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Clinical Trial Summary

Sodium can be buffered in the skin, which mechanism is altered during aging and in certain diseases such as hypertension. High salt environment can promote autoimmunity by expanding pathogenic IL-17 producing T helper (Th17) cells. Psoriasis is a relapsing and remitting inflammatory autoimmune disease affecting the skin and joints and involves proinflammatory Th17 cells. Here we tested the hypothesis if psoriatic skin has a higher sodium content in humans.


Clinical Trial Description

The cytokine interleukin-17A (IL-17A) is a crucial player in the pathogenesis of the autoimmune disease of psoriasis. This neutrophil recruiting cytokine is produced by IL-17A producing CD4+ T cells (Th17) and gamma/delta T cells of the skin and evokes an inflammation circuit finally leading to the classical clinical picture of psoriasis with hyper- and parakeratosis, erythema, scaling and neutrophil abscess formation.

Besides genetic factors, lifestyle factors are relevant and decide if an autoimmune disease becomes manifest. It was shown previously that increased salt (sodium chloride, NaCl) concentrations boost the induction of murine and human Th17 cells. However, more - and also clinical - studies are needed to understand the correlation between salt content and IL-17A in autoimmune diseases.

This study investigates the hypothesis if skin sodium content in human psoriasis is increased in order to get further insight into the IL-17A-salt-interplay. ;


Study Design


Related Conditions & MeSH terms


NCT number NCT04095130
Study type Observational
Source Charite University, Berlin, Germany
Contact
Status Completed
Phase
Start date July 1, 2015
Completion date September 17, 2019

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