Zycortal Symposium Proceedings

syndrome). Histology of the adrenal glands revealed lymphocytic adrenalitis with complete destruction of the zona fasciculata and zona reticularis while the zona glomerulosa was preserved. Adissu et al 26 reported a case of a 4-year-old Great Pyrenees with hypothyroidism and hypoadrenocorticism with normal sodium and potassium concentrations. Histology revealed almost complete replacement of the zona fasciculata and reticularis by lymphocytes, plasma cells and macrophages, whereas the zona glomerulosa was spared. Frank et al 27 examined the adrenal glands of 33 dogs with adrenalitis or adrenocortical atrophy by means of histopathology. Three of the dogs had diffuse atrophy of the zona fasciculata and reticularis with segmental sparing of the zona glomerulosa. One of the dogs had normal sodium and potassium, one dog had hyponatremia and hyperkalaemia and in another one electrolyte concentrations are unknown. Friedenberg et al 28 characterised the lymphocytes within the adrenal glands in three dogs with “typical” and two dogs with “atypical” hypoadrenocorticism as being primarily CD4+. In one of the latter two dogs the intensity of the inflammation within the adrenal cortex was milder than in the other dogs, the different zones, however, were not specified. Buckley et al 29 described a 2-year-old German Shephard with “atypical” hypoadrenocorticism which was euthanised due to progressive weakness and neurological deficits. Post-mortem examination revealed intravascular lymphoma. In both adrenal glands the architecture of the zona fasciculata and zona reticularis was disrupted by blood vessels congested with neoplastic T-lymphocytes, whereas the zona glomerulosa was normal. Unfortunately, aldosterone had not been determined in any of those cases. It therefore remains unknown, if those with (partially spared) zona glomerulosa or mild inflammation had normal secretory function. Evaluation of aldosterone is not routinely included in the work-up of dogs with suspected hypoadrenocorticism. In dogs with confirmed “typical” hypoadrenocorticism it seems logical that not only the cortisol, but also the aldosterone, secretory capacity is affected. Until recently aldosterone concentrations had only been measured sporadically and it was therefore unknown if there are differences in aldosterone concentrations between dogs with mild, and dogs with severe, electrolyte abnormalities. We investigated aldosterone concentrations in 70 dogs with primary hypoadrenocorticism, in 22 dogs with diseases mimicking hypoadrenocorticism and in 19 healthy control dogs 3 . Sodium and potassium concentrations in the 70 dogs with hypoadrenocorticism ranged from normal (four dogs) to severely abnormal. Baseline and post- ACTH aldosterone concentrations were significantly lower in dogs with hypoadrenocorticism than in the other two groups of dogs. In 64/70 dogs with hypoadrenocorticism baseline and post-ACTH aldosterone concentrations were below the detection limit of the assay (RIA). In 6/70 dogs post-ACTH aldosterone was below or in the lower half of the reference interval, all six dogs had hyponatremia and 3/6 had additional hyperkalaemia. Interestingly, in all four dogs with “atypical” hypoadrenocorticism baseline and post-ACTH aldosterone concentrations were below the detection limit of the assay. After the study was published we measured baseline Aldosterone concentrations in dogs with ‘typical’ and ‘atypical’ hypoadrenocorticism

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