Addison's Disease and Skin Changes in Dogs: What to Watch For

By Emiel Maddens · Reviewed in consultation with licensed veterinary professionals · Updated August 2026 · 9 min read

What Is Addison's Disease in Dogs?

Addison's disease, known clinically as hypoadrenocorticism, is a deficiency of the hormones produced by the adrenal cortex, principally cortisol (a glucocorticoid) and aldosterone (a mineralocorticoid). In dogs it is most often caused by immune-mediated destruction of adrenal cortical tissue, and clinical signs typically do not appear until roughly 90% of the cortex has been destroyed.

It is uncommon, with reported prevalence in the general dog population around 0.06% to 0.28%, and it is diagnosed most frequently in young to middle-aged dogs, with a median age at diagnosis of about four years and a marked female predominance in most case series (Klein and Peterson, 2010). Breeds with documented genetic predisposition include the Standard Poodle, Portuguese Water Dog, Bearded Collie, Nova Scotia Duck Tolling Retriever, Leonberger, and Great Dane.

The dermatologic relevance of Addison's is unusual and worth stating plainly, because it runs opposite to what owners expect from an endocrine disease. Hypothyroidism and Cushing's disease both produce distinctive, recognizable skin patterns that often lead to the diagnosis. Addison's does not. It produces a vaguely unwell dog with a coat that has lost its quality, and the specific skin findings are subtle enough that dermatology is rarely how the case is caught. Understanding what Addison's does and does not do to skin is therefore mainly useful for two purposes: recognizing when a poor coat sits alongside systemic signs that deserve an electrolyte panel, and recognizing when the skin problems that appear later are being caused by the treatment rather than the disease.

What Skin Changes Does Addison's Disease Actually Cause?

The skin changes attributable to hypoadrenocorticism itself are non-specific and reflect chronic systemic illness rather than a distinct dermatosis.

Poor coat quality. Owners typically describe a coat that has gone dull, dry, and brittle, sometimes with increased scaling. Cortisol contributes to normal keratinocyte proliferation and lipid production, and a dog that is chronically cortisol-deficient, intermittently dehydrated, and often mildly anorexic is not directing resources toward a metabolically expensive tissue like hair.

Delayed hair regrowth. Hair that is clipped for a blood draw or surgery may take noticeably longer to return. Unlike hypothyroidism, this is a generalized sluggishness rather than the symmetrical truncal alopecia with a rat tail that defines classic endocrine hair loss.

Slow wound healing. Chronic illness, poor perfusion during hypovolemic episodes, and negative nitrogen balance all slow tissue repair.

Hyperpigmentation. This is emphasized in human Addison's, where high pituitary ACTH drives melanocyte stimulation and produces the characteristic bronzing. In dogs it is reported far less consistently, and diffuse darkening of canine skin far more commonly reflects chronic inflammation or yeast overgrowth than adrenal failure. It should not be treated as a reliable sign.

The critical point is what Addison's does not cause. There is no signature alopecia pattern, no comedone formation, no calcinosis cutis. A dog with dramatic bilaterally symmetrical hair loss and thin skin is far more likely to have hyperadrenocorticism or hypothyroidism, and the comparison between those two is covered in Cushing's vs Hypothyroidism: Comparing Skin Changes in Dogs.

How Do Veterinarians Diagnose Addison's Disease?

Diagnosis rests on hormone testing, not on skin findings, and the dermatologic examination serves mainly to rule other conditions in or out.

Screening bloodwork. Classic findings are hyperkalemia and hyponatremia, producing a sodium-to-potassium ratio below 27:1, though ratios below 24:1 raise suspicion considerably. Roughly a third of dogs also show azotemia, and a lack of a stress leukogram in a visibly sick dog is a meaningful clue. Importantly, atypical Addison's, in which only glucocorticoid production is lost, leaves electrolytes entirely normal, so a normal sodium and potassium does not exclude the disease.

Basal cortisol as a rule-out. A resting cortisol above 2 micrograms per deciliter makes hypoadrenocorticism very unlikely and is a reasonable screening step. A value below that threshold is not diagnostic and requires confirmation.

