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Canine Atopic Dermatitis: A Clinical Review for the Practicing Veterinarian

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11
Sep

A scientific review on pathogenesis, clinical presentation, differential diagnosis from cutaneous adverse food reaction, diagnostic confirmation, nutritional management, and multimodal control

Abstract

Canine atopic dermatitis (CAD) is one of the most frequently diagnosed pruritic skin diseases in small animal practice. It is a genetically predisposed, chronically relapsing inflammatory disorder driven by the interaction of epidermal barrier dysfunction, IgE-mediated hypersensitivity to environmental allergens, and cutaneous microbial dysbiosis. Because no single laboratory test is conclusive, diagnosis remains clinical, built on history, breed predisposition, distribution of lesions, and the systematic exclusion of other pruritic dermatoses  most importantly cutaneous adverse food reaction (CAFR), ectoparasitism, and secondary infection. This article reviews the current understanding of CAD pathophysiology, presents a structured approach to differentiating CAD from CAFR, summarizes confirmatory allergy testing (used for allergen identification rather than diagnosis), discusses the evidence for nutritional intervention including therapeutic skin-barrier diets, and outlines a multimodal, stepwise treatment strategy consistent with the International Committee on Allergic Diseases of Animals (ICADA) guidelines.

1. Introduction and Definition

Canine atopic dermatitis is defined by the International Committee on Allergic Diseases of Animals as a genetically predisposed, primarily pruritic, inflammatory skin disease with characteristic clinical features, most commonly associated with IgE antibodies directed against environmental allergens.¹ Reported prevalence in the general canine population ranges widely across studies (roughly 3–15%), but it is consistently cited among the top reasons for dermatology referral.

Historically considered a purely “atopic” (IgE-driven, triggered) condition, current consensus recognizes CAD as a multifactorial disease resulting from the interaction of three elements: (1) an impaired epidermal barrier that facilitates percutaneous allergen penetration, (2) an abnormal immune response to environmental allergens (house dust mites, storage mites, pollens, molds..etc), and (3) a disrupted cutaneous microbiome that favors colonization by Staphylococcus pseudintermedius and Malassezia pachydermatis.²

2. Pathogenesis

2.1 Skin barrier dysfunction

The stratum corneum’s “bricks and mortar” architecture depends on corneocytes embedded in a lipid matrix of ceramides, cholesterol, and free fatty acids. In dogs with atopic dermatitis, both lesional and clinically normal-appearing skin show reduced ceramide content, disorganized intercellular lipid lamellae, and increased transepidermal water loss (TEWL) compared with healthy dogs.³ This barrier defect is thought to be present from early life and is worsened by chronic allergen exposure and self-trauma, creating a cycle in which barrier impairment promotes further allergen penetration and sensitization.

2.2 Immune dysregulation

Percutaneous absorption of environmental allergens by Langerhans cells triggers a predominantly Th2-polarized response. T helper-2 cells are a key subset of T lymphocytes that drive humoral immunity, with interleukins 4, 13, and 31 driving IgE production, eosinophil recruitment, and pruritus. IL-31 in particular has emerged as a key pruritogenic cytokine and is the therapeutic target of the monoclonal antibody lokivetmab.

2.3 Microbial dysbiosis

Barrier disruption and altered innate immunity allow overgrowth of commensal organisms. Secondary bacterial and Malassezia infections are now understood as amplifiers of pruritus and lesion severity rather than incidental findings; this is one reason corticosteroid-responsive pruritus and recurrent yeast or bacterial infections feature prominently in diagnostic criteria.

3. Clinical Presentation and History

3.1 Signalment

Onset is typically before 3 years of age, although this is not universal.
Breed predispositions reported across studies include the West Highland White Terrier, French Bulldog, Boxer, Labrador and Golden Retriever, German Shepherd Dog, Shar Pei, and Bulldog, among others, supporting a heritable component.

3.2 Distribution of lesions The hallmark presentation is seasonal or non-seasonal pruritus affecting the face (periocular skin, muzzle), pinnae (concave aspect, with sparing of the margins), paws (ventral and interdigital), axillae, ventral abdomen, flexor surface of the elbows, and perineal region, typically with relative sparing of the dorsolumbar area. Primary lesions are often subtle (mild erythema).
Most visible changes – self-induced alopecia, excoriations, lichenification, hyperpigmentation, and pododermatitis – are consequences of chronic scratching, licking, and secondary infection.

