English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

Summary   Background  Glucocorticoids ( GC s) are first‐line treatment for keloid disease ( KD ) but are limited by high incidence of resistance, recurrence and undesirable side‐effects. Identifying patient responsiveness early could guide therapy.    Methods  Nineteen patients with  KD  were recruited at week 0 (before treatment) and received intralesional steroids. At weeks 0, 2 and 4, noninvasive imaging and biopsies were performed. Responsiveness was determined by clinical response and a significant reduction in vascular perfusion following steroid treatment, using full‐field laser perfusion imaging ( FLPI ). Responsiveness was also evaluated using (i) spectrophotometric intracutaneous analysis to quantify changes in collagen and melanin and (ii) histology to identify changes in epidermal thickness and glycosaminoglycan ( GAG ) expression. Biopsies were used to quantify changes in glucocorticoid receptor ( GR ) expression using quantitative reverse transcriptase polymerase chain reaction, immunoblotting and immunohistochemistry.    Results  At week 2, the  FLPI  was used to separate patients into steroid responsive ( n  =   12) and nonresponsive groups ( n  =   7). All patients demonstrated a significant decrease in  GAG  at week 2 ( P  <   0·05). At week 4, responsive patients exhibited significant reduction in melanin,  GAG , epidermal thickness (all  P  <   0·05) and a continued reduction in perfusion ( P  <   0·001) compared with nonresponders. Steroid‐responsive patients had increased  GR  expression at baseline and showed autoregulation of  GR  compared with nonresponders, who showed no change in  GR  transcription or protein.    Conclusions  This is the first demonstration that keloid response to steroids can be measured objectively using noninvasive imaging.  FLPI  is a potentially reliable tool to stratify  KD  responsiveness. Altered  GR  expression may be the mechanism gating therapeutic response.

An abnormality in glucocorticoid receptor expression differentiates steroid responders from nonresponders in keloid disease