Calcinosis cutis is skin disorder that forms calcium deposits in the skin. It involves calcium salt deposits in skin and tissues.
Calcinosis cutis is classified into the four types as:
Dystrophic
Metastatic
Iatrogenic
Idiopathic
Dystrophic is common type occurs with normal calcium and phosphate levels that arises in damaged or inflamed tissue from trauma or infection.
Metastatic calcinosis cutis arises from abnormal calcium/phosphate metabolism disorders. Iatrogenic calcinosis cutis arises from medical treatments.
Some rare forms are classified as dystrophic or idiopathic including various types of calcinosis cutis.
Calcinosis cutis pathogenesis remains unclear with various factors leading to different clinical scenarios.
In all cases of calcinosis cutis, insoluble compounds of calcium are deposited within the skin because of local or systemic factors.
Epidemiology
Incidence and frequency data are scarce while Hungary study reported 6.67% prevalence in patients.
Subepidermal calcified nodules are common in children as calcinosis occurs later in life. Calcinosis cutis universalis appears in the second decade and tumoral calcinosis in the first.
No sex preference mentioned. Tumoral calcinosis prevalent in South Africans.
Anatomy
Pathophysiology
Metabolic and physical factors are crucial for calcinosis development with ectopic calcification arising in hypercalcemia or hyperphosphatemia exceeding 70 mg²/dL².
Elevated extracellular levels may increase intracellular calcium-phosphate precipitation. Damaged tissue allows calcium influx to cause elevated intracellular levels and crystalline precipitation.
Tissue damage causes proteins to bind phosphate preferentially. Calcium reacts with phosphate forms calcium phosphate precipitation.
Oxidative stress in diseases accelerates tissue damage and calcification. Vessels calcify from hyperphosphatemia and hyperparathyroidism.
Prognosis depends on underlying disease where calcinosis cutis is usually benign.
Complications are rare but morbidity depends on calcification size and location.
Lesions cause pain, restrict mobility, or compress nerves. Ulceration and infection may lead to ischemia and organ necrosis.
Clinical History
Clinical History:
Collect details including presenting symptoms, family and medical history to understand clinical history of patient.
Physical Examination
Skin examination
Systemic examination
Joint and soft tissue examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Calcifications in the skin, joints, or soft tissues, slowly developing hard, subcutaneous nodules or plaques.
Differential Diagnoses
Milia
Genital Warts
Molluscum Contagiosum
Osteoma Cutis
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Calcinosis cutis treatment is limited to address the underlying issue is essential for improvement.
Intralesional corticosteroids reduce inflammation and fibroblast activity effectively.
Magnesium or aluminium antacids effectively bind phosphate in hyperphosphatemia.
Sodium etidronate and bisphosphonates inhibit bone turnover and crystal growth.
Myo-inositol hexaphosphate inhibits calcium salt crystallization.
Diltiazem use over 5 years shows variable benefits in patients. IV sodium thiosulfate stabilized dystrophic calcinosis cutis but did not definitively reduce calcified lesions.
Surgical removal is indicated for pain, recurrent infection, ulceration, or functional impairment while pre-operative treatment is advised due to potential calcification and recurrence risks.
Extracorporeal shockwave lithotripsy (ESWL) shows anecdotal success in treating calcinosis cutis, venous insufficiency, and scleroderma.
use-of-phases-in-managing-calcinosis-cutis
In the acute diagnosis phase, the focus is to control symptoms and manage complications.
Pharmacologic therapy is effective in the treatment phase as it includes the use of antacids, diphosphonates, calcium-channel blockers, and calcium-channel blockers, and calcimimetics.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional therapies.
The regular follow-up visits with the dermatologist are scheduled to check the improvement of patients along with treatment response.
Calcinosis cutis is skin disorder that forms calcium deposits in the skin. It involves calcium salt deposits in skin and tissues.
Calcinosis cutis is classified into the four types as:
Dystrophic
Metastatic
Iatrogenic
Idiopathic
Dystrophic is common type occurs with normal calcium and phosphate levels that arises in damaged or inflamed tissue from trauma or infection.
Metastatic calcinosis cutis arises from abnormal calcium/phosphate metabolism disorders. Iatrogenic calcinosis cutis arises from medical treatments.
Some rare forms are classified as dystrophic or idiopathic including various types of calcinosis cutis.
