Calcinosis Cutis

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Background

Calcinosis cutis is a term used to describe a group of disorders in which calcium deposits form in the skin. Virchow initially described calcinosis cutis in 1855. Calcinosis cutis is classified into the following four major types according to etiology:

A few rare forms have been variably classified as either dystrophic or idiopathic. These include calcinosis cutis circumscripta, calcinosis cutis universalis, tumoral calcinosis, and transplant-associated calcinosis cutis.[1]

Pathophysiology

In all cases of calcinosis cutis, insoluble compounds of calcium are deposited within the skin as a consequence of local or systemic factors. These calcium salts consist primarily of hydroxyapatite crystals or amorphous calcium phosphate. The pathogenesis of calcinosis cutis is not completely understood, and the variety of contributing factors allows different clinical scenarios to occur.

Metabolic and physical factors are pivotal in the development of most cases of calcinosis. Ectopic calcification can occur in the setting of hypercalcemia or hyperphosphatemia when the calcium-phosphate product exceeds 70 mg2/dL2, without preceding tissue damage. These elevated extracellular levels may result in increased intracellular levels, calcium-phosphate nucleation, and crystalline precipitation.

Alternatively, damaged tissue may allow an influx of calcium ions, which leads to an elevated intracellular calcium level and subsequent crystalline precipitation. Tissue damage also may result in denatured proteins that preferentially bind phosphate. Calcium then reacts with bound phosphate ions, resulting in precipitation of calcium phosphate.

Etiology

Disorders of calcinosis cutis may be categorized according to the type of calcification process involved (ie, dystrophic, metastatic, iatrogenic, or idiopathic). Dystrophic calcification, the most common type, occurs in the setting of normal serum calcium and phosphate levels. The primary abnormality is damaged, inflamed, neoplastic, or necrotic skin. Tissue damage may be from mechanical, chemical, infectious, or other insults.

Dystrophic calcification: localized tissue damage

Extraosseal calcification can occur in the setting of many local and destructive processes, including (but not limited to) burns, arthropod bites, acne lesions, varicose veins, and rhabdomyolysis.

Infections

Necrotic tissue produced by an infectious process may subsequently become calcified. Some infectious granulomas produce 1,25-vitamin D. Infections that may result in calcinosis cutis include onchocerciasis, cysticercosis, histoplasmosis, cryptococcosis, and intrauterine herpes simplex.

Tumors

Benign and malignant tumors may develop calcification. Pilomatrixoma, or calcifying epithelioma of Malherbe, is the most common tumor that becomes calcified. Epithelial cysts and syringomas also have a significant tendency to calcify. Foci of calcification commonly are seen in histologic sections of basal cell carcinomas. In rare cases, melanocytic nevi, malignant melanomas, atypical fibroxanthomas, hemangiomas, pyogenic granulomas, seborrheic keratoses, neurilemmomas, and trichoepitheliomas show foci of calcification.

Dystrophic calcification: generalized tissue damage

Connective-tissue diseases

Examples are dermatomyositis[2, 3] ; lupus erythematosus[4, 5, 6, 7] ; systemic sclerosis; and CREST (calcinosis, Raynaud phenomenon, esophageal dysfunction, sclerodactyly, telangiectasia) syndrome.

Calcification occurs three times more commonly in the juvenile form of dermatomyositis than in the adult-onset form and may be seen in 30-40% of patients. In the setting of dermatomyositis, calcinosis cutis is associated with longer disease duration, fingertip ulcers, and NXP-2 autoantibodies. There is a negative association with transcriptional intermediary factor 1-γ antibodies.[8] Typically, calcification is accentuated over joints, sparing the digits. Aggressive corticosteroid therapy decreases the incidence of calcification.

In lupus erythematosus, calcification is rare and is usually an insignificant incidental radiologic finding. It occurs most frequently with long-standing systemic disease. Although calcification may develop in lesions of lupus profundus, it usually is not associated with panniculitis; however, an associated myositis may be present. Lesions characteristically are on the extremities.

Systemic sclerosis and CREST syndrome are related diseases frequently associated with the late development of tissue calcification.

