Calcinosis in dermatomyositis.

Srijana Davuluri, Christian Lood, Lorinda Chung

Journal: Current opinion in rheumatology 2024;36(6):453-458

PMID: 39120537

Abstract

PURPOSE OF REVIEW

To provide the most recent literature on our understanding behind the pathogenesis and the treatment of calcinosis in dermatomyositis.

RECENT FINDINGS

Early diagnosis and controlling the overall disease activity are cornerstones to prevent calcinosis in juvenile dermatomyositis. Observational cohort studies showed that prolonged state of inflammation and features of vascular dysfunction like digital ulcers and abnormal nailfold capillaries are associated with calcinosis. Neutrophil activation and mitochondrial dysfunction have recently emerged as potential mechanistic pathways involved in calcinosis pathogenesis. Few recent case series have alluded to the efficacy of topical and intralesional sodium thiosulfate, while JAK inhibitors appear to be newer promising therapy in juvenile dermatomyositis.

SUMMARY

Calcinosis in dermatomyositis consists of deposition of insoluble calcium compounds in the skin and other tissues. It is prevalent in up to 75% of patients with juvenile dermatomyositis and up to 20% in adult dermatomyositis. While it leads to significant patient morbidity, we do not yet understand the pathogenesis in its entirety. Surgical excision although palliative is the mainstay of treatment and should be offered to patients. All available treatment options are only based on very low level of evidence.

Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.

Address: Stanford School of Medicine Division of Rheumatology.; Stanford School of Medicine & Palo Alto VA Healthcare System, Division of Immunology & Rheumatology, Palo Alto, California.; University of Washington, Division of Rheumatology, Seattle, Washington, USA.
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