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Dermatology Challege: Severe facial pruritus in a Boston terrier
The internal medicine service at the Veterinary Medical Teaching Hospital at the University of Wisconsin School of Veterinary Medicine requested a consultation on a 7-year-old intact male Boston terrier in which pituitary-dependent hyperadrenocorticism had been diagnosed one month earlier.
The internal medicine service at the Veterinary Medical Teaching Hospital at the University of Wisconsin School of Veterinary Medicine requested a consultation on a 7-year-old intact male Boston terrier in which pituitary-dependent hyperadrenocorticism (PDH) had been diagnosed one month earlier. At the time of the initial diagnosis, the dog had exhibited classic signs of hyperadrenocorticism, including calcinosis cutis on the dorsum. The laboratory test results (i.e. ACTH stimulation testing, low-dose dexamethasone suppression testing, and abdominal ultrasonography) confirmed the diagnosis.
At the time of dermatologic examination, the dog was receiving maintenance mitotane therapy and was being monitored with periodic ACTH stimulation tests. Both the owner and internists were pleased with the dog's response to mitotane therapy; however, severe facial pruritus of 10 days' duration had developed, prompting the consultation. Reviewing the dog's medical records and dermatologic history form and questioning the owner revealed that the dog had no history of pruritus or other skin diseases.
1. The skin in the dorsal scapular area of the dog in this case. Note the alopecic area, which was palpably hard.
Dermatologic examination revealed bilaterally symmetric hair loss on the trunk, mild generalized scaling, thin abdominal skin, comedones on the ventral abdomen and thorax, and diffuse areas of calcinosis cutis on the cranial dorsal trunk. The skin in these regions was hard and erythematous (Figure 1). Mild exudation was present on the lesions' margins. Bilateral hair loss, erythema, and an erythematous papular eruption were present on the face. Several focal areas of exudation were also noted. The facial skin felt thickened but was not palpably hard as were the areas of calcification on the dorsum. The inflammatory lesions on the dog's face were not present at the time of initial diagnosis one month earlier. The results of an otic examination were normal. Raised, hard erythematous plaques compatible with a clinical diagnosis of calcinosis cutis were present in the left inguinal region (Figure 2).
2. The skin in the dog inguinal region. Note the erythematous alopecic areas with well-demarcated borders. These areas were palpably hard.
This patient's primary dermatologic problem was facial pruritus. Atopy and food allergy are commonly associated with facial pruritus and would have been considered as differential diagnoses if the dog had had a prior history of skin disease. The differential diagnoses primarily were infections and infestations secondary to the immunosuppression associated with PDH: demodicosis, dermatophytosis, bacterial pyoderma, and Malassezia pyoderma. Drug reactions were also considered, but hard skin has not been reported as a clinical sign of a drug reaction. The thin skin, hair loss, calcinosis cutis, and scaling were most likely due to PDH.
To rule out demodicosis, numerous deep skin scrapings of the face and body were performed, and the results were negative. Ear swab cytology revealed mild ceruminous debris. A repeat otic examination again revealed a normal ear canal. Impression smears of the facial lesions showed a neutrophilic exudate with intracellular and extracellular cocci; Malassezia organisms were not seen, and the results of a bacterial culture of a ruptured papule were positive for Staphylococcus intermedius. The results of a Wood's lamp examination were negative. A toothbrush technique was used to obtain a sample from the face for fungal culture, and no pathogens were isolated from the culture. Skin biopsy samples were obtained from the face, dorsum, and inguinal region. Histologic examination of the trunk and inguinal lesions revealed large areas of hypereosinophilic, fragmented collagen fibers in the dermis (Figure 3). The pathologists reported that this finding is common in cases of calcinosis cutis. Histologic examination of the facial lesions revealed an ulcerated epidermis, mixed inflammatory infiltrate in the dermis, and small deposits of mineralization; a von Kossa's stain was positive for calcium.
3. A photomicrograph of dermis with calcinosis cutis. The dark hypereosinophilic areas represent dystrophic mineralization of collagen (hematoxylin-eosin; original magnification 400X).
The diagnoses were PDH with calcinosis cutis of the face, trunk, and inguinal area and a secondary bacterial infection. The presence of the neutrophilic exudate with cocci from the face was compatible with a secondary bacterial infection; the diagnosis of a bacterial infection was further supported by the results of culture and sensitivity testing of the papule. Two possible causes of the facial pruritus were considered most likely: a staphylococcal bacterial infection secondary to immunosuppression from the PDH or inflammation from the calcinosis cutis. The problem with the latter diagnosis was that at the original examination there was no mention of calcinosis cutis on the face and no evidence of pruritus at the two other sites of calcinosis cutis, the dorsal trunk and inguinal region.
The dog continued receiving maintenance mitotane therapy for the PDH. Cephalexin (30 mg/kg orally every 12 hours for 21 days) was prescribed along with daily bathing of the face with an antipruritic oatmeal shampoo. Patient reexamination was scheduled for three weeks later, but after only 10 days of antibiotic and topical therapy, the owner reported that the dog's pruritus had worsened and that the dog was mutilating its face (Figure 4). In addition, the dorsal and inguinal lesions were pruritic and self-traumatized. The pruritus had become so severe that the dog was not sleeping or eating. Patient reexamination revealed severe erythema, exudation, and ulceration and a white, gritty material extruding from the skin in these areas, particularly the face. It was suspected that the original and continuing cause of the dog's facial pruritus was resolving calcinosis cutis. (Samples of the gritty material were examined histologically and were confirmed to be calcium deposits.) Twice-daily whole-body hydrotherapy in tepid water was instituted at home until the dog was able to sleep comfortably and was not observed to mutilate itself (at least three weeks).
4. The lateral aspect of the dog's face after increasingly severe pruritus developed. Note the erythematous alopecic areas.
Treating the pruritus was difficult; it did not respond to antihistamines (neither hydroxyzine nor diphenhydramine 2 mg/kg orally every eight hours for seven to 10 days), essential fatty acids (Derm Caps—DVM Pharmaceuticals; 1 capsule/5 kg/day for 10 days), or hydrotherapy. Marked relief from the pruritus was obtained only after topical dimethyl sulfoxide (DMSO) and betamethasone were applied to the affected areas' margins in the evening after the second hydrotherapy. The DMSO and betamethasone were applied once a day for three weeks and then every other day for three weeks. An Elizabethan collar was not used because the owner did not permit it. The dog's pruritus decreased markedly over the next six weeks, and a marked decrease in the calcinosis cutis was noted. Complete resolution of the calcinosis cutis took six months, and after the initial six weeks of DMSO and betamethasone therapy, the owner used the mixture intermittently when lesions became pruritic. The addition of this topical treatment did not affect the therapy and monitoring of the PDH. The dog continued to do well while receiving maintenance mitotane therapy.
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.