Are You Confident of the Diagnosis?
Calcinosis cutis may be triggered by multiple diverse etiologies, ranging from chronic illnesses to acute traumatic and iatrogenic insults to the skin. Calcinosis cutis is classified as dystrophic, metastatic, iatrogenic, or idiopathic based on these causative agents.
Dystrophic calcification results from localized trauma or inflammation in patients with normal serum calcium and phosphate levels, some of whom may have connective tissue disorders or benign or malignant neoplasms. Metastatic calcinosis cutis presents with altered calcium and phosphorus metabolism, typically in the setting of chronic renal disease. Iatrogenic depositions develop after a medical intervention leads to the inadvertent placement of calcium-containing solutions, such as extravasated intravenous calcium gluconate, within the dermis. Lastly, idiopathic calcinosis cutis lacks any definable trigger.
What you should be alert for in the history
A detailed review of systems, past medical history, and exploration of recent medical interventions or hospitalizations are crucial to eliciting the causative agent. Practitioners should inquire about any personal or family history of autoimmune connective tissue disease (ACTD), such as dermatomyositis, scleroderma, CREST (calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, telangiectasia) syndrome, mixed connective tissue disease, systemic lupus erythematosus (SLE), or renal insufficiency. Patients may also report spontaneous extrusion of chalky white-yellow material from the lesions.
Characteristic findings on physical examination
On physical examination, calcinosis cutis’ dermal calcium deposits present as numerous, firm dermal or subcutaneous papules, nodules, or plaques with either a white or yellow coloring (Figure 1, Figure 2). The lesions may be tender to asymptomatic. The depositions may ulcerate and express their contents. Local erythema and necrosis may also be present.
Lesion distribution in calcinosis cutis is closely connected to its etiology. Dystrophic calcinosis cutis presents in areas of recent trauma, such as acne, burns, or inflammatory processes like granulomatous infections. Dystrophic depositions associated with ACTD tend of affect the hands and feet; other common areas include the elbows and knees, arms and legs, torso, and face. Some patients with ACTD may experience calcinosis universalis with widespread calcification of the subcutaneous tissue, muscles, and tendons.
Metastatic calcinosis cutis may involve visceral calcifications as well as potentially generalized dermal or symmetrical periarticular distribution. Visceral involvement most commonly involves the lungs, stomach and kidneys. Tumoral calcinosis presents as large, painless periarticular calcifications, most commonly in the hips and shoulders. Iatrogenic lesions will be located at the site of a recent medical intervention, such as an IV, electrode placement, or repeated heel stick in a neonate.
Idiopathic calcinosis cutis has no characteristic distribution, but is typically localized to one area, such as the breast or vulva. Some subtypes of idiopathic calcinosis cutis, however, do have distinct distributions, such as a subepidermal calcified nodule that presents most often as a solitary verrucous nodule on the head or neck of a young child.
Scrotal calcinosis has traditionally been classified as a type of idiopathic calcinosis cutis that presents as multiple, firm nodules on the scrotum. However, more recently a close connection between the calcium depositions and epithelial cysts, many with evidence of inflammation, has been demonstrated. This association raises the question as to whether scrotal calcinosis would be more appropriately classified as a type of dystrophic calcinosis cutis.
Expected results of diagnostic studies
On histopathology, calcium depositon appears basophilic with hematoxylin-eosin (H&E) staining, black with von Kossa stain, and red with Alizarian red stain (Figure 3). The deposition may be within the dermis or subcutaneous tissue with larger depositions found in the subcutaneous tissue. A giant-cell foreign body reaction, necrosis, or fibrosis may or may not be present.
Given the connection between metastatic calcinosis cutis and disorders of calcium and phosphorus metabolism, assessing serum calcium, phosphorus, and parathyroid hormone levels as well as a urine analysis, are crucial. These values will be normal in non-metastatic types of calcinosis cutis.
If one suspects extensive involvement of subcutaneous and fascial tissues, plain films would show the extent of the calcification. Tumoral calcinosis’ large depositions typically appear lobulated and cystic.
Patients presenting with symptoms of connective tissue disorders should have anti-centromere, anti-SCL-70, creatine phosphokinase (CPK), aldolase, and antinuclear antibody (ANA) levels checked with a referral to a rheumatologist if these values are abnormal.
