If you or a family member suffer from severe eczema (atopic dermatitis), you may feel like you have been living in the Dark Ages. Every time you go to the doctor, you hope for some new therapy, but it has always been the same answers for the last 10 years with a variety of creams, foams, and gels that more or less left you scratching your itchy skin.
It is now the dawn of a new era in eczema therapy. Molecular targets have been identified as targets of new drugs. In other words, the immune system of people with eczema is overly active in certain ways, and medicines have been developed that hone in on those particular elements of the immune system that are too active. One medicine that has just been approved is dupilumab, a target of two interleukins involved in stimulating eczema. The medicine has been approved for adults, and phase III clinical trials for children are underway. The study looked at adults who started out with severe eczema, i.e., some of the toughest cases out there. 36-38% of them were "clear or almost clear" at the end of 16 weeks. The studies also measured something called the EASI score, which stands for Eczema Area and Severity Index. Around 50% of patients saw a 75% improvement in their EASI score. These results left me pretty impressed. If even half of my severe eczema patients can feel and look 75% better, that's a treatment victory.
Dupilumab is an injectable medication that the patient can self-administer at home. If that sounds intimidating or scary, don't worry too much. A nurse educator can train you on how to give yourself the shots. That temporary prick of the needle may be well worth it in the long run if your eczema is better controlled.
The side effect profile of dupilumab was not too alarming. The most common side effect was pain and redness at the injection site, but no one dropped out of the trial due to this side effect. The second most common side effect was conjunctivitis, or eye redness and irritation. There was also increased incidence of herpes virus infections. We are still learning more about how to manage the side effects, but it will be important to mention to your doctor if you have a history of cold sores or genital herpes. Your doctor may want to prescribe an antiviral medication for you.
Not everyone's immune system is the same, and there will be other molecular targets that can be targeted too. Several other agents are in phase III clinical trials now for FDA approval targeting other molecules involved in triggering eczema.
There was also a new topical medicine that was approved for eczema this year, crisaborole. It is a boron-based medication that inhibits an enzyme called phosphodiesterase that can trigger inflammation. As opposed to topical steroids, it won't thin the skin over time. I generally will plan to use this medication in addition to topical steroids so that there can be days when steroid creams are not used but the eczema is still being actively treated.
Treatment of Staph infection or even carriage of this bacteria in the nose is another point I want to reiterate. Many patients have benefitted from a regimen that includes a dilute bleach bath just a little stronger than swimming pool water once or twice a week. The Staph bacteria seem to really love to colonize the impaired skin barrier of eczema patients. In turn, this stimulates the immune system and the eczema gets worse, and that is why decreasing the numbers of Staph bacteria on the skin is so important.
Finally, don't throw away all of your topical steroid creams yet. Topical steroid creams for flares and regular use of emollient creams will continue to be the standard for treating eczema. Not everyone will be a candidate for dupilumab or other molecular targeted therapies. However, it may be a great time to review your current therapy with your dermatologist to make sure you are receiving the most appropriate regimen for your skin.
For further reference:
Simpson EL, Bieber T, Guttman-Yassky E, et al. SOLO 1 and SOLO 2 Investigators. Two phase 3 trials of dupilumab versus placebo in atopic dermatitis. N Engl J Med. 2016; 375: 2335-2348.