Calcinosis cutis


Calcinosis cutis

Description, Causes and Risk Factors:

ICD-10: L94.2.

Alternative Name: Dystrophic calcinosis.

Calcinosis cutis is the abnormal deposition of calcium in the skin. It usually consists of multiple lesions, which develop slowly and are often free of symptoms, appearing as firm, whitish-yellow papules, plaques or nodules on the skin. Over time, lesions may ulcerate and become tender, and affected persons may experience discharge of a whitish material consisting of varying forms of calcium.

Calcinosis cutis

Calcinosis cutis is classified into four subtypes: Dystrophic, metastatic, idiopathic, and iatrogenic.

Dystrophic calcinosis cutis occurs in an area where there is damaged, inflamed, neoplastic or necrotic skin. Tissue damage may be from mechanical, chemical, infectious or other factors. Normal serum calcium and phosphate levels exist. Conditions that can cause dystrophic calcinosis cutis may include:

    Trauma.

  • Acne.

  • Varicose veins.

  • Infections.

  • Tumours (pilomatrixoma, cysts, basal cell carcinomas and others).

  • Connective tissue disease (dermatomyositis, systemic sclerosis, cutaneous lupus erythematosus).

  • Panniculitis.

  • Inherited diseases of connective tissue (Ehlers-Danlos syndrome, Werner syndrome, Pseudoxanthoma elasticum, Rothmund-Thomson syndrome).

Metastatic calcinosis cutis occurs in the setting of abnormal calcium and phosphate metabolism and is often associated with hypercalcemia and/or hyperphosphatemia. Conditions that can cause metastatic calcinosis cutis may include:

    Primary or secondary hyperparathyroidism.

  • Paraneoplastic hypercalcemia.

  • Destructive bone disease, e.g. Paget disease.

  • Milk-alkali syndrome.

  • Excessive vitamin D intake.

  • Sarcoidosis.

  • Chronic renal failure.

  • Calciphylaxis.

Idiopathic calcinosis cutis generally occurs in the absence of any known tissue injury or systemic metabolic defect. Calcification is usually localized to one general area.

Iatrogenic calcinosis cutis arises secondary to a treatment or procedure, e.g. parenteral administration of calcium or phosphate, calcium deposition in newborns from repeated heel sticks.

Symptoms:

The signs and symptoms of calcinosis cutis vary according to the underlying cause.

    In many cases the lesions gradually develop and are often symptomless.The lesions usually appear as firm, whitish/yellowish papules, plaques or nodules on the surface of the skin.

  • Lesions may become tender and ulcerate, discharging chalk-like creamy material consisting mainly of calcium phosphate with a small amount of calcium carbonate.

  • Fingertip lesions may be painful, while lesions at other sites may restrict joint mobility and limit movement due to stiffening of the skin.

  • In severe cases cutaneous gangrene may occur.

Diagnosis:

Differential diagnosis may include:

    Milia.

  • Molluscum contagiosum.

  • Mycetoma.

  • Osteoma Cutis.

  • Genital warts.

  • Xanthomas.

Laboratory tests are performed to determine any metabolic abnormalities that may give rise to elevated calcium and phosphate levels. Radiological examinations including plain film x-ray, CT scanning and bone scintigraphy are useful in demonstrating the extent of tissue calcification.

Biopsy of cutaneous lesions is used to confirm diagnosis. On histology, granules and deposits of calcium are seen in the dermis, often with a surrounding foreign-body giant cell reaction. Calcium deposits may also be found in subcutaneous tissue.

Treatment:

In general, treatment of calcinosis remains a challenge. No controlled studies have yet succeeded in defining the ideal treatment. In addition to aluminum hydroxide and diltiazem, which have been used to treat the condition, various other compounds such as probenecid, warfarin, colchicine and the bisphosphonates have also been tried; however, results have been highly controversial.

Surgical removal of symptomatic lesions is considered as a last resort, since local trauma may stimulate calcification further, leading to a recurrence or exacerbation of the condition. Small, superficial lesions may be removed by CO2 laser.

Cyclosporine, intravenous immunoglobulin, tacrolimus and TNF-alpha inhibitors are some examples of promising possibilities for treatment that are currently undergoing evaluation. They are being used in patients with systemic autoimmune diseases of difficult control, and a reduction in secondary calcinosis has been achieved in some cases.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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