This study which is ahead of full publication in Arthritis Research and Therapy looked at new psoriatic arthritis patients and suggest that a better understanding is needed as to why they don't stay on first treatments for a long period.

Quote:

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Introduction:
This study aimed to describe treatment changes (discontinuation, switching, and therapy add-on) following the initiation of a biologic or nonbiologic oral disease-modifying antirheumatic drugs (DMARDs) in psoriatic arthritis (PsA) patients.


Methods:
Adult patients with 2 PsA diagnoses from physician office visits, initiated on a biologic or non-biologic oral DMARD, were selected from the Truven Health Analytics MarketScan Research Database (2005 to 2009). Patients were required to have continuous insurance coverage 6 months prior to and 12 months post index date (first prescription fill date). Treatment discontinuation, treatment switch, and therapy add-on were captured over the 1 year period following the index date. Treatment changes were described separately for patients initiated on nonbiologic and biologic DMARDs.

Results:
A total of 1,698 and 3,263 patients were initiated on an oral nonbiologic DMARD and biologic DMARD respectively. For patients initiated on nonbiologic DMARDs, 69% had 1 therapy change over the 12 month study period (median time 85 days). Among patients who had a therapy change, 83% discontinued, 29% switched therapy (64% switched to a biologic DMARD), and 25% had a therapy add-on (76% added-on with a biologic DMARD). For patients initiated on a biologic DMARD, 46% had 1 therapy change (median time 110 days). Among patients who had a therapy change, 100% discontinued, 25% switched therapy (92% switched to another biologic DMARD), and 7% had a therapy add-on with a nonbiologic DMARD.

Conclusion:
This study suggests that PsA patients newly initiated on a nonbiologic/biologic DMARD do not remain on the index treatment for a long period of time. A better understanding of factors related to these early treatment changes in PsA patients are needed.

LINK REMOVED

Here an article on scientific research and the flaws in it. If this is the status of real scientific research, how shall we weight the results of pharma paid research on their own products then?

Seems life is kind of a roulette...

The market for treatments of psoriatic arthritis therapies will grow nearly 66 percent increasing to $3.7 billion in 2023 do to increased uptake of premium-price biologics and novel therapies that are expected to launch during the 2013 to 2023 forecast period.

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Decision Resources Group finds that the market for psoriatic arthritis (PsA) therapies will grow nearly 66 percent, increasing to $3.7 billion in 2023, owing to the continued uptake of premium-price biologics and novel therapies that are expected to launch during the 2013 to 2023 forecast period. In 2013, five marketed TNF-alpha inhibitors dominated sales in the PsA market with over 90 percent of the $2.3 billion major-market total; adalimumab (AbbVie/Eisai's Humira) was the overall sales leader. Over the next decade, TNF-alpha inhibitors will retain their sales-leading position, but recently launched treatments ustekinumab (Janssen's Stelara) and apremilast (Celgene's Otezla), together with noval therapies—which include the anti-interleukin-17 monoclonal antibodies secukinumab (Novartis), ixekizumab (Eli Lilly), and brodalumab (Amgen/AstraZeneca/Kyowa Hakko Kirin) and the Janus-kinase inhibitor tofacitnib (Pfizer's Xeljanz)—will account for approximately 21 percent of 2023 PsA sales combined in the United States, France, Germany, Italy, Spain, United Kingdom and Japan.

Of the five agents entering the PsA market, tofacitinib (Pfizer's Xeljanz) will experience the most uptake during the forecast period. Tofacitinib and recently launched apremilast feature oral formulations and unique mechanisms of action, thus allowing them to compete for TNF-alpha inhibitor-refractory patients, as well as experience uptake as "stop gaps" for conventional DMARD failures before stepping up to treatment with biologics.

Less-expensive biosimilar versions of several biologics will launch beginning in 2015 and will erode biologics' sales through 2023, with the largest impact on the TNF-alpha inhibitor class.

Interviewed thought leaders report that conventional DMARDs and TNF-alpha inhibitors are the clinical mainstays for mild and moderate-to-severe PsA, respectively, and will face only moderate loss of patient shares to recently launched and incoming novel therapies.

