Case 4 - 180629-4

Eleven-year-old, female, spayed Portuguese water spaniel.

Euthanized for metastatic hemangiosarcoma. Diagnosed with atypical Addison’s previously.

The adrenal glands are 2 x 0.4 x 0.4 cm and 2.5 x 0.7 x 0.3 cm. On cut section the cortices are markedly narrower, limited to a thin rim, compared to the medulla.

This slide has two sections of adrenal gland, both of which are characterized by a markedly thinned adrenal cortex, which is limited to isolated islands of zona glomerulosa. Infiltrating the overlying adrenal capsule and occasionally within the glomerulosa are small numbers of lymphocytes and plasma cells. There are multifocal aggregates of cells with a cytoplasm distended with gold-gray pigment (presumed lipofuscin), which are along the corticomedullary junction and extend into the medulla.

N/A

Adrenal glands (bilateral): severe, diffuse, cortical atrophy with mild lymphoplasmacytic adrenalitis and lipofuscinosis

The histologic lesions of the adrenal gland in this case matched the clinical history of atypical Addison’s disease. With atypical Addison’s disease, there is a lack of glucocorticoid production but continued production of mineralocorticoids due to the sparing of the zona glomerulosa. The underlying cause and trigger leading to destruction of the adrenal cortex is generally unknown. However, it is speculated, at least in humans, to be triggered by a number of factors coupled with a genetic susceptibility. Participants brought up the point that we often don’t see affected organs until end-stage and thus there is no remaining evidence of ongoing destruction. This was compared to cases of diabetes mellitus in which all that is identified histologically is the absence of pancreatic islets.

H Eystein and K lovas. “Pathogenesis of primary adrenal insufficiency.” Best practice & research clinical endocrinology & metabolism. 2009. 23(2): 147-157.