Atopic dermatitis in dogs is characterized by chronic pruritus and a typical distribution of skins lesions. It is generally associated with IgE antibodies against environmental, food, and/or microbial allergens to which susceptible dogs are genetically predisposed to become sensitized. Diagnosis is based on clinical signs, history, and exclusion of other causes of pruritus. Treatment involves a combination of therapies to relieve pruritus, improve skin barrier function, and control secondary infections; allergens should be avoided when possible.
In 2023, the International Committee on Allergic Diseases of Animals (ICADA) introduced a new definition of atopic dermatitis in dogs to reflect newly acquired knowledge of this disease. ICADA defines canine atopic dermatitis as "a hereditary, typically pruritic, and predominantly T-cell-driven inflammatory skin disease involving interplay among skin barrier abnormalities, allergen sensitization, and microbial dysbiosis” (1).
Etiology and Pathogenesis of Atopic Dermatitis in Dogs
The etiology and pathogenesis of atopic dermatitis in dogs is complex and involves a genetic predisposition, impairment of the normal barrier function of the skin, microbial dysbiosis, and immunological aberrations.
As is the case in other species, dogs with atopic dermatitis are thought to be genetically predisposed to become sensitized to environmental and/or food allergens.
Allergens are proteins that, when inhaled or absorbed through the skin, respiratory tract, or GI tract, evoke allergen-specific IgE production. These allergen-specific IgE molecules affix themselves to tissue mast cells or basophils. When these primed cells come in contact with the specific allergen again, mast cell degranulation results in the release of proteolytic enzymes, histamine, bradykinin, and other vasoactive amines, leading to inflammation (erythema, edema, and pruritus), recruitment of inflammatory cells, and further production of inflammatory and itch mediators.
The term "atopic-like dermatitis" (alternatively, "intrinsic atopic dermatitis") refers to cases that clinically resemble cases of IgE-mediated atopic dermatitis but lack detectable IgE sensitization.
The skin is the primary target organ of atopic dermatitis in dogs; however, rhinitis and GI signs can also occur. Neuronal itch stimulation plays an important role in the initiation and perpetuation of pruritus.
IL-31 is an important pruritogenic cytokine. IL-31 stimulates neurons via its receptors and activation of enzymes of the Janus kinase (JAK) family. IL-31 is the target of some therapies for atopic dermatitis in dogs.
Epidemiology of Atopic Dermatitis in Dogs
Multiple dog breeds are predisposed to atopic dermatitis; however, the prevalence within a breed largely depends on the genetic pool and geographical region.
Dog breeds predisposed to development of atopic dermatitis include the following:
Boston Terrier
Boxer
Chinese Shar-Pei
Dalmatian
Golden Retriever
Labrador Retriever
Lhasa Apso
Scottish Terrier
Shih Tzu
West Highland White Terrier
Wire Fox Terrier
The age of onset is generally between 6 months and 3 years. There is no sex predisposition.
Clinical signs of atopic dermatitis in dogs can be seasonal, nonseasonal, or nonseasonal with seasonal flares.
Clinical Findings of Atopic Dermatitis in Dogs
Pruritus is the characteristic clinical sign of atopic dermatitis in dogs. The paws, face, ears, flexural surfaces of the front legs, axillae, and abdomen are the most frequently affected areas; however, lesion distribution can vary by breed.
Primary lesions of atopic dermatitis in dogs are uncommon and consist of erythematous macules, patches, and small papules.
Most lesions develop secondary to self-trauma and are due to the presence of secondary infections and chronicity of the disease. Secondary lesions include alopecia, erythema, scaling, hemorrhagic crusts, excoriations, lichenification, and hyperpigmentation.
Secondary skin and ear infections with Staphylococcus spp and Malassezia spp are common and often worsen the clinical signs. Chronic or recurrent otitis may be the only clinical sign in a small number of patients.