Decision Resources Group Director Bingnan Kang, Ph.D.
"The addition of the TNF-alpha inhibitors to the PsA treatment algorithm represented a significant step forward in the management of this heterogeneous disease. Despite advances in the diagnosis and treatment of PsA, significant opportunity remains for developers of additional disease-modifying agents and agents with a high degree of efficacy against multiple disease manifestations."

"Physicians are keen for results of pivotal clinical trials of emerging PsA therapies. Interviewed thought leaders tell us that should ixekizumab and/or tofacitinib prove to be as or more effective than active comparator arms (versus adalimumab) in their respective Phase III trials, these therapies would experience stronger uptake compared with other novel agents entering the PsA market."

"Biosimilar versions of etanercept, adalimumab and infliximab are expected to launch in most or all of the major markets during the forecast period and to account for approximately 36 percent of TNF-alpha inhibitor sales for PsA in 2023. Our primary research indicates that most rheumatologists will feel comfortable prescribing biosimilars for PsA, based on biosimilars' clinical trial data in RA, thereby reducing biosimilars' barrier to entry in this market."

This article published in The International Journal of Rheumatic Diseases measured changes in the serum levels of adiponectin, resistin and visfatin, and the associations of such changes with the extent of disease activity and insulin resistance in Psoriatic arthritis (PsA) patients.

Quote:

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Aim:
Psoriatic arthritis (PsA) is an inflammatory form of arthritis typically associated with psoriasis and/or psoriatic nail disease. Adipocytokines were once thought to influence development of (only) insulin resistance and diabetes mellitus. However, it is now clear that adipocytokines play important roles in development of the inflammation associated with either autoimmune or auto-inflammatory disorders. In the present study, we measured changes in the serum levels of adiponectin, resistin and visfatin, and the associations of such changes with the extent of disease activity and insulin resistance in PsA patients.

Material and methods:
A total of 67 subjects (28 with PsA and 39 healthy controls) without hypertension or diabetes mellitus were enrolled. Adiponectin, resistin and visfatin levels, and the extent of insulin resistance (assayed using the homeostasis model [HOMA-IR]), were measured in all subjects. Assessment of PsA disease activity was done with the Disease Activity Index for Psoriatic Arthritis (DAPSA).

Results:
Psoriatic arthritis patients had considerably higher serum levels of adiponectin, resistin and visfatin than did healthy controls (all P < 0.05). In the logistic regression analysis, the following variables may contribute to complex pathogenesis of PsA: adiponectin (P = 0.001, OR = 3.1, 95% CI = 1.6–6.0), resistin (P = 006, OR = 1.8, 95% CI = 1.2–2.9) and visfatin (P = 0.031, OR = 3.9, 95% CI = 1.1–13.9). In contrast, we have not detected any correlation between DAPSA and adipocytokine serum levels (P > 0.05).

Conclusion:
There is no correlation between adipocytokines and disease activity. Although serum adiponectin, resistin and visfatin levels are higher in patients with PsA, pathophysiological significance of the result has to be evaluated with more extensive studies.

I know that we are each going to be different on this as there are different type of psoriasis and different types of treatment represented here on the forum but as someone recently starting treatment, I'm looking each day at signs of improvement. Some days I think things are looking up and other days I don't feel I'm closer to getting clearer. Since treatment takes time and I doubt anyone woke up to say "I'm clear!" I thought I'd ask if anyone wanted to share what they noticed was happening while they were "clearing up". Did you still have bad days when it looked worse, did it just gradually over time keep improving or did it maybe get worse before getting better?

For me, I haven't noticed a huge improvement yet and yes, I know it's still early for me. Less itching (although sometimes I wonder if that's just me being overly hopeful) and my ears almost cleared... but I was on a steroid medpac and I'm guessing it helped with that as they have since gone back to how they were before. My scalp is peeling more than ever I think, but I don't know if that is a good sign or bad. The "redness" still comes and goes, goes as in not away just not as red some days as others.

Also, maybe how long into treatment before you noticed an improvement? (Again, I know that will vary according to treatment, type of p and just individual person)

Dupuytren contracture (DC) is a fibrocontractile disease of the palms where the fingers bend towards the palm and cannot be fully extended, this study looked at the correlation between psoriasis and dupuytren contracture.

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Aim:
To evaluate the prevalence of DC in the full range of clinical psoriasis phenotypes.

