Eczema pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Edzel Lorraine Co, DMD, MD[2]

Overview[edit | edit source]

The mechanism of disease of eczema involves a complex interplay of abnormalities of skin microbiomes, a dysfunction in the epidermal barrier, and an immune dysregulation. ^[1] There are two main theories on the existence of atopic dermatitis, also known as atopic eczema - the inside-out hypothesis, and the outside-in hypothesis.

Pathophysiology[edit | edit source]

Immunological Dysregulation[edit | edit source]

• Affected skin involves the uptake of antigens and allergens by the epidermal dendritic cells, dermal dendritic cells, and Langerhan cells.
• Sensory nerves are activated by the released cytokines interleukins 4,13 and 31 (IL-4, IL-13, and IL-31), which are responsible for the pruritic sensation.
• As the event becomes chronic, an increased expression of keratinocyte and Th-cell-derived cytokines is achieved, with more pruritogens contributing to itch sensation. ^[1]

Genetic Inheritance[edit | edit source]

• There are 34 genetic loci which are thought to be associated with eczema.
• These regions contain several genes which have important immunological functions, such as T-cell activation, type-2 helper cell differentiation, and innate immunity. ^{[2] [3][4]}

Epithelium Barrier Dysfunction[edit | edit source]

• Multiple factors cause the disruption of epithelial barrier. These include:
  • FLG mutations
  • Constant scratching
  • Microbial dysbiosis brought about by Staphylococcus aureus and Malassezia.
• As a result, an interrupted normal skin barrier with elevated pH, high skin permeability, altered lipid composition, and decreased water retention is observed. ^{[5] [6] [7] [8] [9] [10]}

Hypotheses on Development of Eczema[edit | edit source]

• There are two main theories on the existence of atopic dermatitis, also known as atopic eczema - the inside-out hypothesis, and the outside-in hypothesis.^[11]
• Inside-out hypothesis
  • This hypothesis denotes that some allergic triggers weaken the skin barrier that leads to more introduction of allergens to the area, causing more inflammatory reaction.^[11]
• Outside-in hypothesis
  • This hypothesis suggests that an impairment of the skin barrier should occur first before the onset of atopic dermatitis.
  • This involves the down-regulation of filaggrin genes (FLG) responsible for maintenance of the proper function of skin barrier.^{[11] [12]}

References[edit | edit source]