Mechanism of Repigmentation in Vitiligo

Video

Ted Lain, MD, reviews the rates and patterns of repigmentation of the skin in vitiligo and how the timeline is different for each patient.

Seemal Desai, MD: Ted, let’s go, come back and kind of come back to where we talked a little bit about therapies not just in clinical trials, but let’s just talk about the patient in general. Vitiligo patients have different rates of repigmentation. They come in with different patterns, as we talked about: the confetti, the trichrome, the inflammatory, the patchy, the vitiligo vulgaris if you want to call it, whatever methodology or nomenclature you want to use. Can you talk a little bit about the mechanism of repigmentation? What should a patient look for or a clinician look for as a good prognostic sign or a poor sign, and why do you think these are really slow nonuniform processes?

Ted Lain, MD: It’s a great question. I think most of us when we see repigmentation in the areas that are affected by vitiligo, we start seeing these little islands of pigment that occur and then we hope that they coalesce over time. Those islands of pigmentation occur because of the melanocyte stem cells that are in this immune-privileged site in the bulge of the follicle. So that repigmentation occurs from those stem cells that differentiate into melanocytes that then are able to produce the pigment to repigment. That is one way, and the most common way, and the fastest way. The other way is from the border. So, it’s marginal repigmentation where the melanocytes that are still alive and healthy and able to produce pigment produce the pigment that then marginally migrates from the border of the depigmented area. In terms of why it occurs in such different rates between people, I think I don’t have an answer for that, and I don’t know that anybody has an answer for that. But that translates into expectations of therapy though, Seemal, because as I tell people especially with the JAK [Janus kinase] inhibitors, which I’m sure we’re going to get into, whether topical or systemic, everybody responds to the JAK inhibitors on their own timeframe. It’s what makes them so difficult in some way because there’s so much hand-holding with patients and managing expectations. Usually if we were doing the mini-pulse steroids or the IM [intramuscular] steroids, you could reliably tell a patient you will most likely see results quite quickly, or at least stabilization quite quickly. We know with narrow-band UVB [ultraviolet B] it can take up to 16 to 20 treatments before they start seeing results, maybe even more. But with JAK inhibitors, it’s really something where they may be on therapy for 3 to 4 months before they start seeing results. I tell my patients everyone has their own timeline of response. I don’t know what yours is going to be. We are working on developing different trials to determine whether conjunctive or adjunctive therapy will give us more reproducible results and predictable results. But as of now, I can’t tell you, and that’s what I tell my patients. So unfortunately, long-winded answer to say results happen, we don’t know when they’re going to happen. And unfortunately, we just have to be cheerleaders for our patients.

Seemal Desai, MD: I think that’s a great message. We have to set expectations upfront. Patients come in with so much anxiety when they come to see a pigment expert. They want fixes. They want answers right away. And sometimes you just have to be blunt and say we’re on this journey together. I do not know when we’re going to arrive at the destination. We may never make it there. We may just make the connecting flight, may not make the final one. But we’ll get somewhere, and we’ll get there together and I think that’s really, really important.

Transcript edited for clarity

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