Methods:
In total, 98 patients with psoriasis attending our psoriasis clinic were examined for DC, based on predetermined criteria. In addition, 84 patients with DC, obtained from a specialist hand clinic, were assessed using a validated psoriasis questionnaire. We utilized Bayes theorem and bootstrap simulation to calculate the conditional prevalence of DC, then we used the results to compare the prevalence of DC between patients with psoriasis and a nonpsoriasis population.

Results:
The percentage of patients with DC was 19.6% in the psoriasis population and 3.6% in the nonpsoriasis population. Development of DC showed a phenotypic predilection, with 39.1% of patients with predominantly palmoplantar involvement and 38.9% of patients with intertriginous psoriasis developing DC compared with 12.7% of patients with psoriasis who did not have these two phenotypical presentations.

Conclusions:
Our data show a positive correlation between psoriasis and DC. Patients with the palmoplantar phenotype of psoriasis were more likely to develop DC. By understanding this relationship, dermatologists may diagnose DC early in its onset in patients with psoriasis, prompting referral to hand surgeons when appropriate.

This study although small looked at the possibility of NB-UVB (narrow band ultraviolet-B phototherapy) being used after a bio treatment failure.

Quote:

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Background/Purpose:
Biological therapy has demonstrated a very satisfactory anti-psoriatic effect; however, the loss of response with time has been reported.

Objective:
To evaluate the efficacy of the narrow band ultraviolet-B phototherapy (NB-UVB) as a rescue in patients with moderate to severe psoriasis who have lost efficacy in their biological treatment.

Methods:
A retrospective chart review study was conducted on patients with moderate to severe psoriasis receiving treatment with a biologic, with a good initial response that subsequently had lost efficacy. All the patients received combined treatment with NB-UVB.

Results:
Seventeen patients were included, with a mean age of 44 years. The biologics were: 8 etanercept, 4 adalimumab, 3 ustekinumab, 1 efalizumab, and 1 infliximab. The mean NB-UVB sessions was 25 (7–48 sessions), with a mean accumulated dose of 31.12 J/cm2 (5.2–94.6 J/cm2). Sixteen patients had the following results: 44% PASI 90–100, 31.3% PASI 75–89, and 25% PASI 50–74 response.

Conclusion:
According to this study on clinical practice, it could be considered that the use of NB-UVB along with biological drugs that have lost efficacy in controlling moderate to severe psoriasis in adults could contribute to the recovery of the initial response.

I have had psoriasis since I was 4 years old (yup, not usual...the Dr.s had fun studying me in the sixties). It has been quite a journey going from doctor's office to doctor's office. I used tar and cortizone and anthralin and psoralin and methytrexate and light boxes and sea water. My mother tried every remedy going from shark, seal, whale oil to white turkey meat only to butter from New Zealand to....you get the idea. I drank this kind of drink or that which was supposed to have some healing property. She brought me to this healer and that. The only thing I got from it was the profound feeling that I was defective and not human. Bless her for caring, but the best thing I have found is to simply accept myself with my anomalies.

As I have done so, I have altered my diet and activity. I have gained understanding and compassion for others coping with difficulties. I have also learned to pay attention to my skin as an indicator of the need to balance and improve my life better. It is a great meter for how much stress I am under.

I have found that eating a good diet (including lots of fish - I have gained fishing as a hobby now) helps keep my skin under control. I avoid all stimulants (no chocolate, caffeine, etc.), I avoid nightshades, only fish and nuts for protein (although I have not learned to avoid cheese that well yet), no fried foods, no sugar (I do use raw honey), whole grains only, few or no processed foods. Menopause caused a flareup, but I am getting things back in order by living the healthy eating principles more strictly. I also make sure that I am outside as much as possible being active in the sunshine (I walk 3-5 miles a day). The side effect of a diet like this is lots of energy, and not being able to eat out at fast food restaurants very much.

I am careful to study all that is given to me by anyone now. I have learned that most natural oils help with the lesions but do not remove it. I have also learned that some remedies have a backlash effect, meaning that the psoriasis comes back worse than ever if you do not increase the dosage or usage (some drugs and remedies will do this and will cause any number of side effects from being sick all the time to sending the individual on an emotional rollercoaster in addition to causing birth defects if you are the child-bearing type). Do your own homework and decide about the risks you will take. I am currently trying out a Vitamin D.

