Anticonvulsant-induced Toxic Epidermal Necrolysis: Monitoring the Immunologic Response.
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Elsevier BV
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Abstract
Background Toxic epidermal necrolysis is a severe reaction with skin involvement induced by different drugs and other agents. The mechanisms implicated in the induction of the reaction are poorly understood.
Objective To study the involvement of T lymphocytes and other immunocompetent cells in the peripheral blood, blister fluid, and affected skin of 3 patients who developed a severe reaction after receiving anticonvulsant medication.
Methods Quantification of T lymphocytes expressing the skin homing receptor (cutaneous lymphocyte-associated antigen [CLA]) in peripheral blood, skin and skin blister fluid and assessment of other adhesion molecules, activation markers and inflammatory interleukins by flow cytometry, immunohistochemistry and RT-PCR.
Results An increase in CD3+CLA+ cells paralleling the severity of the disease was observed in both peripheral blood and skin, tending to normalize as soon as patient’s condition improved. E-selectin was detected in endothelial vessels in parallel with CLA expression on lymphocytes. An overexpression of TNF-, IFN- and IL-2 was also observed in peripheral blood mononuclear cells. The expression of the different markers changed over the course of the disease.
Conclusions. These data show an increase in activated T cells expressing the skin-homing receptor in both tissue and peripheral blood accompanying clinical symptoms, with a recruitment of macrophages and an overexpression of cytokines. All these results suggest an important role for T cells in the production of toxic epidermal necrolysis.
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This work was supported in part by Grants CICYT SAF 96/0240 from the Consejería de Salud de la Junta de Andalucía and FIS 98/0861. Laura Leyva has a FIS fellowship 98/5061.
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Leyva L, Torres MJ, Posadas S, Blanca M, Besso G, O'Valle F, del Moral RG, Santamaría LF, Juárez C. Anticonvulsant-induced toxic epidermal necrolysis: monitoring the immunologic response. J Allergy Clin Immunol. 2000 Jan;105(1 Pt 1):157-65
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