Canine atopic dermatitis
The atopic dermatitis ( AD ) of the dog is a frequent, allergic reaction of the skin caused by intense itching is characterized. Later on, self-traumatization and concomitant diseases can lead to severe skin changes. Atopic dermatitis in dogs usually develops within the first three years of life. The treatment is often successful, but very tedious. It is based on several pillars such as allergen avoidance or reduction, specific immunotherapy and / or the administration of immunosuppressive agents.
Classification
In the more recent literature, atopic dermatitis is further subdivided in the broader sense:
- feed-induced atopic dermatitis (FIAD, see feed allergy )
- non-feed-induced atopic dermatitis (NFIAD)
Clinically, the forms cannot be differentiated from one another; this article will further discuss atopic dermatitis in the narrower sense.
Occurrence and cause
Atopic dermatitis is a common skin condition in domestic dogs . About 10–15% of dogs suffer from atopic dermatitis ( Lit .: Peters, 2004). Dogs between the ages of six months and three years are particularly affected, and an initial disease beyond the age of six is unlikely. More commonly affected breeds are Boxers , Dalmatians , English Setters , Golden Retrievers , Irish Setters , Labrador Retrievers , Lhasa Apso , Shar-Pei , Shih-Tzu, and Terriers .
As with atopic dermatitis in humans , the cause and development of the disease is not yet fully understood. A genetically determined hypersensitivity to foreign substances is suspected, which leads to the onset of the disease through interaction with environmental factors. The disease is triggered by an allergic reaction of the immediate type , which is mediated by immunoglobulin E. It is assumed that other immunological processes involving immunoglobulin G , Langerhans cells , T lymphocytes , eosinophils and mast cells are also involved.
The allergenic substance (allergen) is mainly absorbed through the skin (percutaneously) , but also through inhalation or oral intake. Numerous antigens such as house dust mites , storage mites , pollen , molds , grasses , insects , animal hair and others come into consideration as allergens , mites being responsible for around 60% of cases. While atopy caused by mites occurs all year round, forms caused by pollen and grasses are mainly observed in spring and summer. The disease is probably based on a disruption of the skin's barrier function, which enables allergens to penetrate. Above all, the number of lipids between the cells of the horny layer is reduced, and in some forms less filaggrin is present.
Clinical picture
The most important and initially only symptom of atopic dermatitis is itching (pruritus) . Itching also occurs in numerous other skin diseases, but the lack of itching rules out atopic dermatitis. Primary skin changes ( primary lesions ) are at most in the form of redness ( erythema ) or nodules ( papules ), but these can also be completely absent ( pruritus sine materia ). The intensity of the itching can change depending on the amount of antigen (“ wax and wane ”) and only exceed a threshold value due to additional factors such as ambient temperature, stress, humidity or parasite infestation.
The itching is particularly evident in regions with thin skin and increased mechanical stress, since microscopic skin injuries (microtraumas) apparently promote the entry of allergens. The most common locations are the head ( lips , eye area , ear ) and / or paws . The flexors of the elbow , pastern and ankle , axilla , groin and abdomen can also be affected. In Boxers, Staffordshire Bull Terriers and Newfoundlands the underside of the neck is considered to be the breed-specific localization . The back, on the other hand, is never primarily affected.
In the further course, secondary skin changes ( secondary fluorescences) quickly occur due to scratching, rubbing, licking (fur discoloration) or gnawing the itchy skin areas. Practically all secondary fluorescences ( superficial skin defects , nodules , pus vesicles , strong flaking ) can occur here , and hair loss and skin thickening can occur for a longer period of time . A secondary bacterial infection can cause purulent inflammation of the skin ( pyoderma ), and excessive development of the skin flora can lead to malassecant dermatitis . Chronic ear inflammation ( otitis externa ) can develop in the ear , and chronic pododermatitis in the feet .
Similar to humans, atopic dermatitis predisposes the development of mycosis fungoides (a T-cell lymphoma of the skin). The mechanism is not known, nor is there any direct causal relationship at all. The disease occurs in dogs with a previous atopy with a twelve-fold higher probability.
diagnosis
The diagnosis is difficult to make clinically. Early forms are often not recognized by the owner or not taken seriously, so that the vet is usually presented with animals with advanced atopic dermatitis and unspecific secondary lesions. Inclusion criteria are:
- Start before the age of three
- predominant attitude in the house
- itching responsive to glucocorticoids
- chronic or recurring malassezia dermatitis
- Front paws are affected
- Auricles are affected
- The edges of the ears are not affected
- The back is not affected.
