Calcinosis has been described as a manifestation of various rheumatic diseases. Chemically, it consists of hydroxyapatite, a physiological component of bones and teeth.1 Hypoxia, microtrauma, and genetic predisposition are presumed factors in its pathogenesis, which remains poorly understood.2,3
A 50-year-old woman with systemic sclerosis, diagnosed at age 36, presented with progressive calcinosis of the hands, first noted at age 44. Two years later, she developed swelling, pain, and ulcerations of the left hand and was diagnosed with a deep soft tissue Mycobacterium haemophilum infection, confirmed by PCR of biopsy material. Azathioprine was discontinued and she received triple therapy with azithromycin, ciprofloxacin, and rifampicin for 1 year. Although the infection-related symptoms resolved, calcinosis progressed, predominantly affecting the volar side of the left hand, around the second and fourth metacarpophalangeal joints and the second and third proximal interphalangeal joints. Its extent and asymmetry were evident on radiographs (Figure 1A) and dual-energy computed tomography (Figure 1B; Supplementary Material, available with the online version of this article), performed 4 years after diagnosis of the infection. Although no established mechanistic model explains how local mycobacterial infection may promote calcinosis, the observed spatial and temporal cooccurrence suggests an aggravating effect of the infection.
(A) Posteroanterior radiograph of both hands. (B) 3D reconstruction of a dual-energy CT scan of both hands, volar view. CT: computed tomography.
The quality of life of those affected by calcinosis is severely impaired by pain, foreign body sensation, loss of function, ulcerations, and recurrent wound infections. Despite numerous and very different approaches, no effective therapy has yet been identified.4 For superficial calcinosis, some patients report temporary relief with topical application of sodium thiosulfate and/or manipulative evacuation (ie, self-performed manual expression). There remains an urgent unmet medical need in the treatment of calcinosis.
Footnotes
CONTRIBUTIONS
JSC: conceptualization, investigation, writing - original draft, visualization. TD: resources, writing - review & editing, visualization. GK: writing - review & editing, supervision. RB: conceptualization, resources, investigation, writing - review & editing, visualization, supervision.
FUNDING
The authors declare no funding or support for this work.
COMPETING INTERESTS
The authors declare no conflicts of interest relevant to this article.
ETHICS AND PATIENT CONSENT
Institutional review board approval is not required according to the authors’ institutions. Written informed consent for publication was obtained from the patient and is available upon request.
- Copyright © 2026 by the Journal of Rheumatology
SUPPLEMENTARY DATA
Supplementary material accompanies the online version of this article.
