Home » other animals » Lupus in your dog: how to recognize and treat it? [Bow. vet. Krystyna Skiersinis

Lupus in your dog: how to recognize and treat it? [Bow. vet. Krystyna Skiersinis

Dog lupus erythematosus (Lupus Erythematosus / LE) is an insidious and malignant autoimmune disease of connective tissue.

Lupus in a dog

Lupus erythematosus can be generalized (as Systemic Lupus Erythematosus / SLE) and cutaneous (as Discoid Lupus Erythematosus / DLE) along with different types of these forms.

The etiology of this disease has not been known to this day; the body for unclear reasons - instead of supporting the animal in the fight against the disease, it begins to attack its own cells and tissues, which may lead to the failure of many organs and even the death of the dog.

This may be due to faulty gene recording, which under the influence of certain factors (e.g. solar radiation) activates and results in the appearance of clinical symptoms of the disease.

Unfortunately, lupus is still an undiscovered disease that still causes many diagnostic problems and causes therapeutic failures.

As the disease itself is classified as incurable (although there are remissions), management is based on relieving clinical symptoms and preventing their spread.

In this study, the Reader will find information about this unpredictable and extremely troublesome disease, which is lupus erythematosus.

Various types of lupus are described here, the possibilities of their diagnosis, as well as therapeutic methods that are taken to combat this disease.

Before we begin our discussion of dog lupus erythematosus in earnest, however, it is worth first asking why the disease develops at all - what happens when a revolt breaks out on board.

I cordially invite you to read!

  • The immune system as the body's military
  • The immune system as a "good policeman "
    • Congenital and acquired defense of the body
  • The immune system as a bad cop
  • Autoimmune disease - a consequence of disorders of the immune system
    • Factors predisposing to immune diseases
    • Drugs used in the treatment of immune diseases
    • Systemic immunosuppressive therapy
    • Local immunosuppressive therapy
  • Dog lupus erythematosus
  • Systemic lupus erythematosus / SLE
    • Etiology and pathogenesis of lupus erythematosus
    • Pathomechanism of the disease
    • The occurrence of the disease
    • Systemic lupus erythematosus symptoms
    • Diagnosis of SLE
    • Differential diagnosis
    • Systemic lupus erythematosus treatment
    • Prognosis
  • Cutaneous lupus erythematosus (CLE)
  • Discoid lupus erythematosus / DLE
    • Etiology and pathogenesis
    • The occurrence of the disease
    • Discoid lupus erythematosus symptoms
    • Clinical symptoms of GDLE
    • Recognition
    • Differential diagnosis
    • Discoid lupus erythematosus treatment
    • Prognosis
  • Mucocutaneous lupus erythematosus (MCLE)
    • The occurrence of the disease
    • Clinical symptoms of mucocutaneous lupus erythematosus
    • Diagnosis of MCLE
    • Differential diagnosis
    • Treatment of mucocutaneous lupus erythematosus
    • Prognosis
  • Exfoliative cutaneous lupus erythematous / ECLE
    • The occurrence of the disease
    • Exfoliative lupus erythematosus symptoms
    • Diagnosis of exfoliative lupus erythematosus
    • Differential diagnosis
    • Exfoliating lupus erythematosus treatment
    • Prognosis
  • Vesicular cutaneous lupus erythematosus / VCLE
    • Occurrence
    • Vesicular cutaneous lupus erythematosus symptoms
    • Diagnosis
    • Differential diagnosis
    • Vesicular cutaneous lupus erythematosus treatment
  • Lupus Onychodystrophy (symetrical lupid onychodystrophy, lupoid onychitis)
    • Causes and occurrence
    • Lupus Onychodystrophy clinical symptoms
    • Lupus Onychodystrophy diagnosis
    • Differential diagnosis
    • Lupus Onychodystrophy treatment

The immune system as the body's military

The immune system can be likened to a mighty army that guards the order and security of the organism as well as its integrity and indivisibility.

It is designed in such a way to detect and destroy invading pathogens, as well as learn and gain experience in order to prevent repeated hostile attacks.

This looks like a fairly simple task to perform, but it is often difficult to tell friend from foe, especially when pathogens have developed a variety of strategies to avoid detection by systemic defenses.

There is a very complex, integrated system established in the body that guarantees the ability to identify most pathogens and take appropriate remedial measures against them.

However, as in any conflict, sometimes the decisions made are wrong and the consequences are very harmful to the body.

In the military nomenclature, there is a very neat term, bluntly and briefly describing the accidental firing of own or allied forces - it is the so-called. "Friendly fire " (friendly fire). As a result of a mistake in the identification of the target or low accuracy, an accidental attack on "his " occurs, despite the fact that the intention was to cause damage to the opponent.

An autoimmune disease can just be described as such a "friendly fire" in which cells and molecules designed to attack pathogens are directed against the host. Just like in war - the damage caused in this way not only occurs unexpectedly, but is usually severe and leads to the appearance of pathologies and various types of clinical diseases.

The immune system as a "good policeman "

All organisms have what can be called an innate immune system.

Even the bark of a tree and the cell wall of bacteria play an important role in protecting their host. The immune system protects the body against bacterial, fungal and viral infections.

To achieve this, however, there is a complex system of humoral and cellular mechanisms that work closely together to provide the desired protection.

Often the body has to react aggressively and ruthlessly to the impending danger, and the reaction must be immediate, therefore the defense mechanisms are strong, and in the case of innate immunity - non-specific.

The readiness to defend the organism must therefore be based on one of the most important assumptions of immunological protection, which is distinguishing "your " from "foreign ".

A key role in the immune system of vertebrates is played by the major histocompatibility complex (MHC), which encodes a collection of immune and non-immune molecules. If this fails, development occurs diseases of the immune system.

The body has the ability to react to almost anything that connects to the receptors of the immune system. Molecules recognized by receptors on lymphocytes are generally called antigens and can range from small chemical structures to highly complex molecules.

The ability to distinguish one's own cells and tissues from foreign structures is acquired during fetal development.

In the primary organ of the lymphatic system, the thymus gland, the fetal thymus lymphocytes are "trained" and then enter the periphery where they mature.

Recognition of self from strangers involves the contact of naive, immature thymic lymphocytes with thymic epithelial cells. These cells present a variety of tissue antigens as well as major histocompatibility antigens (MHC II and MHC I).

Immature T cells are "tested" for their ability to bind to their own MHC antigens.

Those that do not bind at all undergo apoptosis induction and are eliminated.

Those that are too tight are also disposed of.

T cells that recognize their own MHC antigens, but do not bind tight enough to cause a cytotoxic effect, are arrested.

Such cells become CD4 or CD8 T cells and can bind to the MHC class II or MHC class I antigens, respectively, while their T cell receptor (TCR) for the antigen has specificity for some foreign epitopes.

TCRs are checked to see if they are able to respond to randomly presented tissue antigens in thymic epithelial cells, and those that react with any of these antigens are induced to apoptosis and eliminated from the T cell pool.

The remainder will enter the circuit to "vaccinate" secondary lymphoid organs.

Most B cells become tolerant and therefore do not adversely respond to self antigens; Thus, checking for these cells is less stringent than for T cells.

Thus, there are B lymphocytes present in the body that are capable of recognizing and binding to certain epitopes.

However, the lack of T cells reacting with these antigens keeps B cells in check as B cells require the help of T cells to initiate an immune response and produce antibodies.

Thus, T cells that do not adversely react with the host cells and tissues but are able to help eliminate pathogens and other foreign cells enter the periphery.

However, there are situations in which an immune response may be generated, not necessarily beneficial for the body, during which the body's own tissues are attacked.

These types of responses are known as autoimmune responses and depend on which types of autoantigens (i.e. tissues or organs) the immune response is directed against.

Usually, clinical symptoms of the disease appear that may affect the function of these target tissues / organs.

Congenital and acquired defense of the body

The immune system is the body's defense and surveillance system.

It is an extremely complex organization of cells and molecules with a specialized role in defending against infection.

This system recognizes foreign substances on the basis of their molecular characteristics and eliminates them from the body.

The immune system can generally be divided into two parts, depending on how specific their functions are: the innate system and the adaptive system.

Innate immune system

The innate immune system responds to rapid reaction forces that quickly recognize an invader and mobilize defense mechanisms to repel an attack, i.e. a developing infection.

  • In the interaction between the organism and the environment, epithelial cells, such as keratinocytes or mucosa epithelial cells, constitute the first line of defense.
    They have pattern recognition receptors that can detect the presence of foreign organisms or tissue damage, and can initiate further defense systems of the body due to the release of antimicrobial peptides, pro-inflammatory mediators (e.g. Interleukin 1) and chemokines (e.g. Interleukin - 6).
  • In the blood, white blood cells carry out their patrols, which, if signs of infection are found, are ready to immediately attack the enemy.
    • In the case of acute inflammation, neutrophils, i.e. neutrophils, are quickly recruited to inflammatory sites, where - by phagocytosing pathogens and releasing antimicrobial substances and pro-inflammatory mediators - they are perfect for fighting off an attack and preventing bacterial infection.
    • One of the subdivisions of "armed forces " of the body are monocytes, which in a healthy animal circulate in the blood, and at some point leave the circulation and enter the tissues.
      Monocytes can differentiate into the so-called. dendritic cells (such as. Langerhans cells in the epidermis), which are a kind of immune "sentinels": in the presence of pathogens they become professional antigen presenting cells, check the tissue microenvironment, and report the obtained results to the immune system in the lymph nodes.
      In addition, monocytes can transform into tissue macrophages, i.e. "cleaners" or workhorses, involved in the remodeling of tissues in a healthy host, which are divided into the M1 type (pro-inflammatory type) and M2 (anti-inflammatory type).
      Macrophages are often recruited along with neutrophils for antimicrobial defense, especially in chronic lesions.
  • Other populations of white blood cells - eosinophils (eosinophils) and basophils (basophils) are important in the inflammatory response of the body, and are especially active in preventing parasitic invasions.
  • NK cells (ang. Natural Killer are able to detect and destroy virus-infected host cells.

In the fight against invaders, the organism also has a number of innate immunity mediators, which are important in preventing pathogens. These are:

  • Type 1 interferons.
    They are released from cells attacked by viruses to alert neighboring cells to the impending attack of new virus particles.
    As a result, cells that are still healthy can increase the regulation of the antiviral defense system and thus have a better chance of preparing for an attack.
    The indicators of virus infection and a strong source of type 1 interferons are cutaneous plasmacytoid dendritic cells.
  • Acute phase proteins adhere to microorganisms and increase their uptake by phagocytosis.
  • The complement system is a very important part of the antimicrobial defense that leads to inflammation, opsonization (that is, attaching to the surface of the pathogen and thus facilitating phagocytosis by phagocytosis) and the destruction of microbes by the complex attacking the membrane (as a result of its action, cell death occurs).
  • In addition, the coordinated cooperation of various cytokines and chemokines released by the host cells leads to the integration of all the above-mentioned "units" into an effective defense regiment.

Adaptive immune system

Why, despite such precise defense mechanisms of the organism, microbes often manage to bypass the host's entanglements and win the fight?