Diagnosis of Atopic Dermatitis in Dogs
Clinical evaluation
History
Exclusion of other causes of pruritus
Diagnosis of atopic dermatitis in dogs is challenging and is based on signalment, clinical signs, history, and the exclusion of other pruritic skin diseases, not on laboratory tests.
The following clinical features, known as the Favrot criteria, are compatible with a diagnosis of atopic dermatitis in dogs:
affected ear pinnae (but not pinnal margins)
affected front paws
age of onset < 3 years
chronic or recurrent yeast infections
corticosteroid-responsive pruritus
mostly indoor lifestyle
nonaffected dorsolumbar area
pruritus without skin lesions at onset
The sensitivity and specificity of this set of diagnostic criteria for atopic dermatitis in dogs have been reported to be 85% and 79%, respectively, when five of the criteria are fulfilled (2). These criteria do not apply to cases of food-induced atopic dermatitis. Atopic dermatitis in dogs is very likely if at least five of the criteria are present and other differential diagnoses have been ruled out.
Allergy testing (intradermal or serological) is a diagnostic aid that measures increased concentrations of tissue-bound or circulating IgE; alone, allergy testing is not diagnostic but rather reflects exposure.
The primary reason to pursue intradermal or serological allergy testing is to identify the offending allergens in an individual animal and to formulate allergen-specific immunotherapy. Test results are important only if the offending allergens identified are compatible with the history or seasonality of pruritus.
Pearls & Pitfalls
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The most important differential diagnoses for atopic dermatitis in dogs include other pruritic skin conditions, such as the following:
Treatment of Atopic Dermatitis in Dogs
Allergen avoidance
Allergen-specific immunotherapy
Pruritus control
Treatment of secondary infections
Identification and control of flare factors
Atopic dermatitis in dogs cannot be cured; in most cases, however, the disease can be managed to improve the quality of life of dogs and their owners.
Owner education is important, because atopic dermatitis in dogs is a chronic disease requiring lifelong management and regular progress checks.
Management options depend on the severity of clinical signs and whether pruritus is seasonal or year-round.
Avoidance of allergens is ideal for managing atopic dermatitis in dogs; however, allergen avoidance is difficult (if not impossible) to achieve, even when a specific allergen or allergens can be identified.
Allergen-Specific Immunotherapy for Atopic Dermatitis in Dogs
Allergen-specific immunotherapy (ASIT) is the only treatment for atopic dermatitis in dogs that can change a dog's immune response to allergens and induce remission of clinical signs. It remains the treatment of choice of most veterinary dermatologists.
ASIT attempts to increase a patient's tolerance to environmental allergens by inducing the development of anti-inflammatory cytokines, such as IL-10. IL-10 has been has been associated with production of IgG and decreased IgE concentrations. In humans with atopic dermatitis, early administration of ASIT prevents progression of the disease.
ASIT consists of administering increasing doses of the offending allergens until a maintenance dose is reached. ASIT can be administered via subcutaneous injections or orally (ie, sublingually). Both methods are equally effective; therefore, clients should choose the method they find easiest (see also the table ).