3.3 History

A thorough history should capture: age of onset; seasonality versus year-round pruritus; indoor/outdoor lifestyle; positive response to prior glucocorticoid treatment; history of recurrent otitis or pyoderma; and, critically, a complete and honest dietary history, including treats, flavored medications, and table scraps, since this underpins the ability to design a valid elimination diet trial later.

3.4 Favrot’s clinical criteria

Because no single test confirms CAD, Favrot et al. (2010 study by Dr. Claude Favrot and colleagues) developed and validated clinical criteria to help clinicians estimate the probability of the diagnosis.⁴ The most widely used current version requires that the dog be pruritic and satisfy at least 5 of the following 8 criteria, yielding a reported sensitivity of approximately 85% and specificity of approximately 80%:⁵

  • Onset of signs before 3 years of age
  • Mostly indoor dog
  • Corticosteroid-responsive pruritus
  • Pruritus sine materia at onset (i.e., pruritus preceding visible lesions)
  • Affected front feet
  • Affected ear pinnae
  • Non-affected ear margins
  • Non-affected dorsolumbar area

These criteria discriminate CAD from other pruritic dermatoses reasonably well but were never intended to distinguish food-induced from non-food-induced atopic dermatitis, nor to replace exclusion of differentials.⁶

4. Differentiating Canine Atopic Dermatitis from Cutaneous Adverse Food Reaction

This is one of the most clinically important – and most frequently confused – distinctions in veterinary dermatology, because CAFR and environmentally-driven cAD are clinically indistinguishable in a large proportion of cases and can also coexist in the same patient.

4.1 Why they look alike

Both conditions can produce facial, pedal, and ear pruritus; both can be accompanied by recurrent Malassezia otitis and pododermatitis, and both are typically non-seasonal when the causative allergens are constant (house dust mites) or year-round (food). Favrot’s own prospective study found that most clinical features overlapped substantially between food-induced and non-food-induced atopic dermatitis, with only a few statistically significant differences (e.g., a higher frequency of gastrointestinal signs and lesions outside the classic distribution in food-induced disease), none of which were reliable enough to use individually to distinguish between CAFR and CAD.⁵

4.2 Clues that favor CAFR

  • Age of onset at either extreme (younger than 1 year or older than 6 years), which is less typical for pure environmental atopy.
  • Non-seasonality from the very first episode (though constant-allergen CAD is also non-seasonal (Dust mites), so this is supportive, not confirmatory).
  • Concurrent gastrointestinal signs — vomiting, diarrhea, increased frequency of defecation — reported in a meaningful subset of CAFR cases.⁷
  • Poor or partial response to otherwise appropriate anti-allergic therapy.
  • Recurrent bilateral otitis externa as the sole or predominant sign, which is described in a large proportion of CAFR cases across studies.⁸

4.3 Why history and testing cannot make this call alone

No serum IgE, IgG, intradermal, or “hair/saliva” test has adequate sensitivity or specificity to diagnose CAFR; several studies have specifically shown that serologic and intradermal food-antigen testing does not correlate reliably with elimination-challenge outcomes.⁹ Point-of-care hair and saliva allergy tests marketed directly to owners have no validated diagnostic value for food or environmental allergy in dogs and should not be used to guide clinical decisions. Consequently, the only validated diagnostic tool remains the elimination-diet trial with challenge, described below.

5. Diagnostic Confirmation

Diagnosis of cAD is, and remains, a diagnosis of exclusion built on a compatible history and Favrot criteria, after ruling out other causes of pruritus. The diagnostic workup should proceed in a logical order:

5.1 Step 1 — Rule out ectoparasites

Skin scrapings, coat combings/clear acetate tape preparations, and a strict flea-control (given how closely flea allergy dermatitis can mimic cAD) are mandatory first steps, since Sarcoptes, Demodex, Cheyletiella, and fleas are all common, treatable causes of pruritus that must be excluded before allergy is pursued.

5.2 Step 2 — Identify and treat secondary infection

Cytology from affected skin and ears (impression smears, tape preparations) to identify and quantify bacterial cocci/rods and Malassezia yeast is essential, because uncontrolled secondary infection alone can account for a large proportion of a patient’s pruritus; re-assessment after infection resolution is required before judging.

For the otitis externa that so frequently accompanies CAD, Mometamax Ultra[SCT1]  (gentamicin, posaconazole, and mometasone furoate otic suspension) offers a practical in-clinic option: a single 0.8 mL in-clinic administration per affected ear treats otitis externa associated with susceptible strains of Malassezia pachydermatis, Staphylococcus pseudintermedius, and Pseudomonas aeruginosa.24

Shifting administration from the owner to the clinic removes a major compliance barrier in a disease where recurrent, poorly-treated otitis is itself a driver of chronic discomfort and repeated flares.

