POMÁHÁME AKITÁM S SA V NOUZI 

Akita help in an emergency

Sebaceózní Adenitida: Co to je a jak ji léčit

Autor - MVDr. Jan Rybníček

Sebaceózní adenitida u psů je vzácné seboroické a alopetické onemocnění postihující výlučně mazové žlázy kůže, které jsou v průběhu procesu naprosto zlikvidovány. Přestože postižen může být jakýkoli pes, plemenně predisponovaná plemena jsou pudli, akita - inu, viszla, samojed, a čau čau. V některých chovech může být postiženo větší množství zvířat (v současné době je sebaceózní adenitida relativně často v ČR pozorována u plemene akita inu). Byly popsány ojedinělé případy u koček. Onemocnění je geneticky podmíněné, u pudlů byla prokázána autozomálně recesivní dědičnost, u akit na základě genetických studií populace je autozomálně recesívní dědičnost téměř jistá. U geneticky predisponovaných zvířat dochází k autoimunitnímu buněčně zprostředkovanému poškození mazových žláz. U onemocnění nebyl doposud prokázán přesný antigen proti kterému je namířena imunitní reakce, současně též nebyly prokázány cirkulující ani tkáňově vázané autoprotilátky, nicméně imunohistochemickými studiemi byl prokázán přímý buněčně zprostředkovaný útok proti buňkám mazových žláz. Na počátku onemocnění dojde k poškození mazových žláz cytotoxickými T lymfocyty a histiocyty a postupně jsou sebocyty a celé mazové žlázy totálně zlikvidovány. Proces je nevratný. V důsledku abnormalit a absenci mazu často dochází k sekundárním bakteriálním infekcím.

Klinické příznaky: První klinické příznaky se mohou objevit již v pozdějším štěněčím věku nebo kdykoli během života zvířete. Klinické příznaky u akity jsou charakterizovány zejména nadměrným šupinatěním, tvorbou folikulárních odlitků, vypadáváním srsti a sekundární pyodermií s různě vyjádřeným pruritem. Sekundárně může srst působit dojmem mastnoty. Lokalizace procesu bývá obvykle na místech s množstvím mazových žláz, tj. na hlavě, zejména na uších, krku, ocase a dorsální straně trupu. Ojediněle u pacientů též dochází k celkovým klinickým příznakům, zejména k febrilii, apatii, nechutenství apod. Podobné klinické příznaky se vyskytují u samojeda a čau - čaua. U pudla se nejčastěji vyskytuje zvýšené šupinatění, chlupy bývají obaleny tzv. folikulárními odlitky, později dochází k vypadávání srsti ve stejných oblastech jako u akity. Rozdílné klinické příznaky jsou u krátkosrstých plemen (viszla aj.), kdy se tvoří erytematózních papuly a plaky, zejména na obličeji. Tyto léze šupinatějí a následuje vypadávání srsti. Proces se může šířit dále na trup a generalizovat. U krátkosrstých plemen může docházet k intermitentním otokům pysků, nosu a víček.

Diagnostika: Diferenciální diagnóza je široká a zahrnuje folikulitidy (demodikóza, bakteriální folikulitida, dermatofytóza), keratinizační defekty (idiopatická seborea, dermatózy reagující na podávání zinku a vitamínu A), folikulární dysplazie, některé hormonální dermatózy, u krátkosrstých plemen také epiteliotropní lymfom. Diagnóza je stanovena na základě anamnézy, klinických příznaků a zejména histopatologie, která je zcela diagnostická. Vyšetřením krevního vzorku nelze získat diagnózu, jedná se t.č. o výzkumnou metodu.

Histopatologie: Na počátku onemocnění lze pozorovat lymfohistiocytární, granulomatózní zánět orientovaný pouze na mazové žlázy, později v důsledku jejich likvidace nelze mazové žlázy zachytit, perifolikulárně lze pozorovat pouze fokální fibrózu v místech jejich původní lokalizace. Veškeré ostatní struktury nevykazují v počátcích onemocnění žádné změny. Sekundární změny jsou časté zejména u chronických případů a zahrnují hyperkeratózu, keratózu folikulů, příznaky superficiální pyodermie a perivaskulární dermatitidu. Pro výzkumné účely u sebaceózní adenitidy se využívá imunofluorescenční vyšetření.

