What is the pathophysiology of guttate psoriasis?

Updated: Oct 16, 2020
  • Author: Kirstin Altman, MD; Chief Editor: Dirk M Elston, MD  more...
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The exact pathophysiologic mechanism in guttate psoriasis is undetermined. Guttate psoriasis is believed to result from an immune reaction triggered by a previous streptococcal infection in a genetically susceptible host. [12]  

Studies indicate the importance of chromosome 6 in determining the resultant psoriatic phenotype. HLA-Cw*0602–positive patients are more prone to develop the guttate form. Interactions of HLA-C with killer immunoglobulin–like receptors (KIR) on natural killer cells or natural killer T cells can be deregulated by streptococcal infection. T lymphocytes and cytokines are believed to cause the characteristic inflammatory changes appreciated on histopathologic examination of lesions. [13]

Psoriasis was originally classified as a Th1 disease, but Th17 cells have also been recognized to have an important role. Studies are also proposing a role for antimicrobial peptides and dendritic cells in the pathogenesis of psoriasis. Cathelicidin LL-37 is especially thought to lead to activation of dendritic cells, inducing production of interferons. Elevated levels of the cathelicidin LL-37 have been reported in patients with plaque and guttate psoriasis compared with healthy controls. [14, 15] Levels of inflammatory cytokines interleukin (IL)‒1RA, IL-2, IL-23, and interferon (IFN)‒gamma were also elevated in these patients. There was no significant difference in serum levels of inflammatory cytokines and LL-37 between the plaque type and guttate psoriasis group, but a positive correlation between disease activity and cytokine levels was noted. [14]

An autoimmune phenomenon has also been postulated to underlie guttate psoriasis because some streptococcal products and components have been found to cross-react with normal human epidermis. [16, 17] Electron microscopic studies of guttate psoriasis have shown that mast cell degranulation is an early and constant feature in the evolution of guttate psoriatic lesions. Furthermore, Langerhans cell migration appears to be impaired during an acute episode of guttate psoriasis. [18]

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