5.3 Step 3 — Rule out cutaneous adverse food reaction

Because no laboratory test reliably diagnoses CAFR, an elimination diet trial using either a novel, single-source protein the dog has never eaten or a hydrolyzed-protein diet is the diagnostic gold standard.¹⁰ Based on the systematic evidence review by Olivry, Mueller, and Prélaud, more than 80% of dogs with CAFR show remission of signs by 5 weeks, but a full 8-week trial is needed to meet 90% response. This means shorter tests can miss real success. the trial should therefore be fed exclusively (no treats, flavored chews, or table scraps) for a minimum of 8 weeks, followed by ideally an individual-ingredient re-challenge to confirm the diagnosis and identify the specific offending allergen(s).¹¹The best evidence available as of January 16, 2015 suggests that the most likely food allergens contributing to canine CAFRs are beef, dairy products, chicken, and wheat. The most common food allergens in cats are beef, fish and chicken.¹²

Diet selection for the trial matters clinically, because the reliability of an elimination trial depends entirely on how completely the chosen protein avoids recognition by the patient’s existing IgE.


Among commercially available hydrolyzed diets, Royal Canin Anallergenic is the diet to consider as the first-choice option for the trial. It is formulated with extensively hydrolyzed poultry feather protein rather than the hydrolyzed meat- or organ-derived proteins used in most other hydrolyzed diets. 99% of proteins provided in the formulation have a molecular weight  <1kDa; 100% are <3kDa. This represents hydrolysis beyond the 3–15 kDa range typical of standard hydrolyzed chicken- or soy-based diets.²⁶


In a study, serum from dogs with the highest anti-poultry IgE levels showed no recognition of the extensively hydrolyzed feather protein extract, comparable to a beef negative control, and in a clinical challenge, none of ten chicken-allergic dogs reacted after two weeks on the diet (Royal Canin Anallergenic), versus a 40% flare rate on a hydrolyzed chicken-liver diet in the same comparative work.²⁷ This supports feather-protein hydrolysate as a rational choice.

5.4 Step 4 — Confirm and characterize environmental allergy

Once ectoparasites, infection, and CAFR have been reasonably excluded (or addressed) and the Favrot criteria are satisfied, allergen-specific testing can be pursued — not to diagnose cAD, but to select allergens for allergen-specific immunotherapy (ASIT). Two validated methods exist:

  • Intradermal testing (IDT): considered by many dermatologists the reference method for identifying clinically relevant environmental sensitizations, performed with a standardized allergen panel and interpreted alongside positive and negative controls, ideally performed when the patient is symptomatic and has been off antihistamines/glucocorticoids for an appropriate washout period.
  • Allergen-specific serum IgE testing: a practical, less operator-dependent alternative, with comparable utility to IDT for selecting immunotherapy allergens, though agreement between the two methods for individual allergens is imperfect.¹³

Both tests can produce positive results in clinically normal dogs and therefore must always be interpreted in light of clinical relevance and history rather than used as a stand-alone diagnostic tool for cAD itself.¹

6. The Role of Nutrition in Managing Canine Atopic Dermatitis

Given that epidermal barrier dysfunction is a central pathogenic feature of cAD, nutritional strategies that support barrier lipid composition and modulate cutaneous inflammation form a legitimate and evidence-supported pillar of management, complementary to pharmacologic control and allergen avoidance.

6.1 Rationale: feeding the skin barrier

Ceramides, cholesterol, and free fatty acids are the structural lipids of the stratum corneum. Dietary intake of essential fatty acids – linoleic acid (omega-6) and alpha-linolenic acid together with the long-chain omega-3s eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) – supplies substrate for cutaneous lipid synthesis and modulates inflammatory process.¹⁴ Clinical and experimental studies have shown that:

  • Total ceramide content is significantly reduced in both lesional and non-lesional skin of atopic dogs compared with healthy dogs, and this reduction correlates with increased TEWL.¹⁵
  • Oral essential fatty acid supplementation has demonstrated a measurable lower maintenance dose of prednisolone to control pruritus in dogs with cAD in a randomized controlled trial.¹⁶
  • Topical and oral strategies that combine ceramides, free fatty acids, have shown improvement in TEWL and clinical scores in several controlled studies.¹⁷

