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.
In this case, early lesions of calcinosis cutis were not obvious (i.e. hard, firm nodules) at examination but were most likely present in the skin of the face. It is interesting to note that
the pruritus started and was most severe in the areas with minimal calcification. The reason for this is unknown.
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.
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.