ACTH stimulation test, the diagnostic standard. Cortisol is measured before and after synthetic ACTH administration. A dog with Addison's shows a low baseline and, critically, essentially no rise after stimulation, with both values typically under 2 micrograms per deciliter. This flat response is the confirming finding.

Distinguishing skin signs from other causes. Because the coat changes of Addison's are non-specific, a dog presenting primarily for skin disease needs surface cytology to identify bacterial or yeast overgrowth, and thyroid testing where a symmetrical hair loss pattern is present. Working through which pattern fits before an appointment is easier with the Dog Skin Condition Checker, though hormone testing is what settles the question.

Signs and Symptoms to Watch For

The reason Addison's earns the nickname the great pretender is that its signs are vague and waxing-waning, often improving briefly with fluids or a course of steroids given for something else, which delays diagnosis by months.

Treatment, and Why the Skin Problems Often Start Afterward

Treatment is lifelong hormone replacement, and it is generally very successful. Dogs with well-managed hypoadrenocorticism have a near-normal life expectancy, which is unusual among endocrine diseases and worth knowing at the point of diagnosis.

Mineralocorticoid replacement is provided either by injectable desoxycorticosterone pivalate, typically dosed around every 25 to 30 days with the interval and dose individualized from electrolyte monitoring, or by oral fludrocortisone. Glucocorticoid replacement is usually low-dose oral prednisone, and this is where dermatology re-enters the picture.

The most common skin problem in a treated Addisonian dog is iatrogenic, meaning treatment-induced. Physiologic replacement doses of prednisone are low, and current guidance favors titrating to the lowest dose that controls signs. When the dose sits higher than the dog actually needs, whether from cautious dosing or from stress-dose increases that were never tapered back, the result is functionally the same as Cushing's disease: thinning skin, comedones, poor wound healing, and suppressed local immunity that permits recurrent superficial pyoderma. The paradox is real, a disease defined by too little cortisol frequently produces skin lesions caused by too much. Corticosteroids for Dog Skin: Types and Side Effects explains this dose relationship in detail.

Managing the secondary bacterial infections. When steroid-associated pyoderma develops, the aim is to control the bacterial burden topically while the veterinarian reassesses whether the glucocorticoid dose can come down, because systemic antibiotics in a dog on long-term immunosuppressive-range steroids invite resistance without addressing the cause. Chlorhexidine Spray contains 2% chlorhexidine gluconate, a cationic biguanide that binds the negatively charged bacterial cell wall, disrupts membrane integrity, and causes precipitation of cytoplasmic contents. It is active against Staphylococcus pseudintermedius, the organism responsible for the large majority of canine superficial pyoderma, and has useful residual activity because it binds to the stratum corneum and keeps working after application. It targets focal lesions without adding systemic drug exposure to a dog whose hormonal balance is already being carefully titrated, and it is an FDA-registered OTC veterinary drug listed on DailyMed rather than a cosmetic. Background on the active is in our chlorhexidine for dogs guide, and Dog Immune System and Skin Health Connection covers why immunosuppressed dogs develop recurrent surface infection.

How Do You Monitor an Addisonian Dog Long Term?

Long-term management is a monitoring problem more than a treatment problem, and the skin is a useful early indicator that dosing has drifted.

Electrolyte monitoring on schedule. Sodium and potassium are checked frequently during the initial stabilization period and then at longer intervals once stable, with the mineralocorticoid dose adjusted to keep them in range. Many dogs are eventually maintained on lower doses than they started on.

Watch for the signs of glucocorticoid excess. Increased thirst and urination, increased appetite, panting, a developing pot-bellied appearance, thinning skin, or a new recurrent pyoderma all suggest the prednisone dose is higher than this dog requires. Report these rather than accepting them as normal for an Addisonian, because they are usually correctable with a dose adjustment made by your veterinarian.

Understand stress dosing, and understand tapering back. Dogs with hypoadrenocorticism cannot mount their own cortisol response to stress, so surgery, boarding, illness, or travel typically warrants a temporary increase in glucocorticoid, often two to three times the maintenance dose for a short period. The step that gets missed is returning to baseline afterward. Repeated stress doses that are never tapered are a frequent route into iatrogenic skin disease.