If one suspects extensive involvement of subcutaneous and fascial tissues, plain films would show the extent of the calcification. Tumoral calcinosis’ large depositions typically appear lobulated and cystic. Dual-energy computed tomography (DECT) is a modern technique that has been used to detect monosodium urate deposits in gout; it along with multidetector computed tomography (MCT) and ultrasonography have been proposed as potential additional modalities to evaluate calcinosis of the hands.
The differential diagnosis of calcinosis cutis includes:
Milia (which will be differentiated based on the type of material expressed and histopathology)
Calciphylaxis (which is more likely to be painful, on the lower extremities, and be associated with livedo mottling and calcification of subcutaneous blood vessels)
Molluscum contagiosum (which will appear as multiple umbilicated pink papules and should be ruled out in children who present with multiple lesions of subepidermal cutaneous nodules)
Xanthomas which may have a similar appearance of a yellowish nodule but will contain lipid-filled histiocytes, not dermal calcium deposits, on biopsy)
Verruca (which may be confused with the verrocous appearance of some subepidermal cutaneous nodules)
Osteoma cutis or cutaneous ossification(which may occur after calcification and will appear as formed bone histologically)
Gout (whose tophaceous nodules may resemble calcifications but whose uric acid crystals will appear negatively birefringent under polarizing light)
Tenosynovitis (whose calcifications will present with a history of repetitive use or injury to a specific joint)
Cutaneous nodular amyloidosis (which will demonstrate apple-green birefringence under polarizing light after staining with Congo red)
Who is at Risk for Developing this Disease?
The risk factors for calcinosis cutis vary based on the specific etiology of the calcifications. Patients with ACTD, such as CREST, dermatomysitis, and scleroderma are at increased risk for developing dystrophic calcinosis cutis. Children with dermatomyositis are more likely than adults with the disease to develop calcinosis cutis, with between 30-70% developing the condition.
In general, patients with dermatomyositis and scleroderma are at increased risk for extensive calcinosis universalis. In patients with scleroderma, male sex and the presence of digital ulcers have been correlated with higher risk for calcinosis progression. Calcinosis circumscripta is another variant of more limited and localized calcifications seen primarily in patients with scleroderma. Of the few patients with SLE and calcinosis cutis, most develop calcifications after long-standing SLE. A few cases of calcinosis cutis in the setting of Sjögren’s syndrome have been reported.
Benign or malignant neoplasms may also serve as inciting events for dystrophic calcifications. Pilomatricomas present most frequently with calcifications. Bites, burn scars, acne, and infections are also potential triggers. Dystrophic calcinosis cutis may result from panniculitis or fat necrosis, such as from a pancreatic adenocarcinoma triggering a pancreatic enzyme-induced panniculitis, or following neonatal subcutaneous fat necrosis.
Dystrophic calcinosis cutis may also occur in the setting of pseudoxanthoma elasticum, Ehlers-Danlos syndrome, Werner syndrome, porphyria cutanea tarda, and Rothmand-Thompson syndrome. Some patients have also experienced localized calcinosis cutis after exposure to calcium chloride salts in de-icing products causes, which causes local trauma by its exothermic reaction after making contact with skin.
Metastatic calcinosis cutis occurs most commonly in patients with conditions such as renal failure and hyperparathyroidism, leading to hypercalcemia and/or hyperphosphatemia. Similar disruptions in calcium and phosphorus metabolism leading to metastatic calcinosis may be seen in hypervitaminosis D, milk-alkali syndrome, tumor lysis syndrome, osteolytic neoplasms, and sarcoidosis.
Metastatic calcinosis cutis has also been reported to occur in a few patients after liver or lung transplantation, possibly related to the calcium load such patients receive in blood products during their surgery and the potential for disordered metabolism of calcium and phosphorus during the post-operative period.
Tumoral calcinosis is another variant of calcinosis typically associated with hyperphosphatemia and observed to have a familial pattern with African-American patients being at increased risk.
Iatrogenic calcinosis cutis develops after patients have recently had invasive procedures involving calcium-containing solutions, such as intravenous calcium gluconate, injections of calcium-containing low-molecular-weight heparin, the application of electrodes with calcium-containing paste, or the use of calcium alginate dressings on wounds.
Idiopathic calcinosis cutis has no known risk factors other than young age for subepidermal calcified nodules or Down syndrome for milia-like idiopathic calcinosis cutis of the extremities.
What is the Cause of the Disease?