Select Therapeutic Agents for Atopic Dermatitis in Dogs
Agent | Dosagea | Key Points |
|---|---|---|
Allergen-Specific Immunotherapy (ASIT) | ||
Injectable ASIT: subcutaneous allergen-specific immunotherapy (SCIT) | Various protocols exist; patient-specific recommendations are typically provided by the serum manufacturer on the basis of testing results, patient history, allergen cross-reactivity, and geographical location. | Very specific targeted effect Slow onset of action (up to 12 mo) Not useful for acute flares Most common adverse reaction: worsening of pruritus |
Oral ASIT: sublingual allergen-specific immunotherapy (SLIT) | Pump dispenser directly onto oral mucosa, between lip and gum, q 12 h | Most common adverse reactions: face rubbing, transient worsening of pruritus, GI signs |
Topical Glucocorticoids | ||
Triamcinolone acetonide 0.015% | Topically q 12–24 hb | Indicated for acute flares and localized lesions Apply to the affected area Best suited for short-term use (7–14 d) Potential adverse effects of note: cutaneous atrophy, calcinosis cutis |
Hydrocortisone aceponate 0.0584% | Topically q 12–24 hc | |
Betamethasone valerate (various concentrations) | Topically q 12–24 hd | |
Mometasone furoate (various concentrations) | Topically q 12–24 hd | |
Oral Glucocorticoids | ||
Prednisone or prednisolone | Induction or initial dose: 0.5–1.1 mg/kg, PO, q 24 he Target dose after tapering: 0.25–0.5 mg/kg, PO, q 48 he | Indicated for acute flares Fast acting Broad, nonspecific anti-inflammatory response Many potential adverse effects |
Calcineurin Inhibitors | ||
Cyclosporine | Initial dose: 5 mg/kg, PO, q 24 h; tapered to the lowest dose that controls the diseasee | Indicated for long-term management Can take 4–6 wk to achieve clinical improvement Not suitable for treatment of acute flares Most common adverse effects: GI signs Indicated for localized lesions Appears safe for short-term use |
Tacrolimus 0.1% ointment | Topically q 12–24 hb | |
Phosphodiesterase Inhibitors | ||
Pentoxifylline | 20 mg/kg, PO, q 8 hf | May be best suited as adjunctive therapy for chronic conditions Slow onset of action (4–6 wk) Not suited for acute flares Good safety profile |
Antihistamines | ||
Fexofenadine | 18 mg/kg, PO, q 24 hg | Helpful for mild pruritus Best as part of combination therapy Preventive role Sparing agents for glucocorticoids Not suitable for acute flares |
Hydroxyzine | 2 mg/kg, PO, q 12 hh | |
Hydroxyzine + chlorpheniramine | (20.9 mg + 0.7 mg)/10 kg (divided), PO, q 12 hi | |
Cetirizine | 0.5–1 mg/kg, PO, q 12 hh | |
Essential Fatty Acids | ||
High-quality fish oil (with EPA and DHA) | 65–90 mg/kg, PO, q 24 h j,k,l | No evidence of superior efficacy of any particular combination, dosage, ratio, or formulation to improve skin and coat quality and decrease pruritus |
Janus Kinase Inhibitors | ||
Oclacitinib maleate (tablet or chewable tablet) | 0.4–0.6 mg/kg, PO, q 12 h for 2 wk, then q 24 he | Indicated for acute flares and long-term management of pruritus in dogs 12 mo or older Fast onset of action (within 24 h) for pruritus control Most common adverse effects: GI signs Contraindicated in dogs with serious infections or neoplasia May increase susceptibility to infections, demodicosis, and neoplastic conditions Acute kidney injury possible with toxic doses (eg, 27.3 mg/kg)m |
Ilunocitinib | 0.6–0.8 mg/kg, PO, q 24 hn | Indicated for control of pruritus associated with allergic and atopic dermatitis in dogs 12 mo or older
|
Monoclonal Antibodies | ||
Lokivetmab | 2 mg/kg, SC, q 4–8 wko | Indicated for acute flares and long-term management Fast onset of action (1–3 d) for pruritus control Most common adverse effects: lethargy, vomiting |
Adapted from Sandra Koch. What is new in the diagnosis and management of canine atopic dermatitis. Today’s Veterinary Practice. May/June 2015:95-102. | ||
