Case
A 57-year-old man with past medical history significant for hypertension and atopy presented with a flare of atopic dermatitis. Although a lifelong problem, his eczema had recently worsened with widespread pruritic, erythematous, scaly, excoriated patches on his trunk, antecubital and popliteal fossae, arms, and lower legs. He had no recent medication changes and had been taking hydrochlorothiazide, lisinopril, amlodipine, ranitidine, and hyoscyamine for several years. The rash did clear with a 6-day course of prednisone prescribed by his primary care physician; unfortunately, it rebounded upon tapering. Allergy evaluation revealed an eosinophilia of 11%, elevated IgE level of 2880 IU/ml, and numerous environmental allergies. He was diagnosed with adult atopic dermatitis (AD) and started on a soak-and-smear routine with triamcinolone ointment (0.1%).Although initially responsive to this conservative therapy regimen, he experienced frequent exacerbations over the next few years and eventually developed prurigo nodularis (PN) on his arms, legs, and upper back (Figure 1). Although the background AD improved, the prurigo nodules were refractory to clobetasol (0.05% ointment), topical tacrolimus (0.1%), diphenhydramine (25-50 mg), cetirizine (10-20 mg), doxepin (25 mg), gabapentin (300 mg TID), wet dressings with triamcinalone (0.1%), intralesional triamcinolone injections (10 mg/ml), oral prednisone courses (10-80 mg), doxycycline (100 mg BID), cryotherapy, and narrow-band ultraviolet B light therapy. Ultimately, an integrative medicine specialist (author JN) was consulted and the patient was offered treatment with the natural anti-pruritogen quercetin (1000 mg BID). After three months with no improvement on quercetin, he was switched to isoquercetin (500 mg BID). After four weeks of isoquercetin treatment, the patient noted significant reduction in his pruritus with improved sleep and considerable skin healing. He maintained this improvement with isoquercetin and topical steroids for the next two years of follow-up in our clinic (Figure 2).
DISCUSSION
Atopic dermatitis (AD) and prurigo nodularis (PN) result from a complex interaction between immunologic dysregulation, epidermal barrier dysfunction, decreased epidermal defenses, environmental allergens, and patient response to lesions (eg, scratching or rubbing). The mediators of itch in AD and PN have not been clearly defined and neural mechanisms of itch are not well understood. Galli and colleagues suggest that the pruritus and erythema present in atopic dermatitis following allergen exposure might be related to substances released by mast cells with allergen-specific IgE.1 However, studies of plasma histamine levels in AD patients have been inconsistent and typical antihistamines are only mildly helpful in alleviating pruritus, which suggests that histamines cannot be the only pruritogen.2-5Quercetin, a natural polyphenol flavonoid consisting of three rings and five hydroxyl groups, is found in various fruits and vegetables including yellow onions, curly kale, leeks, cherry tomatoes, broccoli, apples, green and black tea, black grapes, blueberries, cauliflower, and cabbage.4 It has antioxidant properties that include free radical scavenging, interfering with inducible nitric oxide synthase activity, inhibiting xanthine oxidase activity, and inhibiting TNF-alpha release. Its potential therapeutic utility has been studied in cardiovascular disease, ischemia-reperfusion injury, ocular disease, allergic disease, arthritis, diabetes, gastrointestinal disease, and cancer. There are several mechanisms by which it could minimize pruritus in atopic patients. In vitro research has shown that quercetin inhibits histamine release from human basophils as well as rat, mouse,