Terapie: Neexistuje žádná terapie, která by umožnila regeneraci mazových žláz, veškeré fromy terapie jsou pouze udržovací a řeší spíše komplikace. Pacienta lze dlouhodobě udržovat v remisi pomocí řady terapeutických postupů jako je zabránění sekundární bakteriální infekce, lokální aplikace emolientií, celkově lze využít do určité míry glukokortikoidy, vitamín A, retinoidy a cyklosporin. Pacienta lze udržovat v dobrém klinickém stavu, avšak vyžaduje to maximální péči ze strany majitele. Lehčí případy lze řešit pouhou aplikací látek nahrazujících do určité míry maz (urea, 50% propylenglykol ad. či jejich kombinace) ve formě denního celotělového sprejování nebo oplachů. Chronické a těžké případy vyžadují celkovou léčbu, kdy asi jako nejvhodnější se v současné době jeví vysoké dávky vitamínu A, který má normalizační efekt na keratinocyty, v dávce 1000 m.j./kg ž.hm. p.p. 2x denně celoživotně. Velmi dobrý efekt je patrný minimálně u 50% případů. Retinoidy (isotretinoin nebo etretinate) nebo cyklosporin jsou sice též účinné, avšak zcela limutující je jejich cena a rizika vedlejších účinků (rohovkové defekty, celkové potíže, imunosuprese ad.). Účinnost těchto látek se v závislosti na různých studiích udává od 50 do 80%. Imunosupresní dávky glukokortikoidů bývají na počátku onemocnění relativně efektivní, avšak vzhledem ke svým výrazným potenciálním vedlejším účinkům, by u tohoto onemocnění (nejedná se o život ohrožující stav), neměly být pokud možno používány. Obvykle k jejich použití přikročíme v případech, kdy majitel není ochoten používat dražší léky a jedinou další alternativou je euthanasie. U velmi ojedinělých případů v počátečních stadiích byla zaznamenána i spontánní remise.

Onemocnění má špatnou prognózu co se týče vyléčení, neboť dochází k totální destrukci mazových žláz. K jejich regeneraci nemůže dojít. Nicméně jedná se ve většině případů o onemocnění, u něhož lze pacienta udržovat na přijatelné zdravotní úrovni.

Prevence: Vzhledem k tomu, že se jedná o geneticky podmíněný defekt, postižená zvířata a jejich přímí příbuzní, zejména rodiče by neměli být zařazováni do chovu.

Pozn.: Bioptické vzorky kůže lze zasílat na adresu uvedenou v hlavičce. Dermatologické vyšetření lze provést na obědnání na klinice Jaggy Brno (tel. 545234035), Praha (235097540) a ve Veterinární nemocnici Libuš, Praha (244470704).

Autosomálně recesivní dědičnost SA:

Ze spojení dvou zdravých rodičů jsou vždy zdraví potomci - 100%

Ze spojení rodičů - jeden zdravý a jeden přenešeč se narodí pouze zdravá štěňata a další přenašeči - 50% - 50%

Ze spojení dvou rodičů přenašečů se narodí zdravá štěňata, další přenašeči i nemocná štěňata - 50% přenašečů - 25% zdravých - 25% nemocných

Ze spojení rodičů - jeden přenašeč a jeden nemocný se narodí pouze přenašeči a nemocná štěňata - 50% - 50%

Ze spojení dvou nemocných rodičů jsou vždy nemocná štěňata - 100%

Procentuální vyjádření není přesné - když uvádíme 50% neznamená to, že jedno štěně je zdravé a druhé zákonitě přenašeč atd., toto vyjádření se týká dlouhodobého sledování velkého počtu objektů
Převzato z haguro.cz