Calcinosis cutis may be triggered by several different processes that ultimately lead to dermal or subcutaneous deposition of insoluble calcium phosphate. Dystrophic calcinosis cutis results from increased local concentrations of calcium following trauma or inflammation. In ACTD, chronic inflammation and vascular hypoxia are thought to increase a patient’s propensity towards this type of posttraumatic calcification. Patients with dystrophic calcinosis cutis will typically not have elevated serum calcium or phosphorus levels.
In metastatic calcinosis cutis, elevated serum calcium and phosphorus levels provoke insoluble calcium crystal formation. Most often, this disordered calcium and phosphorus metabolism is caused when the decrease renal clearance of phosphorus and intestinal absorption of calcium in renal disease triggers a secondary hyperparathyroidism. Increased levels of parathyroid hormone lead to the reabsorption of calcium and phosphorus from bone, increasing the serum concentrations of each.
In iatrogenic calcinosis cutis, the extravasation of calcium-containing solutions into the dermis triggers local injury and inflammation that results in even more calcium being deposited into the effected skin from the cellular reaction. The concentration of calcium within the effected dermis is many times greater than the calcium concentration in the original solution that has extravasated, suggesting an inflammatory response that triggers a more significant movement of calcium into the dermis.
In idiopathic calcinosis cutis, the etiology is unknown.
Calcinosis cutis’ dermal and subcutaneous deposition of insoluble calcium salts results after the traumatic, metastatic, or iatrogenic inciting event leads to the elevated levels of mitochondrial calcium phosphate with subsequent crystant formation and cell death. In idiopathic calcinosis cutis, the triggering mechanism for increased amounts of calcium phosphate within mitochondria is unknown. Once released from the apoptotic cell, the calcium crystals form in the extracellular space along collagen and elastin fibers.
Changes in the balance of extracellular proteins in patients with ACTD may explain their propensity to calcification. The bone matrix proteins osteonectin and matrix gamma carboxyglutamic acid protein (MGP) were found to be increased in the skin of patients with scleroderma compared to healthy controls, with osteonectin being increased in scleroderma patients with calcinosis compared to scleroderma patients without calcinosis.
An association between tissue hypoxia and development of dystrophic calcinosis has been observed: skin biopsies of patients with scleroderma-associated calcinosis display increased levels of hypoxia-associated glucose transporter molecule, along with advanced glycation and lipoperoxidation end products, markers of oxidative stress.
Pyrophosphate has been shown to play a role in antimineralization. Mouse models of generalized arterial calcification of infancy display phenotypic similarities with metastatic and dystrophic calcinosis; such mice have mutations in ENPP1 genes and lack nucleotide pyrophosphatase phosphodiesterase 1, an enzyme involved in the formation of pyrophosphate. ENPP1-/- mice develop severe dysregulation of calcium/phosphate homeostasis, suggesting that pyrophosphate inhibition of hydroxyapatite crystal formation plays an integral role in disease progression.
In familial cases of tumoral calcinosis, defects in fibroblast growth factor (FGF23) and its cofactors have been found to decrease renal clearance phosphorus, leading to the hyperphosphatemia seen in a subset of tumoral calcinosis cases.
Systemic Implications and Complications
Calcinosis cutis may be a symptom of numerous systemic diseases that should be excluded based on the treatment options discussed below. Patients with metastatic calcinosis cutis may also be at risk for calciphylais and visceral involvement.
The ulcerating depositions of calcinosis cutis may also become sources of infection. In a study of French patients with dermatomyositis and polymyositis, calcinosis cutis infections were the second most common cause of pyogenic infections after aspiration pneumonia.
The lesions may be widespread in the subcutaneous tissues. Children with dermatomyositis have been reported to develop extensive depositions along fascial planes, resulting in a debilitating exoskeleton of calcifications.
Treatment options are summarized in Table I.
|Low calcium or phosphorus diet with the addition of Sevelamer if patient has abnormalities of those electrolytes||Erbium:Yag laser therapy followed by curettage of material|
|IVIG (intravenous immunoglobulin)|
Optimal Therapeutic Approach for this Disease
Obtain a detailed history of any antecedent trauma or inflammation with accompanying past medical and family history to elicit systemic disease that may increase the patient’s propensity towards calcification. Diagnostic studies include (1) serum calcium and phosphorus, urine analysis, and parathyroid hormone levels to rule out underlying calcium disturbances as a cause of metastatic calcinosis cutis; (2) ANA testing along with CPK, aldolase, anti-SCL-70, anti-centromere, ANA to exclude underlying connective tissue disorders; and (3) X-ray and CT to rule out visceral calcifications if systemic disease is suspected.