If five of the eight criteria apply, atopic dermatitis is likely. The sensitivity is then 0.85, the specificity 0.79. This means that in 15% of the animals atopic dermatitis is wrongly excluded and in almost 20% it is wrongly suspected. If six criteria are met, the sensitivity is only 58%, but the specificity increases to 89%.
In the differential diagnosis, other allergies such as flea infestation, flea and food allergies , which can also occur at the same time as atopy , as well as mange mite infestation , pyoderma of other origins and demodicosis , the latter primarily proceeding without itching, must be excluded . An exclusion diet makes sense in any case to delimit feed-related allergies.
The determination of the allergen can the so-called Fcε receptor test done with the free IgE - antibodies in the serum can be detected. An intracutaneous test is more meaningful , in which various allergens are injected into the skin and - in the positive case - trigger a reaction at the relevant point. Both allergy tests serve to identify factors that trigger allergies; the actual diagnosis of "atopic dermatitis" is always made clinically. However, both healthy dogs and atopics can react equally to the intracutaneous test. About 30% of atopic patients show a false negative intracutaneous test. This detection method is negatively affected primarily by various drugs, including through antihistamines , glucocorticoids , β2 - agonists and bronchodilators . In contrast, the Fcε receptor test is more robust; a waiting period of 28 days is only recommended when long-term corticosteroids are administered.
therapy
Atopic dermatitis is most effectively by a therapy , treated, which is based on multiple columns.
Allergen avoidance and desensitization
Because the triggering allergen is either unknown or cannot be removed from the dog's environment, eliminating the cause is rarely possible. In any case, combating house dust mites (a common cause of atopic dermatitis) can be attempted.
If the allergen is known through allergy tests , a desensitization can be carried out. The attempt is made to stop the allergic reaction by slowly increasing the administration of the allergen. The treatment is lengthy and requires a lot of willingness to cooperate and patience on the part of the dog owner, but the success rate is around 50 to 80%, around half of the dogs require additional symptomatic treatment, at least temporarily. New technical approaches to desensitization are the administration of the allergen via the oral mucosa ( sublingual immunotherapy , SLIT) or into a lymph node (intralymphatic immunotherapy) or the use of chemically modified allergens ( allergoids ) . While SLIT has fewer side effects than classic injection administration, the other two methods seem to achieve faster desensitization with just a few injections.
Medical therapy
The third treatment option is to combat itching.
Oral administration of prednisolone is most effective , although the dose and frequency of administration must be reduced as quickly as possible. Since prednisolone weakens the immune system , symptoms can suddenly intensify again after initial successes, as naturally occurring bacteria, malassezia and demodex mites suddenly trigger a clinically manifest skin disease. There is also a high risk of causing diabetes . Success with prednisolone is quick, but the treatment has numerous side effects and should therefore be limited to a maximum of three months.
Alternatively, antihistamines such as cetirizine , chlorpheniramine , hydroxyzine or terfenadine can be used, but histamine only plays a subordinate role in dogs as a mediator of itching, so that antihistamines are only effective in a few cases. In pyoderma they are completely ineffective.
Oral administration of cyclosporine , which greatly reduces the inflammatory reactions in the skin and thus can effectively eliminate the itching, is very promising . As with prednisolone therapy, the dose is gradually reduced. However, the treatment is relatively expensive and has side effects such as vomiting and diarrhea in around a quarter of patients . Tacrolimus , which is applied locally to the skin, shows a similar spectrum of activity .
The Janus kinase -1 inhibitor oclacitinib, which came onto the market in 2013, inhibits inflammation and itching and has already proven itself many times in the treatment of atopic dermatitis. The active ingredient shows no interaction with other active ingredients and also not with allergy tests, but it should not be used in severe infections, demodicosis or neoplasias . Lokivetmab, a monoclonal antibody against interleukin 31, has been available since 2017 , which is significantly involved in the development of itching in dogs. The treatment is practically free of side effects and is carried out by monthly subcutaneous injection.
The administration of pentoxifylline inhibits the release of cytokines due to its immunomodulating effect and usually leads to a reduction in itching and thus a clinical improvement. Interferons reduce the activity of Th2 cells and thus IgE production. Whether they are suitable as the sole long-term therapy requires further research. In a current study, the administration of cholecalciferol (vitamin D 3 ) was able to bring about a significant reduction in itching and skin changes.