Panniculitis

Subcutaneous fat necrosis of the newborn typically affects full- or post-term newborns within the first few days to weeks of life. Necrosis of subcutaneous tissues, predominantly on the shoulders and buttocks, results in nodules and plaques that may become calcified. The cause is unknown. Possible inciting events include obstetric trauma, maternal preeclampsia or diabetes, and neonatal hypothermia or hypoxia. Pancreatitis or pancreatic malignancy may result in inflammation of the panniculus. The combination of fatty acids released by damaged fat cells and calcium may lead to calcium salt formation.

Inherited disorders

Examples are Ehlers-Danlos syndrome, Werner syndrome, pseudoxanthoma elasticum, and Rothmund-Thompson syndrome.

Ehlers-Danlos syndrome is a group of inherited disorders of collagen metabolism. Individuals with Ehlers-Danlos type I may develop calcification in healing surgical scars and subcutaneous nodules.

Werner syndrome is an inherited disorder of premature aging. Soft tissue calcification may involve the ligaments, tendons, synovia, vasculature, and/or subcutaneous tissue.

Pseudoxanthoma elasticum is a disorder of abnormal elastic fibers. Calcification occurs in the elastic fibers, causing rupture. Late in the disease, collagen fibers may become calcified.

In Rothmund-Thomson syndrome, small yellow papules of calcification may be numerous on the extremities.

Metastatic calcification

Metastatic calcification arises in the setting of abnormal calcium or phosphate metabolism and is generally associated with hypercalcemia or hyperphosphatemia.

Primary or secondary hyperparathyroidism

In primary hyperparathyroidism, the parathyroid glands become hyperplastic and autonomously overproduce parathyroid hormone (PTH). Secondary hyperparathyroidism is a functional response to hypocalcemia. The causes of hypocalcemia may be numerous, but the most common cause is chronic kidney disease (CKD; or chronic renal failure [CRF]).

Paraneoplastic hypercalcemia

Hypercalcemia may occur as part of a malignancy syndrome due to bony metastases or the production of an abnormal hormone that directly affects calcium and bone metabolism.

Destructive bone disease

Malignancy and other conditions, such as Paget disease, may induce enough bone destruction to cause hypercalcemia.

Milk-alkali syndrome

Uncommon today, this syndrome is caused by excessive consumption of sodium bicarbonate and calcium-containing compounds. The result is a metabolic alkalosis with hypercalcemia, hyperphosphatemia, nephrocalcinosis, and renal failure.

Excessive vitamin D

Overconsumption of vitamin D may increase gastrointestinal (GI) calcium absorption, as well as renal calcium reabsorption, giving rise to hypercalcemia. This mechanism is relatively uncommon.

Sarcoidosis

The sarcoidal granuloma may overproduce 1,25-vitamin D, with subsequent hypercalcemia and an elevated calcium-phosphate product.

Chronic kidney disease

This is the most common setting in which metastatic calcification occurs. CKD affects many factors in calcium metabolism. Hyperphosphatemia due to decreased renal clearance occurs relatively early. Hypocalcemia is the direct result of this hyperphosphatemia and worsened by vitamin D deficiency due to renal failure. As a compensatory measure, excessive PTH is produced. This augmentation results in increased calcium and phosphate mobilization; an elevated solubility product; and, subsequently, the formation and precipitation of calcium salts.

Calciphylaxis

Calciphylaxis is a poorly understood, highly morbid process that most commonly affects patients with end-stage renal disease (ESRD). Calcification occurs in the intima of the blood vessels and subcutaneous tissue. Microthrombi formation is a frequent finding. The exact mechanism remains unknown, but the most common unifying disorders are renal failure, hypercalcemia, hyperphosphatemia, and hyperparathyroidism.

Iatrogenic calcification

Iatrogenic calcinosis cutis arises secondary to a treatment or procedure.[9, 10, 11, 12]

Parenteral administration of calcium or phosphate

Intravenous (IV) administration of solutions containing calcium or phosphate may cause the precipitation of calcium salts and lead to calcification.

Parental inorganic phosphate

This has been implicated in the development of iatrogenic calcification.