Conservative management with elevation, intralesional triamcinolone or sodium sulfate with alternating heat and cold application may be sufficient for limited iatrogenic calcifications. Supportive measures such as proper wound care, antibiotics for infections, and analgesics for pain should be undertaken. General prophylactic measures are aimed at improving blood flow to the extremities through advising the patient to avoid cold exposure, trauma, smoking, and stress.
Calcium-channel blockers may treat calcinosis cutis by stopping the inward flow of calcium ions into the cells of affected tissues and local macrophages, preventing subsequent crystallization within the mitochondria and cell death. Diltiazem is the most frequently used medical treatment for calcinosis; case reports have shown benefit with diltiazem dosed 240 to 480mg/day for 1-12 years for calcinosis in patients with scleroderma.
Bisphosphonates reduce bone resorption and may help inhibit macrophage cytokine production, potentially reversing the calcification process. In patients with dermatomyositis, intravenous infusion of pamidronate has been described as effective for treating calcinosis in severe cases. In a recent mouse model, high doses of etidronate but not alendronate significantly reduced mineralization. A recent case report demonstrated the efficacy of etidronate in treating calcinosis of juvenile dermatomyositis.
Warfarin has been studied as a potential agent given that in patients with calcinosis, abnormally high levels of vitamin K have been implicated in the calcium-binding process. However, the current evidence surrounding warfarin’s efficacy is conflicting, and warfarin as a therapeutic agent in calcinosis warrants further study.
Probenacid and aluminum hydroxide work to lower serum phosphate levels, thus reducing calcification. These agents have decreased calcinosis deposits in patients with dermatomyositis.
Sodium metabisulfite, which reacts with oxygen to become sodium sulfate, inhibits calcium oxalate agglomeration. In a case series, topical sodium metabisulfite has been shown to reduce calcinosis in patients with ACTD.
Biologic agents counteract inflammatory processes that might play a role in progression of calcinosis. In several case reports of patients with ACTD, the anti-TNF agent rituximab and the anti-CD20 antibody infliximab have shown therapeutic efficacy ranging from limiting disease progression to complete resolution of calcinosis.
Discuss a surgical approach for symptomatic lesions. Immediate symptomatic relief often occurs with excision or curettage of the lesions, but lesions may reoccur after the trauma of surgery. Symptomatic improvement may occur even if residual calcinosis, as seen by radiographic studies, remains at the excision or curettage site.
Low calcium and/or phosphorus diets with the addition of the antacid Sevelamer HCl to decrease intestinal absorption of phosphorus may be of benefit in patients with hypercalcemia or hyperphosphatemia. Culture any lesions suspicious for secondary infections and treat with topical antibiotics.
Patients with milia-like idiopathic calcinosis cutis often experience involution of the lesions with time. For intractable cases of calcinosis universalis, IVIG may be warranted to reduce morbidity although some authors report no benefit to IVIG in these cases.
Explain the relatively benign nature of calcinosis cutis and the potential for symptom relief with therapy. If patients have not experienced any spontaneous ulceration and discharge from the lesions, they should be counseled that this is possible. Counsel that new lesions may develop, even with treatment. Caution that even with the excision of lesions, new depositions may reoccur in the same location as the excision itself will be traumatic to the dermis.
Describe treatment options. With the variety of medical and surgical approaches to symptomatic lesions of calcinosis cutis, patients have a choice of modalities. Encourage adherence to treatment for any underlying systemic disease. Patients with metastatic calcinosis cutis often experience symptomatic improvement with the normalization of serum calcium and phosphorus. Patients with calcinosis cutis in the setting of underlying ACTD similarly experience amelioration of the calcification with appropriate management and treatment of their connective tissue disease.
Advise the patient to call their primary medical doctor with any signs of local or systemic infection.
Unusual Clinical Scenarios to Consider in Patient Management
With local nerve compression, calcinosis cutis may cause neuropathic pain, and the presence of adjacent nerves should be a consideration in any excision of a deposition.
Valenzuela, A, Chung L., Calcinosis. “pathophysiology and management”. Curr Opin Rheumatol. vol. 27. 2015 Nov. pp. 542-8. (The authors present an overview of recent studies regarding the epidemiology, pathophysiology, diagnosis, and treatment of calcinosis cutis in patients with systemic sclerosis.)