I guess that's it for now. Thank you for this forum where no one is trying to sell me anymore snake oil! I am grateful I get to hear and explore some of the more natural ways of living and being healthy with my skin.

Hello!

My name is Elvi and I have psoriasis on my hands, feet, scalp, arms and legs. It is worst on my calves. Currently I am using corticosteroids but I have tried all sorts of horrendous forms of treatment - I wish my skin would normalise!

It started approximately five years ago when my husband and I started divorcing (he ran off with a woman - older unusually!), my daughter also took a job abroad around the same time and I felt totally alone after 27 years of marriage! The stress of this triggered patches on my scalp and hands but it soon spread to my feet, legs and arms. I ignored it for awhile in the stress of trying to find a new house, job etc but eventually I went to see a doctor, who sent me to this lovely dermatologist - she has prescribed me a cocktail of treatments over the last five years and so far nothing clears it completely - corticosteroids work when there is a crisis to get me back to a mild case.

I really would love your suggestions and solutions - I just want to wear dresses again and not feel so shy about it - I am 62 and should not have to feel shy about anything! SO PLEASSSEEE let me know or direct me to other threads with ideas that might help! I would be very appreciative!

This article published in The Journal of the European Academy of Dermatology and Venereology looked at the use of Bio treatments for psoriasis in the over 65s and found no differences in the risk association between young and the elderly.

Quote:

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Background:
Psoriasis patients over 65 years-old (elderly) constitute a growing group, underrepresented in clinical trials, and likely to be more prone to adverse events.

Objective:
To describe safety of systemic psoriasis therapy in patients over 65 years-old compared to younger patients.

Methods:
Patients registered in Biobadaderm, a Spanish national registry of psoriasis patients treated with systemic therapy, were grouped in elderly (≥ 65 years old) and younger patients. Rates of adverse events were described by severity and type, and the risks compared in both groups, taking into account exposure to classic or biologic drugs, using Cox regression.

Results:
175 (9.8%) of 1793 patients were elderly. Overall risk of adverse events was not higher in elderly (drug group adjusted HR 1.09 (95%CI: 0.93-1.3)). Serious adverse events were more common in elderly (drug group adjusted HR 3.2 (95%CI: 2.0-5.1)). Age adjusted HR of all adverse events was lower for patients exposed to biologics compared to classic drugs in the whole sample (HR 0.7 (95%CI: 0.6-0.7)). Age did not seem to modify the effect of therapy (biologic vs. classic) in the risk of adverse events (likelihood ratio test for interaction, p = 0.12 for all adverse events, p = 0-09 for serious adverse events).

Conclusions:
Serious adverse events are more common in elderly patients, although they may be related to other variants that are associated with this age group and not due to the treatment itself. Use of biologics was associated with lower risk of adverse events in the whole group. We found no differences in this association between young and elderly. These results are reassuring, although uncontrolled confounding could not be excluded as an explanation for these findings, and the power of the study to detect differences was low.

Hi just made a mistake and another post was posted as me..it repeated the other post... It starts out I'm 37 year old and thought psoriasis was hereditary ... I hope it can be delegated!

Just getting the hang of this new site.

Any way I hope to get this straightened out. Sorry for the mistake.


I hope I haven't caused too much trouble.

Hi, I am the snorkel horse my name is Quest4Cure .
I have psoriasis and psoriatic p. Have a whole mixed bad. The plaque P. I've had since a child, it isn't quite as bad and palmoplanter P. Hand and feet are the worse . Also just this year developed Inverse P. So 4 out of 6 types of P . Sun shine helps this time of year for plaque . I just look like I have white freckles.
Palmoplanter It comes every winter like clock work . Water is my biggest enemy.. For Hands and feet. So sharing ideas and talking with others & sharing what they do to help control their P. Or palmoplantar. Or al types of P. PustularP and plaque P.

Thank goodness Derms have become better at treating this disease and better meds have come along the past few years.

My right hand had surgery last yr for one finger as it turned out it caused what they call the Keobler effect and and caused a flair from surgery causing all my fingers to curl and remain stiff. Has anyone else experienced the Keobler effect ?

I highly recommend a hand spa with wax to keep hands and feet moisturizers during cold dry winters.