They have an evolutionary advantage in the form of a very fast rate of mutation, which allows them to acquire new traits and adapt to changing conditions.

Thanks to this, they manage to outsmart, avoid and bypass their innate immune defenses. Therefore, the adaptive immune system has developed a different pathogen detection strategy that is much more difficult to bypass the recognition of a foreign antigen (usually a structural protein) by various types of lymphocyte receptors.

  • B lymphocytes are trained to detect a foreign antigen present in the extracellular fluid (they are responsible for the so-called. humoral immunity) and react by releasing antibodies - immune projectiles designed to surround the enemy target and initiate further destruction mechanisms.
    The isotype of the antibody can be modified to best suit the current pathogen.

    • In the case of viruses, neutralizing antibodies work best (IgG for systemic defense, IgA for protection of mucous membranes).
    • Against bacteria, attacks of IgM (agglutinating and activating complement) and IgG (neutralizing, opsonizing and activating complement) antibodies are particularly beneficial.
    • IgE antibodies are directed against large parasites, which sensitize mast cells to their presence and facilitate degranulation and release of destructive and inflammatory mediators.
  • T cells constitute the cellular front of adaptive immunity.
    • CD8 T cells+
      • T effector cells (CD8 +) seek out and destroy virus-infected cells, thereby interacting with the virus neutralizing antibody to eliminate the germ from both intra- and extracellular fluid.
      • Killer T cells (CD8 +) can detect viral peptides presented on the surface of an infected cell in combination with MHC class I molecules, and the cytotoxic (damaging) effect is mediated by the induction of apoptosis (programmed cell death).
      • Resident T cells (CD8 +) are often found in the epidermis.
    • CD4 + T cells are usually found in the dermis and vary in function.
    • Type 1 T-helper lymphocytes (Th-1 / ang. T-helper type 1).
      They release interferon γ to "superactivate" tissue macrophages, thus increasing their ability to remove microorganisms.
      Especially important in the case of intracellular microorganisms such as mycobacteria or Leishmania.
    • Type 2 helper lymphocytes (Th-2) release cytokines, including Il-4, Il-5 and Il-13, which help B lymphocytes mature and decide what type of antibodies to produce.
    • Type 3 helper lymphocytes (Th-3) release cytokines including transforming growth factor β (TGF-β).
      They are especially important for mucosal immunity and driving the production of IgA antibodies by B lymphocytes in the lymphoid tissues associated with the mucosa.
    • Type 17 helper lymphocytes (Th17).
      They release cytokines such as interleukin -17.
      They are important in activating epithelial cells to produce AMP and in recruiting neutrophils to the site of bacterial or fungal infection.
    • T-22 (Th-22) helper cells release interleukin 22, which can stimulate the proliferation or hyperplasia of keratinocytes.
      Il-22 appears to play an important role in barrier function, enhancing antimicrobial defense, inflammation and repair.
    • Regulatory T cells.
      Generated in the thymus or circumference.
      Release cytokines such as IL-10 - a natural suppressive cytokine to suppress potentially harmful pro-inflammatory immune responses.

The immune system as a bad cop

As you can see, this immune armory the body has at its disposal to use against invading pathogens is really worthy.

However, the same cells and mechanisms can be activated in the absence of infection, which can cause serious pathology.

In the pursuit of maintaining balance and relative tolerance, huge expenses of immune energy are incurred, thanks to which these highly self-reactive lymphocytes are eliminated, some reactive cells are turned off and regulatory cells are recruited, which are a kind of military gendarmerie of the immune system army.

Autoimmune disease results from a serious misunderstanding by the body of the difference between "its own " and "foreign ", which is additionally exacerbated by the failure of regulatory factors.

Autoimmunity is otherwise referred to as a tissue self-antigen hypersensitivity response. It is usually initiated by the adaptive immune system, but abnormalities most often show innate immune mechanisms (inflammation and tissue damage).

  1. Type II hypersensitivity.
    It is mediated by the binding of antibodies (usually IgM or IgG) with "fixed" own antigen on the cell surface or in the extracellular matrix.
    This antibody binding leads to further effects such as:

    • neutralization of protein functions,
    • increased phagocytosis by macrophages,
    • complement activation,
    • antibody-dependent cellular cytotoxicity (by NK cells).
    • Type II hypersensitivity is particularly important in the case of autoimmune skin diseases in which binding of autoantibodies to cell adhesion molecules (desmosomes or hemidesmosomes) or basement membrane antigens leads to dysfunction and pathology.
  2. Type III hypersensitivity.
    It involves the binding of the antibody (usually IgM or IgG) to its own antigen "soluble ".
    Immune complexes are formed locally in tissues or in the circulation.
    Systemic immune complex formation causes vasculitis.
    Depending on where the circulating immune complexes (skin, synovium, glomeruli) settle, various clinical symptoms appear.
  3. Type IV hypersensitivity.
    Unlike previous hypersensitivity reactions, this type is mediated by T cells - usually Th -1 (CD4 +).
    Tissue reactive Th-1 cells release interferon γ, which in turn activates tissue macrophages to secrete pro-inflammatory mediators, reactive molecules (e.g. nitric oxide) and destructive enzymes (e.g. matrix metalloproteinases).

Autoimmune disease - a consequence of disorders of the immune system

Autoimmune diseases

Autoimmune disease occurs as a result of impaired immune response at its various stages.

The causes of the disease can be both excessive complement activation (specific component of the immune response) and non-specific component (abnormal maturation of immune cells in the thymus and peripheral area, inappropriate expression of MHC antigens, disorders of idiotypic regulation and suppression, participation of external environment factors such as viruses, bacteria, drugs).

The body recognizes and treats as foreign components of its own cell membranes, cytoplasm, cell nuclei, but also hormones, enzymes and many other substances.

Factors predisposing to immune diseases

Susceptibility to autoimmune diseases is controlled by the interplay of environmental and hereditary factors (the latter include the genes of the major histocompatibility complex MHC).

Genetic factors

Inbreeding can lead to various disorders, immune system dysregulation and autoimmunity, and even cancer.


It is hypothesized that sterilization reduces the incidence of autoimmune diseases in females, while male castration may increase it.

Other immune disorders may also underlie many autoimmune diseases.

If a given breed or even line of dogs suffer from one immune disease, they will have an increased incidence of a number of other immune disorders, e.g. dogs with systemic lupus erythematosus may also show autoantibody-associated cytopenia.

An infectious disease

Infections can cause allergies, immune complex formation, cell disorders, gammopathies, or immunodeficiency.


Medicines given to dogs with certain genetic predispositions can trigger a variety of immune responses.

Drugs used in the treatment of immune diseases

The goal of treating most immune diseases is to control the symptoms of the disease while minimizing the side effects of medications.

The therapy of each patient should be adjusted individually and adjusted to the symptoms, comorbidities, and the caregiver's finances.

Since immunosuppressants are used in the treatment of this type of disease, it is important to identify the causative agent, as well as any coexisting disease processes before introducing them.

Regular check-ups are also needed to check the response to treatment and to identify any side effects from the medication.

The latter often cause more problems than the disease itself.

Side effects may appear both as noticeable clinical symptoms, but also as changes in the results of hematology and biochemistry of blood serum. Any secondary infections should be treated.

Systemic immunosuppressive therapy


Prednisolone or methylprednisolone are the mainstay of therapy for most autoimmune skin diseases.

In dogs, they can be combined with azathioprine. There are various schemes for their use. According to Hill (2004):

  • Prednisolone - induction dose in a dog: 2-4 mg / kg / day orally in two divided doses; maintenance dose: 0.5-2 mg / kg every 48 hours orally.
    The tapering of the induction dose to the maintenance dose should be gradual and the dog should receive the full dosing every other day before extending the period to 48 hours for effect.
    Dose tapering starts when a good clinical response is obtained.
    Decreasing the frequency - from daily immunosuppressive doses to every other day immunosuppressive dosing - may take several months, depending on the individual patient.
    Only after dosing the dog every 48 hours and remission, the dose should be reduced to the lowest possible level.
  • Methylprednisolone - induction dose in dogs: 1.5-3 mg / kg / day in divided doses.
    Maintenance dose: 0.4-1.5 mg / kg every 48 hours.
  • Dexamethasone can be used in cases that do not respond to prednisolone or methylprednisolone.
    Induction dose: 0.2-0.4 mg / kg every 24 hours.
    Maintenance dose: 0.05-0.1 mg / kg every 48-72 hours.

As the dose of the immunosuppressant increases, the severity of side effects also increases.

This effect can be reduced by reducing the dose of the drug, but it is important that the drug still has the desired therapeutic effect. With glucocorticosteroids, their immunosuppressive effects decrease when the dose is reduced, but long-term side effects may still occur chronically.

Many cases of iatrogenic skin calcination have been observed in dogs treated with low doses of daily glucocorticosteroids, but less frequently when medications are applied every 48 hours or less.

Undesirable effects of glucocorticosteroids

Immediate side effects with glucocorticoid use include:

  • increased thirst,
  • polyuria,
  • voraciousness (polyphagia),
  • panting,
  • behavior changes,
  • diarrhea.

Chronic side effects from glucocorticoid use can include:

  • muscle atrophy,
  • abdominal enlargement,
  • enlarged liver,
  • fat redistribution,
  • cutaneous calcinosis,
  • alopecia,
  • reduced wound healing,
  • recurrent pyoderma or malasesiosis,
  • demodicosis,
  • blackheads,
  • urinary tract infections,
  • pyelonephritis,
  • diabetes,
  • osteoporosis.

Abrupt discontinuation of glucocorticoid use in dogs during long-term treatment should be avoided.

Drugs that protect the gastric mucosa

These are not drugs for the treatment of immune diseases, but should be given with high doses of glucocorticosteroids.

  • Proton pump inhibitors, e.g. omeprazole for up to 8 weeks.
  • Histamine receptor antagonists, e.g.:
    • cimetidine,
    • ranitidine;
  • Sucralfate - can be given together with a proton pump inhibitor or antihistaminic, but at a different time of the day.


It is a cytotoxic agent that is best administered in relation to the body surface area. Gloves should be worn before administration to avoid contact with the skin.

Induction dose: 50 mg / m2 or 2 mg / kg every 24 hours orally until remission is achieved.

Maintenance dose: 50 mg / m2 or 2 mg / kg every 48 or 72 hours orally.

Chrysotherapy (gold salts; aurothiomalate, aurothioglucose)

Initially, a test dose is administered.

Test dose: dogs weighing 10 kg m.c. - 5 mg intramuscularly.

Induction dose: 1 mg / kg m.c intramuscularly once a week for up to 12 weeks and increase to 1.5-2 mg / kg m.c. intramuscularly once a week.

Maintenance dose: 1-2 mg / kg m.c intramuscularly every 2-4 weeks.

Treatment usually lasts 6-12 weeks.

Pain at the injection site is a common problem. Side effects include thrombocytopenia and drug reactions that can be fatal.

Not used simultaneously with azathioprine.