6.2 Therapeutic: skin-barrier diets

Veterinary therapeutic diets designed for dermatologic support (for example, the Royal Canin Skin Care[SCT1] range) are formulated with an optimised omega-6:omega-3 ratio, providing linoleic acid together with EPA and DHA, marketed specifically to nutritionally support the skin’s natural barrier function and coat quality in dogs with dermatosis.¹⁸

It is worth noting that this class of diet is a barrier-support strategy and is distinct from the hydrolyzed-protein diets used specifically to diagnose or manage a confirmed or suspected CAFR. The two serve different clinical purposes and, in a dog with diagnostic uncertainty regarding food involvement, a hydrolyzed elimination diet should take diagnostic priority before a barrier-support diet is chosen long-term.

6.3 Practical: integration

Nutritional intervention should always be framed to owners as one component of a multimodal plan, not a stand-alone cure.

  • In dogs with confirmed environmental-only cAD (CAFR excluded), a skin-barrier-support maintenance diet enriched in essential fatty acids can be a reasonable long-term nutritional component.
  • In dogs where CAFR has not yet been excluded, prioritize a strict elimination trial with a novel-protein or hydrolyzed diet for the full 8-week diagnostic window before introducing other dietary products, treats, or supplements that could confuse the trial.
  • Nutritional intervention should always be framed to owners as one component of a multimodal plan, not a stand-alone cure.

7. Multimodal Management of Canine Atopic Dermatitis

The 2015 ICADA treatment guidelines remain the reference framework and explicitly recommend a combined, individualized approach rather than reliance on a single intervention, because treatment approach varies between dogs and within the same dog; between the acute flare and chronic maintenance phases.²⁰

7.1 Identify and control flare factors

  • Strict, year-round flea control regardless of visible fleas.
  • Confirmed or suspected food triggers avoided per elimination-trial results.
  • Environmental allergen avoidance where practical (e.g., house dust mite control measures, HEPA air filtration, minimizing grass contact during peak pollen exposure).

7.2 Restore and maintain skin/coat hygiene

Regular bathing with mild, non-irritating (and where indicated, antimicrobial) shampoos reduces allergen load on the skin surface, supports barrier hydration, and helps manage secondary infection; this is recommended as a foundational, low-risk intervention in both the 2010 and 2015 ICADA guidelines.²⁰

Within this category, DOUXO S3 CALM CEVA is a topical option purpose-built for the barrier pathophysiology. Its active ingredient, Ophytrium is described as acting on three fronts simultaneously – physically reinforcing the barrier, supporting a balanced microbial flora, and calming irritated skin. The shampoo/mousse leave-on protocol is designed to be used together for sustained skin contact.²⁹ In a European/US field study of dogs with atopic dermatitis, the combined shampoo-and-mousse protocol was associated with a reported 58% reduction in extent/severity of lesions based on CADESI scoring (Canine Atopic Dermatitis Extent and Severity Index) and a 41% reduction in pruritus, with responses apparent from around day 7 and best results by day 21.29

7.3 Control acute flares

First-line options for acute pruritus and lesion flares include: A topical application; DUOXO S3 CALM CEVA or topical glucocorticod spray

Systemic Pruritis control:
Oral Pruritis control; glucocorticoids or an oral Janus kinase (JAK) inhibitor.alongside identification and elimination of the precipitating cause.²⁰

Most recently, Numelvi® [SCT1] (atinvicitinib), a second-generation, JAK1-highly selective inhibitor, was authorized in the EU and in the US and in UAE recently, for control of pruritus associated with allergic dermatitis, including CAD, from 6 months of age.²⁵ Its selectivity profile – reported as at least 10-fold greater for JAK1 than for JAK2, JAK3, or TYK2 – is intended to limit interference with hematopoietic and immune functions dependent on the other JAK enzymes while still delivering rapid antipruritic effect.

7.4 Manage chronic disease

For long-term control, the medications with the strongest evidence base are:

  • Oral glucocorticoids (effective but limited long-term by adverse effects).
  • Oral ciclosporin, an effective steroid-sparing option for chronic cases, with a delayed onset of action (typically 4–6 weeks).
  • Numelvi (atinvicitinib), the newer second-generation JAK1-highly selective inhibitor, dosed once daily and safe to use from 6 months of age; field-trial data indicated a normal serological response to core vaccination when given at the recommended dosage — both practically useful properties for dogs on long-term, combination management.²⁵
  • Lokivetmab, a monoclonal antibody targeting IL-31, given as a monthly subcutaneous injection. Lokivetmab is licenced for dogs and randomized controlled trials describe a rapid onset of antipruritic effect with a good safety profile.
  • Essential fatty acid (EFA) supplementation.

