Worldwide medical and scientific journal for animal health professionals

Issue number 31.2 Other Scientific

Canine hyperadrenocorticism

Published 04/11/2021

Written by Fiona Scholz and Sam Crothers

Also available in Français , Deutsch , Italiano and Español

Dogs with hyperadrenocorticism can often present with dermatological signs; this paper reviews the diagnosis and treatment of a common canine disease.

Generalised bilateral symmetrical alopecia of the trunk with consequent intense hyperpigmentation of the skin due to exposure to UV light.

Key points

Pituitary-dependent hyperadrenocorticism is the most common cause for spontaneously occurring hypercortisolism in dogs.


The clinical signs of hyperadrenocorticism are wide and varied, but the various cutaneous changes are often obvious and dramatic. 


A variety of diagnostic procedures can be performed, but it is important to also identify the origin of the hyperadrenocorticism to appropriately guide the management and therapeutic plan.


Treatment of hyperadrenocorticism should also encompass therapy for any intercurrent disorders in order to improve the patient’s quality of life.


Introduction

Canine hyperadrenocortisolism is a relatively common condition which may occur either spontaneously or via an iatrogenic route. The spontaneous etiologies include hypersecretion of endogenous glucocorticoids from a functional adrenal tumor or hypersecretion of corticotropin or corticotropin-like substances from an idiopathic functional pituitary tumor, whilst exogenous glucocorticoid administration can lead to iatrogenic disease. Approximately 85% of dogs with spontaneous hypercortisolism have pituitary-dependent hyperadrenocorticism (PDH), which results from excessive corticotropin secretion arising from either a microadenoma or a macroadenoma of the pituitary gland 1. Approximately 90% of all pituitary tumors are functional, with the hypersecretion of corticotropin resulting in bilateral adrenal hyperplasia.

The hypothalamic-pituitary-adrenal axis 

The adrenal cortex is composed of three distinct anatomical regions, the zona glomerulosa, zona fasiculata and zona reticularis, with glucocorticoids being produced in the zona fasiculata under the control of the hypothalamic-pituitary-adrenal (HPA) axis. The hormone corticotropin (or adrenocorticotropic hormone, ACTH) is secreted by the adenohypophysis of the pituitary gland, with the primary function of stimulating the adrenal cortex. Secretion occurs in a pulsatile manner and is stimulated by stress, but is normally controlled by the negative feedback of serum glucocorticoid levels. Corticotropin in turn is controlled by release of corticotrophin releasing hormone (CRH), secreted by the hypothalamus, again in a pulsatile manner 23. CRH secretion is inhibited by glucocorticoids and stimulated by serotonin and epinephrine.

Diagnosis

Since diagnosis of canine hyperadrenocorticism can be complex and none of the screening tests are 100% accurate, an integrated approach to the diagnosis is required. Signalment, history, clinical findings, screening tests and specific assays for the hypophyseal-adrenal axis should all be considered carefully in a collective manner to avoid misdiagnosis and to ensure concomitant disorders are not overlooked.

Signalment, history and clinical signs 

Hyperadrenocorticism typically affects middle-aged to old, small breed dogs, with no apparent gender bias. Whilst any breed can develop the disease, Poodles, Dachshunds and Terriers appear to be at increased risk. The clinical signs are generally slow to develop and progress, and many owners consider the early stages as part of the normal aging process of their dog. Various cutaneous changes, as shown in Table 1, are often significant.

 

Table 1. Cutaneous signs of hyperadrenocorticism.
Bilateral, symmetrical hypotrichosis/alopecia
Coat color change 
Hyperpigmentation 
Thin, hypotonic skin 
Comedones 
Calcinosis cutis
Poor wound healing 
Phlebectasia (venous dilation)
Bruising (petechiae and ecchymoses) 
Seborrheic dermatitis
Suppressed immune function (Chronic recurrent superficial pyoderma, Malassezia dermatitis, demodicosis, dermatophytosis)

 

These include the classic textbook appearance of generalized bilateral symmetrical truncal alopecia (Figure 1), often accompanied by hyperpigmentation (Figure 2). Thinning of the skin (Figure 3) and calcinosis cutis are also commonly seen (Figure 4) and suppression of the immune system can contribute to chronic dermatitis and furunculosis (Figure 5). Other systemic signs are also commonly encountered, as set out in Table 2 4. It is important to question an owner about recent corticosteroid administration (topical, oral, and injectable) to rule out a possible iatrogenic cause for hyperadrenocorticism before attempting to diagnose the spontaneous form of the disease.

 

Table 2. Systemic signs of hyperadrenocorticism.
Polyuria/polydipsia 
Abdominal distension 
Polyphagia 
Panting 
Weakness and lethargy 
Muscle atrophy 
Neuromuscular signs (pituitary macroadenomas may cause seizures, circling or blindness) 
Reproductive abnormalities (persistent anestrous, testicular hypoplasia) 
Recurrent urinary tract infections 
Diabetes mellitus 
Acute pancreatitis 

 

General health profile findings

If a dog is suspected of having hyperadrenocorticism after collecting the signalment, history and performing a physical examination, then blood and urine sampling (hematology and biochemistry panels, plus urinalysis and culture) is indicated. Routine laboratory findings in dogs with hyperadrenocorticism are shown in Table 3. 

                                

Table 3. Routine laboratory findings in dogs with hyperadrenocorticism.
Hematology
Stress leukogram (neutrophilia, lymphopenia and eosinopenia)
Erythrocytosis
Serum biochemistry panel
Elevated alkaline phosphatase (ALKP)*
Elevated alanine transferase (ALT)
Hypercholesterolemia
Hyperlipidemia
Hyperglycemia
Low blood urea nitrogen (BUN)
Urinalysis and urine culture
USG: hyposthenuric (often < 1.008) providing drinking water has not been withheld
Glucosuria (if concurrent diabetes mellitus)
Possible bacteruria and proteinuria, often without pyuria
 
*85-90% of dogs with hyperadrenocorticism exhibit elevated ALKP 57

 

Owners may believe that some of the signs that can develop with hyperadrenocorticism, such as bilateral trunk hypotrichosis.

Figure 1. Owners may believe that some of the signs that can develop with hyperadrenocorticism, such as bilateral trunk hypotrichosis (one of the most common signs of the disease), are a normal part of aging. Unusually, in this dog some hair regrowth is visible along the Blaschko lines. © Christoph klinger

Generalised bilateral symmetrical alopecia of the trunk with consequent intense.

Figure 2. Generalised bilateral symmetrical alopecia of the trunk with consequent intense hyperpigmentation of the skin due to exposure to UV light. © Christoph klinger

The abdomen of a dog with Cushings disease. Note the thin skin with superficial blood.

Figure 3. The abdomen of a dog with Cushings disease. Note the thin skin with superficial blood vessels easily visualized, and an area of hypocollagenosis where the skin appears to be torn. © Christoph klinger

Calcinosis cutis (white spots) and comedone formation (black spots) which can be typical.

Figure 4. Calcinosis cutis (white spots) and comedone formation (black spots) which can be typical of Cushing’s disease. © Christoph klinger

A dog with severe furunculosis on the right hind limb; this was due to ruptured inflamed.

Figure 5. A dog with severe furunculosis on the right hind limb; this was due to ruptured inflamed hair follicles with free hair shafts in the dermis leading to a foreign body reaction at the affected areas. © Christoph klinger

Ready to access more content?

Register

Already registered? Log in here