Gold salts are contraindicated in the treatment of systemic lupus erythematosus due to the potential of both the drug and disease to cause glomerulonephritis.


It inhibits the activity of T cells by reducing the production of IL-2 by inhibiting calcineurin.

Used at a dose of 5-10 mg / kg every 12-24 hours.

Side effects include:

  • frequent vomiting and diarrhea,
  • urinary tract infections,
  • purulent dermatitis,
  • gum hyperplasia,
  • papilloma,
  • suppression of bone marrow function can occur especially at high doses.

Tetracycline (tetracycline, oxytetracycline, doxycycline) and niacinamide (nicotinamide)

Since 1992, a combination of tetracycline and niacinamide (nicotinamide) has been used to treat a variety of immunological and sterile granulomatous dermatoses in dogs.

This combination has numerous anti-inflammatory and immunomodulatory properties.


  • tetracycline or oxytetracycline: 25 mg / kg every 8 hours orally or doxycycline 10 mg / kg every 24 hours orally
  • plus niacinamide:
    • dogs over 10 kg: 500 mg every 8 hours orally,
    • dogs under 10 kg: 250 mg every 8 hours orally.

When using this combination, side effects may occur, which are usually attributed to niacinamide:

  • gastrointestinal disorders,
  • lack of appetite in the dog,
  • apathy,
  • vomiting,
  • diarrhea.

Tetracyclines are contraindicated in dogs with hepatic insufficiency.

These drugs are given with food to minimize gastrointestinal side effects.

However, this combination should not be administered with dairy products or vitamin or mineral supplements as divalent and trivalent cations such as calcium, aluminum, magnesium, zinc, iron bind tetracycline, thus reducing its bioavailability.

Medicines administered with food are rarely associated with side effects.

The action of tetracycline and niacinamide is relatively slow, the therapeutic effect is visible within 3-8 weeks of administration.

Vitamin E

Served at a dose of 400-800 IU every 12 hours (two hours after eating).

Local immunosuppressive therapy


Hydrocortisone aceponate spray can be used as an adjunct to treatment. It is especially useful in cases of localized lesions. Wear gloves when using.

Tacrolismus (protopic 0.1% cream). Used twice a day for localized lesions, especially for cutaneous lupus.

There are many autoimmune skin conditions that affect pets.

They vary from relatively mild, topical dermatoses to severe, systemic diseases.

Their therapy can often be tedious and very frustrating for both dog handlers and the veterinarian. This group of diseases includes lupus erythematosus.

Let's find out what the disease is and how to deal with it.

Dog lupus erythematosus

Dog lupus erythematosus

As the disease can come in various forms (more "mild" or more severe), the classification of lupus erythematosus may be as follows:

  • Systemic lupus erythematosus. Systemic Lupus Erythematosus, SLE):
    • systemic lupus erythematosus with skin lesions,
    • systemic lupus erythematosus without skin changes.
  • Cutaneous lupus erythematosus. Cutaneous Lupus Erythematosus, CLE):
    • discoid lupus erythematosus. Discoid Lupus Erythematosus, DLE),
    • mucocutaneous form of lupus erythematosus. Mucocutaneous Lupus Erythematosus, MCLE),
    • exfoliative cutaneous lupus erythematosus. Exfoliative Cutaneous Lupus Erythematosus, ECLE),
    • cutaneous vesicular lupus erythematosus. Vesicular Cutaneous Lupus Erythematosus, VCLE).

The exact pathogenesis of this group of diseases is unknown.

It is known that they form antigen-antibody complexes and then deposit them in small vessels and the basement membrane zone of the skin (SLE and DLE) and in various organ systems (SLE).

Lupus aetiology has been linked to genetic factors, T-cell defects, B-cell hyperactivity, hormonal changes, and virus-induced immune complex formation.

Lupus erythematosus develops more often in dog breeds:

  • Scottish sheep-dog,
  • German Shepherd,
  • Siberian husky,
  • Shetland sheepdog,
  • british spaniel,
  • German shorthaired pointer,
  • Alaskan malamute,
  • chow chow, and their crosswords.

Systemic lupus erythematosus / SLE

It is a multi-system autoimmune disease in which numerous tissues and organs are affected because the body treats them as if they were foreign.

Systemic lupus erythematosus can affect the joints, skin, kidneys, platelets, and red blood cells.

This form of lupus is characterized by the presence of numerous autoantibodies, especially antinuclear antibodies (ANAb). The formation and deposition of circulating immune complexes by these antibodies is responsible for many of the changes found in SLE.

Systemic lupus erythematosus in humans has been known since the 19th century, but was not diagnosed in dogs until 1965.

The prevalence of SLE in dogs and cats has not yet been estimated, in humans the incidence is approximately 5 per 100,000 population; the disease much more often (as much as 75%) affects women. There was no such predilection in dogs.

Systemic lupus erythematosus most commonly affects dogs between 2 and 8 years of age.

Etiology and pathogenesis of lupus erythematosus

The cause of SLE is unknown.

In SLE, antibodies are produced that complex with antigens (proteins) on or in the cells of the body. These immune complexes get trapped in the blood vessels of certain organs, such as the joints and kidneys, and cause an inflammatory response.

The body tries to cope with the inflammatory response, but these attempts actually make things worse.

The cause of the loss of tolerance to the body's own structures and control over the immune system is unknown. To date, it has not been possible to determine why the body begins to produce antibodies against its own tissues.

In the etiology of the disease, genetic factors, viruses, immune disorders, pharmacological factors and environmental factors were suspected.

Genetic factors are important from the etiological point of view.

Dog colonies with systemic lupus erythematosus were experimentally established.

Quimby et al. suggests that genes may play a role in SLE: those that determine the disposition to autoimmunity (class I) and those that define the disease phenotype (class II).

Permissive alleles of class I genes are associated with antibody production, while class II genes determine disease symptoms. The development of SLE is to result from the interaction between genes of both classes.

Several studies have also linked the onset of SLE to infectious agents such as viruses, parasites, and other infectious agents.

SLE viral background was suspected from a study in which puppies were injected with acellular filtrates from SLE cases, resulting in the production of antinuclear antibodies. However, none of the animals in this study developed clinical signs of SLE disease.

Evidence that an immune disorder contributes to the pathogenesis of SLE comes from studies of New Zealand black and New Zealand white mice.

These mice are an animal model for studying SLE in humans and have been shown to lose T-suppressor activity with age. Loss of this activity is associated with the emergence of clinical symptoms of lupus.

Many drugs have been reported to cause the production of anti-nuclear antibodies in humans.

Hydralazine has also been shown to cause the production of antinuclear antibodies in dogs, although the dogs in this study remained clinically healthy.

The onset of symptoms typical of SLE in dogs may be provoked by:

  • procainamide,
  • hydantoin derivatives,
  • isonicotinic acid hydrazide.

In such cases, immunoglobulin deposits appear in the skin, and antibodies against single-stranded DNA in the blood serum, which disappear after drug discontinuation.

It has been suggested that environmental influences may also play a role as the disease worsens when exposed to sunlight in dogs and humans.

For example, ultraviolet light is believed to exacerbate changes in SLE.

Pathomechanism of the disease


Autoimmune disease is caused by an immune response against its own tissues.

Autoantibodies that appear in the course of lupus are able to react directly with cells and penetrate them inside.

SLE patients develop antibodies against a wide range of nuclear, cytoplasmic, and cell membranes.

In SLE, autoantibodies are directed against:

  • nuclear antigens, including native RNA, DNA, histones and nucleoproteins, centromere, spindles;
  • cell surface antigens on leukocytes, erythrocytes and platelets;
  • certain cytoplasmic antigens such as ribosomes, lysosomes, mitochondria, Golgi apparatus, microsomes;
  • membrane antigens, such as phospholipids (the so-called. the phospholipid syndrome, the occurrence of which causes the occurrence of thrombotic changes), cardiolipin;
  • immunoglobulins (rheumatoid factor - antibodies to IgG).

In a broader sense, the occurrence of autoantibodies in the course of SLE is observed for:

  • platelets,
  • lymphocytes,
  • granulocytes and red blood cells,
  • follicular epithelial cells,
  • cells of the reticular layer of the adrenal cortex,
  • gastric parietal cells,
  • smooth muscle cells and cardiomyocytes,
  • vascular endothelial cells.

Own antibodies can damage tissues directly or damage them by forming immune complexes.

In the case of continuous production of autoantibodies against self-antigens, an overload of the mononuclear phagocyte system may occur.

Circulating immune complexes build up in the walls of blood vessels where there is a physiological outflow of fluids (e.g. in the glomeruli, synovium and choroid plexus).

Immune complexes

The tissue damage mechanism in SLE is primarily a type III hypersensitivity reaction in which immune complexes are deposited in various tissues, mainly along blood vessels and basement membranes.

Immune complexes are composed of autoantibodies and antigens that activate complement. Complement activation, in turn, attracts neutrophils to induce an inflammatory response.

Hematopoietic autoantibodies cause type II hypersensitivity, in which the autoantibodies bind to the cell involved (e.g. erythrocyte) and either induce cell lysis through complement activation or cause cell phagocytosis.

In SLE, IgM and IgG autoantibodies bind complement producing a direct cytotoxic effect or make cells susceptible to phagocytosis.

Complement fixation by immune complexes is a central step in the pathogenesis of tissue damage seen in SLE. Complement activation induces the production of anaphylatoxin and infiltration of neutrophils. The latter cause phagocytosis of immune complexes and the release of lysosomal enzymes and oxygen free radicals.

Autoantibodies can bind to platelets or red blood cells, which explains the anemia caused by the immune system and the thrombocytopenia found in SLE.

Immune complexes also lead to platelet aggregation and Hageman factor activation, which in turn contributes to the inflammatory process, local ischemia and necrosis.

Immune complexes are deposited in various tissues such as the vascular endothelium, glomeruli, synovial membranes and joint capsule, as well as the basement membrane of the epidermis.

In the case of vascular lesions, autoantibodies to vascular endothelial cells play an important role in the pathogenesis.

Deposits of immune complexes build up in the capillaries and prehairia of the skin, joints and kidneys.

Transient, local inflammatory processes arise from chronic activation of infiltrative cells, release of cytokines and other inflammatory mediators.

The emerging vascular urticaria is the result of the accumulation of immune complexes in the vessels and antibodies to Clq (leukoclastic vasculitis).

The occurrence of the disease

Systemic lupus erythematosus is uncommon in dogs, with the exception of German Shepherd Dogs, Collies, Shetland Dogs and their crossbreeds, which appear to be predisposed to the disease.

The disease was much more common in some research cultures, more often than can be attributed to genetics.

In fact, SLE has been linked to some molecules of the major class I histocompatibility complex in German Shepherds.

Many dog ​​breeds can develop SLE, but German Shepherds do appear to be predisposed. Young and middle-aged dogs are most often affected.

Systemic lupus erythematosus symptoms

Systemic lupus erythematosus most often evolves as a chronic multiorgan disease with exacerbations, and sometimes as a subacute disease.

The clinical symptoms encountered are not necessarily observed simultaneously, but are often successively observed as the disease progresses. The symptoms are extremely variable.