Palmitoylethanolamide (PEA) is a bioactive lipid that is formed by damaged skin cells and reduces inflammation and itching. A study with oral administration of PEA led to a significant improvement in skin changes and a reduction in itching. However, PEA is not yet available in Germany.
Probiotics can improve the skin's barrier function and reduce interleukin-10 secretion. Their use in atopic dermatitis shows contradicting results. Treatment with eggs from roundworms such as Trichuris vulpis (dog whipworm) or Uncinaria stenocephala can - similar to the use of eggs from Trichuris suis in humans - lead to an improvement in symptoms in severe skin changes.
If prednisolone, oclacitinib, lokivetmab or ciclosporin show no or insufficient effect, the use of masitinib can also be considered, although moderate to severe side effects are to be expected in 16% of cases.
Supportive measures
Supportive measures make sense in any case, but are rarely sufficient as sole therapy. The administration of essential fatty acids (high-quality edible oils, special preparations) can significantly improve the symptoms after a few weeks. A ratio of omega-3 to omega-6 fatty acids of 5–10: 1 is considered optimal.
A shampooing is always supportive sense. It should be done twice a week. Shampoos based on chlorhexidine in particular prevent secondary comorbidities caused by malassezia or bacteria. In addition, they remove allergens, sweat and inflammation products from the surface of the skin and support the healing of skin damage and thus the creation of the skin's natural barrier function.
literature
- Beat Bigler: Skin Diseases . In: Peter F. Suter and Hans G. Nobody (eds.): Internship at the dog clinic . Paul-Parey-Verlag, 10th edition 2006, ISBN 3-8304-4141-X , pp. 332-391.
- Favienne Dethioux: The Challenge: Canine Atopic Dermatitis. Waltham Focus, Special Edition, 2006, 55 pp.
- Chiara Noli and Fabia Scarampella: Atopic Dermatitis . In: Practical Dermatology in Dogs and Cats . Schlütersche Verlagsanstalt, 2nd edition 2005, ISBN 3-87706-713-1 , pp. 252-259.
- Stefanie Peters: Atopic dermatitis in dogs. Long-term therapy on several pillars. In: Small animal concrete 7 (5) / 2004, pp. 20–26.
Individual evidence
- ↑ a b c C. Favrot et al .: A prospective study on the clinical features of chronic canine atopic dermatitis and its diagnosis. In: Vet. Dermatol. 21 (2010), pp. 23-31.
- ↑ a b c d e Katrin Timm and Petra Roosje: The atopic dermatitis of the dog . In: Kleintierpraxis 57 (2012), pp. 588–608.
- ↑ a b c d Ariane Neuber: Canine Atopic Dermatitis (CAD) - Part 1: Diagnosis. In: Kleintierpraxis Volume 64, Issue 8, 2019, pp. 458–476.
- ↑ D. Santoro et al .: Investigation on the association between atopic dermatitis and the development of mycosis fungoides in dogs: a retrospective case-control study. In: Veterinary Dermatology 18 (2007), pp. 101-106.
- ↑ Ralf S. Müller: Intradermal reactions against the storage mite Lepidoglyphus destructor in normal dogs and dogs with atopic dermatitis. In: Kleintierpraxis 56 (2010), pp. 5–10.
- ↑ P. Hensel at al .: Canine atopic dermatitis: detailed guidelines for diagnosis and allergen identification. In: BMC veterinary research. Volume 11, August 2015, p. 196, doi : 10.1186 / s12917-015-0515-5 , PMID 26260508 , PMC 4531508 (free full text) (review).
- ↑ a b c d Chiara Noli: Atopic Dermatitis in Dogs - Current Therapeutic Approaches . In: The practical veterinarian . tape 96 , no. 10 , 2015, p. 996-1007 .
- ↑ H. Moyaert et al .: A blinded, randomized clinical trial evaluationg the efficacy and safety of lokivetmab Compared To ciclosporin in client owned dogs with atopic dermatitis. In: Vet. Dermatology 2017
- ↑ CJ Klinger et al .: Vitamin D shows in vivo efficacy in a placebo-controlled, double-blinded, randomized clinical trial on canine atopic dermatitis. In: The Veterinary Record. Volume 182, number 14, 04 2018, p. 406, doi : 10.1136 / vr.104492 , PMID 29419484 .
- ^ Ralf S. Müller: Immunomodulating therapies for canine atopic dermatitis . In: Kleintierpraxis 56 (2011), pp. 642–648.