Looking foreword to meeting new people and sharing experiences with living with P.
Thanks Quest4Cure

Hi
I've been on fumaderm for a year now and have reduced my dose from 2 tablets OD to 1 tablet once a day. We are trying every other day at the moment but it's starting to come back quite quickly.
Fumaderm has transformed me and my skin. It has had it's side effects but a very small price to pay and all manageable. I'm concerned what the long term implications will be, my dermatologist has said I can only be on it for 2 years and due to a lack of evidence for long term care I'm starting to feel a little anxious at it all returning again.
Has anyone been on it long term? Advise appreciated please
Charlotte x

Hi there,
Me again, but really feel the need to moan. So still waiting on the appointment for rheumatology, still waiting for dermatology appointment. Laying in bed in pain, hands, feet, knees, neck, feel like they are on fire. Pain in all joints and psoriasis everywhere. I have never had it on my face before and now suddenly here it is! I cannot quite describe how I feel at this moment in time except to say I have had enough! I itch all over and I mean all over, my feet and ankles are covered, swollen. My hands look like I have leprosy. Right now I really don't know what to do with myself. I really don't! I can literally peel my skin off in sheets, my husband can't believe it! It is reproducing so quickly I can't keep up with it. None of my usual stuff is making a difference.
Sorry, I know all I can do is wait for appointments, but I think tonight I have reached my limit in pain, itch and actually how revolting I look!

The first time I went to the dermatologist, he prescribed fluocinolone acetonide and told me it "should" come with a shower cap, to wear it overnight. Well, what I got from the pharmacist was fluocinolone acetonide BODY oil, no shower cap. Plus the derm told me to use on all spots so it seemed right. I didn't think anything of it other than perhaps they no longer put the shower cap with it. I used it and it did help soothe, but didn't help a lot with itchiness, it didn't clear up anthing however so next visit he put me on meds as mentioned in other posts.

Anyway, I told him I was low on the oil so he gave me another prescription for the same thing. THIS time, the pharmacy gave me fluocinolone acetonide SCALP oil. (I'm thinking it was what he prescribed the first time and the pharmacy just got it wrong.) It appears to be pretty much the same thing but the scalp oil is a little thicker (I think) and it did come with a shower cap.

I ran out of the first bottle (the body oil, although I didn't realize at this time there was a difference) and opened the second one. When I saw the shower cap, I thought they had just left it out of the first one but I looked and saw the first one said BODY oil and the second specifically said SCALP oil. So anyway I used the scalp oil for the first time this last Thursday (I was told not to use topicals on days of light therapy)

Anyway, it helped a lot! I moistened my scalp, applied the oil, put on the shower cap (wouldn't win any fashion awards for that one!) and left it on for 4 hours. No way can I sleep with it as I'm too restless and that cap would be off within half and hour. Wearing the cap really helped with keeping the moisture in and after washing out the oil, I gently ran a comb along the scalp and descaled. The scales were rolling off practically. I didn't force it as didn't want to irritate my scalp and make it sore. For the first time in a LONG time, my scalp was barely itchy at all. I had light therapy yesterday and today my skin is "tightening" up and I can feel the dry scales. I plan on using this a couple of times a week on days I don't have light therapy and hope it continues to relieve some of the itching.

I wanted to mention this as anyone suffering from scalp psoriasis and severe itching might want to ask their dermatologist if this would be something they could try. Just make sure you ask about the SCALP oil.

The FDA (U.S. Food and Drug Administration) says “Psoriasis has a great emotional impact on some patients. But it doesn’t have to, given the right care and treatment.”

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The more scientists learn about psoriasis, the more therapeutic options are becoming available for patients with this skin disease.

“As we better understand the disease, researchers know more about what specific factors to target in order to develop effective treatments,” says Melinda L. McCord, M.D., a dermatologist at the Food and Drug Administration.

The treatment for psoriasis has changed from the previous gradual step-by-step approach. Today, doctors seek to optimize treatment from the first visit—whether with phototherapy or systemic therapies—based on the specific needs of each patient.

“Tomorrow’s treatments will become even more personalized because the drugs in development now are targeting different aspects of the immune system,” McCord notes.

Psoriasis is an immune system disorder characterized by inflammation and the rapid overproduction of skin cells, creating scaling, pain, swelling, heat and redness. About 7.5 million Americans have psoriasis, a skin condition that can create significant physical and emotional discomfort.