a For most antipruritic agents used to treat dogs with atopic dermatitis (glucocorticoids, calcineurin inhibitors, phosphodiesterase inhibitors, antihistamines, essential fatty acids, Janus kinase inhibitors, monoclonal antibodies), therapy typically continues until clinical signs have resolved. However, in many cases, long-term therapy is required to maintain control of clinical signs. When long-term therapy is required, medications should be tapered to the lowest dose and frequency that maintains remission of clinical signs. b Olivry T, Foster AP, Mueller RS, McEwan NA, Chesney C, Williams HC. Interventions for atopic dermatitis in dogs: a systematic review of randomized controlled trials. Vet Dermatol. 2010;21(1):4-22. doi:10.1111/j.1365-3164.2009.00784.x c Nuttall TJ, McEwan NA, Bensignor E, Cornegliani L, Löwenstein C, Rème CA. Comparable efficacy of a topical 0.0584% hydrocortisone aceponate spray and oral ciclosporin in treating canine atopic dermatitis. Vet Dermatol. 2012;23(1):4-10, e1-2. doi:10.1111/j.1365-3164.2011.00992.x d Anecdotal evidence. e Olivry T, DeBoer DJ, Favrot C, et al. Treatment of canine atopic dermatitis: 2015 updated guidelines from the International Committee on Allergic Diseases of Animals (ICADA). BMC Vet Res. 2015;11:210. doi:10.1186/s12917-015-0514-6 f Singh SK, Dimri U, Saxena SK, Jadhav RK. Therapeutic management of canine atopic dermatitis by combination of pentoxifylline and PUFAs. J Vet Pharmacol Ther. 2010;33(5):495-498. doi:10.1111/j.1365-2885.2009.01146.x g Alja P, Silvestra K, Domanjko-Petric A, Kotnik T. The efficacy of antihistamine fexofenadine versus methylprednisolone in the treatment of atopic dermatitis in dogs. Slov Vet Res. 2009;46(1):5-12. h Bizikova P, Papich MG, Olivry T. Hydroxyzine and cetirizine pharmacokinetics and pharmacodynamics after oral and intravenous administration of hydroxyzine to healthy dogs. Vet Dermatol. 2008;19(6):348-357. doi:10.1111/j.1365-3164.2008.00697.x i Eichenseer M, Johansen C, Mueller RS. Efficacy of dimetinden and hydroxyzine/chlorpheniramine in atopic dogs: a randomised, controlled, double-blinded trial. Vet Rec. 2013;173(17):423. doi:10.1136/vr.101907 j Saevik BK, Bergvall K, Holm BR, et al. A randomized, controlled study to evaluate the steroid sparing effect of essential fatty acid supplementation in the treatment of canine atopic dermatitis. Vet Dermatol. 2004;15(3):137-145. doi:10.1111/j.1365-3164.2004.00378.x k Schäfer L, Thom N. A placebo-controlled, double-blind study evaluating the effect of orally administered polyunsaturated fatty acids on the oclacitinib dose for atopic dogs. Vet Dermatol. 2024;35(4):408-417. doi:10.1111/vde.13246 l Müller MR, Linek M, Löwenstein C, et al. Evaluation of cyclosporine-sparing effects of polyunsaturated fatty acids in the treatment of canine atopic dermatitis. Vet J. 2016;210:77-81. doi:10.1016/j.tvjl.2015.11.012 m Damone JM, Lister S, Lyons BM. Oclacitinib (Apoquel) toxicosis resulting in acute kidney injury in a dog. J Am Vet Med Assoc. 2025;263(9):1-2. doi:10.2460/javma.25.04.0240 n Kuntz EA, Gabor L, Toutain CE. Safety of ilunocitinib tablets (Zenrelia™) after once daily oral administration in dogs. BMC Vet Res. 2025;21(1):144. doi:10.1186/s12917-025-04579-1 o Michels GM, Ramsey DS, Walsh KF, et al. A blinded, randomized, placebo-controlled, dose determination trial of lokivetmab (ZTS-00103289), a caninized, anti-canine IL-31 monoclonal antibody in client owned dogs with atopic dermatitis. Vet Dermatol. 2016;27(6):478-e129. doi:10.1111/vde.12376 | ||
For injectable ASIT, also known as subcutaneous immunotherapy (SCIT), the interval between maintenance dosages varies with different protocols; adjustments in the interval are based on the animal’s response and can vary from a few days to 3–4 weeks.
