Rebound phenomenon to systemic corticosteroid in atopic dermatitis

Allergol Immunopathol (Madr). 2005 Nov-Dec;33(6):307-11. doi: 10.1016/s0301-0546(05)73248-1.

Abstract

Three patients with atopic dermatitis, one boy and two girls, aged between 6 and 17 years, presented eczematous skin, pruritus, scarifications, lichenification and a family history of atopy. During exacerbations, the patients sought emergency care and were prescribed oral corticosteroids for a period of approximately 15 days. Initially, the patients improved but after cessation of therapy or dose reduction, marked worsening occurred with the development of lesions with extreme pruritus, several confluent lesions, scarification and intense exudates, as well as fever and dehydration. The patients' condition was so severe that two were admitted to the allergy unit. The medication was withdrawn and intravenous hydration was administered, together with hydrating skin creams and antihistamine therapy. In addition, weak topical corticosteroids were applied on the most severely affected areas. All three patients progressively improved. We conclude that the patients with atopic dermatitis described herein presented a rebound phenomenon after the use of corticosteroids. We believe that systemic corticosteroids may exacerbate the acute phase of atopic dermatitis, mediated by IgE, accentuating the Th2 pattern in these patients.

Publication types

  • Case Reports

MeSH terms

  • Acute Disease
  • Administration, Oral
  • Adolescent
  • Adrenal Cortex Hormones / administration & dosage
  • Adrenal Cortex Hormones / adverse effects*
  • Adrenal Cortex Hormones / therapeutic use
  • Anti-Allergic Agents / administration & dosage
  • Anti-Allergic Agents / adverse effects*
  • Anti-Allergic Agents / therapeutic use
  • Child
  • Dermatitis, Atopic / drug therapy*
  • Dermatitis, Atopic / immunology
  • Female
  • Humans
  • Immunoglobulin E / immunology
  • Male
  • Recurrence
  • Th2 Cells / immunology

Substances

  • Adrenal Cortex Hormones
  • Anti-Allergic Agents
  • Immunoglobulin E