Systemic lupus erythematosus is classically described as having 4 syndromes:

  1. Autoimmune hemolytic anemia;
  2. Thrombocytopenia;
  3. Symmetrical polyarthritis;
  4. Membraneous glomerulonephritis induced by immune complexes;

Dermatological changes occur very often, in as much as 32-54% of cases.

The skin symptoms associated with SLE include:

  • ulcerative stomatitis,
  • seborrheic mucocutaneous ulceration,
  • finger pad ulcers,
  • inflammation of the fatty tissue,
  • hives,
  • purpura.

The non-cutaneous symptoms of SLE include:

  • polyarthritis,
  • fever,
  • glomerulonephritis,
  • hemolytic anemia,
  • thrombocytopenia,
  • polymyositis,
  • neurological symptoms,
  • myocarditis,
  • lymphadenopathy.

Pleurisy, meningitis, and gastrointestinal disorders such as ulcerative colitis are much less common.

The disease in an individual animal may have one or all of the above syndromes and the development of the various clinical signs may occur in any order.

Initially, non-specific symptoms may appear, such as:

  • weight loss,
  • lethargy,
  • decreased appetite,
  • mild lameness.

The most common symptom is an irregular, cyclical fever.

Many reports indicate the presence of increased internal body temperature at the level of 39.5-41.0 ° C.

The fever may be intermittent or constant.

Musculoskeletal symptoms

Musculoskeletal symptoms are often seen in dogs with systemic lupus.

There are two forms of involvement of the musculoskeletal system:

  • polyarthritis,
  • polymyositis.


Polyarthritis, which is polyarthritis, generally develops as one of the first symptoms in approximately half of dogs with SLE.

It is characterized by difficulty moving and warm and painful joints.

SLE-related arthritis, unlike rheumatoid arthritis, is non-erosive, affecting the intervertebral articular surfaces, wrist, tarsus, and in the event of disease progression - the temporomandibular joint.

About 50% of dogs in SLE have more than 5 joints involved. These patients experience gait stiffness and a shortened step; some animals refuse to walk.

Dogs with fewer joints affected may show hind limb weakness and migratory lameness.

Some dogs may appear to have only one joint involved, but synovial fluid testing often shows damage to several joints, one with more intense inflammation than the other.

It is common that clinical symptoms vary over time.

An enlargement of the outline of the joints is often visible, especially in the area of ​​the wrist and tarsus.

The leukocyte count in the synovial fluid averages 74,500 cells / mm3, with the majority of cells being neutrophils.

Radiography shows no abnormalities in the joints, although swelling of the soft tissues can be observed.

Histopathologically, it is found that the synovium is thickened as a result of infiltration of inflammatory cells. The greatest number of cells is in the vicinity or in the layer of synovial cells.


Polymyositis is much rarer than polyarthritis.

The most common clinical symptoms of polymyositis are:

  • muscle atrophy,
  • weakness,
  • giant esophagus dysphagia.

Pathological changes include:

  • necrosis of muscle fibers,
  • phagocytosis,
  • perivascular and interstitial infiltrates of mononuclear cells,
  • degeneration and vacuolization of myofibrils type I and II.

Dermatological symptoms

Skin lesions may occur in up to 50% of dogs with systemic lupus erythematosus.

Symptoms are highly variable and their preferred location is in areas of fine skin that are poorly protected by hair, such as the nose, head and auricles.

Skin lesions often show symmetry.

The main irregularities are:

  • alopecia with or without dermatitis,
  • erythema,
  • less often ulceration,
  • occasional hyperkeratosis of the skin,
  • at a later stage of the disease - crusts and scars.

Sometimes acute, extensive facial swelling is observed, as well as vitiligo, localized to the nasal plate.

Cheek ulcers are rare but quite distinctive.

The dog has a bullous phase which is transient but the lesions are rarely ulcerative.

Changes that indicate a chronic bacterial skin disease are also possible, but the condition does not respond to antibiotics.

Dogs also suffer from another form of the disease, discoid lupus erythematosus (DLE), in which the lesions are usually limited to the nose area and may include ulceration of the tongue. However, unlike SLE, DLE is usually negative in both Antinuclear Antibody (ANA) and Cell Assay (LE) tests, and does not involve any other (than skin) systems.

Histopathological examination shows hyperkeratosis and keratin blockage around the appendages.

There is hydropic degeneration in the basal cells of the epidermis and swelling of the dermis with fibrinoid deposits around the collagen.

Extravasation of erythrocytes in the upper layers of the dermis may be visible, as well as pigment incontinence (leakage).

Kidney symptoms

Dogs with kidney involvement may initially show no clinical signs.

In the event of significant kidney damage, the following may occur:

  • increased thirst
  • increased urination,
  • muscular dystrophy,
  • nausea,
  • vomiting.

Kidney damage is often seen in severe cases.

Glomerulonephritis due to the build-up of immune complexes causes proteinuria and sometimes microscopic hematuria.

It is accompanied by normal specific gravity, at least at the beginning of the disease, before tubular function is involved.

This can lead to hypoalbuminaemia with subsequent edema.

Renal symptoms are often responsible for the death of an animal due to terminal renal failure.

Histopathological evidence shows thickening of Bowmann's capsules and hyalinization of the glomeruli.

Hematological symptoms

Immune thrombocytopenia (platelet factor 3 / PF-3 positive) can cause symptoms such as:

  • ecchymoses and haemorrhages in the skin and mucous membranes,
  • hematuria,
  • bloody stools,
  • epistaxis.

Research suggests that approximately 10% of dogs with immune thrombocytopenia also have SLE (based on positive LE cell test). Platelet levels drop below 100,000 platelets / mm3 and megakaryocytes are abundant in the bone marrow.

Autoimmune hemolytic anemia (AIHA) occurs in approximately 30% of dogs with systemic lupus erythematosus.

It is a more frequent manifestation of SLE than thrombocytopenia, giving a positive result in the Coombs test.

About 17% of dogs with AIHA suffer from SLE.

Animals with AIHA show signs of weakness, pallor, and possible jaundice.

Anemia is accompanied by spherocytosis, multicolor and reticulocytosis.

Hyperbilirubinemia can also be detected in which more than 50% of the total bilirubin is unconjugated. In such cases, the plasma protein content will usually be normal or increased.

Normocytic and normolour anemia may also occur. About 70% of people with SLE suffer from anemia as a result of chronic disease and a similar frequency is suspected to occur in dogs.

Leukopenia may occur in SLE as a result of complement activation and the generation of chemotactic fragments. However, dogs with lupus with AIHA or with complicated infections will have leukocytosis with a shift to the left.

Other disorders

The other symptoms may include:

    • generalized enlargement of the glands and enlargement of the spleen,
    • pleurisy and pericarditis,
    • chronic pneumonia,
    • damage to the central nervous system,
    • polyneuritis, characterized by hyperalgesia.

Diagnosis of SLE

Diagnosing SLE can be an extremely difficult challenge due to the variety of clinical syndromes that make up the disease.

Since there is no specific diagnostic test to definitively diagnose SLE, diagnosis is based on clinical signs, pathological abnormalities, serological criteria, and specialized immunoassays.

In humans, SLE is diagnosed after the detection of a minimal number of diagnostic criteria, including clinical symptoms and laboratory results.

Several similar diagnostic schemes have been proposed to help diagnose SLE in dogs.

Diagnosis of SLE based on clinical symptoms:

Main symptoms:

  • skin changes (bullous dermatitis),
  • non-damaging (non-erosive) polyarthritis,
  • hemolytic anemia,
  • glomerulonephritis,
  • polymyositis,
  • leukopenia,
  • thrombocytopenia,
  • proteinuria,
  • hemolytic anemia.

Secondary symptoms:

  • fever of unknown origin,
  • central nervous system symptoms,
  • mouth ulcers,
  • enlargement of peripheral lymph nodes,
  • pleurisy,
  • endocarditis,
  • pericarditis,
  • stupor,
  • epilepsy.

A positive test result accompanying the presence of two major symptoms or one major and two secondary symptoms allows the diagnosis to be made.

Systemic lupus erythematosus is also considered if there are two main symptoms with a negative serological test result or one main symptom with a positive serological test result.

Serological tests

The serological tests used to diagnose SLE in dogs are the ANA test and the LE cell test.

The titer of antinuclear antibodies

Antinuclear antibody titer is the procedure used to detect antibodies to various nuclear antigens.

To perform the ANA test, serum dilutions from the suspected patient are applied to a substrate, such as a layer of mouse cells; after appropriate incubation time, the specimen is rinsed.

Fluorescein-conjugated anti-canine IgG serum is then added, the entire system is incubated, then the slide is rinsed again.

Both a fluorescence pattern (ring or spotted) and a titer are obtained.

Titers vary from lab to lab and also depending on the media used. Normal sera will have significant titers from time to time, therefore the ANA test cannot be used as the sole basis for diagnosis.

This test is positive in most SLE cases, however the actual proportion of patients who report significant titers ranges from 40-100% (depending on reports).

The highest titers appear in the most severe clinical cases.

The ANA titer is relatively constant and relatively resistant to corticosteroids. After clinical remission is achieved, titers decline.

Therefore, the ANA titer can be used as an index of disease activity. A high titer indicates an exacerbation of the disease.

LE cell assay

The LE cell test is another important criterion used to diagnose SLE. The LE cell is a neutrophil that has phagocytized (engulfed) nuclear material.

The circular structure representing the phagocytic material is located in the cytoplasm of the neutrophils, compressing the nucleus on one side of the cell.

Occasionally, LE cells are seen in the synovial fluid from an animal with SLE, but this is primarily a laboratory phenomenon.

Preparation of LE cells requires a lot of time and experience.

The procedure involves passing both serum and clot through a fine wire mesh.

The collected material is then placed in a Wintrobe hematocrit tube and centrifuged for 10 minutes at high speed.

The sheepskin coat is used to make smears that are stained and tested for LE cells.

When two or more LE cells are found, the test is positive.

The incidence of the LE-cell phenomenon in naturally occurring SLE varies across studies.

Overall, 60-90% of SLE cases are positive. The LE cell assay is more specific to SLE than the ANA assay. In turn, the ANA test is considered a more sensitive test.

In contrast to the titre of antinuclear antibodies, the LE cell test quickly becomes negative during treatment with corticosteroids.

Examination of a tissue section

Immunoassays can also be performed on skin, kidney and joint tissue biopsies.

Fluid can be taken from inflamed joints and sent for analysis and culture.

Histopathological findings in the skin include epidermal and cutaneous lesions and may include leukocytoclastic vasculitis and cellulitis with mononuclear cell infiltration.

Direct immunofluorescence testing is a specialized procedure to help diagnose SLE.

Direct immunofluorescence (DIF) is used to detect immunoglobulin and complement embedded in the basement membrane zone at the dermal-epidermal junction or in the glomerular capillaries.

When DIF is applied to the skin it is known as "lupus band test ". It is a sensitive indicator of lupus erythematosus in the affected skin.