ASIT is not useful for acute flares of atopic dermatitis, because the time to response can vary greatly, from 3 months up to 12 months.
Studies vary in the reported efficacy of immunotherapy in dogs with atopic dermatitis. A 2022 retrospective study of 664 dogs treated with SCIT showed an improvement in clinical signs (> 50% decrease in pruritus) for approximately 60% of dogs treated for at least 9 months. Approximately half of the dogs with clinical improvement still required concomitant medication for control of clinical signs. Concurrent glucocorticoids appeared to decrease the response to SCIT (3).
For oral ASIT, also known as sublingual immunotherapy (SLIT), the administration is once or twice a day; however, protocols vary between veterinary dermatologists. Dog owners are advised not to expect much response for 6 months and are asked to commit to at least 1 year of therapy before deciding on its usefulness. The best assessment of response is to compare the degree of disease or discomfort between similar seasons. A 2020 study showed that SLIT may be inferior to SCIT or intralymphatic immunotherapy for the treatment of atopic dermatitis in dogs (4); however, other studies have reported good response rates (5).
Adverse effects of ASIT are uncommon; increased pruritus is the most commonly reported one. Most of these cases respond to premedication with an antihistamine, but some require dose adjustment. Less common adverse effects include pain at the injection site, urticaria, lethargy, and, very rarely, anaphylaxis. Owners should be asked to administer ASIT when able to monitor their dogs for at least 30 minutes after administration.
Owner education is essential when initiating ASIT. The need to perform the treatment for at least 12 months before evaluating the response, the best route of administration, the protocol, and the rate of success should be discussed in detail. The success rate of ASIT in dogs with atopic dermatitis is approximately 70% (6), and some patients may require additional therapies, such as regular bathing, essential fatty acids, and antihistamines.
Transdermal immunotherapy is an emerging ASIT option for the treatment of atopic dermatitis in dogs. One study evaluated clinical response and serum IgE concentrations in six dogs treated with transdermal immunotherapy for dust mites, ragweed, and timothy grass over 6 months. The study showed a decrease in IgE concentrations and decreased clinical lesions (7). Further studies with larger sample sizes and longer treatment intervals are needed to elucidate the validity of these findings.
Pruritus Relief in Atopic Dermatitis in Dogs
By definition, atopic dermatitis in dogs is a pruritic skin disease. Pruritus can be relieved via antipruritic drugs alone, while waiting for allergen-specific immunotherapy (ASIT) to be effective, or in combination with ASIT in partially responsive cases.
For most antipruritic therapies, treatment typically continues until clinical signs have resolved. However, in many cases, long-term therapy is required to maintain control of clinical signs. When long-term therapy is required, medications should be tapered to the lowest dose and frequency that maintains remission of clinical signs.
Several topical interventions are effective in relieving pruritus (see also the table ):
Topical glucocorticoids (eg, triamcinolone, hydrocortisone aceponate, betamethasone, mometasone) are best suited for acute flares and localized lesions. They should be applied to the affected area. See the table for specific concentrations and dosages. Prolonged use can cause changes consistent with iatrogenic hyperadrenocorticism (eg, cutaneous atrophy or calcinosis cutis).
Topical tacrolimus ointment (0.1% ointment, every 12–24 hours [8]) can be used for long-term management of localized lesions.
Bathing can decrease allergen load and is often the most effective way to implement allergen avoidance. Weekly to biweekly baths are recommended. In dogs with a history of flares caused by microbial overgrowth, routine use of antimicrobial shampoos can help decrease the incidence of secondary infections. Choosing the active ingredient in a shampoo to targetthe most likely cause of the observed problem adds extra benefit; for example, in cases of superficial pyoderma, an antimicrobial product such as chlorhexidine will likely give the best results.