Sebaceous adenitis: What is it and how to treat it

Author - DVM. Jan Rybníček

Sebaceous adenitis in dogs is rare and seborrheic alopetické disease affecting only the sebaceous glands of the skin that are in the process completely destroyed. Although it may be affected by any dog ​​breeds are predisposed stud poodle, akita - inu, Viszla, Samoyed, and bye bye. In some breeds may be affected by a larger number of animals (currently sebaceous adenitis relatively frequently observed in CR breed Akita). Isolated cases have been reported in cats. The disease is genetically determined, the Poodle has been demonstrated autosomal recessive inheritance, in Akita based on genetic studies of populations is an autosomal recessive inheritance almost certain. In genetically susceptible animals leads to cell-mediated autoimmune damage to the sebaceous glands. For the disease has not yet demonstrated the exact antigen against which it is directed immune response, whilst also been demonstrated circulating or tissue-bound autoantibodies, however, immunohistochemical studies have shown a direct cell-mediated attack against cells of the sebaceous glands. Early in the disease there is damage to the sebaceous glands by cytotoxic T lymphocytes and histiocytes and gradually are sebocytes and sebaceous glands throughout totally destroyed. The process is irreversible. As a result of abnormalities and absence of sebum often leads to secondary bacterial infections.

Clinical signs: The first clinical symptoms may appear as early as later in the puppy age or at any time during the life of the animal. Clinical signs in Akitas are mainly characterized by excessive popping, the formation of follicular casts, hair loss and secondary pyoderma variously expressed pruritus. Secondarily, the coat can give the impression of grease. Localization of the process is usually in places with many sebaceous glands, i.e. on the head, especially on the ears, neck, tail and dorsal side of the hull. Occasionally, patients also leads to an overall clinical symptoms, in particular fever and lethargy, loss of appetite, etc. Similar clinical signs occur in Samoyeds and Chow - Chow. At the bottom line is most prevalent increased scaling, hairs are coated so. Follicular casts later leads to hair loss in the same areas as the Akita. Different clinical symptoms are short-breeds (Viszla et al.), Which forms erythematous papules and plaques, particularly on the face. These lesions šupinatějí, followed by hair loss. The process can be spread further to the hull and generalize. For shorthaired breeds may experience intermittent swelling of the lips, nose and eyelids.

Diagnosis: Differential diagnosis is wide and includes folliculitis (demodicosis, bacterial folliculitis, dermatophytosis), keratinization defects (idiopathic seborrhoea, dermatitis respond to the administration of zinc and vitamin A), follicular dysplasia, some hormonal dermatoses, for the short breeds also epiteliotropní lymphoma. Diagnosis is based on history, clinical symptoms, and histopathology in particular, which is completely diagnostic. Examination of the blood sample can not get a diagnosis, it is at present, a research method.

Histopathology: At the onset of the disease can be observed lymphohistiocytic, granulomatous inflammation oriented only on the sebaceous glands, later as a result of the liquidation of the sebaceous glands can not capture, peri can be seen only focal fibrosis in places of their original location. All other structures show early in the disease no changes. Secondary changes are frequent, especially in chronic cases and include hyperkeratosis, keratosis follicular pyoderma and symptoms superficial perivascular dermatitis. For research purposes by the sebaceous adenitis is used immunofluorescence tests.

