Enhanced Platelet Activation in Patients with Atopic Eczema/Dermatitis Syndrome
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Enhanced Platelet Activation in Patients with Atopic Eczema/Dermatitis Syndrome Alicja Kasperska-Zaja¸c,1,2 Marek Nowakowski,1 and Barbara Rogala1
Abstract—Data gathered prove that circulating platelets are activated upon human allergic inflammation, partly as a result of direct IgE-mediated process. It has been indicated that platelets may contribute to pathogenesis of atopic eczema/dermatitis syndrome (AEDS). Authors of the recent study have investigated systemic platelet activation in patients with AEDS on the basis of blood level of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4), which are recognized markers of platelet activation, also belonging to C-X-C chemokine family. Plasma levels of beta-TG and PF4 were measured by enzyme-linked immunoassay (ELISA) in 18 AEDS patients with moderate disease activity and 23 healthy, nonatopic individuals. No differences in peripheral platelet count of the two groups were noted. Only four (33.3%) AEDS patients represented beta-TG and PF4 within the control range; plasma beta-TG and PF4 were significantly increased (p < 0.001) in the AEDS group compared as a whole with the control subjects. No association between circulating concentrations of beta-TG or PF4 and total IgE levels in AEDS patients was proved. The results suggest that some patients with AEDS may have enhanced blood platelet activity as expressed by beta-TG and PF4 level. KEY WORDS: platelet activation; beta-thromboglobulin; platelet factor 4; atopic eczema/dermatitis syndrome.
INTRODUCTION
Few studies have examined platelet function in AEDS patients. Evidence, in animals, suggests that PF4 may contribute significantly to the development of atopic dermatitis (7). Throughout their preliminary studies the authors have recorded increased plasma level of PF4 in 9 male AEDS patients. However, small number of AEDS subjects restricts conclusions, which could be drawn from the results (8). There are also controversial data concerning platelet activity in patients suffering from various allergic diseases. The purpose of the recent study was to evaluate in vivo platelet activity as expressed by plasma beta-TG and PF4 in patients with moderate AEDS.
Platelet activation results from direct IgE-dependent process and secondarily as caused by other pathways of allergic inflammation (1–3). The platelets play essential role in allergic inflammation, partly due to their participation in cell recruitment to tissue and release of inflammatory mediators, including chemokines. Best recognized platelet chemokine family members are beta-TG and PF4. They are released from blood platelets following their activation and may play certain role upon allergic inflammatory reactions particularly in control of eosinophils activity (4, 5). Moreover, evaluation of plasma beta-TG and PF4 appears as valuable indicator of in vivo platelet release reaction (6).
MATERIAL AND METHODS Subjects
1 Chair
and Clinical Department of Internal Diseases, Allergology and Clinical Immunology, Medical University of Silesia, 3-go Maja 13-15, 41-80
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