Corticosteroids — prednisone, prednisolone, dexamethasone, methylprednisolone, triamcinolone, and the rest — are among the most useful and most prescribed drugs in veterinary medicine. They quiet the inflammation of allergic skin disease, suppress immune-mediated destruction of blood cells and joints, control the swelling of the brain and spinal cord, and manage addisonian crisis. They are also the drug class owners fear most, for reasons that are not entirely wrong: the side effects of long-term steroids are visible, sometimes dramatic, and well documented.

This article analyzes 32,938 adverse-event reports naming at least one glucocorticoid active ingredient in the FDA Center for Veterinary Medicine (CVM) animal drug adverse-event database — spanning 1987 through early 2026 and covering prednisone, prednisolone, dexamethasone, methylprednisolone, triamcinolone, betamethasone, hydrocortisone, and budesonide in animals. Every number below comes from a direct computation of the FDA CVM adverse-event reports (analysis run date: 2026-06-14).

Three things these numbers do not mean

Before the data, three caveats that apply to every pharmacovigilance analysis:

1. Reports are not causal proof. The FDA states explicitly that reports in this database have not been verified for causality. A report linking prednisone to elevated liver enzymes does not mean prednisone caused it — the dog was on prednisone for a disease that may itself raise enzymes.
2. Volume reflects usage. Prednisone has been the workhorse veterinary steroid for decades, prescribed across dozens of conditions. It will accumulate more reports than a narrowly used drug like budesonide simply because far more animals have taken it.
3. Under-reporting is substantial. The FDA acknowledges that only a fraction of adverse events are ever reported. The known, expected side effects of steroids — the increased drinking and urination every owner recognizes — are rarely reported at all, which means the database skews toward the serious and the unexpected.

The glucocorticoid ingredients by report count

The database contains 32,938 reports naming at least one veterinary glucocorticoid active ingredient. The breakdown by ingredient (a single report naming two steroids is counted under each):

Prednisone and prednisolone alone account for more than half of all glucocorticoid reports — a reflection of how broadly they are used, not necessarily of any single safety signal.

The reactions: a textbook steroid profile

When the analysis is narrowed to systemic glucocorticoids (prednisone, prednisolone, dexamethasone, methylprednisolone, excluding combination ear and eye products where a steroid is paired with an antibiotic or antifungal), the reaction list reads almost exactly like the glucocorticoid side-effect chapter of a pharmacology textbook. That is reassuring rather than alarming: the database is capturing the effects veterinarians already expect and counsel owners about.

The most common reactions reported with systemic glucocorticoids (17,965 reports) include:

A UK VetCompass study of dogs on short-term prednisone or prednisolone found that by day 14, roughly 90% of dogs showed one or more side effects, with polyuria and polydipsia the most consistently reported — a finding that lines up precisely with the reaction signal in the FDA data. Behavior changes, including restlessness and in some cases aggression, were also documented and are the side effect owners find most surprising.

One signal worth separating: hearing loss in combination ear products

When all glucocorticoid reports are pooled together (including combination otic products such as betamethasone with gentamicin and an antifungal), "deafness" and "loss of hearing" appear among the top reactions — with well over 2,000 reports. This is not a steroid effect. It is the signature of aminoglycoside antibiotics (gentamicin, neomycin, amikacin) administered into the ear of a dog whose eardrum may be ruptured, where the drug reaches the inner ear and causes ototoxicity. The steroid in those products is along for the ride.

This matters for two reasons. Clinically, it is why a veterinarian checks the tympanic membrane before prescribing an ear product containing an aminoglycoside — a ruptured eardrum converts a routine otic treatment into an ototoxic risk. And analytically, it is a reminder that pooling a drug class across combination products can make a reaction look like it belongs to the wrong ingredient. The clean steroid signal lives in the systemic-only data above.

Species differences: cats tolerate steroids differently

Across all glucocorticoid reports, dogs dominate the volume (about 71% of reports versus 17% for cats), again reflecting relative use. But the outcome data point to a real species difference that clinicians already respect:

Among systemic glucocorticoid reports specifically, the serious-event rate is comparable between dogs and cats (about 46–47%), but the reported fatal-outcome rate is higher in cats (about 20% versus 14% in dogs). The caveat above applies — these are reports, not causation, and cats in the database are often sicker patients on steroids for serious immune-mediated disease — but the direction is consistent with what veterinarians already know: cats are more likely than dogs to develop steroid-induced diabetes, they do not tolerate the polyphagia and muscle wasting of chronic steroids well, and their margin for error on long-term corticosteroids is narrower. Cats also process prednisone poorly compared with prednisolone (cats lack the hepatic conversion efficiently), which is why prednisolone is the preferred oral glucocorticoid in that species.