Therapy: There is no therapy that would allow the regeneration of sebaceous glands, all Froma therapies are only maintenance and solves rather complications. The patient may in the long term to maintain remissions in a series of therapeutic procedures such as preventing secondary bacterial infections, topical emollients, generally can be used to a certain extent glucocorticoids, vitamin A, retinoids and cyclosporin. The patient can be maintained in good clinical condition, but it requires the utmost care by the owner. Mild cases can be solved by the mere application of alternatives to some extent wax (urea, 50% propylene glycol, etc., Or a combination thereof) in the form of daily whole-body spraying or rinsing. Chronic and severe cases require systemic treatment, which probably is the most suitable at present seems high doses of vitamin A, which has a normalizing effect on keratinocytes, at 1000 m.j./kg bw AET 2x daily for life. A very good effect is noticeable at least 50% of cases. Retinoids (isotretinoin or etretinate) or cyclosporine are indeed also effective but completely limutující is the cost and risk of side effects (corneal defects, major problems, immunosuppression ad.). The effectiveness of these substances was based on various studies indicates from 50 to 80%. Immunosuppressive doses of glucocorticoids are early in the disease relatively effective, but given its significant potential side effects, would in this disease (not a life-threatening condition) should not be used if possible. They usually use proceed in cases where the owner is not willing to use more expensive drugs and the only other alternative is euthanasia. In very rare cases in the early stages was recorded spontaneous remission.

The disease has a poor prognosis with regard to cure, because there is a total destruction of the sebaceous glands. The regeneration can not occur. However, it is in most cases of disease in which the patient can be maintained at an acceptable level of health.

Prevention: Since it is a genetically determined defect affected animals and their direct relatives, especially parents should not be placed into breeding.

Note .: skin biopsy specimens should be sent to the address specified in the header. Dermatological tests can be performed to order separately clinic Jaggy Brno (tel. 545 234 035), Prague (235,097,540) and the Veterinary Hospital Libus (244,470,704).

