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roid cats are approximately 20% larger than healthy cats. Diabetes mellitus does not cause adrenal gland enlargement in cats, but acromegaly does. Computed tomography or magnetic resonance imaging (brain)
Approximately 50% of PDH cases are pituitary mac- roadenomas that can be detected using CT or MRI.
Treatment
Trilostane
Usually causes a reduction, but not resolution, of clinical signs and insulin doses if diabetic, as well as improved ACTH stimulation test results. Doses used for treatment of feline HAC range from 10 to 30 mg per cat orally SID to BID, however lower starting doses of 1-2mg/kg/day have been suggested more recently. A 2-4 h post-trilostane ACTH stimulation cortisol measurement of 50-150 nmol/L is recom- mended. Adverse effects include anorexia, lethargy, weight loss, pancreatitis and hypoadrenocorticism. Trilostane is mostly well tolerated and is the most efficacious drug currently available for treatment of feline HAC.
complications do not occur. For cats with pituitary macroadenomas, neurological signs usually improve after radiation, and some, but not all have improved signs of HAC after radiation therapy, and reduced insulin requirements or diabetic remission. Cats with diabetes mellitus may have reduced insulin requirements or diabetic remission if they respond to treatment for HAC.
Sex-steroid secreting adrenal tumours
Tumours may secrete one or more adrenal
sex steroids, e.g. progesterone, oestradiol
or testosterone, alone or in combination.
Typical clinical presentations include clinical signs of HAC, diabetes mellitus and behaviour change (aggression). Some adrenal tumours in cats co-secrete aldosterone and adrenal sex steroids, e.g. progesterone and aldosterone. These cats can present with clinical signs of
HAC as well as behaviour changes and signs
of hyperaldosteronism such as weakness and hypertension. Alternatively, overproduction of sex steroids can result in presentation with signs of oestrus or virilisation of neutered males e.g. urine spraying, aggression, skin thickening and penile spines.
Diagnosis
Diagnosis is on the basis of high basal and post- ACTH stimulation sex-hormone levels, detected on adrenal sex-steroid panels and adrenal imaging. Serum cortisol levels are usually low due to lack
of enzymes within the adrenal tumour to convert progesterone to cortisol, or hypothalamic–pituitary– adrenal axis suppression of cortisol by sex-steroids. Adrenalectomy of the neoplastic gland is curative with regression of clinical signs over weeks to months
References:
Boland L, Barrs VR. Peculiarities of Feline Hyperadrenocroticism. Journal of Feline Medicine and Surgery 2017, 19: 933-947. doi: 10.1177/1098612X17723245.
Niessen SJ, Church DB, Forcada Y. Hypersomatotropism, acromegaly, and hyperadrenocorticism and feline diabetes mellitus. Vet Clin North Am Small Anim Pract 2013;43:319- 350.
Mitotane
Not recommended for therapy since it is far less effective than trilostane, clinical signs often prog- ress and ACTH stimulation test results remain unchanged.
Adrenalectomy
Unilateral adrenalectomy is the treatment of choice for feline ADH. Bilateral adrenalectomy is curative for PDH but is associated with a relatively high com- plication rate due to poor wound healing, immuno- compromise and skin fragility.
Hypophysectomy
Microsurgical transsphenoidal hypophysectomy for PDH is an increasingly reported curative treatment for PDH. Complications included oronasal fistula, soft palate dehiscence, transient reduction in tear production and recurrence of HAC due to pituitary remnants.
Radiation
Radiation therapy for PDH generally involves multi- ple fractionated treatments. Availability of a gamma knife or a stereotactic capable linear accelerator can reduce this to a single treatment.
Prognosis
Trilostane is the medical treatment option with the longest reported survival times. Cure can be achieved with adrenalectomy or transsphenoidal hypophysectomy if immediate surgical
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