A number of systemic antipruritic treatments are also effective (see also the table ):
Oral glucocorticoids (eg, prednisone or prednisolone at an initial dose of 0.5–1.1 mg/kg, PO, every 24 hours, with a taper [9]) are best suited for severe, acute flares, as they are fast acting. Long-term use of these drugs presents a high risk for adverse effects. For long-term use, the dosage should be tapered to the lowest effective dose and frequency (see Corticosteroids in Animals).
Oral cyclosporine (5 mg/kg, PO, every 24 hours) is best for long-term management of pruritus (9), as it has a slow onset of effect (up to 4–6 weeks). The most common adverse effects are GI upset (vomiting, diarrhea, anorexia); however, other adverse effects, including secondary infections, hypertrichosis, gingival hyperplasia, psoriasiform lichenoid dermatosis, and papillomatosis can occur.
Oral pentoxifylline (20 mg/kg, PO, every 8 hours), in combination with oral polyunsaturated fatty acids, improved pruritus and clinical lesion scores in a small study (10). Few adverse effects were noted.
Antihistamines have very little efficacy for acute flares but can be useful, in conjunction with other treatments, in controlling chronic disease. Antihistamines work best if given before a flare, to block effects of histamine. Several antihistamines may need to be tried before finding the most efficacious one for an individual patient (9).
Essential fatty acids (EFAs) are not useful for controlling acute flares of atopic dermatitis in dogs, as they can take up to 2 months to take effect. EFAs are most helpful as adjunctive therapy, and several studies have shown that they both increase the efficacy and decrease the required dosage of concurrent medications (glucocorticoids, cyclosporine, oclacitinib) (11, 12, 13).
Janus kinase (JAK) inhibitors, such as oclacitinib and ilunocitinib, are fast-acting antipruritic and mildly anti-inflammatory agents useful for both acute flares and control of chronic atopic dermatitis in dogs. Both drugs are licensed for dogs > 12 months old. The most common adverse effects are GI disturbances. Other adverse events associated with both oclacitinib and ilunocitinib include infections and hematologic changes, such as leukopenia, lymphopenia, and liver enzyme elevations. Acute kidney injury is possible with toxic doses of oclacitinib (eg, 27.3 mg/kg) (14).
Lokivetmab, a monoclonal caninized antibody that targets IL-31 (a pruritogenic cytokine), has a quick onset of effect, making it effective for both acute flares and control of chronic atopic dermatitis in dogs. There are no age restrictions or reported drug interactions with lokivetmab. The most common adverse effects are lethargy and GI disturbances.
Recognition and Control of Flare Factors in Atopic Dermatitis in Dogs
A relapse of clinical signs of atopic dermatitis in dogs whose disease is otherwise well controlled should prompt investigation into the cause of the pruritic exacerbation. Recognized flare factors include fleas, food and environmental allergens, and secondary infections such as Malassezia dermatitis, superficial pyoderma, and otitis externa. These need to be investigated and addressed, and the level of pruritus must be reevaluated before choosing long-term antipruritic therapy.
For acute flares, the patient's current flea control protocol should be reviewed and, if needed, flea control should be implemented. Steps should be taken to determine whether there is an increase in allergen counts and to identify and address any secondary skin and ear infections.
Key Points
Atopic dermatitis in dogs is a genetically predisposed chronic inflammatory and pruritic allergic skin disease with characteristic clinical features.
Diagnosis is based on clinical signs, history, and exclusion of other causes of pruritus.
Management includes treatments that relieve pruritus, treatment and control of secondary infections, allergen-specific immunotherapy, and avoidance of allergens.
Client education and monitoring are key for treatment success.
For More Information
Nuttall TJ, Marsella R, Rosenbaum MR, Gonzales AJ, Fadok VA. Update on pathogenesis, diagnosis, and treatment of atopic dermatitis in dogs. J Am Vet Med Assoc. 2019;254(11):1291-1300.
Miller J, Simpson A, Bloom P, et al. 2023 AAHA management of allergic skin diseases in dogs and cats guidelines. J Am Anim Hosp Assoc. 2023;59(6):255-284.
