The first day of the DERM2019 NP/PA CME Conference kicked off with a bang! Exciting talks and lively panel discussions from April Armstrong, David Cohen, Adam Friedman, Kara Gooding, and Joe Gorelick were the mainstay of the day.

Psoriasis Pathogenesis and Treatment Targets Presentation from April W. Armstrong

Recap by Leigh Ann Pansch, NP

She did it yet again! Dr. Armstrong presented on “Psoriasis Pathogenesis and Treatment Targets” and laid out a concise and simple understanding of the disease state and pathways. While these systemic therapies can feel daunting, Dr. Armstrong breaks myths and dispels fear with cold, hard facts!  Current best evidence suggests the native T cell (not the keratinocyte) becomes TH1 and TH17 in the psoriatic patient and is the most specified target. Current target molecules on the playing field for biologic systemic therapy include TNF-α, IFN-gamma, IL-17A, IL-17F, and IL-23.  Don’t these look familiar!? Dr. Armstrong suggested these cytokines and receptors may be the best targets in psoriatic disease.  Infliximab, adalimumab, certolizumab and etanercept target TNF-a. Further, ustekinumab targets IL-12/23 by targeting a mutual P40 subunit.  Molecules which target only IL-23 include guselkumab, tildrakizumab, risankizumab, and mirikizumab.  The players for IL-17 targets include bimekizumab, brodalumab, secukinumab, and ixekizumab. 

STOP THE BUS! We all need to re-think our medication monitoring! The National Psoriasis Foundation recommends pre-screening with CBC differential, CMP, TB, and Hepatitis B and C with yearly re-screening only for TB.  These molecules are safe and, unlike other systemic therapies, do not appear to carry the same risks of malignancy.  It’s an exciting time in systemic therapies for psoriasis!  This research gives hope there is an effective treatment option for everyone; and in a field that is directed to “first do no harm,” we can feel confident in safety profiles for these medications as a whole.

Psoriasis Immunology and Treatment Targets Presented by April Armstrong

Recap by Jayme M. Heim MSN, FNP-BC, West Michigan Dermatology

From 2009 to 2019, our ability to treat our patients with biologic agents has grown exponentially. In fact, there are now eleven FDA approved biologic medications used for the treatment of psoriasis. However, not all of these biologic medications are FDA approved for the treatment of psoriatic arthritis.

When we examine immunopathogenesis and therapeutic targets, we are targeting specific cytokines that are responsible for psoriasis and psoriatic arthritis. The key cytokines are TNF-Alpha, IL-12, IL-23, and IL-17. Biologic agents target the receptor sites on these key cytokines.  Other therapies used to treat psoriasis include topical medications, phototherapy, and oral systemic medications.

Choosing a biologic therapy can be very challenging. In April of 2019, the AAD-NPF Psoriasis Guidelines were published in the Journal of the American Academy of Dermatology.  The guideline was published as a reference for providers who treat psoriasis patients. Areas highlighted today included laboratory monitoring before starting a biologic, dose escalation of biologic therapy, different subtypes of psoriasis, and strength of clinical recommendations.

Baseline labs prior to starting biologic therapy include TB, CBC, CMP, hepatitis B and C.  HIV testing is at the provider’s discretion. With ongoing therapy, annual TB testing is recommended. It is important to keep in mind that these are minimum recommendations and that additional monitoring is at the discretion of the provider. 

Dose escalation has been done in clinical practice and is considered an off label use of a medication. However, this new guideline looks at dose escalation for certain biologic agents. The Biologic agents identified for treatment in escalated dosing include: Etanercept, Adalimumab, Infliximab, Secukinumab, Ixekizumab, and Ustekinumab. This is important because some patients require dose escalation to maintain control of their disease. 

Dr. Armstrong concluded her presentation with data presented at the American Academy of Dermatology discussing the malignancy risks of oral drugs, phototherapy, and biologics.  A red, yellow, green, and no color system was used to identify risk. The greatest risk of malignancy is in the red category.  These medications include Cyclosporine, Azathioprine, and PUVA therapy. Medications with insufficient data or mixed data include UBV, Methotrexate, Etanercept, and Adalimumab.  Acitretin is the only medication in the green group which has the potential for preventing malignancy. The white category represents those therapies with no known increased risk for the patient. This includes: Apremilast, Certolizumab, Ustekinumab, Secukinumab, Ixekizumab, Brodalumab, Guselkumab, Tildrakizamab, and Risankizumab.

Many insights were gained during this presentation.  One thing is certain; our understanding of therapies for psoriasis will continue to guide us in the future and provide the best outcomes for our patients.