Tumor lysis syndrome

Cutaneous calcification associated with tumor lysis syndrome is due to several factors, including chemotherapy-induced tissue damage with resultant hyperphosphatemia, hypocalcemia, hyperuricemia, and the potential for acute kidney injury (AKI; or acute renal failure [ARF]). Hypocalcemia frequently requires parenteral calcium use, increasing the possibility of tissue calcification.

Repeated heel sticks in the newborn

Calcium salt deposition may occur in newborns at sites of repeated heel sticks.

Prolonged use of calcium-containing electrode paste

Prolonged placement of electrode pastes containing calcium on abraded skin in diagnostic procedures such as electroencephalography (EEG), electromyography (EMG), or brainstem auditory evoked potential testing may result in calcium deposition at the placement site.

Idiopathic calcification

Idiopathic calcinosis cutis occurs in the absence of known tissue injury or systemic metabolic defect.

Idiopathic calcinosis of scrotum, penis, or vulva

Calcification may occur after trauma, or it may occur in the absence of known tissue injury. Calcinosis cutis of the penis may also result from calcification of an epidermal cyst.

Milialike idiopathic calcinosis cutis

Many cases have been associated with Down syndrome and/or syringoma formation.[13, 14, 15, 16] Lesions are usually multiple and occur on the trunk, limbs, and face. The etiology remains controversial, but some evidence of calcium deposition in the sweat glands is present.

Subepidermal calcified nodule

This lesion usually develops in early childhood and is typically solitary, though multiple lesions can also be present. The nodule most commonly occurs on the face, though it may occur anywhere. The pathogenesis is unknown, but the lesion may be due to calcification of components of adnexal structures.

Tumoral calcinosis

This may be caused by an error in renal phosphate metabolism that results in hyperphosphatemia. General characteristics of the calcified nodules are as follows:

The most common locations of calcification are the hip, elbow, scapula, foot, leg, knee, and hand. Tumoral calcinosis is often familial, and the hereditary pattern suggests that it is an autosomal recessive trait. Vitamin D deficiency may also be associated with hyperphosphatemia.

Calcinosis cutis circumscripta and calcinosis universalis

These forms are rare and may be due to altered ground substances. Calcinosis cutis circumscripta generally occurs earlier and tends to involve the extremities, whereas calcinosis universalis occurs later and is usually more widespread. Both have been associated with trauma, foreign body reaction, and (on occasion) scleroderma.

Transplant-associated calcinosis cutis

In addition to calciphylaxis, numerous cases of calcinosis cutis have been described in transplant recipients.[17, 18, 19] Although calcinosis cutis appears to be most common after renal transplantation, it is also described in liver, heart, and lung transplantation. The etiology of this calcification is unknown. Perhaps patients are infused with large numbers of blood products containing citrate and calcium that create an environment favoring calcification. The roles of other factors remain to be elucidated.

Epidemiology

Dystrophic calcinosis cutis is the most common type. Specific incidence and frequency data are generally unavailable. A study from Hungary cited a prevalence of 6.67% in patients with connective-tissue diseases (most frequently systemic sclerosis).[20]

Subepidermal calcified nodules are more common in children. Calcinosis cutis circumscripta tends to arise in the second half of life. Calcinosis cutis universalis occurs in the second decade of life. Tumoral calcinosis usually arises in the first or second decade of life.

No sex predilection is documented.

Tumoral calcinosis is more common in Blacks of South African heritage.

Prognosis

The prognosis is determined by that of any underlying disease. Calcinosis cutis alone usually is benign. Severe complications are infrequent. Morbidity, when present, is related to the size and location of the calcification.

Lesions may become painful, limit mobility of an adjacent joint, or compress adjacent neural structures. Ulceration and secondary infection may occur. Vascular calcification may result in ischemia and necrosis of the affected organ.

History

Most lesions of calcinosis cutis develop gradually and are asymptomatic. However, the history and evolution of the lesions depend on the etiology of the calcification. Patients with dystrophic calcification may provide a history of an underlying disease, a preexisting dermal nodule (which represents a tumor), or an inciting traumatic event. Patients with metastatic calcification most frequently have a history of chronic kidney disease (CKD; or chronic renal failure [CRF]). Those who develop iatrogenic calcinosis cutis generally have a history of recent hospitalization. Cases of idiopathic calcinosis cutis usually are not associated with previous trauma or disease.  

