A 26-year-old man presented with a severe, life-long history of atopic dermatitis, with a fluctuating disease course, refractory to conventional therapy such as emollients, topical corticosteroids, oral antihistamines, psoralen UV-A, rifampicin and azathioprine. He had symptoms of nasal congestion and ocular complication of keratoconus, for which corneal transplantation was performed in the previous 2 years. The patient had been treated with depot corticosteroid (betamethasone valerate) for approximately 1 year. Any attempt to discontinue corticosteroid therapy led to new flares; the current relapse had begun 20 days before the time of admission. The physical examination showed exudative erythroderma involving more than 90% of his body surface area with erythematous desquamative plaques, marked lichenification, and evidence of secondary skin infection (Figures 1 and 2). The patient had facial and lower extremity edema and inguinal lymphadenopathy. The blood eosinophilic count (20%) and total serum immunoglobulin E (IgE) (2250 IU) were significantly higher and accompanied by hypoproteinemia (54 g/L) and hypoalbuminemia (25g/L). Systemic corticosteroid therapy of 20-mg methylprednisolone daily was administered to cope with the severe symptoms. As an alternative approach to avoid corticosteroid dependence, 10 days after the beginning of this therapy, the cysteinyl leukotriene receptor antagonist montelukast (10 mg daily) was introduced in an adjunctive manner. The patient's condition improved quickly and gradual reduction of methylprednisolone was undertaken with a step of 4-mg per 5 days, which allowed discontinuation of the corticosteroid for a period of 1 month. At that time the patient's symptoms subsided to several patches involving less than 15% of his body surface area (Figure 3). Montelukast treatment continued for an additional 2 weeks and at the end of the course of treatment a complete remission was achieved (Figure 4). At that time the eosinophils and total IgE level dropped to 15% and 2050 IU, respectively. The patient remained on topical emollient therapy only and at the follow-up visit, 2 months after the end of montelukast treatment, complete remission was sustained.
DiscussionThe pathogenesis of atopic dermatitis is not completely understood. Increasing evidence supports the potential role of soluble mediators including leukotrienes in some of the pathogenic variants of the disease. 1,2The leukotrienes are metabolites of the arachidonic acid pathway. Leukotriene synthesis begins with the translocation of activated 5lipoxygenase to the cell membrane, where it forms a complex with a special protein and catalyzes the metabolism of arachidonic acid to 5hydroperoxyeicosatetraenoic acid and subsequently to leukotriene A4 (LTA 4 ), which may be converted to leukotriene B4 (LTB 4 ) or conjugated with glutathione to form leukotriene C4 (LTC 4 ) and their derivatives-leukotriene D4 (LTD 4 ) and leukotriene E4 (LTE 4 ).Cysteinyl leukotrienes (LTC 4 , LTD 4 , LTE 4 ) are potent inflammatory eicosanoids that act...