7.5 Prevent flares long-term

Two interventions are specifically highlighted by ICADA as capable of preventing or delaying flare recurrence rather than simply treating active disease:

  • Allergen-specific immunotherapy (ASIT), based on IDT (intradermal Testing) or serum IgE results, remains the only treatment with the potential for long-term disease modification and is particularly attractive for dogs requiring lifelong management or with drug-related contraindications.
  • Proactive, intermittent topical glucocorticoid application to previously affected sites, shown to reduce flare recurrence when applied 2–3 times weekly between flares.²⁰ as well as DOUXO S3 Calm shampoo and leave on foam.

7.6 Putting it together

A realistic multimodal plan for a newly diagnosed, moderately affected dog typically layers:
(1) confirmed flea control, (2) treatment of any active secondary infection; including, where bacterial and/or Malassezia otitis is present, an in-clinic single-dose option such as Mometamax Ultra to remove compliance as a variable, (3) a completed elimination-diet trial if food involvement has not already been excluded, (4) a barrier-support skin diet and/or EFA supplementation, (5) a fast-acting antipruritic -the newer JAK1-selective Numelvi, or lokivetmab, or short-course glucocorticoids – to control the current flare, and (6) discussion of ASIT for dogs with confirmed environmental sensitization and an expected long disease course. Reassessment intervals and PVAS (Pruritus Visual Analog Scale) scoring at each recheck help objectively track response and guide step-down or step-up adjustments over time.

8. Conclusion

Canine atopic dermatitis is best understood as a barrier-immune-microbiome disease rather than a single-cause allergy, and its diagnosis remains clinical and exclusionary, anchored by a compatible history, Favrot’s criteria, and systematic ruling-out of ectoparasites, infection, and cutaneous adverse food reaction via a properly conducted 8-week elimination diet trial.
Allergy testing (intradermal or serum IgE) confirms allergen specificity for immunotherapy and will not establish the diagnosis alone.
Nutritional support targeting skin barrier lipid composition is a well-supported adjunct within a broader multimodal strategy that combines flare-factor control, hygiene, appropriately chosen antipruritic therapy, and, where suitable, allergen-specific immunotherapy for durable long-term control.

