Part 2: Advancing the Treatment Landscape in Severe Alopecia Areata

In Part 2 of our expert roundtable, Drs Brittany Craiglow, Brett King, and Maryanne Senna explore how treatment for severe alopecia areata (AA) has evolved from limited topical therapies to powerful, FDA-approved JAK inhibitors. Drawing from landmark clinical trials and their own practices, the panel outlines when and how to initiate these therapies, how to counsel patients on risk, and why early intervention can dramatically improve outcomes.

Dr Craiglow: Now we’re going to move on to treatment, which is really exciting—we finally have some options for patients. We’ll talk a bit about how treatment has evolved alongside our understanding of the pathophysiology of the disease, and we’ll touch on some common clinic questions. Treating alopecia may seem straightforward but, in reality, it often isn’t. There’s a lot of nuance involved. So, let’s talk through some clinical scenarios that require thoughtful decision-making.

Brett, you often speak about where we used to be in our understanding of alopecia and what tools we had available then, compared to now. Maybe you can walk us through a brief history of treatment?

Dr King: Yeah, I think it’s fascinating how quickly things have changed. A great way to look at this is through Jerry Shapiro’s JAAD CME reviews on alopecia areata every 8–10 years. In 2010, the CME covered topical corticosteroids, intralesional triamcinolone, topical minoxidil, DPCP, SADBE, systemic corticosteroids, methotrexate, cyclosporine, and counseling. Each of these got about a paragraph of attention.

Then by 2018, the CME included JAK inhibitors—off-label, of course—but it was already clear they were transforming the treatment paradigm. And suddenly, counseling wasn’t mentioned. For those of us treating these patients frequently, it was obvious that treatment had arrived.

Then—holy cow—2022, baricitinib is FDA approved; 2023, ritlecitinib; and 2024, deuruxolitinib. Now, you look at the clinical trial landscape and there are 6, 7, 8, 9, even 10 trials underway or completed. Twelve years ago, pharma didn’t even know what alopecia areata was. Now it’s a hotbed for targeted immunological therapies—all trying to match or outperform oral JAK inhibitors. It’s really exciting.

Dr Craiglow: Yes, we’ve come a long way in a short time. As long as someone hasn’t been missing hair for many years, alopecia areata is largely a treatable disease. I don’t think the whole dermatology community is there yet, but hopefully within the next 5 years, the perception will shift: “Oh yeah, this is treatable. You don’t have to live with this forever.”

Maryanne, can you talk to us a bit about JAK inhibitors—how you think about selecting candidates and how you approach it?

Dr Senna: Absolutely. I completely agree with Brett. For all those treatment paragraphs listed up until 2018, the problem was that none of those treatments actually worked. JAK inhibitors changed everything. That one paragraph has allowed us to treat an entire population of patients with severe alopecia areata that we previously couldn’t help. It was an incredibly exciting time during the clinical trials, and now with FDA approval, our ability to help patients has been absolutely transformative.

When do I consider a JAK inhibitor? Usually when someone has about 25% to 30% scalp hair loss and isn’t responding to other treatments. If it’s clearly impacting their life, and I can see that the disease is progressing—whether slowly or quickly—I begin thinking, This is someone who needs a JAK inhibitor.

Of course, we screen carefully—any history of solid malignancy, stroke, heart attack, etc., requires caution. But by and large, this is a healthy patient population. And nothing works quite like a JAK inhibitor. Clinical trial data also shows that earlier treatment leads to better outcomes. Waiting until someone has total scalp loss or 10+ years of disease reduces the chance of a meaningful response. So, I’ve started treating people earlier, and the outcomes have been fantastic.

Dr Craiglow: Yes, and it’s so rewarding—not just seeing them look different, but feel different. We don’t talk about that enough, but it’s genuinely fun to treat patients with JAK inhibitors because the transformation is dramatic. There may still be hesitancy among some clinicians, but once you do it a few times, you’re hooked.

Dr Senna: Totally. And both short-term and long-term safety data are very reassuring. We don’t have 20 years of data in AA yet, but we do have good safety data from other indications. Given the efficacy we see in alopecia areata, it makes sense to use these when appropriate.

Dr Craiglow: A lot of people are curious how to structure the conversation with patients—how to discuss the boxed warning and address concerns about risks. Brett, could you walk us through what that looks like in your office?

Dr King: Sure. First, it’s essential that we as clinicians understand the safety data ourselves. We can’t have a meaningful discussion with patients if we don’t understand and feel comfortable with the numbers.