Sebaceous Adenitis in the Akita : "The Mysterious Skin Disease" PD Dr. Ina Pfeiffer Sara Baila cand. Dipl.-Biol. Feb 2015 Current Overview Sebaceous Adenitis (SA) in dogs is primarily an advancing inflammatory destruction of the sebaceous glands of the skin. This disease occurs in various dog-breeds with certain breeds showing a higher predisposition. Most frequently affected are e.g. Akitas, American Akitas, Poodles, Vizslas, Samoyedes, Chow Chows and English Springer Spaniels. Furthermore cases of SA have been found in cats, rabbits, horses and humans (Bensignor & Guaguère, 2012). Within this context, the current scientific knowledge about sebaceous adenitis, specifically in the Akita (Fig), will be discussed. Fig. 1: On the left a healthy Akita, on the right an Akita with sebaceous adenitis 2 Anatomy of the skin The Sebaceous Glands As already mentioned, the sebaceous glands of the skin (glandulae sebaceae) play a major role in this condition. Figure 2 (Fig.:2) shows in detail the anatomical structure of the skin as well as the precise localisation of the gland. The Glandulae sebaceae can be found in the dermis and opens via a small duct horizontally into the cavity containing the hair follicle. The glandular product, the sebum, is secreted from the sebaceous glands via the follicular duct to the surface of the skin. The fatty substances subsequently spread, as a kind of protective film, on the surface of the skin and the hair. I addition to the lubrication of the skin, the sebum functions as a physicochemical barrier protecting the skin from potential pathogens. Salts and several proteins are also found in the produced sebum, e.g. glycoproteins, interferons and immunoglobulines, in order to ensure a specific protection (Sousa, 2006). Furthermore other fatty acids support the barrier effect. The sebaceous glands can be found all over the dogs skin with exception of the teats, nose leather and the soles of the paws. Depending on the region of the body, there are variations of sebaceous glands e.g. in size, number and occurrence. Extremely large glands are located in the regions of the chin, neck and the tail. Fig. 2: Schematic illustration of the anatomic structure of the skin (Fabre, 2014) 3 Clinical Signs Idiopathic (= without detectable cause) sebaceous adenitis can be characterized by an inflammation of the sebaceous glands leading to a total destruction of the gland. (Bensignor & Guaguère, 2012). As a result, the production of the sebum decreases in the affected skin areas causing numerous negative effects on the skin and coat. How the lack of the secretion influences hair growth, is still unknown (Sousa, 2006). Microscopic examinations shows a dry and scaly skin-surface and some SA-dogs even demonstrate blisters (Fig 4 C) and pustules (Fig 4 D) (Simpson & McKay, 2012). Moreover keratin casts, an agglomeration of brown crusts and scales stucked together at the hair shaft, are typical characteristics for sebaceous adenitis in the Akita-dogs (Fig 3). In addition to the loss of undercoat, the fur is described as dry, dull, and fragile (Sousa, 2006). The loss of sebum generally triggers a broad range of secondary skin infections: Bacteria, viruses, or fungi (Bensignor & Guaguère, 2012). Typically a bad odor, like socks worn for several days, accompanies the individual appearance of SA. Fig. 3: Agglomerated brownish coloured follicular casts Box 1: Clinical signs of sebadenitis in Akita (Bensignor & Guaguère, 2012; Simpson & McKay, 2012) symptoms  Keratin cast (Fig 4 A/B) on hair line  Itching (pruritus) of the skin, generally caused by fungi and bacteria  In case of acute pyoderma (bacterial skin infection with pus formation): o blisters (papules) (Fig 4 C) o pustules (Fig 4 D) o inflammatory collarette (FigE)  Symmetric hair loss (alopecia) up to complete hair loss  Hair: o brittle o dull o as if eaten by moths  White-haired dogs develop a brown-red colouring caused by brownish crust formation 4 In general, the first clinical symptom will most often appear on the dogs head. More precise on the outer ear as a brown crumbling residue which can be mistaken for mites. Later on, the SA-signs spread all over the body to the tail (Simpson & McKay, 2012). During the chronic phase of disease, the coat appears thinner - as if eaten by moths (Simpson & McKay, 2012) - while the remaining hair shows a grayish cast and resembles a "puppy coat". Especially in Akitas, a diffuse hyperkeratosis (Greek: hyper "over", keratos "keratin", an overproduction of keratin in the skin) can be seen sometimes, appearing similar to symmetric alopecia (loss of hair) (Bensignor & Guaguère, 2012). In Akitas, both, male and female dogs are affected. There appears to be no correlation between SA and the coat colour of the dog. In general, the first symptoms usually appear with the beginning of sexual maturity. A significant correlation between the duration of the disease and