P.R.G. Monteiro; B.M.P. Coelho; K.K. Kanayama; D.M.N. Simões; V.A.B.F. Wirthl; M.M. Kogika
Hypoadrenocorticism results from reduced production of glucocorticoids and mineralocorticoids by adrenal cortex. The disease is relatively rare and it is classified as spontaneous (primary and secondary) and iatrogenic (adrenalectomy or use of mitotane). The disease is more commonly observed in young to middle age bitches. Poodle seems to be predisposed to develop the disease and it is linked to autosomal recessive genes. The clinical signs are nonspecific, acute or chronic. The electrolyte disorders are marked. The prognosis is good when the diagnosis and treatment are early established to avoid metabolic crisis. The present study evaluated 34 dogs of various breeds, presenting spontaneous or iatrogenic (secondary to the use of mitotane) hypoadrenocorticism, aging from 2 to 12 y-old (mean of 5.6 years). The diagnosis was based on clinical and laboratory findings, and confirmed by ACTH stimulation test. The cases were assisted at Small Animal Internal Medicine Service, Veterinary Teaching Hospital, FMVZ/USP, from 1996 to 2008. Spontaneous hypoadrenocorticism was detected in 26 dogs and iatrogenic in 8 cases. Regarding to breeds, 67.6% of the dogs were purebred (n=23); among the breeds, poodle (52.2%) was more frequent, followed by Teckel (8.7%), Maltese (8.7%) and other breeds represented by White Shepherd, Cocker Spaniel, Pointer, Fox Paulistinha, Pit Bull, Yorkshire and Samoyed (4.3% each one). Mongrel dogs were observed in 32.4%. Females and males were represented in 23 (67.6%) and 11 cases (32.4%), respectively. The most frequent clinical signs observed were lethargy (84.4%), vomiting (84.4%), bradycardia (48.4%), dysorexia (46.9%), dehydration (45.2%), hypothermia (41.9%), anorexia (40.6%) and polyuria and polydipsia (15.6%). Laboratory abnormalities more common were: increase of serum urea (96%), acidosis (87.5%), sodium-potassium ratio < 27 (86.7%), hyponatremia (80%), hyperkalemia (78.8%), hypoglycemia (69.6%) and increase of serum creatinine (53.8%). Laboratories exams were not performed in all dogs, except ACTH stimulation test. Treatment was based on fluid, glucose and steroids. Twenty-two of 34 dogs were evaluated as the disease progressed during the period of 2 to 108 months, and were stable, under treatment. Six of 34 dogs died and it was not related to the disease. The findings suggest that main clinical signs are not specific for the disease, and symptoms related to gastrointestinal and urinary systems should be considered in the differential diagnosis, mainly when it is associated with azotemia.