References

  1. International Committee on Allergic Diseases of Animals (ICADA). Consensus statement on the terminology and diagnostic criteria for canine atopic dermatitis. Vet Dermatol.
  2. Olivry T, Mueller RS. Critically appraised topic on adverse food reactions of companion animals (1): duration of elimination diets. BMC Vet Res. 2015;11:225.
  3. Kwochka KW. Defective skin barrier in canine atopic dermatitis [review]. Cited studies include: Marsella R, Samuelson D. Unraveling the skin barrier: a new paradigm for atopic dermatitis and house dust mites. Vet Dermatol. 2009;20:533–540.
  4. Favrot C, Steffan J, Seewald W, Picco F. A prospective study on the clinical features of chronic canine atopic dermatitis and its diagnosis. Vet Dermatol. 2010;21:23–31.
  5. Favrot C, Steffan J, Seewald W, Picco F. A prospective study on the clinical features of chronic canine atopic dermatitis and its diagnosis. Vet Dermatol. 2010;21:23–31. (Sensitivity/specificity data as summarized in subsequent validation literature.)
  6. Le Mignon E, et al. Canine atopic dermatitis diagnostic criteria: evaluation of four sets of published criteria among veterinary students. J Vet Med Educ. Advance online, PMID 25588943.
  7. Mueller RS, Olivry T. Critically appraised topic on adverse food reactions of companion animals (7): signalment and cutaneous manifestations of dogs and cats with adverse food reactions. BMC Vet Res. 2019;15:140.
  8. Olivry T, Mueller RS. Critically appraised topic on adverse food reactions of companion animals (3): prevalence of cutaneous adverse food reactions in dogs and cats. BMC Vet Res. 2017;13:51.
  9. Bethlehem S, Bexley J, Mueller RS. Patch testing and allergen-specific serum IgE and IgG antibodies in the diagnosis of canine adverse food reactions. Vet Immunol Immunopathol. 2012;145(3–4):582–589.
  10. Mueller RS, Unterer S. Adverse food reactions: pathogenesis, clinical signs, diagnosis and alternatives to elimination diets. Vet J. 2018;236:89–95.
  11. Olivry T, Mueller RS, Prélaud P. Critically appraised topic on adverse food reactions of companion animals (1): duration of elimination diets. BMC Vet Res. 2015;11:225.
  12. Mueller RS, Olivry T, Prélaud P. Critically appraised topic on adverse food reactions of companion animals (2): common food allergen sources in dogs and cats. BMC Vet Res. 2016;12:9.
  13. 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.
  14. Popa I, Watson AL, Solgadi A, Butowski C, Allaway D, Portoukalian J. Linoleate-enriched diet increases both linoleic acid esterified to omega hydroxy very long chain fatty acids and free ceramides of canine stratum corneum without effect on protein-bound ceramides and skin barrier function. Arch Dermatol Res. 2018;310(7):579–589.
  15. Marsella R. Are transepidermal water loss and clinical signs correlated in canine atopic dermatitis? A compilation of studies. Vet Dermatol. 2012;23:238-e49.
  16. Vet Times. Using essential fatty acids in canine atopic dermatitis [review of randomized controlled trial data on EFA glucocorticoid-sparing effect].
  17. Marsella R, Cornegliani L, Ozmen I, Bohannon M, Ahrens K, Santoro D. Randomized, double-blinded, placebo-controlled pilot study on the effects of topical blackcurrant emulsion enriched in essential fatty acids, ceramides and 18-beta glycyrrhetinic acid on clinical signs and skin barrier function in dogs with atopic dermatitis. Vet Dermatol. 2017;28:577-e140.
  18. Royal Canin. Skin Care and Sensitive Skin Care veterinary/therapeutic diet product information (manufacturer product documentation).
  19. Royal Canin. Skin Care dry dog food — analytical constituents and composition (manufacturer product documentation). 
  20. International Committee on Allergic Diseases of Animals (Olivry T, DeBoer DJ, Favrot C, Jackson HA, Mueller RS, Nuttall T, Prélaud P). Treatment of canine atopic dermatitis: 2015 updated guidelines from the International Committee on Allergic Diseases of Animals (ICADA). BMC Vet Res. 2015;11:210.
  21. Forster S, et al. Comparative efficacy and safety of ilunocitinib and oclacitinib for the control of pruritus and associated skin lesions in dogs with atopic dermatitis. Vet Dermatol. 2025.
  22. Michels GM, et al. Efficacy and safety of lokivetmab (Cytopoint®) for the control of pruritus and skin lesions in dogs with atopic dermatitis. Vet Dermatol.
  23. Clinical efficacy of oclacitinib and lokivetmab in dogs with canine atopic dermatitis. J Vet Clin (Korean Society of Veterinary Clinics).
  24. Heuer C, et al. Clinical safety and efficacy of a single-dose gentamicin, posaconazole and mometasone furoate otic suspension for treatment of canine otitis externa. Vet Rec. 2024. (Mometamax Ultra/Mometamax Single; MSD/Merck Animal Health.)
  25. MSD Animal Health / Merck Animal Health. NUMELVI® (atinvicitinib) Tablets for Dogs — product and pivotal field-trial data presented at the 35th European Veterinary Dermatology Congress, Bilbao, Spain, September 2025; EU marketing authorization July 2025; US FDA approval February 2026.
  26. Bizikova P, Olivry T. A randomized, double-blind crossover trial testing the benefit of two hydrolyzed poultry-based commercial diets for dogs with spontaneous cutaneous adverse food reactions. Vet Dermatol. 2016;27:289-e70; and Jackson HA, et al./Olivry T, et al. Extensive protein hydrolyzation is indispensable to prevent IgE-mediated poultry allergen recognition in dogs and cats. BMC Vet Res. 2017;13:251.
  27. Olivry T, et al. Extensive protein hydrolyzation is indispensable to prevent IgE-mediated poultry allergen recognition in dogs and cats. BMC Vet Res. 2017;13:251.
  28. Royal Canin. Skin Care dry dog food — patented Skin Barrier complex (select B-vitamins and amino acid) and analytical constituents (manufacturer product documentation).
  29. Gatellet M, Ahman S, Bruet V, Cadot P-M, Mueller R, Noli C, Nuttall T, Ollivier E, Blondel T, Savelli N. Performance of combined shampoo and mousse applications containing Ophytrium in dogs with sensitive, itchy and irritated skin: a European field trial. Vet Dermatol. 2020;31(Suppl 1):33. (Ceva Animal Health/DOUXO® S3 CALM field-trial data.)
August 20, 2026