the severity of the disorder could not be demonstrated. Additionally there was no correlation observed between the degree of illness and the age of the dog. The progression of SA does moreover not follow a rigid pattern: Some individuals demonstrate a rapid progression (2 months), while others progress over a period of many years (Reichler, et al., 2001). Fi Fig. 4: A-E: Depiction of the symptoms of sebadenitis in Akita dogs: A: "featherlike" keratin cast (Bensignor & Guaguère, 2012), B: keratin casts at the hairline (red circle), C: blisters (papules) (Noli, 2008), D: pustules (Noli, 2008), D : collarettes (Noli, 2008) 5 In the Akita, it is assumed that SA probably follows an autosomal recessive mode of inheritance (Fig 5) (Reichler, et al., 2001). That is why the term genodermatosis (geno = for genetic reasons, dermatosis = skin disease) is frequently used in relation to SA. Presumably, hormonal changes play a key-role in triggering the disease. But also pregnancy or any stressful situations cannot be totally excluded as a possible contributor for this health issue. Clinical Diagnostics Diagnosing SA is very difficult without a skin biopsy (Histological examination). SA exhibits numerous similarities with other diseases, such as canine demodicosis (skin disorder caused by parasitic mites), dermatophytosis (fungal infection of the skin) folliculitis (inflammation of the follicles) or leishmaniosis (infectious disease) to name a few (Bensignor & Guaguère, 2012). Hence the veterinarians should first investigate and eliminate the above mentioned diseases in order to avoid misdiagnosis. Biopsy A definitive diagnosis can only be found by means of a skin biopsy. In cases of suspected sebaceous adenitis, multiple skin biopsies and samples from different body regions should be taken, in order to identify the varying inflammatory phases of the sebaceous glands. Three phases of sebaceous glands with inflammatory symptoms can be observed: In the first phase the excretory duct of the sebaceous gland is inflamed (Bensignor & Guaguère, 2012). During the second phase various "defensive cells" of the immune system are found in the tissue samples (Fig 7). Fig. 5: Diagram of an autosomal recessive inheritance (Brüggemann, 2014) 6 The so called "defencive cells" were represented by makrophages, lymphocytes, and neutrophilic granulocytes. In more scientific term, representing a perifollicular (= around the follicle) granulosum, i.e. accumulation of many cells without connective tissue (Linek, et al., 2005). In phase 3, the destruction of the gland tissue has taken place, which is probably caused by the infiltrating immune cells. The tissue develops a perifollicular fibrosis (Bensignor und Guaguère, 2012). In other words, in the end only scar tissue remains and can be seen in the inflamed regions (Klöppel, et al., 2008). Because of the complete destruction of the sebaceous glands, the degree of inflammation decreases. It is vital to stress, that SA is not caused by microbial infection - neither an attack of viruses, nor bacteria or fungi can be observed in the affected gland tissue. SA can be seen as a disorder of the autoimmune system which means that the body's own defence attacks its own structures. In conclusion, an auto-immune mediated disease is possibly the main reason for sebaceous adenitis in the Akita. Trichoscopy Using trichoscopy (Greek trichos "hair", ancient Greek skopein "scopy" = method or instrument of observation and examination), a method of evaluating hair microscopically, one can get an overview of the hair density, scaling or formation of pustules, and the characteristic keratin casts (Bensignor & Guaguère, 2012). Treatment There is no treatment available at this time for curing sebaceous adenitis with a certainty of 100 percent remission. (Bensignor und Guaguère, 2012). In other words, there is no treatment available that will totally restore the coat and skin of affected Akita dogs. It appears that the disease typically progresses in periodical cyles. In the beginning the dogs show a massive hair loss. Oil-treatment encourages hair growth almost back to normal. Followed in episodes, by an other loss of hair and the cycle starts again. Fig. 6: Histological image of a sebaceous gland with an inflammatory reaction (Reichler, et al., 2001) 7 The aim of therapy is to slow down the inflammatory process as well as to reduce stress, in order to stabilize the immune system (Simpson & McKay, 2012). Local Treatment Local treatment means the external application of medication. Following the individual step of treatment are outlined. The 4 step procedure is relatively time consuming but - as practice shows - exceptionally promising (Simpson & McKay, 2012). Step one: Removing scales, crusts and keratin casts Using a keratolytic or keratoplastic shampoo, bathe the dog to remove dry scales and crusts as well as keratin casts. Shampoos with ingredients