In a section of macroscopically unchanged skin, immune complexes (lupus band test) are granular deposits at the dermal-epidermal border.

DIF of kidney biopsy specimens will show discontinuous granular deposition on glomerular capillary loops.

Direct (rather than indirect) immunofluorescence is more relevant in diagnosing lupus in dogs, as circulating antibody titers are low.

Other immunological criteria

Other immunological criteria, while not specific to SLE, may aid diagnosis by detecting autoantibodies directed against other tissues.

These tests include the direct Coombs test (anti-erythrocyte antibodies) and the Platelet Factor 3 test (for anti-platelet antibodies).

Other research

Some additional tests are advisable when SLE is suspected.

Hematology, blood chemistry and urinalysis may show different abnormalities depending on the organs involved (other than the skin), e.g. anemia, decreased number of platelets, elevated levels of protein in blood and urine or elevated renal parameters.

Based on the morphology, a decision can be made about the need for a bone marrow biopsy. It should be considered in the presence of non-regenerative anemia and leukopenia and thrombocytopenia.

The Coombs test is used as a routine test for regenerative anemia.

Serum protein electrophoresis can detect an increase in gamma globulin, which corresponds to an increased production of immunoglobulin.

Urinalysis: About half of the SLE patients have proteinuria in the urinalysis.

Glomerular cell proliferation is observed in the early stages of SLE.

The glomerular cells can produce oxygen radicals, proteinases and chemotactic proteins.

Deposits of immune complexes accumulate on the basement membrane and in the mesangium.

If there is significant proteinuria, hematuria, erythrocyte rolleruria and decreased glomerular filtration, renal biopsy is indicated (however, this is not a routine test).

The screening test used when proteinuria is suspected of glomerular origin is urine protein to creatinine ratio. Correctly, this ratio should not exceed the value of 1.

One of the main symptoms of SLE is glomerulonephritis.

The immunochemical test shows the following deposits:

  • IgG,
  • IgM,
  • rarely IgA or IgE,
  • complement components C3 and C1γ,
  • properdin,
  • fibrin.

In patients with disorders of the musculoskeletal system, it is reasonable to perform x-rays of the joints and puncture them.

In SLE, there are no radiographic changes, but there is an increase in the viscosity of the synovial fluid, an increase in the number of cells and the absence of bacteria characteristic of aseptic arthritis.

In the course of SLE there are reactive changes in the joints, transient serous inflammation characterized by increased proliferation of synoviocytes and lymphocytic infiltrates within the fibrous membrane of the articular capsule.

With myositis, the level of creatine kinase is determined. In some cases, a muscle biopsy is also performed.

An X-ray and / or an ultrasound scan of the abdomen may also be indicated.

Systemic lupus erythematosus can also result in changes in the heart, such as. papillary endocarditis of the atrioventricular valves (called. atypical endocarditis of the Libman and Sacs type a) where lesions are present on both surfaces of several valves.

In the valve there are foci of fibrinous degeneration and foci of necrosis, infiltrates of lymphocytes and plasma cells.

Blood clots form on the valves, and the valves become fibrous and regurgitated.

Small coronary arteries narrow as a result of intimal fibrosis, degeneration and necrosis of the vessel wall and endothelial cells, and the formation of blood clots.

In most cases of SLE, sero-fibrinous and fibrinous pericarditis, fibrinous epicarditis, fibrous adhesions with the pericardial surface are found.

Myocardial hypertrophy occurs as a result of hypertension resulting from glomerulonephritis.

The diagnosis of SLE is difficult because no single test for the presence of the disease is available.

It can be said that the atypical change is inherent in the essence of systemic lupus, which has its own rules and attacks the body according to the key known only to itself.

Therefore, it may be necessary to conduct additional tests to rule out other diseases that may cause similar symptoms and produce similar laboratory test results.

These can include infections, other immune diseases, drug reactions, and certain cancers, among others.

Establishing a diagnosis of SLE depends on eliminating these diseases and documenting at least one positive immunoassay and involving at least two different organ systems.

Differential diagnosis

The differential diagnosis of SLE should take into account other changes, characterized by the appearance of lymphocyte and histiocyte infiltration, in the course of which there is no hydropic degeneration of cells in the basal layer of the epidermis and no changes in the basement membrane.

They are e.g. subepidermal bullous diseases, pemphigus erythematosus and common pemphigus, dermatomyositis and superimposition syndromes.

Other polyarticular diseases affecting dogs should also be ruled out, the most common of which are:

  • rheumatoid arthritis,
  • undifferentiated connective tissue disease,
  • primary antiphospholipid syndrome,
  • idiopathic thrombocytopenic purpura,
  • drug-induced lupus,
  • autoimmune thyroid disease.

This disease is also suspected in patients with fever or spleen enlargement and / or lymphadenopathy.

Lupus may occur with local or generalized lymphadenopathy or splenomegaly, but lymphadenopathy is rarely> 2 cm, while splenomegaly is mild to moderate.

In febrile patients with confirmed SLE, leukocytosis, neutrophilia, shivering, and normal levels of anti-DNA antibodies promote infection.

Patients with confirmed or suspected SLE with pronounced lymphadenopathy, massive spleen, or an enlarged population of monoclonal B cells should arouse the suspicion of non-cerebral lymphoma.

Systemic lupus erythematosus treatment

Treatment of SLE focuses on two categories of non-selective, non-specific drugs that modulate cellular function:

  • corticosteroids,
  • cytotoxic agents.

Corticosteroids are used because they suppress the functions of monocytes and macrophages.

On the other hand, cytotoxic agents are used to reduce the production of antibodies.

When used together, these drugs show a complementary effect.


The drug of choice is initially prednisone or prednisolone at a dose of 2-4 mg / kg body weight administered orally and divided into two doses per day.

High doses of immunosuppressants are usually needed to control the disease, so it is important to rule out infectious diseases before starting treatment.

Dosage is reduced as clinical symptoms resolve.

Dose tapering should be done gradually by reducing the dose to half every 2 weeks until a dose is given every other day sufficient to maintain remission.

Treatment may be discontinued as long as the patient is monitored.

If the dog does not respond well to prednisone alone, stronger immunosuppressants are added to the therapy, such as:

  • azathioprine,
  • cyclosporine,
  • cyclophosphamide.

Cytotoxic drugs

Many cases do not respond to corticosteroids alone and require additional cyclophosphamide or azathioprine.

There are many acceptable treatment regimens.

One regimen that can be used is the use of cyclophosphamide at an oral dose of 1.5-2.5 mg / kg once a day for four consecutive days of the week.

Azathioprine is administered at a dose of 2 mg / kg body weight in two divided doses.

After achieving remission, the prednisone dose should be halved.

If clinical symptoms have resolved for one full month then azathioprine may be switched to alternate day dosing.

If remission continues for another 2-4 months, cyclophosphamide and azathioprine may be completely discontinued.

Prednisone can then be reduced.

The most effective treatment is oral administration of glucocorticosteroids in combination with doxycycline, strong local glucocorticosteroids (betamethasone, triamcinolone) and systemic antibiotic therapy with amoxicillin with clavulanic acid or enrofloxacin.

Dexamethasone therapy (0.2 mg / kg m.c.) and cyclosporine (5 mg / kg m.c.).

Patients with haemolytic anemia may require splenectomy as the spleen is the primary site for the destruction of sensitized (antibody) red blood cells and the primary site for antibody production.

However, in dogs, these two functions may be taken over by other sites, and relapses will occur even with splenectomy.

Some reports, however, show that as much as 50% of splenectomies performed in dogs have resulted in a good result in treating AIHA.

A splenectomy (removal of the spleen) can also help treat thrombocytopenia, although test results are variable.

Since SLE is associated with the loss of T-suppressor function, other drugs, in addition to corticosteroids and cytotoxic agents, may also be useful.

Since levamisole is a T cell modulator, it can regenerate some of the lost functions of T cells.

Another drug that can regenerate the regulation by suppressor T cells is the V fraction of thymosin. This drug is derived from the thymus gland of a bovine fetus.

Neither drug has been reported to treat canine SLE, although either can be tried if other treatments are unsuccessful.

Other medications, supplements, and dietary changes may be recommended to relieve proteinuria, joint pain, vomiting, weight loss, and other symptoms.

Long-term monitoring of both the disease and the potential side effects of drugs used to treat it is imperative.

Prednisone usually increases appetite, thirst, and urination, and causes weight gain and has a secondary effect on the liver.

Stronger immunosuppressants may have adverse effects on blood cells, liver and kidney function.

Periodic check-ups and repeated laboratory tests are usually needed throughout a dog's life.


Systemic lupus erythematosus is a chronic, progressive disease that is difficult to control.

Many animals do not or only partially respond to therapy (e.g. skin improves, but kidney disease does not).

Sometimes the answer appears early, but over time the disease becomes more difficult to control.

If kidney damage does occur and begins to fail, prognosis is poor and survival is usually short.

Dogs with SLE live an average of about a year from the onset of clinical signs of disease.

Initially, the symptoms are very non-specific and may suggest other diseases.

Clinicians call this disease "the great mimic" because the clinical picture of SLE can be so diverse that it makes it impossible to diagnose.

It should be remembered that this disease is incurable and although the final diagnosis does not significantly change the management, it allows to determine the prognosis and familiarize the dog owner with the nature of the disease.

Patients with haemolytic anemia and thrombocytopenia are those who will most often require cytotoxic agents and aggressive treatment.

However, most patients without these syndromes respond positively to prednisone therapy and remain in clinical remission for a long time.

The main prognostic factor for patients with SLE is the presence of glomerulonephritis. Many SLE patients with glomerulonephritis progress to renal failure, and uremia is often fatal.

Cutaneous lupus erythematosus (CLE)

Cutaneous lupus occurs in dogs as a variety of clinical skin conditions. These are rare disorders of immune origin.

Histopathological and immunopathological changes observed in their course are very similar or even identical.

Collies, Shetland sheepdogs, German shorthaired pointers, Siberian huskies and Breton spaniels are predisposed to the occurrence of various types of cutaneous lupus, therefore genetic factors probably play a role in the etiology of the disease.

Discoid lupus erythematosus / DLE

Discoid lupus erythematosus is considered to be the second most common autoimmune disease in dogs.

Unlike systemic lupus, this form of lupus is limited to the skin.

The exact pathogenesis of this disease is unknown, but the formation of antigen-antibody complexes with subsequent deposition in small vessels and the basement membrane zone of the skin is observed.

Etiology and pathogenesis

The exact pathogenesis of DLE is not elucidated in dogs and cats. Unfortunately, it is not known what causes the body's own immune system to "rebel" and begin targeting the skin.

However, exposure to ultraviolet light in a group of dogs with clinical signs significantly exacerbated the severity of the disease, while the protection against radiation was improved, so it is safe to assume that UV rays play a role in at least some DLE patients.

There also appear to be dogs that are unaffected by changes in exposure to UV radiation.

The dominant cells that infiltrate the skin in human discoid lupus are T helper cells, and dogs have a large number of B lymphocytes.

In addition, there is a deposition of immune complexes in the basement membrane of the epidermis.