Calcinosis cutis pathogenesis remains unclear with various factors leading to different clinical scenarios.
In all cases of calcinosis cutis, insoluble compounds of calcium are deposited within the skin because of local or systemic factors.
Incidence and frequency data are scarce while Hungary study reported 6.67% prevalence in patients.
Subepidermal calcified nodules are common in children as calcinosis occurs later in life. Calcinosis cutis universalis appears in the second decade and tumoral calcinosis in the first.
No sex preference mentioned. Tumoral calcinosis prevalent in South Africans.
Metabolic and physical factors are crucial for calcinosis development with ectopic calcification arising in hypercalcemia or hyperphosphatemia exceeding 70 mg²/dL².
Elevated extracellular levels may increase intracellular calcium-phosphate precipitation. Damaged tissue allows calcium influx to cause elevated intracellular levels and crystalline precipitation.
Tissue damage causes proteins to bind phosphate preferentially. Calcium reacts with phosphate forms calcium phosphate precipitation.
Oxidative stress in diseases accelerates tissue damage and calcification. Vessels calcify from hyperphosphatemia and hyperparathyroidism.
Prognosis depends on underlying disease where calcinosis cutis is usually benign.
Complications are rare but morbidity depends on calcification size and location.
Lesions cause pain, restrict mobility, or compress nerves. Ulceration and infection may lead to ischemia and organ necrosis.
Clinical History:
Collect details including presenting symptoms, family and medical history to understand clinical history of patient.
Skin examination
Systemic examination
Joint and soft tissue examination
Calcifications in the skin, joints, or soft tissues, slowly developing hard, subcutaneous nodules or plaques.
Milia
Genital Warts
Molluscum Contagiosum
Osteoma Cutis
Calcinosis cutis treatment is limited to address the underlying issue is essential for improvement.
Intralesional corticosteroids reduce inflammation and fibroblast activity effectively.
Magnesium or aluminium antacids effectively bind phosphate in hyperphosphatemia.
Sodium etidronate and bisphosphonates inhibit bone turnover and crystal growth.
Myo-inositol hexaphosphate inhibits calcium salt crystallization.
Diltiazem use over 5 years shows variable benefits in patients. IV sodium thiosulfate stabilized dystrophic calcinosis cutis but did not definitively reduce calcified lesions.
Dermatology, General
Wear protective cloths to minimize pressure and friction. Use mild skincare products to prevent skin irritation.
For ulcerated lesions, the area should be clean and dressed in non-adhesive.
Maintain adequate hydration to support skin health and improve tissue healing.
Avoid activities risking injury or irritation in weight-bearing areas.
Proper awareness about calcinosis cutis should be provided and its related causes with management strategies.
Appointments with a dermatologist and preventing recurrence of disorder is an ongoing life-long effort.
Dermatology, General
Aluminum hydroxide:
It is an effective phosphate binder, but it is not a first-line therapy drug due to potential toxicity risks.
Magnesium oxide:
It treats magnesium deficiencies or magnesium depletion due to malnutrition and alcoholism.
Dermatology, General
Etidronate disodium:
It reduces bone formation and does not alter renal tubular reabsorption of calcium.
Dermatology, General
Diltiazem hydrochloride:
It inhibits calcium ions from entering slow channels of vascular smooth muscle.
Dermatology, General
Cinacalcet:
It increases the sensitivity of the calcium receptor on the chief cell.
Dermatology, General
Surgical removal is indicated for pain, recurrent infection, ulceration, or functional impairment while pre-operative treatment is advised due to potential calcification and recurrence risks.
Extracorporeal shockwave lithotripsy (ESWL) shows anecdotal success in treating calcinosis cutis, venous insufficiency, and scleroderma.
Dermatology, General
In the acute diagnosis phase, the focus is to control symptoms and manage complications.
Pharmacologic therapy is effective in the treatment phase as it includes the use of antacids, diphosphonates, calcium-channel blockers, and calcium-channel blockers, and calcimimetics.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional therapies.
The regular follow-up visits with the dermatologist are scheduled to check the improvement of patients along with treatment response.
Calcinosis cutis is skin disorder that forms calcium deposits in the skin. It involves calcium salt deposits in skin and tissues.
Calcinosis cutis is classified into the four types as:
Dystrophic
Metastatic
Iatrogenic
Idiopathic
Dystrophic is common type occurs with normal calcium and phosphate levels that arises in damaged or inflamed tissue from trauma or infection.