like sulfur or salicylic acid (Scott, et al., 2001) are especially recommendable. In cases with a secondary bacterial folliculitis, shampoos combining the ingredients mentioned above and benzoylperoxide, proved to be very effective. All shampoos should be allowed to infiltrate for 10 minutes (Simpson & McKay, 2012). Step two: Replacing the oily barrier on the outer skin (stratum corneum) Bathe the dog using generic baby oil, olive oil, or calendula oil. A treatment of 50 percent water and 50 percent oil proved beneficial. Apply the emulsion by rubbing from head to tail. Soaking for about two hours. Step three: Removing the excess oil. Step four: Skin care protective Moisturising products, such as conditioners (Vétoquinol Hydra-Pearls™ Shampoo, Virbac EPISOOTHE® Shampoo) and sprays (Virbac HUMILAC® Spray) protect the skin from drying out and support the protective function of the skin (Rosser, 1999). Simpson and McKay (2012) suggest that this four-stage treatment plan be performed once a week for a time period of four to six weeks. The skin and haircoat should show improvement after one to two months. Attention: There is no guarantee for the success of the treatment. The majority of the affected dogs respond very well, showing new hair growth and a certain degree of stabilization. The outer oil treatment is a simple and "low-priced" method to restore the lipid film of the skin. According to the Bensignor and Guaguère's study (2012), olive oil supports the regression of affected skin wounds. As shown by special analyses, the components of olive oil (up to 83 % oleic acid) are very similar to the natural composition of the sebum: 48 % cholesterol ester, 48 %wax, diesters and 4 % free fatty acids as well as a slightly acid pH-value (Bensignor & Guaguère, 2012). This is possibly a reason, why olive oil can simulate the external skin-biofilm and protect against harmful pathogens (Bensignor & Guaguère, 2012). Using antiseborrheic shampoos or giving fatty acids orally (in the form of capsules) is not advisable (Bensignor & Guaguère, 2012). 8 Cyclosporines are often percaved by owners as expensive SA-medications. But they are frequently associated with negative side-effects. These drugs belong to a group of immunosuppressives, used to inhibit the function of the patients own immune system. In the past, only oral treatments with cyclosporin were commonly known. But a recent study showed their use in treatments in the form of sprays resulting in an improvement of the skin, coat and also of the general state of health of the dogs. However, it is not totally clear whether cyclosporines actually have a positive health effect or if other ingredients, such as 1,2-propanediol, vegetable oils, or mineral oils in the spray lead to the regression of SA (Bensignor & Guaguère, 2012). In addition a remedy for the treatment of the dog's ears, namely Ortena® (with the main ingredient 1,2-Propandiol), is being discussed. One of its most important ingredients is the colourless oil "Squalane" (Bensignor & Guaguère, 2012). Nowadays it can be isolated from olive oil whereas in the past, this substance was extracted from shark liver. Also the thought of lipid as intermediate product of the body's own metabolism is of interest (Käser, 2014). For example Squalane has the ability to remove keratin from the stratum corneum and replace it with a lipid film (Bensignor & Guaguère, 2012). Systemic Therapy Systemic therapy can be described as use of medication in form of tablets or injections. This means the agent is transported by blood circulation. Cyclosporine has been used several times as medication for SA. An oral dosage of 5-10 mg cyclosporine per kg body weight has been proved successful. The drug induces an inhibition of the immune systems which blocks all inflammations. Regeneration of the sebaceous glands has been observed to a certain degree, depending on the severity of the SA. In an open study, performed by Bensignor and Guaguère (2012), 12 dogs have been treated with cyclosporine for one year. 60 % of the test-dogs showed a clinical improvement. After a treatment of 8-12 months, a stabilisation of the inflammations was detected. Discentinuing medication lead to a spontaneous recurrence of the SA (Bensignor & Guaguère, 2012). Critical Treatment Several systemic treatment options have resulted in unsatisfactory results in the treatment of SA. Oral fatty acids (capsules) do not lead to any positive effect on the skin conditions (Simpson & McKay, 2012). Likewise a therapy with corticoids showed mainly disappointing results (Bensignor & Guaguère, 2012; Simpson & McKay, 2012 Corticoids belong to a group of steroid hormones which are generated in the adrenal cortex. In addition to influencing many physiological effects, corticoids play a role in the metabolism - especially in the water and electrolyte balance of the body, the cardiovascular system, and the nervous system. They also suppress the immune system, thus having anti-inflammatory effects (Simpson & McKay, 2012). 