Physical Examination

The clinical presentation of calcinosis cutis can vary according to the diagnosis and underlying process. In general, multiple, firm, whitish dermal papules, plaques, nodules, or subcutaneous nodules are found in a distribution characteristic for the specific disorder. (See the first image below.) At times, these lesions may be studded with a yellow-white, gritty substance. Not infrequently, the lesions spontaneously ulcerate, extruding a chalky, white material. (See the second image below.) Most lesions are asymptomatic, though some may be tender, and others may restrict joint mobility. When severe, vascular calcification can cause diminished pulses and cutaneous gangrene.



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Calcinosis cutis appearing as indurated and nodular subcutaneous plaque in patient with systemic lupus erythematosus.



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Ulceration of lesion of calcinosis cutis in patient with systemic lupus erythematosus.

The major types of calcinosis cutis have varying manifestations, as follows:

Complications

Complications of calcinosis cutis include pain, cosmetic disfigurement, ulceration, and mechanical compromise.

The plaques or nodules may impinge on adjacent structures such as joints, resulting in restricted mobility, and nerves, resulting in pain or paresthesia. Destruction of synovial tissue also may result. Vascular occlusion may result in gangrene. Ulceration may be complicated by bacterial infection.

Laboratory Studies

Serum calcium, inorganic phosphate, alkaline phosphatase (ALP), and albumin levels may be helpful. An elevation in serum calcium and ALP levels with a decrease in the inorganic phosphate level is suggestive of hyperparathyroidism. One can further calculate the calcium-phosphate product to determine if the threshold of 70 mg2/dL2 is exceeded. An albumin value is needed to interpret the significance of hypocalcemia or hypercalcemia. Calcium is highly protein-bound, and abnormalities in the albumin concentration may cause clinically insignificant abnormalities of calcium concentration.

The following should also be considered:

Imaging Studies

Radiographic examination may demonstrate the extent of tissue calcification.

Ultrasonography (US) may permit a more precise assessment of the location and size of the mass and its relation to the surrounding tissues. A combination of radiography with US may prove sufficient for diagnosis, though additional imaging (eg, computed tomography [CT] or magnetic resonance imaging [MRI]) may be necessary for masses that are large and in deep locations.[22]

CT allows identification of visceral and nonvisceral calcification. It is infrequently used in evaluating calcinosis cutis and is primarily used in assessing tumoral calcinosis.

MRI is of limited utility in evaluating calcified structures, but calcific deposits have characteristic patterns. The granulomatous foreign body reaction in tumoral calcinosis is evident.

Bone scintigraphy with radiolabeled phosphate compounds (technetium Tc 99m methylene diphosphonate [MDP]) is useful in evaluating nonvisceral soft-tissue calcification; it is more sensitive than plain radiography.[23, 24]

Procedures

Findings on biopsy and histopathologic examination of a cutaneous lesion are diagnostic.

Results of fine-needle aspiration (FNA) cytology of a skin nodule may also be diagnostic.

Histologic Findings

On biopsy, granules and deposits of calcium are seen in the dermis, with or without a surrounding foreign-body giant cell reaction. Alternatively, massive calcium deposits may be located in the subcutaneous tissue. In areas of necrosis, calcium deposition is frequently found within the walls of small and medium-sized blood vessels. Calcium deposition may be confirmed on Von Kossa and alizarin red stains.