Metastatic calcinosis cutis arises from abnormal calcium/phosphate metabolism disorders. Iatrogenic calcinosis cutis arises from medical treatments.
Some rare forms are classified as dystrophic or idiopathic including various types of calcinosis cutis.
Calcinosis cutis pathogenesis remains unclear with various factors leading to different clinical scenarios.
In all cases of calcinosis cutis, insoluble compounds of calcium are deposited within the skin because of local or systemic factors.
Incidence and frequency data are scarce while Hungary study reported 6.67% prevalence in patients.
Subepidermal calcified nodules are common in children as calcinosis occurs later in life. Calcinosis cutis universalis appears in the second decade and tumoral calcinosis in the first.
No sex preference mentioned. Tumoral calcinosis prevalent in South Africans.
Metabolic and physical factors are crucial for calcinosis development with ectopic calcification arising in hypercalcemia or hyperphosphatemia exceeding 70 mg²/dL².
Elevated extracellular levels may increase intracellular calcium-phosphate precipitation. Damaged tissue allows calcium influx to cause elevated intracellular levels and crystalline precipitation.
Tissue damage causes proteins to bind phosphate preferentially. Calcium reacts with phosphate forms calcium phosphate precipitation.
Oxidative stress in diseases accelerates tissue damage and calcification. Vessels calcify from hyperphosphatemia and hyperparathyroidism.
Prognosis depends on underlying disease where calcinosis cutis is usually benign.
Complications are rare but morbidity depends on calcification size and location.
Lesions cause pain, restrict mobility, or compress nerves. Ulceration and infection may lead to ischemia and organ necrosis.
Clinical History:
Collect details including presenting symptoms, family and medical history to understand clinical history of patient.
Skin examination
Systemic examination
Joint and soft tissue examination
Calcifications in the skin, joints, or soft tissues, slowly developing hard, subcutaneous nodules or plaques.
Milia
Genital Warts
Molluscum Contagiosum
Osteoma Cutis
Calcinosis cutis treatment is limited to address the underlying issue is essential for improvement.
Intralesional corticosteroids reduce inflammation and fibroblast activity effectively.
Magnesium or aluminium antacids effectively bind phosphate in hyperphosphatemia.
Sodium etidronate and bisphosphonates inhibit bone turnover and crystal growth.
Myo-inositol hexaphosphate inhibits calcium salt crystallization.
Diltiazem use over 5 years shows variable benefits in patients. IV sodium thiosulfate stabilized dystrophic calcinosis cutis but did not definitively reduce calcified lesions.
Dermatology, General
Wear protective cloths to minimize pressure and friction. Use mild skincare products to prevent skin irritation.
For ulcerated lesions, the area should be clean and dressed in non-adhesive.
Maintain adequate hydration to support skin health and improve tissue healing.
Avoid activities risking injury or irritation in weight-bearing areas.
Proper awareness about calcinosis cutis should be provided and its related causes with management strategies.
Appointments with a dermatologist and preventing recurrence of disorder is an ongoing life-long effort.
Dermatology, General
Aluminum hydroxide:
It is an effective phosphate binder, but it is not a first-line therapy drug due to potential toxicity risks.
Magnesium oxide:
It treats magnesium deficiencies or magnesium depletion due to malnutrition and alcoholism.
Dermatology, General
Etidronate disodium:
It reduces bone formation and does not alter renal tubular reabsorption of calcium.
Dermatology, General
Diltiazem hydrochloride:
It inhibits calcium ions from entering slow channels of vascular smooth muscle.
Dermatology, General
Cinacalcet:
It increases the sensitivity of the calcium receptor on the chief cell.
Dermatology, General
Surgical removal is indicated for pain, recurrent infection, ulceration, or functional impairment while pre-operative treatment is advised due to potential calcification and recurrence risks.
Extracorporeal shockwave lithotripsy (ESWL) shows anecdotal success in treating calcinosis cutis, venous insufficiency, and scleroderma.
Dermatology, General
In the acute diagnosis phase, the focus is to control symptoms and manage complications.
Pharmacologic therapy is effective in the treatment phase as it includes the use of antacids, diphosphonates, calcium-channel blockers, and calcium-channel blockers, and calcimimetics.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional therapies.
The regular follow-up visits with the dermatologist are scheduled to check the improvement of patients along with treatment response.
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