Dima, A, Balanescu, P, Baicus, C. “Pharmacological treatment in calcinosis cutis associated with connective-tissue diseases”. Rom J Intern Med. vol. 52. 2014. pp. 55-67. (A review of pharmacological treatment options for calcinosis in patients with ACTD.)
Del Barrio-Díaz, P, Moll-Manzur, C, Álvarez-Veliz, S, Vera-Kellet, C. “Topical sodium metabisulfite for the treatment of calcinosis cutis: A promising new therapy”. Br J Dermatol. 2016 Jan 22. (Case series of four patients with calcinosis cutis, secondary to dermatomyositis, systemic sclerosis and radiodermitis after breast cancer who were treated with 25% sodium metabisulfite. All patients exhibited a decrease in size, erythema, and pain, with complete resolution of associated ulcers. One patient had a complete response; no adverse effects were observed.)
Wakabayashi, T, Sasaki, N, Chinen, N, Suzuki, Y. “Dramatic Improvement of Subcutaneous Calcinosis by Intermittent, High-Dose Etidronate plus Cimetidine in a Patient with Juvenile Dermatomyositis”. Case Rep Rheumatol. 2015. (Case report of a 17-year-old boy with juvenile dermatomyositis who presented with bilateral lower limb calcinosis. Cimetidine was combined with intermittent administration of high-dose etidronate, leading to marked improvement of both subcutaneous and muscular calcinosis with no skeletal adverse reactions during 5-year follow-up.)
Shahi, V, Wetter, DA, Howe, BM. “Plain radiography is effective for the detection of calcinosis cutis occurring in association with autoimmune connective tissue disease”. Br J Dermatol. vol. 170. 2014. pp. 1073-1079. (A retrospective blinded review of imaging studies of 37 patients assessing for calcinosis cutis associated with ACTD at one institution. Plain radiographs detected calcinosis in all 37 patients; with a nodular pattern of calcification most commonly observed and two or more morphological patterns of calcification present in 19 patients; individual patterns were not specific to a particular ACTD subtype.)
iQ, Sundberg, JP, Levine, MA, Terry, SF. “The effects of bisphosphonates on ectopic soft tissue mineralization caused by mutations in the ABCC6 gene”. Cell cycle (Georgetown, Tx). vol. 14. 2015. pp. 1082-1089. (A mouse model was used to explore the efficacy of bisphosphonates in preventing ectopic calcification caused by ABCC6 mutations seen in Pseudoxanthoma elasticum (PXE) and generalized arterial calcification of infancy (GACI). ABCC6(-/-) mice were fed diets containing etidronate disodium (ETD) or alendronate sodium trihydrate (AST); high-dose ETD significantly reduced mineralization, suggesting that selected bisphosphonates may be helpful for prevention of mineral deposits in PXE and GACI caused by mutations in the ABCC6 gene.)
Mackenzie, NC, Zhu, D, Milne, EM. “Altered bone development and an increase in FGF-23 expression in Enpp1(-/-) mice”. PloS One. vol. 7. 2012. pp. e32177(A detailed phenotypic assessment of a mouse model ENPP1(-/-) lacking nucleotide pyrophosphatase phosphodiesterase 1 (NPP1, an inhibitor of hydroxyapatite crystal formation). ENPP1(-/-) mice show severe disruption in mineralization of long-bones, dysregulation of calcium/phosphate homeostasis and changes in Fgf-23 expression, suggesting a role for pyrophosphate in anti-mineralization.)
Tosounidou, S, MacDonald, H, Situnayake, D. “Successful treatment of calcinosis with infliximab in a patient with systemic sclerosis/myositis overlap syndrome”. Rheumatology. vol. 53. 2014. pp. 960-961. (Case report documenting successful treatment of refractory calcinosis with intravenous infusions of infliximab in a patient with systemic sclerosis/myositis overlap syndrome.)
Lapner, MA, Goetz, TJ. “High-speed burr debulking of digital calcinosis cutis in scleroderma patients”. J Hand Surg. vol. 39. 2014. pp. 503-510. (A retrospective analysis of 9 patients with calcinosis secondary to scleroderma who underwent a debulking procedure using a high-speed micro-burr to soften and express calcific material in the digits; at 2-year follow up, 7 patients had recurrences; patient satisfaction was inversely correlated to the number of digits involved.)