Antibodies included in these complexes are directed against antigens of the epidermis with a molecular weight of 84 and 120 kD.

The occurrence of the disease

German Shepherds, Collies, Shetland Sheepdogs, Siberian huskies are predisposed to the development of the disease. It is a condition that generally affects middle-aged dogs.

Discoid lupus erythematosus is one of the most common autoimmune skin diseases in dogs and humans. In humans, 10% of all DLE patients develop systemic lupus erythematosus.

This probably isn't the case in small animals; only in rare cases will a patient with DLE develop systemic changes.

Discoid lupus has no symptoms of systemic disease, except in very rare potential cases which become more consistent with SLE over time.

In discoid lupus erythematosus, the lesions are skin-related, with the nose and face being the most affected areas.

Direct sunlight and higher altitudes (above sea level) may contribute to the aggravation of the disease, so DLE often worsens during the summer months.

Discoid lupus erythematosus (GDLE) can occur locally as well as recently diagnosed as generalized discoid lupus erythematosus.

  • In the local form of DLE, the changes concern the nasal plate and are manifested by symmetrical discoloration, cracks and ulcerations.
    The lesions spread along the bridge of the nose with the formation of scabs and hyperkeratosis.
    This localized form of lupus is most common in German Shepherds and their hybrids.
  • The generalized form appears in middle-aged and older dogs (5-12 years), mainly in breeds:
    • labrador retriever,
    • Chinese crested dog,
    • miniature pinscher,
    • leonberger,
    • Shih tzu,
    • poodle.

Discoid lupus erythematosus symptoms

The first symptoms appear on the nose and often affect the nasal plate, although changes have also been observed on the eyelids, lips, pads, the concave surface of the auricle and the mouth.

The earliest and mildest symptom of the disease is depigmentation of the affected skin. Initially, the nose - from its usual dark brown or black color - becomes grayish or gray-blue, and over time it becomes discolored.

Then there is erythema and excessive exfoliation of the epidermis.

Over time, the surface of the nasal plate also changes: increased damage to the basal layer of the skin causes atrophy and loss of the normal, paved architecture of the nose - the normal, cobblestone-like surface of the nasal plate becomes smoother and the wrinkle becomes blurred.

In places of discoloration, the lesions are grayish in color.

As the disease continues, the lesions may progress to reveal scabs, erosions and wounds.

The lesions then spread to the dorsal area of ​​the nose, usually towards the eyes.

In severe and chronic cases, erosions, deep ulcers, crusts and scars develop.

With this disease, itching is absent or insignificant, but it is possible to feel pain in the affected areas.

Even after minor trauma to the nasal plate, profuse hemorrhages can occur.

Clinical symptoms of GDLE

  • The initial clinical changes most frequently reported by dog ​​handlers are usually first noticed in the neck and trunk:
    • erythematous spots,
    • lumps,
    • plaques with erosions and peeling.
  • Changes may also be present on:
    • head,
    • belly,
    • medial and lateral surfaces of the limbs,
    • the chest.
  • Generalized hyperpigmentation or discolored spots with an erythematous areola, adherent scales and scarring along with deep erosions or ulcers are possible.
  • Hyperkeratosis with extensive or multifocal alopecia in the dorsal area or symmetrical lesions on the abdomen, thighs, armpits and chest are also common.
    Plaques are often mild to moderate scarring with erosions, depigmentation, or discoloration.
  • An unusual pattern of mesh-like discoloration was also observed on the skin of the abdomen and on the sides of the chest.
  • In about half of the cases, the mucocutaneous area is affected along with typical DLE lamellar lesions, most often appearing in the genital area, in the perineum and anus area.
  • Strong discoloration of the skin, thickening of the stratum corneum, as well as plaque formation and discoloration may appear in the area of ​​the nasal plate, bridge of the nose, eyes and the entire face area.
    The architecture of the nasal plate is destroyed, erosions and ulcers appear.
  • Symmetrical discolored spots or plaques may appear on the edges of the auricles or even on the entire medial surface of the ears, hyperkeratosis and blockage of the hair follicles.

Despite the generalized changes, no systemic or organ symptoms are observed (apart from itching and pain in the lesions), and the results of laboratory tests are normal.


Discoid lupus erythematosus is diagnosed on the basis of history and clinical examination, laboratory tests (blood count, serum biochemistry) and histopathological examination of primary skin lesions, as well as immunofluorescence and immunoperoxidase.

The following criteria are considered in the diagnosis of discoid lupus:

    1. Over 3-month history of generalized skin lesions justifying their chronic or recurrent nature.
    2. The presence of skin lesions: the presence of erosions and scabs within the limited, dye-free lesions. The lesions are located on the nose.
    3. Presence of microscopic lesions typical of cutaneous lupus (lymphocyte-rich dermatitis with basal cell damage).

Laboratory test results are usually normal.

Pap smears can be useful for finding an infection that can occur at any time, especially when the disease is not under control.

For an accurate diagnosis, a biopsy is performed.

Other diseases can mimic many of the changes seen in DLE, but require very different treatment regimens. For this reason, a biopsy is required to confirm the autoimmune nature of the disease before starting treatment.

Determination of antinuclear antibody (ANA) titers and LE cell tests (useful in the diagnosis of systemic lupus) are not tests of choice in the diagnosis of DLE.

The ANA test is positive in approximately 5% of DLE cases. Thus, negative titers do not rule out disease, but positive antinuclear antibody titers could mean that animals could potentially convert to systemic lupus erythematosus and should therefore be closely monitored.

The histopathological examination of the skin section is decisive.

There are aquatic and lichen-like dermatitis at the junction of the dermis and epidermis, damage to the basement membrane and apoptosis of keratinocytes in the deeper layers of the epidermis.

The infiltration of mononuclear cells is located at the dermal-epidermal and perivascular boundaries. It is dominated by lymphocytes and plasma cells, and sometimes mast cells and macrophages may be present.

Mucin build-up is also common.

Pigment is released from damaged cells of the basal layer of the epidermis, which results in its loss.

Final diagnosis usually requires confirmation by immunofluorescence and immunoperoxidase methods.

The lymphocytes infiltrating the skin lesions of dogs with DLE are predominantly B cells.

Differential diagnosis

The diagnostic process takes into account diseases in the course of which the nasal plate is affected. These are:

  • exfoliating lupus erythematosus,
  • deciduous pemphigus,
  • pemphigus erythematosus,
  • mucosal pemphigoid,
  • Familial (congenital) parakeratosis of the Labrador Retriever's nasal plate,
  • nasal and finger pad hyperkeratosis,
  • idiopathic discoloration of the nasal plate,
  • vitiligo,
  • skin-choroid syndrome,
  • drug reactions,
  • vasculitis of the nasal plate,
  • dermatomyositis,
  • zinc-dependent dermatoses,
  • Sun burns,
  • histiocytosis,
  • epitheliotropic lymphoma.

In the differential diagnosis, other likely causes of changes to the dog's nose should also be considered, such as:

  • bacterial infection,
  • tinea,
  • injury,
  • cancer.

Discoid lupus erythematosus treatment

Traditional treatment of canine DLE is usually multi-faceted, aimed at reducing clinical symptoms while reducing unwanted side effects from medications.

There are a number of treatment options available to treat this condition, but their choices will depend on a variety of factors.

These are among others:

  • the stage of the disease,
  • ease of administration of the drug to the animal,
  • response to therapy,
  • potential side effects of medications.

Each animal must be assessed individually, and then the most appropriate drug or combination of drugs is selected after close inspection and consultation with the owner.

Treatment regimens typically include systemic and / or topical glucocorticoids, oral tetracycline, oral niacinamide, and topical tacrolismus.

Topical treatment is usually sufficient for mild lesions or those confined to a small area:

  • Initially, fluocinolone or betamethasone (preferably dimethyl sulfoxide - DMSO) every 12 hours are used to control symptoms and achieve remission.
  • After remission is achieved, creams are applied less frequently (every 48 hours) and / or active substances are changed to less effective ones (e.g. triamcinolone, 1 or 2% hydrocortisone).
  • Cream containing 1% tacrolismus.
    Improvement is seen after about 8 weeks of use.

General treatment is recommended in situations where the lesions cover larger areas or when local treatment is ineffective.

  • Oral glucocorticoids such as prednisolone 2.2 mg / kg orally every 24 hours (dosing can then be limited to every 48 hours).
  • Vitamin E in the dose of 200-800 IU a day, two hours before or two hours after feeding.
  • Omega-3 polyunsaturated fatty acids at a dose of 66 mg / kg m.c.
    Omega-3 unsaturated fatty acids have been suggested to have essential anti-inflammatory properties through their conversion to resolvins and protectins, which act in conjunction with the gamma receptor and the G protein-coupled receptor.
    These properties may make omega-3 fatty acids useful supplements for controlling autoimmune disease.

If this treatment is unsatisfactory, treatment with tetracycline and nicotinamide may be used.

Drugs are administered orally:

  • dogs up to 10 kg - 250 mg of each drug orally every 8 hours;
  • dogs over 10 kg - 500 mg of each drug orally every 8 hours.

The changes gradually disappear within 3 weeks of treatment, but relapses are possible.


Tetracycline is a broad-spectrum antibiotic (i.e. active against many species of bacteria) with significant anti-inflammatory properties.

It can affect:

  • complement activation,
  • production of antibodies,
  • chemotaxis,
  • synthesis:
    • prostaglandins,
    • lipases,
    • collagenase.

Common side effects seen with tetracyclines are gastrointestinal disturbances such as anorexia, vomiting and diarrhea.

These symptoms are usually mild and usually disappear during or after treatment.


Nicotinic acid amide - belongs to the group of vitamins B (the so-called. vitamin PP or B3).

It also has anti-inflammatory properties, and has been used in humans for 50 years to treat many conditions such as acne and rosacea.

It is suspected to work by inhibiting mast cell degranulation and phosphodiesterase.

In dogs, the immunomodulatory combination of niacinamide and tetracycline has been used for 20 years as a glucocorticoid substitute for some proven or suspected autoimmune diseases, especially DLE and pemphigus.

Cyclosporin A in high doses (30 mg / kg m.c.).

The effects are noticeable about 6 weeks after starting treatment.

Often, due to side effects of treatment (e.g. gingival hyperplasia) ciclosporin therapy must be discontinued (usually after about 6 months of treatment).


Azathioprine at a dose of 1-1.5 mg / kg m.c. daily, then every 48-72 hours.

It is used in severe, unresponsive cases.

Topical medications

Once the general therapy has managed to control the clinical symptoms of the disease, long-term topical tacrolismus or glucocorticoid treatment once or twice daily can be initiated to prevent relapse.

Regardless of the treatment program developed individually for each patient, sun avoidance is extremely important (for the success of therapy and further prognosis), as it plays a key role in triggering and strengthening the symptoms of the disease.

In summer, you should avoid walking your dog between 8 a.m. and 5 p.m.

Since it is often a difficult requirement to meet, it is important to use local sunscreen and "protectors " on the nasal plate during periods of sun exposure (you can make a nose cover yourself, modifying the material muzzle accordingly).