Psoriatic Arthritis: Essentials for Dermatology Providers Presented by April W. Armstrong

Recap by Leigh Ann Pansch, NP

Dr Armstrong wants to know if you screen EVERY patient with psoriasis for psoriatic arthritis?  When was the last time your newly treated with systemic therapy psoriatic patient declared, “I feel so much better!  My hands, ankles, (etc.) don’t hurt anymore!”  Do you ever wonder how we’re continuing to miss them?  The reality is we need to be comfortable evaluating for PsA.  While topical therapies and phototherapy may be appropriate for skin disease, those creams and light therapies don’t touch the joints.  The progression of joint disease in PsA is rapid and permanent and can lead to functional disability.  Do we have your attention?

Spondylitis (lower back pain), enthesitis (ankle pain), dactylitis (“sausage-shaped digits”), iritis (eye redness, pain, and blurred vision), mucous membrane ulcers, urethritis, and more extra-articular manifestations are associated with PsA.  This form of joint disease typically presents an oligo-articulate joint (single, solitary, one-sided) and is not typically symmetric like with other types of arthritis.  However, it can present in many ways and mimic other forms of arthritis.  Who knew we could purchase a dactylometer to measure those digits?  The next time you hit your “funny bone,” I dare you to proclaim, “I just hit my ulnar nerve!”  And who knew Dr. Armstrong would have us all doing the robot dance?  Have you seen the CASPAR criteria classification?  This tool offers the provider a highly sensitive way to identify those with PsA who may be slipping through the cracks.  CASPAR suggests any inflammatory articular pain with at least 3 points from the following features should be investigated for PsA:  Current psoriasis (score 2), a history of psoriasis (1), a family history of psoriasis (score 1), dactylitis (score 1), juxta-articular new bone formation (score 1), RF negativity (score 1), and nail dystrophy (score 1).  While examining the skin, pay close attention to the Achilles tendon insertion, plantar facia, and lateral epicondyles for enthesitis.  I can honestly say I am very thankful to Dr. Armstrong for helping me feel more confident making the PsA diagnosis. The National Psoriasis Foundation introduced us to yet another way to identify PsA:  The PEST screening tool.  This instrument has been validated and is simple and easy to use.  The tool contains 5 simple questions supported by the addition of a mannequin for easy patient markup.  Let’s all agree to add these important tools to our toolbox this year!

Atopic Dermatitis: Pathogenesis and Clinical Presentation Panel Discussion with April W. Armstrong, Adam Friedman, and David Cohen

Recap by Leigh Ann Pansch, NP

Oh the dreaded eczema! Or, as Dr. Armstrong noted, the topic of her presentation is that chronic, itchy dermatitis which we all know affectionately and that often appears in conjunction with allergic rhinitis, asthma, food allergies, and allergic conjunctivitis.

Simply stated, this disease state can present from immune dysfunction (Th2 which drives inflammation) and/or barrier dysfunction (fillagrin absence). Dr. Armstrong presented evidence that the immune response (or inflammatory response) is heightened in our atopic patients which seems to drive inflammation.   Additionally, their skin barrier is more like a sponge than a brick wall. Understanding the morphology, or typically presentation (including sites of involvement) can aid in diagnosis and differential across the lifespan.

We all need to re-think peanut avoidance! Don’t limit peanuts or foods. In fact, new evidence suggests we should expose at-risk children (those with family history of food allergies and eczema) to these allergens early in life to help reduce the potential of allergy development. 

So what exactly is the atopic march: Patients that follow a pathway of childhood eczema (usually in infancy), then develop asthma, then allergic rhinitis. Given infection is a concern for these patients, daily bathing (in lukewarm water for no more than 15 minutes followed by thorough application of emollients) may help reduce bacterial colonization. Let’s be proactive out there team!

The next time you consider oral and IM steroids for that atopic flare, Dr. Friedman says consider this a deal with the devil! The risks including infection, rebound flare, and atrophy are dangerous and should be avoided long term. Cyclosporine (which may be a good short-term option but should not be considered long-term due to side effects and malignancy risk), Methotrexate (which newer research indicates is safer than we once thought but may not be an ideal long-term option given concern for liver toxicity), Mycophenolate Mofetil, NBUVB (not ideal for the flared patient), Azathioprine, and Acitretin (no ETOH or in women with childbearing potential) are systemic therapy options which have been available for years. Consider neuropathic mediations and antihistamines for itch. Dupilimumab is an IL-4/IL-13 receptor blocker currently FDA approved for patients (12 years and up) with moderate-severe atopic dermatitis with an excellent safety profile.

Dr. Cohen had the pleasure of updating us on small molecules (oral and topical small molecular weight) in AD. We felt his pain as he discussed psoriasiform spongiotic dermatitis and took away our hope for every being the masters of the differential diagnosis. There are numerous new molecules (anti IL-13, anti IL-31, JAK inhibitors, TYK2) in late-phase testing which offer promise for an optimistic future for this disease state.