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/

Global: Zendy Plus annual

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

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Ann Saudi Med 28(6) November-December 2008 www.kfshrc.edu.sa/annals 466 Systemic lupus erythematosus (SLE) is a multis system chronic autoimmune inflammatory diss ease. SLE has been associated with numerous complement abnormalities including C1q deficiency.1 Patients with SLE and C1q deficiency may have a ses vere multisystem disease, including cutaneous lesions.2,3 Patients with antiphospholipid antibody syndrome often develop cutaneous ulcerations which mimic pyos derma gangrenosum (PG), particularly leg ulcers, and similar lesions have rarely been reported in patients with SLE.4,5 We managed a young girl with familial SLE and C1q deficiency who developed progressive exs tensive ulcerations that were consistent with pyoderma gangrenosum.

Extensive ulcerations due to pyoderma gangrenosum in a child with juvenile systemic lupus erythematosus and C1q deficiency