Therapies for psoriasis include:

Medicines applied to the skin (topical treatment)
Light treatment (phototherapy)
Drugs taken by mouth or injection (systemic therapy)

There is no cure for psoriasis, so the main goals of treatment are to reduce inflammation and to stop the skin cells from growing so quickly.

In the past, doctors treated psoriasis using a “step-wise approach.” Patients with mild to moderate psoriasis would start with topical therapies and, if they did not respond well to that, move on to other treatments, such as systemic therapy or phototherapy. This approach called for treating people with moderate to severe psoriasis with phototherapy or traditional systemic therapies—drugs such as methotrexate and cyclosporine—before offering them biologic therapies (a type of treatment that works with your immune system).

That strategy has changed to a more patient-specific approach. Today, patients and their doctors can choose a treatment based on its effectiveness, the severity of their disease, lifestyle considerations, risk factors, and associated diseases (co-morbidities).

The most recent biologic product approved by the FDA for the treatment of psoriasis is Stelara (ustekinumab). Ustekinumab contains an antibody that’s produced in a laboratory and designed to bind to a specific target in the immune system. “When given to patients, this antibody blocks the action of two proteins (interleukin 12 and 23) that contribute to the inflammation and the overproduction of skin cells. By targeting these proteins, ustekinumab can interrupt the inflammatory pathway,” McCord says.

“Looking forward, the drugs in development are targeting different pathways in the immune system that lead to inflammation. Researchers are exploring the importance of interleukin 17,” McCord says. “They’re also looking at proteins and molecules that can interrupt cellular signaling, which can increase the spreading of the inflammation.”

“As we learn more about the immune pathways that lead to the development of psoriasis, we can target specific molecules for treatment and make more therapeutic options available to patients,” McCord says. “Understanding the disease gives us the opportunity to target specific factors.”

McCord recommends a team approach to treating psoriasis. Patients, families and their health care providers need to work together to address the multiple diseases that may occur in association with psoriasis, including the risk of developing metabolic syndrome (the occurrence of obesity, high blood pressure, high cholesterol and diabetes in one patient), lymphoma, heart disease and/or depression. “We do not completely understand the relationship of these co-morbidities to psoriasis, but it is an area of active research,” she adds.

Because psoriasis is a chronic disease with no cure, patients may need to use treatments for a long time. Many therapies approved by FDA have been evaluated for extended time periods.

Psoriasis has environmental and genetic components. It is more common in adults and can run in families. What triggers it? A virus? Bacteria? Stress? Other environmental factors? “We just don’t know,” McCord says.

The good news is that patients can treat some of the signs and symptoms of psoriasis with simple measures. For example, regular use of moisturizers may improve the itching and scaling. Reducing or limiting tobacco use and alcohol consumption may decrease the number of flares of psoriasis. Lifestyle changes—such as maintaining a healthy weight and being physically active—may help lessen or prevent the development of associated diseases.

McCord advises patients to seek treatment early from a doctor experienced with the disease. A dermatologist can provide patients with the correct diagnosis and information to manage the disease. “If you are diagnosed and treated early, you may avoid the pitfalls of ineffective and inappropriate therapy,” she adds.

Some patients become easily discouraged about treatments, but newer therapies may make them more comfortable. That’s why McCord says patients should investigate treatment options early and educate themselves about their condition. Even if patients have a mild case of psoriasis and decide they don’t want a particular treatment option, there are ways they can decrease their symptoms.

“Psoriasis has a great emotional impact on some patients. But it doesn’t have to, given the right care and treatment,” she says.

After reading a conversation here: RE: Hey fellow sufferers I thought it would be interesting to start a new poll.

Question: Do you think there will ever be a cure for psoriasis? (I'm talking cure as in it's gone from the whole world and will never come back as that is a cure to me)

You can vote in the poll above (open to guests too) Members can also add comments in this thread.

