What is hypoadrenocorticism, and how does primary ‘typical’ hypoadrenocorticism differ from primary ‘atypical’ hypoadrenocorticism?
Hypoadrenocorticism is a disorder resulting in clinically significant adrenocorticolysis. It is often from immune-mediated destruction of the adrenal cortex, occasionally from adrenal gland haemorrhage, neoplasia infiltration, or rarely granulomatous inflammation.
In the typical form of this disease, the destruction occurs at both zona glomerulosa and fasciculata, resulting in a reduced capacity to produce cortisol and aldosterone. In the atypical form, there is selective destruction of the zona fasciculata, so only reduced capacity of cortisol production is detected, and mineralocorticoid production is preserved.
What are the presenting signs for hypoadrenocorticism?
The presenting signs of hypoadrenocorticism are highly variable, often mimicking other illnesses such as intestinal or kidney disease. These dogs can present in an emergency with acute collapse, hypovolaemic and dehydration, but most often, they have a longer duration of intermittent non-specific clinical signs such as lethargy, weakness, reduced appetite, vomiting, or diarrhoea.
What are the clinicopathological changes for hypoadrenocorticism dogs?
In the typical hypoadrenocorticism dogs, the classic electrolytes abnormalities such as hyponatraemia and hypokalaemia, together with acidosis and azotaemia, are often identified. In contrast, electrolytes derangement is not seen in dogs with atypical hypoadrenocorticism because there is no reduction in mineralocorticoid production.
Cortisol deficiency alone causes more subtle clinicopathological changes that may be overlooked, such as the absence of stress leukogram, anaemia, eosinophilia, lymphocytosis, hypoalbuminaemia, hypoglycaemia and hypocholesteroraemia.
How is a hypoadrenocorticism case diagnosed?
The index of suspicion of hypoadrenocorticism is increased if resting cortisol is below 55 nmol/L. However, this does vary slightly between laboratories and the demonstration of minimal cortisol response to exogenous ACTH administration is required to confirm the diagnosis. Serum aldosterone is within the reference in dogs with atypical hypoadrenocorticism but is not routinely performed.
How do you treat or manage dogs with hypoadrenocorticism?
Intravenous fluid replacement is the single most important component of treatment to stabilise these dogs when they presented in an acute crisis. Glucocorticoid is usually supplemented using hydrocortisone intravenously until the patients start to eat, and then we switch them to oral glucocorticoid and mineralocorticoid supplementation for typical hypoadrenocorticism dogs. Even though mineralocorticoid supplementation is not necessary for patients with atypical hypoadrenocorticism at the time of diagnosis, it is recommended that electrolytes be monitored every three months because some dogs develop mineralocorticoid deficiency in a couple of months after the initial diagnosis.
How common is atypical hypoadrenocorticism?
In the early studies, most of the reported hypoadrenocorticism cases are dogs with the typical form. However, more and more dogs are recognised to have the atypical form of this disease in recent years. In the latest study, nearly half of the population of hypoadrenocorticism dogs were diagnosed with atypical hypoadrenocorticism. This is likely due to increasing clinician awareness of the disease rather than increased prevalence of the disease in the population. So, watch out for this great pretender and make sure you do not let it falls through the cracks!