Medical Care

Medical therapy for calcinosis cutis is limited and of variable benefit. When the underlying problem is identified, it should be corrected.[25, 26]

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 other bisphosphonates may reduce bone turnover and inhibit the growth of ectopic hydroxyapatite crystals. However, prolonged treatment is necessary, and paradoxical hyperphosphatemia may result. A retrospective study by Rauch et al reported objectively beneficial effects of pamidronate in approximately half of the cases examined.[27]

Myoinositol hexaphosphate is a dietary substance shown to inhibit the crystallization of calcium salts. Animal studies demonstrated a reduction in calcinosis cutis lesions with topical myoinositol hexaphosphate, suggesting a potential benefit in humans.[28, 29]

Warfarin has shown benefit in some. Low-dose warfarin should not be used, in that no benefit has been established.[30]

Rituximab and tumor necrosis factor (TNF) inhibitors may be beneficial alternatives in patients with dermatomyositis.[30]

The use of the calcium-channel blocker diltiazem over at least 5 years has shown variable benefits. The therapeutic effect is believed to be the antagonism of the calcium-sodium ion pump.[31, 32, 33]

Use of intravenous (IV) sodium thiosulfate should be considered, on the grounds that it has been shown to be effective in many cases of calciphylaxis. This would be regarded as off-label and experimental therapy.[34]  Reports have suggested that ulcerative calcinosis cutis and tumoral calcinosis may respond to topical or intralesional sodium thiosulfate 25%.[35, 36, 37, 38]  

In a case series (N = 5) by Bruns et al, IV sodium thiosulfate was used to treat dystrophic calcinosis cutis; although a reduction in calcified lesions could not be definitively established, the disease was stabilized.[39]  In a retrospective study (N = 7) by Robert et al, partial responses to systemic (IV or oral) sodium thiosulfate was noted in four of the seven patients; although no complete responses were recorded, reductions in pain, ulceration, and frequency of inflammation were noted, and further progression of disease was prevented in the four responders.[40]

Minocycline may be another treatment option. In a study by Robertson et al, nine patients with cutaneous calcification associated with limited systemic sclerosis were treated with 50-100 mg/day of minocycline.[41] In eight of the nine, improvement was noted within 1-7 months. Although lesional size was only moderately improved, ulceration and inflammation were markedly reduced.

Theoretically, in extraordinarily severe cases of calcinosis cutis, associated with one of several connective-tissue diseases, autologous hematopoietic stem cell transplantation (HSCT) may be considered. Risks and benefits must be thoroughly investigated, but some studies have suggested remission of some connective-tissue diseases with HSCT, which, in theory, should help with calcinosis cutis.[42]

Surgical Care

Indications for surgical removal include pain, recurrent infection, ulceration, and functional impairment. Because surgical trauma may stimulate calcification, a test site should be treated before the decision is made to pursue a large excision. Recurrence is common after excision.

Extracorporeal shockwave lithotripsy (ESWL) has been anecdotally successful in treating calcinosis cutis associated with dermatomyositis, as well as venous insufficiency and scleroderma.[43, 44, 45]  In one example, only minimal reduction in the size of the calcification was achieved, but the associated pain was completely relieved; in another, near-complete resolution of calcium deposition was achieved. The physiology underlying the effect of ESWL on calcinosis is unknown.

Diet

Dietary alteration is of minor benefit in most cases. However, the following changes may be tried:

Activity

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

Prevention

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

Consultations

A nephrologist, a rheumatologist, a hematologist, or some combination thereof should be consulted, as indicated by the underlying disease.

Medication Summary

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

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

Clinical Context:  Aluminum hydroxide is an effective phosphate binder; it is not considered first-line therapy because of its potential for toxicity.

Magnesium oxide (Maox, Mag-ox)

Clinical Context:  Magnesium oxide treats magnesium deficiencies or magnesium depletion due to malnutrition, restricted diet, alcoholism, or magnesium-depleting drugs.

Class Summary

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

Etidronate disodium (Didronel)

Clinical Context:  Etidronate disodium reduces bone formation and does not alter renal tubular reabsorption of calcium. It does not affect hypercalcemia in patients with hyperparathyroidism.

Class Summary

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.

Diltiazem hydrochloride (Cardizem)

Clinical Context:  Diltiazem hydrochloride is used for the management of angina, supraventricular tachycardia, and hypertension. During depolarization, it inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

Class Summary

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

Cinacalcet (Sensipar)

Clinical Context:  Cinacalcet directly lowers parathyroid hormone (PTH) levels by increasing the sensitivity of the calcium-sensing receptor on the chief cell of the parathyroid gland to extracellular calcium. This also results in concomitant serum calcium decrease.

