.
Psorinovo is also, but then unlike Fumaderm without additives. Would make it even worse for your stomach and intestines if.... it was not enteric coated and slow release, but it is....
Which means that it will not be released in the stomach and is slowly released in the intestines. The effect of this is that:
1) almost no cramps, less diarrhea
2) limited flushes, I have them by day about once a week (20 minutes) and sometimes at night
3) higher doses than 6x120mg are possible

Psorinovo is also, like fumaderm I guess, based on the research of dr schweckendieck, but improved by dr L. Kunst into the current form.
Currently a scientific investigation is started in the large medical centers in holland, initiated by the patients community already using Psorinovo, in order to place it better on the map as a very well working treatment to beat psoriasis.

hello everyone i am new here happened to find this when i was doing my own researching online and thought it might be beneficial to see what everyone else is doing

Wow amazing!

Had 2 letters last week telling me I could wait upto 13 weeks for an appointment.

Just got off the phone with the booking service........

Can I come in tomorrow?

yeah!

Janssen Biotech, Inc. and Janssen Biologics B.V. announced today the submission of a supplemental Biologics License Application (sBLA) to the United States Food and Drug Administration (FDA) and a Type II Variation to the European Medicines Agency (EMA) requesting approval of STELARA® (ustekinumab) for the treatment of adult patients with active psoriatic arthritis.  

It is estimated that more than two million people in the U.S. and approximately 4.2 million people across Europe are living with psoriatic arthritis, a chronic autoimmune disease characterized by both joint inflammation and psoriasis skin lesions, for which there is no cure.

"We are pleased to present applications to health authorities in the U.S. and Europe seeking approval of STELARA for the treatment of active psoriatic arthritis, a chronic, debilitating immune-mediated inflammatory disease," said Jerome A. Boscia, M.D., Vice President, Head of Immunology Development, Janssen Research & Development, LLC.  "The efficacy and safety of STELARA, an anti–interleukin-12/23 antibody, have been evaluated in a large Phase 3 clinical development program for the treatment of active psoriatic arthritis, a disease for which tumor necrosis factor inhibitors are currently the only approved biologic therapies, and additional therapeutic options are needed."

The applications are supported by findings from Phase 3 Multicenter, Randomised, Double-blind, Placebo-controlled trials of Ustekinumab, a Fully Human anti–IL-12/23p40 Monoclonal Antibody, Administered Subcutaneously, in Subjects with Active Psoriatic Arthritis (PSUMMIT I and PSUMMIT II), which evaluated the efficacy and safety of subcutaneously administered STELARA 45 mg or 90 mg at weeks 0, 4 and then every 12 weeks.  The trials included patients diagnosed with active psoriatic arthritis who had at least five tender and five swollen joints and C-reactive protein (CRP) levels of at least 0.3 mg/dL in spite of previous treatment with conventional therapy.  PSUMMIT II also included patients with previous exposure to tumor necrosis factor (TNF) inhibitors.  The primary endpoints for both studies were the proportion of patients demonstrating at least a 20 percent improvement in arthritis signs and symptoms [American College of Rheumatology (ACR) 20] at week 24.  Secondary endpoints at week 24 included in the submissions were: improvements in Health Assessment Questionnaire Disability Index (HAQ-DI) scores, a 50 or 70 percent improvement in arthritis signs and symptoms (ACR 50 or ACR 70), and at least a 75 percent improvement in psoriatic skin lesions as measured by the Psoriasis Area Severity Index (PASI 75) in patients with at least three percent body surface area involvement at baseline.

Source: NO LINKS ALLOWED

PSUMMIT I report: Stelara and Psoriatic Arhtritis Phase 3 data

PSUMMIT II report: Stelara Significantly Reduced Psoriatic Arhtritis

Stelara (ustekinumab)

Just wondered if anyone can advise me

I am currently waiting for my derm appt, which will take up to 13 weeks.

I have a large percentage of coverage, including face, scalp, palms and soles of my feet.
I have plaques and lots of small patches, so I struggle with putting on topicals.

My question is this: am I likely to be offered anything other than topical treatments while I am trying to get pregnant?

This affects members accounts that have never been used.

By default accounts not activated within 24 Hrs are deleted, but we still have some accounts that have been activated yet no posts or further log-ins have been made. This is a ploy sometimes used by spammers, so from now on I will be deleting any accounts with zero posts that have not logged-in in the past twelve months.

How will this affect me?

• Members with at least one post: Your account will remain open and you don't need to do anything.
  
• Members who have logged-in at least once in the past twelve months: Your account will remain open and you don't need to do anything.
  
• Members with zero posts who have not logged-in in the past twelve months: Your account will be deleted.