title: Cetirizine modulates adhesion molecule expression in a double-blind controlled study conducted in psoriatic patients.
abstract: Psoriasis is a chronic inflammatory T-cell-mediated immune dermatosis, characterized by the cutaneous expression of adhesion molecules belonging to the beta1 and beta2 integrin subfamilies, such as intracellular adhesion molecule (ICAM)-1, ICAM-3, lymphocyte function associated antigen (LFA)-1, vascular cell adhesion molecule (VCAM)-1 and endothelial adhesion molecule (ELAM)-1. Cetirizine is a nonsedating, selective H1-receptor antagonist, whose therapeutic efficacy is probably the result of its effect on both the immediate allergic reaction and the late-phase allergic response. The aim of this study was to investigate adhesion molecule expression (ICAM-1, ICAM-3, VCAM-1, LFA-1 and ELAM-1) by using an immunophosphatase alkaline (APAAP) technique in a double-blind controlled study. Nineteen patients with active psoriasis vulgaris minima were randomized into two groups: group A (two men and six women, aged 22-59 years) was treated with cetirizine (30 mg a day, 3 times a day for 15 days) and group B (three men and eight women, aged 24-72 years) were administered placebo. Positive cells were counted by two independent and blinded observers and at least three adjacent high-power fields (250 X) were analyzed. In group A, ICAM-1-positive cells decreased from 75.8 (SE +/- 15.12) to 38.8 (SE +/- 7.57) ICAM-3-positive cells decreased from 61.7 (SE +/- 12.72) to 45.2 (SE +/- 9.44) and LFA-1 decreased from 103.9 (SE +/- 17.34) to 66.5 (SE +/- 8.63) after cetirizine treatment (p = 0.02). In group B, a nonsignificant reduction was found after placebo administration in the expression of adhesion molecules except for ELAM-1, which showed a slight variation, from 23.4 (SE +/- 3.56) to 21.5 (SE +/- 3.26). The reduction in the expression of adhesion molecules in psoriasis after cetirizine treatment suggests a possible inhibitory effect of this drug on some cell surface proteins and subsequently on the migration of inflammatory cells in psoriatic skin lesions. Our findings support its antiinflammatory effect in addition to its H1-blocking activity.
authors.affiliation: Department of Dermatologic Science, University of Florence, Florence, Italy.
authors.forename: E
authors.initials: E
authors.lastname: Pestelli
authors.forename: I
authors.initials: I
authors.lastname: Floriani
authors.forename: P
authors.initials: P
authors.lastname: Fabbri
authors.forename: M
authors.initials: M
authors.lastname: Caproni
mesh_terms: D000328:Adult; D000368:Aged; D015815:Cell Adhesion Molecules / Q000096:biosynthesis / Q000187:drug effects*; D017332:Cetirizine / Q000627:therapeutic use*; D004311:Double-Blind Method; D019040:E-Selectin / Q000096:biosynthesis / Q000187:drug effects; D005260:Female; D039563:Histamine H1 Antagonists, Non-Sedating / Q000627:therapeutic use*; D006801:Humans; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis / Q000187:drug effects; D016169:Lymphocyte Function-Associated Antigen-1 / Q000096:biosynthesis / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D011565:Psoriasis / Q000188:drug therapy*; D012867:Skin / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis / Q000187:drug effects
chemical_list: D015815:Cell Adhesion Molecules; D019040:E-Selectin; D039563:Histamine H1 Antagonists, Non-Sedating; D016169:Lymphocyte Function-Associated Antigen-1; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D017332:Cetirizine