What a veterinarian is watching for on long-term steroids

For a dog or cat on more than three to four months of corticosteroids — particularly at immunosuppressive doses — the monitoring conversation is not optional. The Merck Veterinary Manual lists the long-term glucocorticoid risks the database reflects: polyuria and polydipsia, polyphagia and weight gain, muscle wasting and steroid myopathy, thin skin and calcinosis cutis, poor wound healing, and increased susceptibility to infection. One landmark finding owners rarely hear is urinary tract infection: a JAVMA study of dogs on long-term corticosteroids for chronic skin disease cultured bacteria from the urine of roughly 39% of treated dogs, and in about 68% of those infected dogs there were no clinical signs at all — which is why urine cultures every three to six months are recommended for animals on chronic treatment, not just urinalysis.

The operational principles that reduce this burden are the same ones that govern every glucocorticoid decision: the lowest effective dose, the shortest effective duration, alternate-day dosing once the condition is controlled (to spare the adrenal axis), and a plan to taper rather than stop abruptly. For dogs whose condition allows it — allergic airway disease, for example — transitioning from oral steroids to a non-steroid alternative (an Apoquel-type targeted therapy, a Cytopoint monoclonal antibody, or an inhaled steroid) is the single most effective way to remove the systemic side-effect burden while keeping the disease controlled.

What these reports do not change

The pharmacovigilance data does not argue against corticosteroids. It argues for the discipline that experienced clinicians already apply: use them when the disease demands it, at the dose that works, for as short a time as the diagnosis allows, and monitor for the effects the database confirms are real. The increased drinking and urination, the panting, the behavior change, the creeping liver enzymes, the silent urinary infection — these are not surprises to a veterinarian managing a steroid patient. They are the known cost of a drug class that, used well, controls disease almost nothing else can.

Sources

• U.S. FDA, Center for Veterinary Medicine, animal drug adverse-event database (openFDA Animal & Veterinary Adverse Events) — analysis of reports naming glucocorticoid active ingredients, analysis run date 2026-06-14, https://www.fda.gov/animal-veterinary/safety-health/reporting-problem-fda/veterinary-adverse-event-drug-experience-reporting
• Merck Veterinary Manual, "Hormonal Treatment for Integumentary Disease in Animals" (glucocorticoid adverse effects: PU/PD, polyphagia, infections, GI ulceration, pancreatitis, osteoporosis, steroid myopathy, calcinosis cutis), https://www.merckvetmanual.com/pharmacology/systemic-pharmacotherapeutics-of-the-integumentary-system/hormonal-treatment-for-integumentary-disease-in-animals
• Ihrke PJ, Norton AL, Ling GV, Stannard AA, "Urinary tract infection associated with long-term corticosteroid administration in dogs with chronic skin diseases," J Am Vet Med Assoc 186(1):43-46, 1985 (39% UTI prevalence; ~68% of infected dogs showed no clinical signs), https://avmajournals.avma.org/view/journals/javma/186/1/javma.1985.186.01.43.pdf
• McGonigle E, et al., "Perception and usage of short-term prednisone and prednisolone in dogs" (VetCompass; ~90% of dogs showed ≥1 side effect by day 14; PU/PD most common; behavior change including aggression), PubMed Central (PMC10364361), https://pmc.ncbi.nlm.nih.gov/articles/PMC10364361
• VCA Animal Hospitals, "Steroid Treatment — Long-term Effects in Dogs" (short- and long-term glucocorticoid side effects; lowest-dose principle), https://vcahospitals.com/know-your-pet/steroid-treatment-long-term-effects-in-dogs
• Merck Veterinary Manual, "Addison Disease (Hypoadrenocorticism) in Animals" (iatrogenic hyperadrenocorticism signs; prednisone tapering), https://www.merckvetmanual.com/endocrine-system/the-adrenal-glands/addison-disease-hypoadrenocorticism-in-animals