Many of our patients come in already informed. The AA community is incredibly connected online. They’ll say, “I read about these medicines and the warnings—who would agree to take that?”

But that perception—“grow your hair back but risk cancer, stroke, heart attack, clots, infections, and death”—is not accurate. Those warnings stem from a trial in older rheumatoid arthritis patients with cardiovascular risk factors—a worst-case scenario. They were typically over 60, obese, with comorbidities, and taking multiple immunosuppressants. That’s not who we’re treating.

Even in that trial, the difference was small: 4% of the JAK group had an event vs 3% in the TNF group—and again, this is in high-risk RA patients. This doesn’t indicate the drug is unsafe; it means that with simple patient screening, we can use these medications safely.

You can explain all of that to a patient in under 2 minutes. Most patients respond, “That’s helpful,” and many say, “If you think this is right for me, I want it.” We aren’t saying nothing bad ever happens—but the risk is so low that most of us will never even see it in practice.

Dr Senna: Right, and one thing I find helpful is showing patients that the incidence of these adverse events is roughly the same as in the general population—in other words, being on a JAK inhibitor doesn’t suddenly multiply your risk tenfold.

And for patients who want to dive deeper, I always refer them to the National Alopecia Areata Foundation. They have excellent videos and resources—you, Brit, and I have contributed to some of them—and they walk through the data in a patient-friendly way. It’s great for folks who are more anxious or when time is tight in clinic.

Dr Craiglow: I agree. And even if there were a slightly elevated risk, many of these patients are willing to accept that. Our role is not to be gatekeepers—it’s to provide clear information and let patients decide what’s right for them. Also, some risk factors are modifiable: weight, blood pressure, lipids. Managing those can lower baseline risk and help patients feel empowered. So, conversations about safety can be productive and even motivating.

Let’s shift to some clinical scenarios. Not everyone responds quickly. Some patients respond partially, and hair behaves differently from skin diseases like atopic dermatitis or psoriasis.

Brett, could you talk about how long we should wait before calling a treatment a failure? And how this differs from other conditions?

Dr King: Gladly. What’s great is that we now have clinical trial data to guide us—not just expert opinion. From the baricitinib and ritlecitinib trials, we know that you can’t confidently determine treatment failure before 9 months, and ideally, you wait up to 12 months.

If you stop at 6 months, you could miss a third of potential responders. That’s huge. Another insight from the baricitinib data: if patients regrow eyebrows or eyelashes by month 9—even if scalp regrowth is slow—that’s predictive. About a third of those patients go on to achieve full scalp regrowth. So, watching lashes and brows is a valuable clue.

Dr Craiglow: Yes, and importantly, we only switch drugs if the patient truly isn’t responding. If they’re still making progress, even slowly, we stay the course. But it gets tricky when someone regrows 40% of their scalp hair and eyebrows, then stalls. In those cases, we often try to optimize growth—maybe with oral minoxidil or intralesional injections.

Maryanne, can you share some of your “art of medicine” in these situations?

Dr Senna: Absolutely. First, I use oral minoxidil with almost every patient—unless they’re already overwhelmed by meds. It helps hair grow faster and more completely alongside JAKs.

Then, I may add intralesional steroids or even consider pulsed or systemic steroids briefly to give them a push and then taper off. These tools can enhance regrowth in real-world settings beyond what we saw in trials.

I haven’t seen success with topicals—especially topical JAK inhibitors—in this population, despite getting asked about them a lot.

Dr Craiglow: Yeah, unfortunately, topical JAKs haven’t been effective for AA. But the good news is that we have multiple options. If one JAK doesn’t work, another might. People metabolize medications differently—trying a different one is totally reasonable, as long as you’ve given the first one enough time.

Before we wrap up, any final pearls?

Dr Senna: Just a quick note on tapering. Patients often ask about it. There’s no major safety difference between 2 mg and 4 mg baricitinib, but if someone insists on tapering, do it very slowly. Wait at least 3 months after each dose change, because that’s how long it can take to see changes in hair.

Dr Craiglow: Thank you for saying that. It’s a really important point. Patients always ask, “Do I have to take this forever?” And while a few might be able to stop and maintain regrowth, most will need chronic therapy.

Because of the lag time in hair regrowth, you can’t just stop or even cut the dose in half—despite what the label says. The fallout won’t happen immediately, but once it does, it’s too late. You’re looking at months or even years to get back to where they were.

If a patient spent 2 or 3 years growing their hair back and stopped wearing their wig, we don’t want to undo all of that. So, if you taper, it should be the slowest taper of your career.