9 As a last resort, a treatment of SA with vitamin A (retinoids) is a possibility. Like previously mentioned medications, vitamin A has a similar anti-inflammatory effect. Retinoids are also involved in the proliferation and differentiation of cells. Under strict medical supervision, several dog breeds showed an 80-90 % improvement after three months. Synthetic retinoids (such as isotretinoin and acitretin) can possibly provide a slight reduction of manifested SA (Simpson & McKay, 2012). A study done by Simpson and McKay (2012) showed that 60 % of dogs treated with synthetic retinoids demonstrate a 50 % percent reduction of hair loss. Although the treatment of above mentioned substances promise a certain recovery, their use is highly controversial because side effects are not yet fully evaluated. Possible side effects are: Digestive disorders, dry eyes due to a lack of lacrimal fluid, diarrhoea, deformities during pregnancy, elevated blood fat levels (triglycerides), a risk factor for cardiovascular diseases or liver poisoning (Bensignor & Guaguère, 2012; Simpson & McKay, 2012). Because of these secondary effects, veterinarians should attentively monitor the chosen therapy (Bensignor & Guaguère, 2012; Simpson & McKay, 2012) very careful. Treatment of secondarily microbial infections Skin lesions in SA-affected Akita dogs can be very often traced back on a secondary skin infiltration of bacteria, viruses or fungi. If a veterinarian confirms this infection, a sufficient treatment with antibiotics (of about 4 to 6 weeks) should be considered (Bensignor und Guaguère, 2012). Research perspective SA in Akitas demonstrates a broad spectrum of unknowns. Therefore the disease opens up multiple fields of research. It is vitally important to cooperate with breeders and dog owners - especially in order to not fall behind: EDTA blood samples (ca. 2ml) only from pure bred SA diagnosed (only by skin biopsy) Akita dogs can be an advance in research. Without this cooperation, a perspective to solve this health concerns seem to be possible. The following question still remains: What is the reasons the defensive cells of the dog attack and destroy the body's own structures in Akitas? A continuous treatment of SA with immunosuppressants (such as cyclosporine) is normally associated with high costs and cannot be considered as a longterm solution because of the undesirable side effects. Open questions for further studies are for example, what kind of substances trigger or cause the autoimmune reactions in the sebaceous glands? Genetic reasons for the defective regulation of the processes should likewise be further investigated. The immune system is a rather complex and not fully understood system Therefore various motives and possibilities have to be considered in SA. The SA-disease can be seen as an eminently multifaceted problem. From the current status of knowledge, a simple and short-termed solution on 10 the genetic level can not be assumed: Several influencing factors such as different genes, the natural dogs environment and maybe several epigenetic side aspects we actually do not know about, play a major role. References Bensignor, E. & Guaguère, E. (2012). Adénite sébacée granulomateuse du chien: une revue. Prat Méd Chir Anim Comp. (47), 51-65. Brüggemann, A. (2014). Tibet Terrier. Retrieved from https://www.tibet-terrier-wissen.de/gesundheit/erbkrankheiten 5 th March 2014 Fabre, P. (2014). Akne muss kein Schicksal sein. Retrieved from https://www.akne-info.ch/allesueber-akne/akne-verstehen/ 15th February 2014 Käser, H. (2014). olionatura. Retrieved from https://www.olionatura.de/_oele/index.php?id=33 4 th March 2014 Klöppel, G., Rudolph, P., Mentzel, T., Cardesa, A., Kreipe, H. H., Slootweg P. J., Remmele, W. (2009). Pathologie (Bd. 1). Springer. Linek, M., Boss, C., Haemmerling, R., Hewicker-Trautwein, M., & Mecklenburg, L. (2005). Effekt of cycloporine A on clinical and histologic abnormalities in dogs with sebaceous adenitis. J Am Vet Med Assoc (226), S. 59-64. Noli, C. (2008). Papeln, Pusteln, Krusten beim Hund-Algorithmus. Ospedale Veterinario Cunesse. Italien. Reichler, I. M., Hauser, B., Schiller, I., Dunstan, R. W., Credille, K. M., Binder, H., Claus T.,Arnold S. (2001). Sebaceous adenitis in the Akita: clinical observations, histopathology and heredity. Veterinary Dermatology (12), S. 243-253. Rosser, E. J. (1999). Therapy for sebacous adenitis. In: Bonagura JD, ed. Kirk's Current Veterinary Therapy XII. PA. WB Saunders, S. 572-573. Scott, D. W., Miller, J. und Griffin, C. E. (2001). Dermatologic therapy. In: Muller and Kirk's Small Animal Dermatology. PA. WB Saunders , S. 241-243. Simpson, A. und McKay, L. (2012). Sebaceous Adenitis in Dogs. Vetlearn , E1-E7. Sousa, C. A. (2006). Sebaceous adenitis. Vet Clin North Am Small Anim Pract (36), S. 243-9