Hey everyone new to this forum but not in regards to P.
I thought I would share my experience with you after starting Acitretin Aug 2014.
Suffered since age 12 and as a veteran of the vast array of meds on offer I am now at the stage of trying Acitretin. My P by the way is on the high end of moderate bordering on severe. Apparently, after bloods, cholestorol etc I am an ideal candidate. This is my second attempt at an oral drug as I reacted adversely to ciclosporin. I will share with you any side effects and effects on skin.
Day 1: 35mg Acitretin taken after breakfast, started to develop a pressure headache, foggy feeling and this didn't stop only respite is when asleep, nightmare.
Day 2: Same strict routine and again now a hazy headache not very alert, with a foggy feeling, after a nap feel brighter continued throughout day again nightmare.
Day 3: Headaches don't seem to be there today no pain and it seems the fogginess is going feel more brighter than last two days. Not sure whether related but my IBS flared badly in the am.
No significant change in skin or anything else will try and update again further along. However, I live in hope this treatment may help me but don't hold out much optimism considering years trying other treatments that have failed, anyway we will see.

Ok folks after a really bad flare over the last few weeks, I've decided to forego the natural remedy route for now and give the Acitrecin and topical steroids a try. I found a nifty back applicator at the pharmacy so I can apply the steroid cream all over. Oh I'm just going to lube myself up and have a party! I'm going to be diligent about sticking with the routine and see if there is any progress in a month when I go back to the Derm. I'm hoping I will tolerate the Acitrecin as I cannot go on biologics because of my cancer history. My Dr. did tell me I could go on methotrexate and wanted to put me on that because he said it would work faster than the Acitrecin but my cancer Dr. says it's poison and to stay away. I know many here have had good luck with Methotrexate and if Acitrecin doesn't work, I'll have to give it a try. Dr. thinks I have about 70% coverage btwn my scalp, face, torso, arms and legs and said he rarely has seen a case spread so fast and be so acute. Lucky me. Also taking Atarax for the itch. I wish I didn't have to deal with any of this and it would just go away on it's own but I know that's not going to happen.

I'll post on the natural remedies board about my experience with Functional Medicine Dr. I had last week.

Following on from this thread Covagen Initiates Phase Ib/IIa Study with COVA322 Janssen today announced it has now acquired Covagen. As for if this is a good thing or a bad thing we will have to wait and see.

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Cilag GmbH International, an affiliate of the Janssen Pharmaceutical Companies of Johnson & Johnson, announced today that it has acquired Covagen AG, a privately-held, biopharmaceutical company specializing in the development of multispecific protein therapeutics through the FynomAb® technology platform. The opportunity was identified and facilitated through the Johnson & Johnson Innovation Center in London. The company's lead product, COVA 322, a bispecific anti-tumor necrosis factor (TNF)-alpha/anti-interleukin (IL)-17A FynomAb, is in Phase 1b study for psoriasis and holds potential as a treatment for a broad range of inflammatory diseases including rheumatoid arthritis. Covagen develops FynomAbs, multi-specific protein therapeutics, by fusing its fully human Fynomer binding proteins to antibodies. Fynomers are small binding proteins engineered to bind to target molecules with the same affinity and specificity as antibodies. The tailored architecture and novel mode of action of FynomAb therapeutics may offer enhanced efficacy in the treatment of a broad range of inflammatory diseases and other conditions. Financial terms of the transaction have not been disclosed.

"Our goal is to translate advancements in immunology science into next-generation therapies that improve patient outcomes," said Susan B. Dillon, Ph.D., Global Therapeutic Area Head, Immunology, Janssen Research & Development, LLC. "Our interest in Covagen stems from the company's scientific acumen, their novel FynomAb platform, and the potential of COVA 322, a bispecific designed to achieve better control of inflammation by blocking two key cytokines that have been implicated in disease pathogenesis and progression. We look forward to progressing COVA 322 development, and to further expanding the potential of multispecific biologics for immunologic and other diseases. This exciting opportunity underscores the value of co-locating scientific innovation leads at our regional hubs in thriving life science communities as part of our strategy to identify and realize new opportunities and build long-term competitive advantage."

Covagen will maintain a research presence in Zurich-Schlieren, Switzerland, and will continue to focus on the further development and application of the Fynomer technology. "We are very excited to further develop our pipeline and innovative FynomAb platform as part of Janssen," said Julian Bertschinger, Ph.D., co-founder and former CEO of Covagen. "Janssen's tremendous knowledge in the research and development of biologics provides us with a great environment to develop novel FynomAb-based therapeutics addressing unmet medical needs."

Covagen was co-founded in 2007 by Julian Bertschinger, Ph.D., and Dragan Grabulovski, Ph.D. as a spin-off company of ETH Zurich, Switzerland.