eMedicine Specialties > Dermatology > Metabolic Diseases

Calcinosis Cutis: Treatment & Medication

Author: Julia R Nunley, MD, Professor, Program Director, Dermatology Residency, Department of Dermatology, Virginia Commonwealth University Medical Center
Coauthor(s): Lydia M E Jones, MD, Staff Physician, Department of Dermatology, Virginia Commonwealth University
Contributor Information and Disclosures

Updated: Jan 27, 2009

Treatment

Medical Care

  • Medical therapy of calcinosis cutis is limited and of variable benefit. When identified, the underlying problem should be corrected.
  • 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.18,19
  • Warfarin has shown benefit in some.
  • 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.20,21
  • Use of sodium thiosulfate may be considered as it has been shown to be effective in many cases of calciphylaxis. It would be considered off-label and experimental therapy.22

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 dermatomyositis-induced tissue calcification.23
    • 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.

Consultations

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

Diet

  • 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

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

Medication

Medical therapy generally has limited benefit. The following medications may be tried.

Antacids

Inorganic salts can bind phosphate in the GI tract and prevent absorption.


Aluminum carbonate (Basaljel)

Increases gastric pH >4 and inhibits proteolytic activity of pepsin. Does not coat mucosal lining but may have local astringent effect. May increase tone of lower esophageal sphincter.

Adult

400-1800 mg PO tid with meals

Pediatric

Not established

Decreases effects of allopurinol, chloroquine, corticosteroids, diflunisal, digoxin, ethambutol, iron salts, H2-antagonists, isoniazid, penicillamine, phenothiazines, tetracyclines, thyroid hormones, and ticlopidine; increases effects of benzodiazepines and dicumarol

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Use in patients with renal insufficiency may result in aluminum toxicity; nausea and constipation are frequent adverse effects; aluminum ions inhibit smooth muscle contraction, inhibiting gastric emptying; caution in gastric outlet obstruction; may cause dose-related rebound hyperacidity by increasing gastric secretion or serum gastrin levels; prolonged use of aluminum-containing antacids in renal failure may result in or worsen dialysis osteomalacia; elevated tissue aluminum levels contribute to dialysis encephalopathy and osteomalacia syndromes


Aluminum hydroxide (ALternaGEL, Alu-Cap, Amphojel, Dialume)

Effective phosphate binder; not considered first-line therapy because of potential for toxicity.

Adult

320-1800 mg PO tid with meals

Pediatric

50-150 mg/kg/d PO divided q4-6h; titrate to maintain normal serum phosphorus levels

Tetracyclines, ranitidine, ketoconazole, benzodiazepines, penicillamine, phenothiazines, digoxin, indomethacin, isoniazids, and corticosteroids decrease effects of aluminum in hyperphosphatemia; absorption of dicumarol and benzodiazepines may increase if administered concurrently

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients with recent massive upper GI hemorrhage; renal failure may cause aluminum toxicity


Magnesium oxide (Maox, Mag-ox)

Treats magnesium deficiencies or magnesium depletion due to malnutrition, restricted diet, alcoholism, or magnesium-depleting drugs.

Adult

140-420 mg PO tid with meals

Pediatric

Administer as in adults

Decreases effects of benzodiazepines, chloroquine, corticosteroids, digoxin, H2-antagonists, hydantoins, nitrofurantoin, tetracyclines, iron salts, ticlopidine, phenothiazines, iron salts; increases the effects of dicoumarol, quinidine, and sulfonylureas

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hypermagnesemia and toxicity may occur in renal impairment when magnesium >50 mEq is given qd because of decreased clearance of magnesium ion; approximately 5-20% of orally administered magnesium salts can be absorbed systemically

Diphosphonates

These agents are used to inhibit bone turnover to lower serum calcium and phosphate levels. These agents also can absorb hydroxyapatite crystal and inhibit growth.


Etidronate disodium (Didronel)

Reduces bone formation and does not alter renal tubular reabsorption of calcium. Does not affect hypercalcemia in patients with hyperparathyroidism.