Also see pet owner content regarding dermatitis and dermatological problems in dogs.
References
Eisenschenk MC, Hensel P, Saridomichelakis MN, Tamamoto-Mochizuki C, Pucheu-Haston CM, Santoro D. Introduction to the ICADA 2023 canine atopic dermatitis pathogenesis review articles and updated definition. Vet Dermatol. 2024;35(1):3-4. doi:10.1111/vde.13183
Hensel P, Santoro D, Favrot C, Hill P, Griffin C. Canine atopic dermatitis: detailed guidelines for diagnosis and allergen identification. BMC Vet Res. 2015;11:196. doi:10.1186/s12917-015-0515-5
Fennis EEM, van Damme CMM, Schlotter YM, et al. Efficacy of subcutaneous allergen immunotherapy in atopic dogs: A retrospective study of 664 cases. Vet Dermatol. 2022;33(4):321-e75. doi:10.1111/vde.13075
Fischer NM, Rostaher A, Favrot C. A comparative study of subcutaneous, intralymphatic and sublingual immunotherapy for the long-term control of dogs with nonseasonal atopic dermatitis. Vet Dermatol. 2020;31(5):365-e96. doi:10.1111/vde.12860
DeBoer DJ, Verbrugge M, Morris M. Clinical and immunological responses of dust mite sensitive, atopic dogs to treatment with sublingual immunotherapy (SLIT). Vet Dermatol. 2016;27:82-e24. doi:10.1111/vde.12284
Fischer NM, Müller RS. Allergen specific immunotherapy in canine atopic dermatitis: an update. Curr Derm Rep. 2019;8:297-302. doi:10.1007/s13671-019-00276-z
Muse R, Rosenberg A; Nicholas J. Evaluation of antibody levels and clinical response to transdermal immunotherapy in six dogs: a pilot study. In: 2025 selected abstracts for NAVDF. Vet Dermatol. 2025;36:533-551. doi:10.1111/vde.13359
Olivry T, Foster AP, Mueller RS, McEwan NA, Chesney C, Williams HC. Interventions for atopic dermatitis in dogs: a systematic review of randomized controlled trials. Vet Dermatol. 2010;21(1):4-22. doi:10.1111/j.1365-3164.2009.00784.x
Olivry T, DeBoer DJ, Favrot C, et al. Treatment of canine atopic dermatitis: 2015 updated guidelines from the International Committee on Allergic Diseases of Animals (ICADA). BMC Vet Res. 2015;11:210. doi:10.1186/s12917-015-0514-6
Singh SK, Dimri U, Saxena SK, Jadhav RK. Therapeutic management of canine atopic dermatitis by combination of pentoxifylline and PUFAs. J Vet Pharmacol Ther. 2010;33(5):495-498. doi:10.1111/j.1365-2885.2009.01146.x
Saevik BK, Bergvall K, Holm BR, et al. A randomized, controlled study to evaluate the steroid sparing effect of essential fatty acid supplementation in the treatment of canine atopic dermatitis. Vet Dermatol. 2004;15(3):137-145. doi:10.1111/j.1365-3164.2004.00378.x
Schäfer L, Thom N. A placebo-controlled, double-blind study evaluating the effect of orally administered polyunsaturated fatty acids on the oclacitinib dose for atopic dogs. Vet Dermatol. 2024;35(4):408-417. doi:10.1111/vde.13246
Müller MR, Linek M, Löwenstein C, et al. Evaluation of cyclosporine‐sparing effects of polyunsaturated fatty acids in the treatment of canine atopic dermatitis. Vet J. 2016;210:77–81. doi:10.1016/j.tvjl.2015.11.012
Damone JM, Lister S, Lyons BM. Oclacitinib (Apoquel) toxicosis resulting in acute kidney injury in a dog. J Am Vet Med Assoc. 2025;263(9):1-2. doi:10.2460/javma.25.04.0240
