Activity of Tumor Necrosis Factor-alpha (TNF-alpha) and its soluble type I receptor (p55TNF-R) in some drug-induced cutaneous reactions

Ann Univ Mariae Curie Sklodowska Med. 2003;58(2):50-6.

Abstract

Plasma concentration of TNF-alpha and its type I receptor (p55TNF-R) was examined in 126 patients with drug-induced skin reactions using immunoenzymatic ELISA method. Patients were subdivided into 6 groups: maculopapular eruptions (ME), erythema multiforme (EM), erythema multiforme coexisting with erythema nodosum (EMN), hyperergic vasculitis (HV), Stevens-Johnson syndrome and toxic epidermal necrolysis (SJS/TEN). In the acute clinical stage highly significant (p<0.001) or significant (p<0.01) elevation of mean plasma concentrations of the cytokine and its receptor was found in all examined groups in comparison with the control. Clearing of clinical symptoms was connected with considerable decrease (p<0.001, p<0.01) of mean plasma levels of the both proteins in comparison with the before treatment values. TNF-alpha concentrations still remained significantly more elevated than those observed in the control. The results indicate that plasma activity of TNF-alpha and its p55 receptor change with the clinical course of the examined drug-induced skin reactions, which suggests the partake of both proteins in the pathogenesis of these diseases.

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Biomarkers / blood
  • Case-Control Studies
  • Drug Eruptions / blood*
  • Enzyme-Linked Immunosorbent Assay
  • Erythema / blood
  • Erythema / chemically induced
  • Etanercept
  • Female
  • Humans
  • Immunoglobulin G / blood*
  • Immunosuppressive Agents / blood
  • Male
  • Middle Aged
  • Parapsoriasis / blood
  • Parapsoriasis / chemically induced
  • Receptors, Tumor Necrosis Factor / blood*
  • Stevens-Johnson Syndrome / blood
  • Stevens-Johnson Syndrome / chemically induced
  • Stevens-Johnson Syndrome / etiology
  • Time Factors
  • Tumor Necrosis Factor-alpha / metabolism*
  • Urticaria / blood
  • Urticaria / chemically induced
  • Vasculitis / blood
  • Vasculitis / chemically induced

Substances

  • Biomarkers
  • Immunoglobulin G
  • Immunosuppressive Agents
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
  • Etanercept