Adult

5 mg/kg/d PO for no longer than 6 mo

Pediatric

Not established

Coadministration with calcium containing products and other multivalent cations decrease absorption

Documented hypersensitivity; hypocalcemia, renal impairment

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse effects dose related and infrequent with 5 mg/kg/d PO; caution in renal insufficiency; maintain adequate intake of calcium and vitamin D during therapy; monitor hypercalcemia-related parameters (eg, serum calcium, phosphate, magnesium, potassium levels)

Calcium-channel blockers

Antagonism of calcium-sodium pump may diminish the intracellular calcium concentration, decreasing crystal formation.


Diltiazem hydrochloride (Cardizem)

For management of angina, supraventricular tachycardia, and hypertension. During depolarization, inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

Adult

240-480 mg/d PO

Pediatric

Not established

May increase carbamazepine, digoxin, cyclosporine, theophylline levels; may cause bradycardia and decrease cardiac output when administered with amiodarone; may increase cardiac depression when administered with beta-blockers; cimetidine may increase levels

Documented hypersensitivity, severe CHF, sick sinus syndrome, second- or third-degree AV block, hypotension (<90 mm Hg systolic)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor blood pressure and heart rate during therapy; caution in renal or hepatic impairment; may increase LFT levels and hepatic injury may occur

Calcimimetics


Cinacalcet (Sensipar)

Directly lowers parathyroid hormone (PTH) levels by increasing sensitivity of calcium-sensing receptor on chief cell of parathyroid gland to extracellular calcium. Also results in concomitant serum calcium decrease.

Adult

30 mg PO qd initially; titrate q2-4wk prn to normalize calcium levels by sequential doses of 30 mg bid, 60 mg bid, 90 mg bid, and 90 mg tid/qid; take with meals or immediately following; do not crush, chew, or cut tab

Pediatric

Not established

Strong CYP450 2D6 inhibitor; may increase serum levels of CYP2D6 substrates (eg, flecainide, vinblastine, thioridazine, TCAs); coadministration with CYP450 3A4 inhibitors (eg, ketoconazole, erythromycin, itraconazole) may decrease clearance

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Serum calcium reduction may cause lowered seizure threshold, paresthesia, myalgia, cramping, and tetany; monitor calcium and phosphorus levels closely within 1 wk following initial dose or dose changes and then monthly (secondary hyperparathyroidism) and q2mo (parathyroid carcinoma); do not initiate treatment if serum calcium level <8.4 mg/dL; adynamic bone disease may occur if iPTH levels suppressed <100 pg/mL; caution with hepatic impairment; common adverse effects include nausea and vomiting

More on Calcinosis Cutis

Overview: Calcinosis Cutis
Differential Diagnoses & Workup: Calcinosis Cutis
Treatment & Medication: Calcinosis Cutis
Follow-up: Calcinosis Cutis
Multimedia: Calcinosis Cutis
References
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Further Reading

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Keywords

cutaneous calcinosis, cutaneous calculi

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Contributor Information and Disclosures

Author

Julia R Nunley, MD, Professor, Program Director, Dermatology Residency, Department of Dermatology, Virginia Commonwealth University Medical Center
Julia R Nunley, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Society of Nephrology, International Society of Nephrology, Medical Dermatology Society, Medical Society of Virginia, National Kidney Foundation, Phi Beta Kappa, and Women's Dermatologic Society
Disclosure: Johnson and Johnson stock holder dividends; Amgen stock holder dividends; Forest Lab, Inc stock holder dividends; Galaxo Smith Klein stock holder dividends; Covidien stock holder dividends; Novartis Grant/research funds Consulting; Biolex  sub-investigator

Coauthor(s)

Lydia M E Jones, MD, Staff Physician, Department of Dermatology, Virginia Commonwealth University
Disclosure: Nothing to disclose.

Medical Editor

James W Patterson, MD, Director of Dermatopathology, Professor of Pathology and Dermatology, Departments of Pathology and Dermatology, University of Virginia Medical Center
James W Patterson, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Medical Association, American Society of Dermatopathology, Medical Society of Virginia, Royal Society of Medicine, Society for Investigative Dermatology, and United States and Canadian Academy of Pathology
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Rosalie Elenitsas, MD, Herman Beerman Associate Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System
Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology and American Society of Dermatopathology
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology
Disclosure: elsevier Royalty Other; american college of physicians Honoraria Other

 
 
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