Class Summary

These agents lower PTH levels by increasing sensitivity of calcium-sensing receptor on chief cell of parathyroid gland to extracellular calcium. Serum calcium also decreases.

What is calcinosis cutis?What is the pathophysiology of calcinosis cutis?How are the causes of calcinosis cutis classified?What is dystrophic calcinosis cutis?What causes localized tissue damage in dystrophic calcinosis cutis?What causes necrotic tissue damage in dystrophic calcinosis cutis?Which tumors that may result in dystrophic calcinosis cutis?What is the role of connective tissue diseases in the etiology of calcinosis cutis?What is the role of panniculitis in the etiology of calcinosis cutis?Which genetic disorders cause calcinosis cutis?What causes metastatic calcinosis cutis?What is the role of hyperparathyroidism in the etiology of calcinosis cutis?What is the role of paraneoplastic hypercalcemia in the etiology of calcinosis cutis?What causes bone destruction in calcinosis cutis?What is the role of milk-alkali syndrome in the etiology of calcinosis cutis?What is the role of vitamin D in the etiology of calcinosis cutis?What is the role of sarcoidosis in the etiology of calcinosis cutis?What is the role of chronic renal failure in the etiology of calcinosis cutis?What is the role of calciphylaxis in the etiology of calcinosis cutis?What causes idiopathic calcinosis cutis?What causes iatrogenic calcinosis cutis?What is the prevalence of calcinosis cutis?What is the racial predilection of calcinosis cutis?What is the sexual predilection of calcinosis cutis?Which age groups have the highest prevalence of calcinosis cutis?What is the prognosis of calcinosis cutis?What is included in patient education about calcinosis cutis?Which clinical history findings are characteristic of calcinosis cutis?Which physical findings are characteristic of calcinosis cutis?What are the possible complications of calcinosis cutis?Which conditions should be included in the differential diagnoses of calcinosis cutis?What are the differential diagnoses for Calcinosis Cutis?What is the role of lab testing in the workup of calcinosis cutis?What is the role of imaging studies in the workup of calcinosis cutis?What is the role of biopsy in the workup of calcinosis cutis?Which histologic findings are characteristic of calcinosis cutis?How is calcinosis cutis treated?What is the role of surgery in the treatment of calcinosis cutis?Which dietary modifications are used in the treatment of calcinosis cutis?Which activity modifications are beneficial for patients with calcinosis cutis?How is calcinosis cutis prevented?Which specialist consultations are beneficial to patients with calcinosis cutis?Which medications are used in the treatment of calcinosis cutis?Which medications in the drug class Calcimimetics are used in the treatment of Calcinosis Cutis?Which medications in the drug class Calcium-Channel Blockers are used in the treatment of Calcinosis Cutis?Which medications in the drug class Diphosphonates are used in the treatment of Calcinosis Cutis?Which medications in the drug class Antacids are used in the treatment of Calcinosis Cutis?

Author

Julia R Nunley, MD, Professor, Department of Dermatology, Virginia Commonwealth University Medical Center

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Board of Dermatology<br/>Author for: Up-to-date.

Specialty Editors

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Disclosure: Nothing to disclose.

Rosalie Elenitsas, MD, Herman Beerman Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System

Disclosure: Received royalty from Lippincott Williams Wilkins for textbook editor.

Chief Editor

Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

James W Patterson, MD, Professor of Pathology and Dermatology, Director of Dermatopathology, University of Virginia Medical Center

Disclosure: Nothing to disclose.

Acknowledgements

Lydia M E Jones, MD Staff Physician, Department of Dermatology, Virginia Commonwealth University

Disclosure: Nothing to disclose.

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Calcinosis cutis appearing as indurated and nodular subcutaneous plaque in patient with systemic lupus erythematosus.

Ulceration of lesion of calcinosis cutis in patient with systemic lupus erythematosus.

Calcinosis cutis appearing as indurated and nodular subcutaneous plaque in patient with systemic lupus erythematosus.

Ulceration of lesion of calcinosis cutis in patient with systemic lupus erythematosus.