Discussion

In my experience, resolving calcinosis cutis lesions often become pruritic. This is perplexing to clinicians because the pruritus from calcinosis cutis may develop before high cortisol concentrations (which usually decrease pruritus) are controlled or because the pruritus develops even while the dog is still clinically symptomatic from the PDH or while there is still evidence of disease in diagnostic test results (e.g. elevated liver enzyme activities). The pathophysiology of dystrophic calcification in dogs with naturally occurring or iatrogenic hypercortisolism is unknown. The cause of the pruritus is also unknown, but some clinicians and pathologists have suggested that it might be related to calcium extruding from the epidermis (i.e. transepidermal elimination).^1,2

Treating pruritus is difficult because it is often severe and nonresponsive to nonsteroidal drugs. It seems contrary to use any form of glucocorticoids in patients with calcinosis cutis because, more often than not, glucocorticoids were involved in the development of the hyperadrenocorticism (naturally occurring or iatrogenic). In this patient, applying the topical glucocorticoid provided relief from the pruritus and did not interfere with treatment. DMSO was used because of its anti-inflammatory effects and to enhance the absorption of the topical glucocorticoid. Topical glucocorticoids may not be appropriate for all patients, and other options should be explored first. Other successful treatments I have used to manage pruritic calcinosis cutis lesions include topical application of a low-dose triamcinolone spray, triamcinolone lotion or ointment, and, more recently, cyclosporine at a dosage of 5 mg/kg given orally once a day for 30 to 45 days or until the lesions have resolved. Keep in mind that calcinosis cutis will spontaneously resolve with appropriate treatment, but in patients experiencing severe pruritus, it may be necessary to provide humane relief from the discomfort.

Calcinosis cutis is most commonly associated with iatrogenic or naturally occurring hyperadrenocorticism.² Other causes of focal dystrophic calcification include calcinosis circumscripta, inflammatory lesions or foreign bodies, follicular cysts, and certain neoplastic lesions (e.g. pilomatricoma).² Widespread dystrophic calcification can occur with diabetes mellitus, hyperadrenocorticism, and percutaneous calcium penetration. In my experience, and that of others, idiopathic calcinosis cutis may occur in young dogs secondary to severe systemic illness.¹ The important take-home messages from this case are that intense pruritus from calcinosis cutis can occur even when the classic dermatologic signs are not yet present and that calcinosis cutis can develop secondary to PDH after diagnosis.

The photographs and information for this case were provided by Karen A. Moriello, DVM, DACVD, Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706.

REFERENCES

1. Gross, T.L. et al.: Veterinary Dermatopathology: A Macroscopic and Microscopic Evaluation of Canine and Feline Skin Disease. Mosby-Year Book, St. Louis, Mo., 1992; pp 223-226.

2. Scott, D.W. et al.: Neoplastic and non-neoplastic tumors. Calcinosis cutis. Muller and Kirk's Small Animal Dermatology, 6th Ed. W.B. Saunders, Philadelphia, Pa., 2001; pp 1398-1399.