Carry documentation. Every Addisonian dog should have written notes on the diagnosis, current doses, and emergency instructions available to any veterinarian who might see them, because an adrenal crisis presenting to an unfamiliar emergency clinic is a genuine risk and prior knowledge changes the response time.

Support coat recovery patiently. Once hormone replacement is stable, coat quality generally improves, but hair follicles cycle slowly and visible change usually takes two to three months. Adequate dietary protein and essential fatty acid intake support that recovery. Do not judge treatment success by the coat at the four-week recheck.

Frequently Asked Questions

Does Addison's disease cause hair loss in dogs?

Not in a characteristic pattern. Unlike hypothyroidism or Cushing's disease, hypoadrenocorticism does not produce bilaterally symmetrical truncal alopecia. What owners usually notice is a dull, dry, poor-quality coat and slow hair regrowth after clipping, which reflects general systemic illness rather than a specific dermatosis.

What are the first signs of Addison's disease in a dog?

Vague and intermittent ones: reduced appetite, weight loss, lethargy, weakness, and episodes of vomiting or diarrhea that resolve then return. This waxing and waning pattern is why it is called the great pretender. Roughly 30% of dogs are instead diagnosed only after presenting in acute collapse.

Can Addison's disease cause skin infections in dogs?

The disease itself rarely does. Recurrent pyoderma in an Addisonian dog usually reflects glucocorticoid over-replacement, because prednisone above the physiologic replacement dose suppresses local skin immunity in the same way Cushing's disease does. It signals a dose review is needed alongside treating the infection.

Which dog breeds get Addison's disease most often?

Standard Poodles, Portuguese Water Dogs, Bearded Collies, Nova Scotia Duck Tolling Retrievers, Leonbergers, and Great Danes have documented predisposition, and heritability is established in several of them. Median age at diagnosis is around four years, with females over-represented in most case series.

Can a dog have Addison's with normal blood electrolytes?

Yes. Atypical hypoadrenocorticism involves loss of glucocorticoid production only, leaving aldosterone and therefore sodium and potassium normal. These dogs are frequently misdiagnosed as having gastrointestinal disease. An ACTH stimulation test is required to exclude the condition, a normal electrolyte panel is not sufficient.

Will my dog's coat improve after Addison's treatment starts?

Usually yes, but slowly. Hair follicles cycle over months, so expect roughly two to three months of stable hormone replacement before coat quality visibly improves. Judging treatment success by coat appearance at a four-week recheck will understate how well the dog is actually doing.

Sources

1. Klein SC, Peterson ME. Canine hypoadrenocorticism: part I. Canadian Veterinary Journal. 2010;51(1):63-69.
2. Klein SC, Peterson ME. Canine hypoadrenocorticism: part II. Canadian Veterinary Journal. 2010;51(2):179-184.
3. Lathan P, Thompson AL. Management of hypoadrenocorticism (Addison's disease) in dogs. Veterinary Medicine: Research and Reports. 2018;9:1-10.
4. Van Lanen K, Sande A. Canine hypoadrenocorticism: pathogenesis, diagnosis, and treatment. Topics in Companion Animal Medicine. 2014;29(4):88-95.
5. Frank LA. Comparative dermatology, canine endocrine dermatoses. Clinics in Dermatology. 2006;24(4):317-325.
6. Hillier A, Lloyd DH, Weese JS, et al. Guidelines for the diagnosis and antimicrobial therapy of canine superficial bacterial folliculitis. Veterinary Dermatology. 2014;25(3):163-e43.

Related Reading

• Cushing's vs Hypothyroidism: Comparing Skin Changes in Dogs
• Corticosteroids for Dog Skin: Types & Side Effects
• Long-Term Immunosuppressive Therapy for Dog Skin Disease: Monitoring and Safety

Emiel Maddens

Founder of Vetified. Develops topical antifungal and antimicrobial formulations for companion animals. Vetified products are listed on DailyMed and manufactured through FDA-registered facilities in the United States.

Veterinary review: All Vetified content is developed in consultation with licensed veterinary professionals and references peer-reviewed research published in journals including Veterinary Dermatology, JAVMA, and Journal of Small Animal Practice.