Iatrogenic Hyperadrenocorticism, Calcinosis Cutis, and Myocardial Infarction in a Dog Treated for IMT

Abstract

An 8 yr old male English bulldog receiving treatment for immune-mediated thrombocytopenia was diagnosed with calcinosis cutis 90 days after initiation of corticosteroid therapy. Twenty-four days later, the patient presented in a comatose state after collapsing and was euthanized. Postmortem examination revealed coronary arteriosclerosis and myocardial infarction leading to congestive heart failure. Calcinosis cutis and myocardial necrosis were most likely complications associated with administration of corticosteroids in this dog. Important implications regarding the classification of calcinosis cutis and the use of immunosuppressive doses of corticosteroids are discussed.

Use of fluorescent light energy for the management of bacterial skin infection associated with canine calcinosis cutis lesions

“…Calcinosis cutis is a skin condition where mineral salts are deposited in the skin and one major cause is iatrogenic hypercortisolism 1–3. Secondary (superficial or deep) bacterial skin infection can occur 3.…”

Minocycline as a treatment of dog with calcinosis cutis

“…Calcification of the skin may occur in a wide variety of disorders. It is most commonly developed as a result of naturally occurring or iatrogenic hyperadrenocorticism (HAC) in dogs [4,12]. The mechanisms of calcification are divided into four categories: dystrophic, metastatic, iatrogenic and idiopathic [4].…”

“…It is most commonly developed as a result of naturally occurring or iatrogenic hyperadrenocorticism (HAC) in dogs [4,12]. The mechanisms of calcification are divided into four categories: dystrophic, metastatic, iatrogenic and idiopathic [4]. Dystrophic calcification is the most common type and it is associated with local tissue damage or disorders in collagenous, elastic, or subcutaneous tissue [8].…”

“…Metastatic calcification is related to the accumulation of calcium salts in normal tissue, associated with aberrant metabolism of calcium and phosphorus [6]. Iatrogenic calcification appears secondary to penetration of calcium containing products and idiopathic calcification is in the absence of identifiable local or systemic factors such as local tissue damage or metabolic disorders [4]. As dystrophic calcification commonly occurs in association with canine HAC that leads to calcinosis cutis [1], diagnoses on hematologic and biochemical profile present hypercortisolism with normal calcium and phosphorus levels typically found [4,5].…”

“…It is the specific type of dystrophic calcium deposits and occurs most commonly secondary to iatrogenic HAC [2,3]. It is probably caused by protein catabolic functions of cortisol which results in damage to the structure within collagen and elastin, predisposing calcium precipitation in the skin [4]. In addition, local tissue damage and necrosis increases cell membrane permeability, allowing cytosolic influx of sufficient calcium that exceeds the capacity of mitochondria.…”