Treatment is usually necessary for the rest of a dog's life.

Some cases of discoid lupus erythematosus respond quickly to therapy, while others are difficult to treat.

There are patients who respond well to only topical treatments (tacrolismus), but many dogs require systemic therapy with steroids, doxycycline in combination with niacinamide or cyclosporine.

Each therapy has advantages and limitations.

The advantage of tacrolismus ointment is that it does not work systemically, but the limitation is that dogs often lick it from the nose, and in addition, this drug is relatively expensive.

The benefit of doxycycline with niacinamide is that the combination is effective in many cases and the risk of side effects is low.

The limitation of this therapy is the fact that - according to some data - it often takes as long as 8 weeks for it to start working and 12 weeks for drugs to achieve maximum effectiveness.

Adverse reactions are usually mild and limited to gastrointestinal disturbances, although hepatotoxicity may rarely occur.

Ciclosporin (5 mg / kg orally every 24 hours) works faster (within 4 to 6 weeks).

It also has a low risk of side effects limited to an upset stomach, gingival hyperplasia, hirsutism, and rarely increased susceptibility to papillomavirus.

The advantage of steroid therapy is that it works quickly; however, it does not work in all cases.

Steroids also have the highest risk of side effects (hepatopathy, muscle wasting, excessive thirst, increased urination, panting, increased appetite), especially if you are on long-term daily therapy.

Systemic corticosteroids are rarely needed in DLE, so should only be used in severe DLE that does not respond to topical therapy.

Topical glucocorticoids applied to the nasal plate are often the only form of steroids needed to treat and control milder cases of DLE.


The prognosis for DLE is usually favorable.

  • Most cases respond well to treatment, and the long-term prognosis is good.
  • If glucocorticosteroids cannot be used, the prognosis is cautious to poor.
  • If the lesions are left untreated, they can become painful and can lead to the development of squamous cell carcinoma (rare).

You should monitor the condition of your dog.

Laboratory tests are performed regularly to monitor potential side effects of medications.

The patient is routinely checked for the severity of lesions, and the therapy - if necessary - is appropriately modified.

Mucocutaneous lupus erythematosus (MCLE)

Mucocutaneous lupus erythematosus is a recurrent version of cutaneous lupus erythematosus.

German Shepherds may be predisposed to this form of lupus: about 50% of dogs with MCLE are representatives of this breed or their hybrids.

The disease was also found in:

  • labradors,
  • belgian shepherd dogs,
  • miniature pinscher,
  • welsh corgi,
  • Jack Russell Terriers,
  • Pyrenean mountain dogs.

The occurrence of the disease

In a study of dogs with mucocutaneous lupus, German Shepherds were 57% of the 21 sick dogs, Labrador Retrievers (2%) and other breeds (Wolfspitz, Miniature Pinscher, Welsh Corgi, Pyrenean Mountain Dog, Belgian Shepherd Tervueren) were 33%. , Jack Russell terrier and hybrids).

The age of skin lesions varies from 3 to 13 years (median: 6 years, mean: 7 years).

The most advanced changes are visible in the "middle" of adulthood, i.e. between 4. a 8. the course of life.

Clinical symptoms of mucocutaneous lupus erythematosus

The changes that appear in the course of MCLE mainly concern the so-called. dermal-mucosal connections, so they are located (sometimes simultaneously):

  • on or around the genitals,
  • in the anus area,
  • on the skin around the eyes,
  • around the nose or mouth,
  • on the lips.

Changes in the mouth are also possible on the gums or the palate, but also on the abdomen and the auricles.

In most dogs, the lesions affect two or more areas of the skin or mucous membranes.

Mucocutaneous lesions in most cases are symmetrical and most often constitute well-delimited areas of erosions and ulcers, erythema and scab.

A rim of intense discoloration is often observed around ulcers or in places of previous lesions.

Change unfolds in many areas at the same time.

Symptoms observed by the owners are most often mucocutaneous wounds, pain during defecation (dyschezia) and / or urination (dysuria), the presence of fresh blood in the stool, constipation, and licking the affected area.

No systemic changes were observed, apart from pain at the site of injury.

Diagnosis of MCLE

The diagnosis of chronic erosive lesions with histopathological features of lupus erythematosus, mainly affecting mucocutaneous junctions, is still relatively difficult.

In dogs, in addition to systemic lupus erythematosus, three other forms of the disease are confined to the skin:

  • discoid lupus erythematosus,
  • exfoliating lupus,
  • follicular lupus.

Therefore, the diagnosis of MCLE takes into account the following criteria:

  • over 2-month history of skin changes, proving their chronic or recurring nature;
  • the presence of erosions or ulcers mainly on the mucous membranes or dermal-mucosal junctions (any);
  • the presence of microscopic changes typical of cutaneous lupus erythematosus;
  • no complete remission after the use of antibiotics and antiseptics.

The entire diagnostic process is typical for cutaneous lupus (information obtained from the owner, nature and location of clinical symptoms, laboratory tests and histopathological examination of the skin specimen).

Differential diagnosis

Purulent dermatomyositis

There are no extensive erosions, but rather erythema and swelling.

Additionally, these changes respond to antibiotic treatment, unlike MCLE, which does not improve with antibiotic treatment.

Bullous pemphigoid

The lesions are deeper in the skin, and there are bubbles and blisters in the mouth.

Erythema multiforme

In addition to epidermal defects, such as erosions, there are also edema lesions, lumps and plaques that take an arcuate shape or the letters "S ".

Systemic lupus erythematosus

It involves disorders of the internal organs, manifested by various clinical symptoms and abnormalities in the results of laboratory tests.

Usually, there is also the presence of antinuclear antibodies (ANA).

Treatment of mucocutaneous lupus erythematosus

In the treatment of the disease, the following are used:

  • Tetracycline (dogs up to 10 kg - 250 mg 2-3 times a day; dogs over 10 kg - 500 mg 2-3 times a day) in combination with vitamin PP 350-750 mg per dog every 12 hours.
    Alternatively, doxycycline 5 mg / kg m may be administered instead of tetracycline.c. every 12 hours.
  • Calcineurin inhibitors (tacrolismus, pimecrolismus) are applied 2-3 times a day on the changed skin.
  • Oral glucocorticosteroids (prednisone 2.2-6.6 mg / kg m.c. every 24 hours).
    After a noticeable improvement, the dose of the drug is reduced and the time intervals are extended, giving the drug every 48-72 hours.
  • In treatment-resistant cases, glucocorticosteroids are combined with azathioprine (1.5-2.5 mg / kg every 24 hours).

Classic immunosuppressive treatment with glucocorticoids (local or systemic), niacinamide with tetracycline or doxycycline, cyclosporine or tacrolismus is almost always associated with a significant improvement or complete withdrawal of disease symptoms.


Immunomodulatory drugs appear to be effective in treating MCLE.

The prognosis for remission is good, however, relapses are frequently observed.

Exfoliative cutaneous lupus erythematous / ECLE

It is an inherited disease (autosomal recessive) formerly known as congenital lupus dermatosis or generalized exfoliative German pointers lupus dermatosis.

It is a familial form of lupus seen in German shorthaired pointers.

Exfoliative lupus erythematosus is an autoimmune disease as it affects the basement membrane zone of the skin (as with all types of lupus erythematosus) with the build-up of immune complexes, leading to an inflammatory response.

The occurrence of the disease

Exfoliating lupus erythematosus occurs exclusively in German shorthaired pointers.

The disease is considered to be genetic as it only occurs in this one breed of dog.

It has also been found that a large number of sick dogs are related to each other.

Clinical signs usually appear in the first year of life, and the disease is more common in females.

Exfoliative lupus erythematosus symptoms

The first symptoms are seen in young dogs between 6 months and 2.5 years of age.

The predominant symptom is excessive, generalized exfoliation of the epidermis with follicular casts and alopecia, which initially affects the skin of the face, auricles and the nose.

Then the lesions appear on the abdomen, limbs, back, and over time, the disease may become more generalized.

Sometimes changes are also present in the area of ​​the tail and perineum.

Occasionally there are scabbed ulcers.

The epidermis along the back is thinned and is easily damaged.

The itching is usually minimal.

The nasal plate becomes discolored which then spreads along the bridge of the nose.

Peeling of the epidermis and ulceration may be accompanied by other symptoms, such as:

  • blood picture disturbances (e.g. anemia),
  • enlargement of the superficial lymph nodes,
  • sometimes the disease is accompanied by intermittent fever,
  • joint diseases;
    lameness may occur in sick dogs, which is most noticeable in the first 10 minutes after the animal is resting;
    dogs may show a hunched posture characterized by a slight dorsal curvature of the spine and a stiffness in the hind limbs;
    X-rays of the limbs and pelvis do not show any abnormalities, as is the examination of the synovial fluid.
  • Spermatogenesis and oestrus cycle disorders are also possible (these symptoms, however, may be related to the administration of immunosuppressants).
  • Sun exposure worsens the progression of the disease.

Diagnosis of exfoliative lupus erythematosus

Diagnosis is made on the basis of information obtained from the owner and typical clinical symptoms.

  • Interview and clinical examination
    • age and breed of the dog,
    • skin symptoms,
    • the occurrence of the disease in related individuals,
    • signs of pain.
  • Hematological examination - thrombocytopenia and lymphopenia may sometimes be observed.
  • Microscopic examination of the hair may show casts of the hair follicles, which are formed as a result of the accumulation of corneocytes at their mouths.
  • Confirmation of the diagnosis is obtained after a histopathological examination.
    Visible are hyperkeratosis, apoptosis of keratinocytes with lymphocytic infiltration on the border of the dermis and epidermis, as well as inflammation of the hair follicles.
    There may be destruction of sebaceous glands and loss of melanin.
  • Immunohistochemistry shows the deposition of IgG immunoglobulins in the basement membrane of the epidermis and around the sebaceous glands.

In the case of ECLE, the antinuclear antibodies typical for SLE are absent or their titers are very low.

There are also no antibodies against the structures of the sebaceous glands and the basal membrane of the epidermis.

Differential diagnosis

  • keratinization disorders (e.g. inflammation of the sebaceous glands),
  • systemic lupus erythematosus,
  • dermatophytosis,
  • zinc-dependent dermatoses.

Exfoliating lupus erythematosus treatment

Treatment of exfoliative lupus erythematosus in dogs is based on balancing the desired drug effects (alleviation of clinical symptoms) and drug toxicity.

Therapy of this form of lupus is largely palliative, however, it is possible to achieve periods of disease remission thanks to the therapy used (prednisolone, azathioprine, local keratolytic and keratoplastic agents).

Treatment aimed at immunomodulation:

  • glucocorticosteroids (prednisolone),
  • cyclosporine,
  • nicotinic acid amide with tetracycline,
  • azathioprine,
  • retinol and synthetic retinoids,
  • leflunomide,
  • adalimumab (TNF-alpha antagonist),
  • hydroxychloroquine,
  • polyunsaturated fatty acids.

The use of keratomodulating, anti-seborrheic and moisturizing shampoos.


