Chapter 12: Contact Dermatitis – Drug Treatment & Care

Contact Dermatitis, which causes approximately 5.7 million healthcare visits yearly, is defined as a skin disorder resulting from exposure to an allergen or irritant, and is primarily categorized as Irritant Contact Dermatitis (ICD) or Allergic Contact Dermatitis (ACD). ICD involves direct cellular damage that disrupts the water–protein–lipid skin barrier through the release of proinflammatory cytokines, while ACD, exemplified by reactions to poison ivy, is a T-cell-mediated immune response that progresses through sensitization and elicitation phases. Atopic Dermatitis, or eczema, is a chronic, pruritic condition strongly linked to genetic factors, particularly mutations in the filaggrin gene (FLG) which compromise the structural integrity of the skin barrier, alongside immune dysregulation. Diagnosis relies on patient history and visual symptoms, which can manifest in acute phases (erythema, vesicles, crusting) or chronic phases (lichenification). Patch testing is considered the definitive method to confirm ACD. The goals of drug therapy focus on restoring the normal epidermal barrier, managing inflammation, and controlling pruritus. First-line treatment emphasizes nonpharmacologic strategies, including patient education, avoidance of triggers, utilizing protective equipment, and the regular use of moisturizers containing emollients, humectants, and occlusive agents to combat dry skin (xerosis). When pharmacologic intervention is required, Topical Corticosteroids (TCSs) are the initial topical agents for localized CD and AD, interfering with antigen processing and suppressing cytokine release. TCS selection requires careful consideration of potency based on the affected area and patient age, as prolonged use can lead to adverse events like skin atrophy or purpura. Second-line options for AD, often reserved as steroid-sparing agents or for facial involvement where atrophy is a concern, include Topical Calcineurin Inhibitors (TCIs) such as tacrolimus and pimecrolimus, or the PDE-4 inhibitor crisaborole, and phototherapy. For widespread or refractory symptoms, systemic therapy is warranted. This involves oral corticosteroids, which must be tapered to prevent rebound flares, or immunosuppressive agents for refractory AD like cyclosporine, azathioprine, methotrexate, or mycophenolate. Notably, methotrexate is specifically contraindicated in pregnant patients due to fetal risk, underscoring the necessity of cautious systemic drug selection in special populations.