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Up until a few years ago, Heather Sullivan’s 14-year-old son, Sawyer, had struggled with eczema his entire life. When he was just a baby, most of his body would be covered in intensely itchy rashes that bled and oozed when he couldn’t help but scratch. His family tried steroid creams, wet wraps, bleach baths, and all of the lotions. They tore up their carpet and replaced their sheetrock in hopes of eliminating triggers. At 15 months, he went on cyclosporine, a powerful immunosuppressant usually given to organ-transplant patients. It cleared him up, but the drug comes with potentially dangerous side effects over time. Doctors, Sullivan recalls, were “just appalled that my child would be on this amount of medicine at this age”—but his eczema came roaring back as soon as he went off it.
When a new eczema drug called Dupixent finally became available to Sawyer a few years ago, his turnaround was fast and dramatic. Within a week, his itchiness and redness started calming down. He felt and looked better. The condition that had dominated their lives began to fade into the background.
Doctors who treat severe eczema now speak of pre- and post-Dupixent eras: “It changed the landscape of having eczema forever,” says Brett King, a dermatologist at Yale. Today, a half dozen novel treatments are available for the skin condition, all of which work by quieting the same biological pathway in eczema; dozens more are in clinical trials. Unlike older drugs, these new ones are precisely targeted and in many cases startlingly effective.
Eczema, also known as atopic dermatitis, is characterized by red, itchy, and inflamed skin. It’s a very common condition, estimated to affect 10 percent of Americans. Of those, a large minority suffer from moderate to severe eczema that seeps into everyday life. “Just imagine scratching endlessly,” King says. “You wake up from sleep scratching. Your sheets are bloody in the morning.” The most basic eczema advice is to moisturize, and moisturize often, to protect the barrier of the skin. But scientists now know that eczema’s cause is not in the skin alone. Many patients also have “an over-reactive or overzealous immune system,” says Dawn Davis, a dermatologist at the Mayo Clinic. Their immune cells release chemicals that irritate nerves, causing itch, and even degrade the skin itself.
Topical steroids, such as over-the-counter hydrocortisone cream, can tamp down the immune reaction that flares in eczema. If these fail, doctors have resorted to more powerful oral steroids, such as prednisone, or other oral immunosuppressants, such as the aforementioned cyclosporine. The drugs can calm eczema, but because they suppress the overall immune system, they also do much more. Prednisone, for example, makes you more prone to infections as well as bone fractures, high blood pressure, and glaucoma when taken in the long term. Of course, for many people, eczema is a chronic condition that requires long-term treatment. “Prednisone is kind of like carpet bombing,” says Peter Lio, a dermatologist at Northwestern University. It blasts eczema away, but at a cost.
In contrast, the newer drugs, Lio says, are more like shotguns that target specific parts of the immune system—with less collateral damage. They fall into two broad classes. Monoclonal antibodies, such as Dupixent, intercept the immune-signaling molecules that trigger itch and skin inflammation. And then JAK inhibitors, which include pills such as Rinvoq and the topical cream Opzelura, scramble the signal after cells have received it. The development of these drugs came after years of research zeroed in on some of the key immune molecules dysregulated in eczema. But serendipity played a role too: The first such drugs were originally developed for other conditions, such as rheumatoid arthritis—only to be repurposed when researchers realized that they targeted the very pathways involved in eczema. The breakthroughs in eczema treatment, in fact, are part of a broader revolution in treating inflammatory disorders; both classes of new drugs are now used to tune the immune system in a whole host of different conditions.
The monoclonal antibodies and oral JAK inhibitors may have their own serious side effects, such as blood clots, which, Lio says, give some doctors unfamiliar with the new drugs—especially the latter type—pause. But the traditional drugs are not great either. “I’m frustrated that a lot of clinicians are very cavalier about prednisone and cyclosporine … They’re like, ‘Oh, they’re our old friends,’” he told me. “Then they get nervous about JAK inhibitors.” In his mind, the new drugs are simply the better option in terms of safety and efficacy.
Jonathan Silverberg, a dermatologist at George Washington University who specializes in eczema, says he now rarely uses the old oral steroids and immunosuppressants. When he does revert to them, it’s not for medical reasons: He ends up prescribing older (that is, generic and therefore cheaper) drugs for uninsured patients who can’t afford the new ones, or for patients who have insurance but are nevertheless denied coverage. “Insurance says, ‘Can it be fixed with a $10 medicine? Or does it really need the $1,000 tube?’” King told me. Getting patients these newer drugs can mean a lot of time fighting with insurance.
For now, these drugs have most dramatically improved the lives of patients with moderate to severe eczema—at least those patients who can access them. But doctors told me that topical JAK inhibitors, which are safer than the oral version, could one day be first-line treatments for mild eczema as well. “In a perfect world, I would love it if I never had to prescribe a topical steroid again,” Silverberg said, citing the side effects that come with long-term use. Topical steroids can thin the skin, causing stretch marks, fragility, and poor healing. But at the moment, steroids are also cheap and easily available. They’re not going anywhere as long as the new treatments still come with hefty price tags.
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Sarah Zhang
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