Calcinosis Cutis Treatment & Management

Updated: Mar 05, 2020
  • Author: Julia R Nunley, MD; Chief Editor: Dirk M Elston, MD  more...
  • Print

Medical Care

Medical therapy of calcinosis cutis is limited and of variable benefit. When identified, the underlying problem should be corrected. [23, 24]

Intralesional corticosteroids may be beneficial because of their anti-inflammatory and inhibitory effects on fibroblast activity.

Probenecid and colchicine have been beneficial in some individuals.

Magnesium or aluminum antacids may be effective phosphate binders in patients with hyperphosphatemia. However, the use of these agents in patients with renal insufficiency may result in magnesium or aluminum toxicity.

Sodium etidronate and diphosphonates may reduce bone turnover and inhibit the growth of ectopic hydroxyapatite crystals. However, prolonged treatment is necessary, and paradoxical hyperphosphatemia may result.

Myo-inositol hexaphosphonate is a dietary substance shown to inhibit the crystallization of calcium salts. Recent animal studies have demonstrated a reduction in calcinosis cutis lesions with topical myo-inositol hexaphosphate. This potentially could be of benefit in humans. [25, 26]

Warfarin has shown benefit in some. Low-dose warfarin should not be used, as no benefit has been established. [27]

Rituximab and tumor necrosis factor inhibitors may be beneficial alternatives in patients with dermatomyositis. [27]

The use of the calcium-channel blocker diltiazem over at least 5 years has variable benefits. The therapeutic effect is believed to be the antagonism of the calcium-sodium ion pump. [28, 29, 30]

Use of intravenous sodium thiosulfate should be considered as it has been shown to be effective in many cases of calciphylaxis. It would be considered off-label and experimental therapy. [31]  Reports suggest that ulcerative calcinosis cutis and tumoral calcinosis may respond to topical or intralesional sodium thiosulfate 25%. [32, 33, 34, 35]

Minocycline may be another treatment option. Nine patients with cutaneous calcification associated with limited systemic sclerosis were treated with 50-100 mg/day of minocycline. Improvement was noted within 1-7 months in 8 of the patients. Although lesional size was only moderately improved, ulceration and inflammation were markedly reduced. [36]

Theoretically, in extraordinarily severe cases of calcinosis cutis, associated with one of several connective-tissues diseases, autologous hematopoietic stem cell transplantation (HSCT) may be considered. Risks and benefits must be thoroughly investigated, but studies exist that suggest remission of some connective-tissue diseases with HSCT, which, in theory should help with calcinosis cutis. [37]


Surgical Care

Indications for surgical removal include pain, recurrent infection, ulceration, and functional impairment. Because surgical trauma may stimulate calcification, initially treat a test site before pursuing a large excision. Recurrence is common after excision.

Electric shock wave lithotripsy is anecdotally successful in treating calcinosis cutis associated with dermatomyositis, as well as venous insufficiency and scleroderma. [38, 39]  Although reduction in the size of the calcification was minimal, the patient's associated pain was completely relieved. The physiology for this effect is unknown.



A nephrologist, a rheumatologist, and/or a hematologist should be consulted, as indicated by the underlying disease.



Dietary alteration is of minor benefit in most cases.

The following changes may be tried:

  • Restrict dietary phosphorous when hyperphosphatemia is present.

  • Restrict dietary calcium intake when hypercalcemia is present.

  • A ketogenic diet that stresses the consumption of free fatty acids may be helpful in some individuals. An accumulation of ketoacids, the metabolic product of fatty acids, may lower tissue pH and prevent crystallization.



Activity is affected only if the calcified plaques and/or nodules are large enough to restrict joint mobility or cause ischemia and/or ulceration.



Prevention or treatment of the underlying disease process, as well as prevention of trauma and factors associated with iatrogenic calcinosis, is optimal.