Psoriasis

[chuckles] Let's start by talking about the pathophysiology of psoriasis, both the skin manifestations and some of the more systemic disease manifestations as well.

Yes.

Thank you very much.

Over the last several years, the dermatology community and medical community at large has learned a great deal about psoriasis.

We were always aware of the basic construct of the skin pathology, and I'll go through that in a moment.

What we didn't appreciate until we had better data was that the same inflammatory cascade that is happening in the skin, we knew it could sometimes happen in the joints.

I think the medical community was aware of psoriatic arthritis, but we weren't aware of the systemic nature of the inflammation impacting the whole person and the need to practice whole-person care when you're managing a patient with psoriasis.

So psoriasis is literally more than skin deep.

And if our colleagues today remember just a couple of things about psoriasis, I would appreciate if they would take home that psoriasis is more than a skin disease.

Psoriasis is a multisystem inflammatory disorder that happens to most commonly manifest in the skin, and that psoriasis comes with multiple comorbidities that have to deal with systemic inflammation aligned with metabolic syndrome.

And so when they see a patient with psoriasis, they should approach that patient similarly to how they approach a metabolic syndrome patient that has chronic liver disease, kidney disease, hypertension, insulin resistance, diabetes, adiposity or obesity, central adiposity or obesity, and things that go along with systemic inflammation that definitely impacts health longevity, life longevity, and quality of life.

In patients who have psoriatic arthritis, does the skin manifestations of psoriasis mirror the activity of the psoriasis, or are they completely independent of each other?

Psoriasis is caused when people have genetic combinations that together give them a predisposition for a code.

It's not a single Mendelian gene disorder.

But people have various combinations of HLA haplotypes and immune haplotypes that make them susceptible to psoriasis.

Then they have a stressor event, either to their immune system or to their skin, that can trigger that predisposition to be exposed and to start the inflammatory cascade.

That manifests as psoriasis on the skin.

What happens is our inflammatory system, our neutrophils, followed occasionally by lymphocytes, come to the dermal epidermal junction and release their chemicals, and the skin is genetically primed to overgrow to protect itself like a callus.

So regular skin will grow, die, shed, and separate every 28 days.

Psoriasis skin is genetically primed that when inflammation reaches the skin, it will hyperproliferate to form a callus, and it will try to die, shed, and separate in three days, 72 hours.

So the reason that we see erythematous scaly patches and plaques on the skin is because our skin is like a wound-up factory that's on overdrive, and it cannot grow, die, and shed fast enough, which is why you see red.

That's the inflammation and the hyperproliferation or overgrowth of the skin.

And then you see the scale because that's the skin that is trying to die, shed, and separate.

Does that necessarily happen in the joints? The same similar inflammatory process happens in the joints, and synovium in, in joint space has epidermal tissue, but it's not the cutaneous glabrous tissue of the skin.

It's synovial tissue that is a skin- Type.