Clinical and immunohistochemical study of the effect of a cosmetic product in patients with asteatotic eczema.

Cutaneous xerosis is a common clinical condition associated with an altered barrier function of the stratum corneum. Xerotic skin appears dry, rough and slightly scaling. Patients complain of pruritus and stinging. Our aim was to investigate the clinical effects of a cosmetic ointment (Scherilan) in patients with circumscribed senile xerosis (also called asteatotic eczema). Moreover, variations in expression of epidermal proteins such as keratin (K)-5 and involucrin, detected by immunohistochemistry, were also evaluated before and after topical treatment. We enrolled 30 patients (11 males, 19 females) with asteatotic eczema. We examined dryness, roughness and desquamation and symptoms such as itching and dryness. A score of 0 to 3 was assigned to each of these parameters. A biopsy was performed in seven patients before and after a 21-day topical treatment. All skin specimens were then immunostained with antibodies to K5 and involucrin. At day 7 or 21 of treatment all signs of xerosis and pruritus were significantly reduced; furthermore, the reduction increased with the duration of therapy. Before treatment K5 was strongly expressed in stratum basale (SB) and stratum spinosum (SS), while involucrin was strongly expressed in stratum granulosum (SG) and the upper portion of SS. In contrast, after treatment immunostaining for K5 was restricted to SB and the lower part of SS, while involucrin showed intense staining in SG. We highlight the importance of treating cutaneous xerosis with an ointment such as this one, which probably induces an increase of lipid content of the SC intercellular matrix.

Cetirizine modulates adhesion molecule expression in a double-blind controlled study conducted in psoriatic patients.

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.

Undifferentiated connective tissue disease and its cutaneous manifestations.

Undifferentiated connective tissue disease (UCTD, also named UCT syndrome, latent lupus or incomplete lupus) is regarded as an autoimmune disorder in which signs and symptoms are widely variable and evocative for connectivitis but not sufficiently evolved to fulfil any of the accepted classification criteria for the defined connective tissue diseases. In this paper we describe the case of a 47-year-old woman affected by UCTD according to the preliminary classification criteria supplied by Mosca et al. in 1999.

Cetirizine reduces the number of tryptase-positive mast cells in psoriatic patients: a double-blind controlled study.

Psoriatic plaque contains an increased number of mast cells that are thought to play an important role in the initiation and maintenance of the disease through the release of mediators such as histamine, proteoglycans, proteinases and cytokines. To verify the possible participation of these cells in the chronic inflammatory cutaneous response in psoriasis, we performed a double-blind controlled study to investigate the presence and activation of tryptase-positive mast cells in the lesional skin of 19 patients affected by active psoriasis vulgaris minima compared with five healthy, age-matched subjects. Psoriatic patients were randomized into two groups (A and B). The first group was treated with cetirizine (10 mg/three times a day for 15 days) and the second one was treated with placebo. Both groups underwent clinical staging [psoriasis area and severity index (PASI) score] and immunohistochemical evaluation [alkaline phosphatase antialkaline phosphatase (APAAP) procedure] before and after treatment. In group A, the PASI score ranged from 3.8 (SE +/- 1.00) to 1.8 (SE +/- 0.68) and in group B, from 5.0 (SE +/- 0.98) to 3.4 (SE +/- 0.47). The mean number of tryptase-positive mast cells for field, mainly distributed in the perivascular and periadnexal sites, ranged from 40.8 (SE +/- 7.15) to 21.6 (SE +/- 3.04) in group A and from 25.1 (SE +/- 3.78) to 26.3 (SE +/- 3.59) in group B (ANOVA test f = 6.95; gl = 1.16; p = 0.02). In our psoriatic patients, cetirizine significantly reduced the expression of tryptase-positive mast cells and produced a clinical improvement in erythema, suggesting a multilevel immunopharmacologic modulation of this antihistamine in psoriasis.

Further support for a role for Th2-like cytokines in blister formation of pemphigus.

Pemphigus vulgaris and pemphigus foliaceus are commonly known as antibody-mediated bullous diseases. However, recently a role for infiltrating cells as contributors to the pathogenesis of these diseases has been suggested. The aims of our study were to characterize the immunophenotype of the cellular infiltrate of pemphigus lesional skin and to study the cytokines secreted. We have therefore performed an immunohistochemical study with a large panel of monoclonal antibodies (to CD3, CD4, CD8, CD25, CD30, myeloperoxidase, eosinophil cationic protein EG2, tryptase, human interleukin (IL)-2, human IL-4, human IL-5, human IL-6, human IL-8, and interferon (IFN)-gamma using the alkaline phosphatase-antialkaline phosphatase procedure on lesional and uninvolved skin of six patients with clinical, histological, and immunofluorescent proven pemphigus. We also performed RT-PCR in order to demonstrate mRNA expression of the cytokines of interest. Our results suggest the presence of a T cell population with a prevalent Th2-like cytokine pattern in lesional skin. In addition, we demonstrate a consistent number of granulocytes and mast cells that show clear signs of activation. These data suggest the involvement of an inflammatory infiltrate in the production of pemphigus lesions. In particular, we assume that Th2 cells may be implicated in the very early stages of autoimmune response, concluding that they exert broad activity in blister formation.