Chamberlain, AJ, Walker, NP. “Successful palliation and significant remission of cutaneous calcinosis in CREST syndrome with carbon dioxide laser”. Dermatol Surg. vol. 29. 2003. pp. 968-70. (Case report of use of carbon dioxide laser on calcinosis cutis deposits on the fingers of a 40-year-old woman with CREST syndrome. The patient experienced re-epithelization within 6 weeks and at the time of publication had experienced at least a 3-year remission.)
Chan, AY, Li, E. “Electric shock wave lithotripsy (ESWL) as a pain control measure in dermatomyositis with calcinosis cutis – old method, new discovery”. Clin Rheumatol. vol. 24. 2005. pp. 172-3. (A 23 year-old male with an 18-year old history of juvenile dermatomyositis received symptomatic relief after two sessions of ESWL to his right leg, each with 3,000 shocks with total energy delivered ranging from 896 to 929 volts. Prior to the ESWL, he experienced ongoing infections of the calcification and pain that ultimately necessitated opioid therapy. The ESWL treatments relieved his pain even though the size of the calcinosis did not change dramatically.)
Davies, CA, Jeziorska, M, Freemont, AJ. “Expression of osteonectin and matrix Gla protein in scleroderma patients with and without calcinosis”. Rheum. vol. 45. 2006. pp. 1349-55. (Comparison of the expression in endothelium cells and dermal fibroblasts of the bone matrix proteins osteonectin and matrix gamma-carboxyglutamic acid protein (MGP) in healthy controls, patients with limited cutaneous scleroderma with and without calcinosis. Scleroderma patients of both types were found to have increased expression of both bone matrix proteins relative to healthy controls while scleroderma patients with calcinosis displayed greater osteonectin expression than scleroderma patients without calcinosis. The authors describe the further need to study MGP in its various states of gamma-carboxylation as a means to understanding how gamma-carboxylation contributes to local calcification.)
Dubey, S, Sharma, R, Maheshwari, V. “Scrotal calcinosis: idiopathic or dystrophic”. Dermatol Online J. vol. 16. 2010. pp. 5(A combination prospective and retrospective histopathologic study of scrotal calcinosis that supports a dystrophic etiology driving scrotal calcinosis from inflamed or ruptured epitelial cysts. Forty-one percent of patients contained intact epithelial cysts with 53% demonstrating intact, inflammed epithelial cysts with calcium material within the lumen of the cyst.)
Meissner, M, Ochsendorf, F, Kaufmann, R. “Therapy of calcinosis cutis using erbium-doped yttrium aluminum garnet laser treatment”. Dermatol Surg. vol. 36. 2010. pp. 727-8. (Authors describe using Er:YAG laser (5 J/cm2, 5 mm diameter, 5 Hz) for calcinosis cutis nodules that were less than 2 cm in diameter to open the skin and allow for the removal of the calciferous materials. The authors report this was well tolerated by patients who were able to have multiple nodules treated at once with only local anesthetic.)
Moss, J, Syrengelas, A, Antaya, R. “Calcinosis cutis: a complication of intravenous administration of calcium gluconate”. J Cutan Pathol. vol. 33. 2006. pp. 60-2. (A case report of a pediatric patient with a sarcoma who developed edema followed a few weeks later by a tender plaque at the site of an intravenous infusion of calcium gluconate. Pathology confirmed calcinosis cutis. This article contains a thorough discussion of the potential pathogenesis of iatrogenic calcinosis cutis following the extravasation of calcium-containing solutions within the dermis.)
Mukamel, M, Horev, G, Mimouni, M. “New insight into calcinosis of juvenile dermatomyositis: A study of composition and treatment”. J Pediatr. vol. 138. 2001. pp. 763-6. (Case study of a 6-year-old boy with a four-year history of juvenile dermatomyositis with large calcinosis cutis deposition in the axilla, hips, and abdominal wall who experienced a reduction of deposition size and improved functionality after the addition of 10mg/d alendronate. The authors theorize that the previously unreported ability of a bisphosphonate to reduce existing calcifications by inhibiting local macrophage activity as a mechanism for the patient's improvement. The authors report no impairment in skeletal growth during the year the patient took alendronate.)
Touart, DM, Sau, P. “Cutaneous deposition disease Part II”. J Am Acad Dermatol. vol. 39. 1998. pp. 527-46. (A thorough review of calcinosis cutis' etiology, histopathology and treatment options. Also contains reviews of deposition conditions seen in cutaneous ossification, alkaptonuria and ochronosis, exogenous ochronosis, and gout.)
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