Counter-regulatory balance: atopic dermatitis in patients undergoing infliximab infusion therapy.
Atopic dermatitis has been characterized as an autoimmune or auto-allergic phenomenon in which environmental allergens resembling human proteins activate auto-reactive T-cells to release pro-inflammatory cytokines of the T-helper 2 (Th2) cytokine profile (IL-4, IL-5, IL-10, and IL-13). Infliximab is a chimeric IgG1 monoclonal antibody that blocks the effects of the inflammatory cytokine tumor necrosis factor (TNF)-alpha. Infliximab has been shown to benefit greatly patients suffering from diseases associated with a Th1 profile (IL-1, TNF-alpha, and IFN-mu), such as psoriasis, Crohn's disease and rheumatoid arthritis. Some researchers have suggested that disrupting the Th1-Th2 balance by downregulating Th1 cytokines may result in manifestations of Th2 disease. Consistent with this hypothesis, we present the cases of three patients who exhibited vivid manifestations of atopic dermatitis after the inception of infliximab induction therapy.
Chan
Joanna L
JL
Department of Dermatology, Stanford University Medical Center, Stanford, California, USA.
Davis-Reed
Linda
L
Kimball
Alexa Boer
AB
D000293:Adolescent; D000911:Antibodies, Monoclonal / Q000009:adverse effects* / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000188:drug therapy; D003424:Crohn Disease / Q000188:drug therapy; D003876:Dermatitis, Atopic / Q000139:chemically induced*; D003879:Dermatologic Agents / Q000009:adverse effects* / Q000627:therapeutic use; D005260:Female; D006801:Humans; D000069285:Infliximab; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D011565:Psoriasis / Q000188:drug therapy
D000911:Antibodies, Monoclonal; D003879:Dermatologic Agents; D000069285:Infliximab