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Examinando G.G. A. Artículos por Autor "Ballut, Juan Carlos"
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Publicación Acceso abierto Diagnóstico de hiperadrenocorticismo adreno-dependiente en una perra poodle(2023-02-27) Arias Hernández, Alberto; Ballut, Juan CarlosCushing’s syndrome is the group of clinical signs caused by hyperadrenocorticism that affects medium to old age dogs, with a predilection in certain breeds and females. In 85% of naturally occurring cases, they are pituitary-dependent and only 15% have their origin in the adrenal glands. An 11.5-year-old Poodle was referred with an uncertain history of possible hyperadrenocorticism. Physical examination and paraclinical examinations revealed the following presumptive signs of hyperadrenocorticism: lethargy, abdominal distension, polydipsia/polyuria, panting, hyposthenuria, lymphopenia, elevated liver enzymes. Two hormonal tests were performed to assess the hypothalamus-hypophysis (or pituitary)- adrenal axis (HHA or HPA): low dose dexamethasone suppression test and measurement of endogenous corticotropic hormone (ACTH). Baseline serum cortisol was slightly elevated with a value of 8.52 µg / dL (normal = 1.8 - 6.0). Cortisol values at 4 and 8 hours post-dexamethasone administration were 2.46 and 6.91 µg/dL, respectively. These results showed a lack of suppression at 4 hours (with concentrations above 1.4 µg/dL) and 8 hours (concentrations >50% the baseline value). Furthermore, because cortisol values were 2.4 µg/dL at 4 hours post-administration of dexamethasone (exceeding the cut-off point of 1.4 µg/dL), the hyperadrenocorticism was not suggestive of pituitary origin but caused by tumor/s in the adrenal glands. The diagnosis was corroborated by an endogenous ACTH test, whose values were below the reference range: 10 pg/mL (15.0 - 60.0 pg/mL). In conclusion, the steps to follow in the diagnosis of hyperadrenocorticism begin with a good clinical and laboratory analysis before performing specific hormonal tests to assess the HPA axis. From the point of view of therapy, it is important to differentiate between hyperadrenocorticism of pituitary and adrenal origin.