Long-term treatment is extremely difficult and the prognosis is cautious or even unfavorable.

Treatment of the disease is usually ineffective as symptoms almost always flare up and periods of remission are short.

Despite the use of many drugs, it is not possible to achieve a satisfactory treatment effect. Unfortunately, dogs are often euthanized. Even the trial of treatment with adalimumab for a long time (16 weeks) was unsuccessful.

In prevention, it is extremely important to prevent the spread of the disease in the population of dogs of this breed and to eliminate individuals with diagnosed disease from further breeding.

Vesicular cutaneous lupus erythematosus / VCLE

The disease is also known as idiopathic ulcerative dermatosis of Collies and Shetland Sheepdogs, previously thought to be a variant of juvenile dermatomyositis found in these breeds.

In 2001, Jackson and Olivry separated this ulcerative dermatosis from dermatomyositis, and in 2004 reported the discovery of circulating anti-Ro antibodies in dogs with VCLE.


There is not yet enough information about canine VCLE to be able to assess the incidence and prevalence of this disease in dogs.

It is known that animals of mature age are predisposed, and the intensification of skin lesions is usually observed in the summer.

This dermatosis is most common in collies, shetland dogs and their crosses.

VCLE develops antibodies against one or more extracted nuclear antigens (ENA). They are detected in a significant percentage of sick animals (73-82% of cases).

Vesicular cutaneous lupus erythematosus symptoms

The disease usually presents with vesicles, blisters (usually for a short time), and polycyclic ulcers.

Changes in the form of annular, multifocal and serpentine erosions or ulcers occur mainly in the hairless areas, such as:

  • armpits,
  • groin,
  • belly,
  • inner surfaces of the auricles.

It happens that eruptions occur not only on the skin, but also on mucous membranes (e.g. in the mouth) and on the border of the skin and mucous membranes.

Apart from the skin lesions, no other clinical signs are present in the affected dogs. Vesicular cutaneous lupus erythematosus is also light-sensitive.


The diagnosis of the disease is made on the basis of information obtained from the owner and clinical symptoms.

The diagnosis can be supported by a histopathological examination.

Skin biopsy shows mainly lymphocytic infiltration at the border of the skin and epidermis, as well as folliculitis and possible formation of sub-epidermal blisters.

In the basal layer, there are apoptotic keratinocytes with features of aquatic degeneration.

Testing for the presence of ANA antinuclear antibodies is almost always negative.

Diagnosis can be performed using the detection of several extractable nuclear antigens (ENA).

Immunohistochemical examination

In a study of eleven dogs suffering from vesicular cutaneous lupus erythematosus, CD3 T cells were found in all patients in epidermal sections.

In two of them, the phenotype of infiltrating skin leukocytes was similar: 25-50% of epidermal leukocytes were T cells expressing alpha-beta receptor, CD3 and CD8; less frequently, epithelial lymphocytes expressed the CD4 receptor.

Other epithelial lymphocytes were identified as CD-1 positive Langerhans cells.

In the dermis, infiltrating cells consist of approximately an equal population of alpha-beta T cells expressing CD4 or CD8-alpha and CD-1 + cutaneous dendritic cells.

CD-21 B cells are rarely found in the dermis+.

Basal layer keratinocytes expressed high levels of ICAM-1 and low levels of major class II histocompatibility molecules, indicating their activated state.


The direct immunofluorescence study showed the deposition of immunoglobulins attached to the skin-epidermal junctions or to the cytoplasm of corneocytes.

The examination revealed the presence of IgG in the basement membrane zone in approximately 50% of the dogs with VCLE. Deposition of IgG around the blood vessels was observed in 93% of the dogs.

Immunobloting enables the detection of autoantibodies against soluble nuclear antigens in the serum.

An ELISA study found that the sera of 73% of dogs contained IgG autoantibodies.

Differential diagnosis

The differential diagnosis should take into account, first of all, other autoimmune diseases, such as:

  • bullous pemphigoid,
  • acquired blistering epidermal detachment,
  • pemphigus vulgaris,
  • systemic lupus erythematosus,
  • erythema multiforme - toxic epidermal necrolysis syndrome.
  • drug reactions.

Vesicular cutaneous lupus erythematosus treatment

Since cutaneous vesicular lupus erythematosus is induced and / or worsened by UV radiation, sun exposure should be minimized as soon as possible after diagnosis.

Therapy is based mainly on immunosuppressive drugs:

  • Glucocorticoids (prednisone 2 mg / kg m.c.) - in 55% of the dogs tested, clinical symptoms resolved after oral administration of prednisone.
  • Azathioprine (1-2 mg / kg m.c.) is added to therapy when the disease does not respond to treatment with glucocorticoids.

Other treatment options:

  • Another option is to administer tetracycline with niacinamide (500 mg of each drug every 8 hours) and vitamin E (400 IU 2 times a day).
  • Pentoxifylline at a dose of 3-30 mg / kg m.c. may bring a slight improvement.
    Pentoxifylline at higher doses in combination with azathioprine at a dose of 2 mg / kg m.c. may be effective in treating the disease, but the response to pentoxifylline has been reported to be poor in studies.
  • Cyclosporin A at the dose of 4 mg / kg m.c. in combination with ketoconazole 4 mg / kg m.c. and prednisolone at a dose of 0.2 mg / kg m.c.
    Ketoconazole leads to an increase in the serum concentration of cyclosporin, therefore it is used to lower the dose of cyclosporine, mainly due to its high cost (however, administration of ketoconazole should be avoided).
  • Combination therapy with dexamethasone (0.2 mg / kg m.c.) and cyclosporine (5 mg / kg m.c.) may prove effective in cases not responding to other forms of treatment.
    Dexamethasone is given for 4 weeks and ciclosporin is continued for another 3 months.
  • Good treatment results were also obtained with the use of hydroxychloroquine sulphate 5 mg / kg m.c. including topical tacrolismus.
    Contraindications to this type of therapy are retinopathies and nephropathies.
  • Antibiotics should be used for a minimum of 4 weeks.
    The treatment includes:

    • amoxicillin with clavulanic acid,
    • cephalexin,
    • oxacillin,
    • enrofloxacin.
  • Antibacterial agents (containing ethyl lactate, benzoyl peroxide, chlorhexidine) are also used topically.
    The duration of antibacterial treatment may be up to 16 weeks.
  • In one dog, the lesions were shown to respond to the immunosuppressive mycophenolate mofetil - the introduction of this drug led to complete remission of skin lesions upon withdrawal of glucocorticosteroids.
  • Some patients benefit from the use of calcineurin inhibitors (tacrolismus, pimecrolismus).
    In these dogs, relapses of clinical signs occurred frequently after dose reduction of ciclosporin, however, with administration of calcineurin inhibitors (singly or in combination) it was possible to achieve long-term remission of symptoms.
    These reports suggest that tacrolismus may be the drug of choice in dogs with VCLE.

The prognosis for follicular cutaneous lupus erythematosus is conservative.

Some dogs are euthanized for not responding to treatment.

Lupus Onychodystrophy (symetrical lupid onychodystrophy, lupoid onychitis)

It is a rare claw disease that was first reported in the United States in a German Shepherd Dog.

In the course of this disease, there is an inflammatory infiltration of the claw bed, consisting mainly of B and T lymphocytes and a few macrophages.

Causes and occurrence

The etiology of lupus deformity of the claws is still unclear.

The disease can be genetically determined as it is most common in certain breeds of dogs, such as:

  • German Shepherds,
  • miniature schnauzers,
  • giant schnauzers,
  • labrador retrievers,
  • border collie,
  • gordon setters,
  • boxers,
  • greyhounds.

Males are predisposed.

It is known that the disease can coexist with other immune or allergic diseases (e.g. atopic dermatitis or food allergy), so it can be a reaction that occurs as a result of the action of various stimuli (e.g. as a post-vaccination reaction).

Currently, the terms symmetrical exfoliation or inflammation of the subungual shaft are used.

Lupus Onychodystrophy clinical symptoms

The disease most often develops in dogs between the ages of 3-8 years.

First, there is a sudden loosening and / or separation of one or more claws from the 3rd phalanx (exfoliation, onychomadesis).

Initially, the disease process affects individual claws, but within a few months it affects all claws.

Sick dogs lick their paws intensively, most likely because they are very sore.

The source of pain is secondary infection or fragmentation of damaged claws.

There is also lameness and reluctance to walk.

The claws that grow back are short, dry, soft, brittle and brittle.

Secondary bacterial infections often appear.

Lupus Onychodystrophy diagnosis

The diagnosis of the disease is based on the clinical symptoms, which are quite characteristic: all or most of the claws are lost.

If the lesions affect one or two claws, the diagnosis is confirmed by biopsy, culture and radiography.

X-rays and cultures are performed to assess secondary infections and check for osteomyelitis.

Cytological examination of the exudate from under the removed claws shows mainly neutrophils, which is useful in assessing the severity of secondary infections.

Histopathological examination reveals inflammation on the border of the skin and epidermis with an inflammatory infiltrate consisting of lymphocytes and plasma cells.

There is also aquatic degeneration in the keratinocytes of the basal layer, necrosis of these cells, pigment incontinence.

There are no systemic symptoms such as anemia, thrombocytopenia or glomerulonephritis in this disease.

Usually, high titers of antinuclear antibodies are not found.

Differential diagnosis

All claw diseases are included in the differential diagnosis:

  • fungal infections of the claws (onychomycosis),
  • bacterial infections,
  • tumors,
  • deciduous pemphigus,
  • systemic lupus,
  • leishmaniasis,
  • nutritional deficiencies.

Lupus Onychodystrophy treatment

There is no specific effective treatment.

Therapy is based on controlling pain and preventing changes to the remaining claws.

Sometimes (unfortunately rarely) there are spontaneous remissions.

Immunosuppressive and anti-inflammatory drugs are used to treat lupus onychodystrophy.

Supplementation with polyunsaturated fatty acids (omega-6, omega-3)

Usually it's helpful, but should be used for at least a few weeks.

When used alone, acids are only effective in some patients.

Unsaturated fatty acids can be administered in combination with tetracycline (or doxycycline) and niacinamide, and with pentoxifylline.

Tetracycline and niacinamide by mouth

This combination is recognized as an effective treatment for:

  • in dogs over 10 kg - 500 mg every 8 hours, in dogs up to 10 kg - 250 mg every 8 hours.

If symptoms improve, drug use can be reduced by administering medications every 12 hours and then once a day.

Instead of tetracycline, doxycycline (5-10 mg / kg m.c. once a day).


Pentoxifylline at a dose of 10 mg / kg m.c. every 8-12 hours and clofazimine 2 mg / kg m.c. every 24 hours can also be effective.

Pentoxifylline should be used in cases where the administration of tetracycline with niacinamide does not bring improvement.

It can be used with azathioprine.


Azathioprine 2 mg / kg m.c. every 24 hours, when improvement is achieved, the dose is reduced to half and given every other day.

In the absence of improvement after the use of these drugs, general administration of glucocorticosteroids (prednisolone 1-2.2 mg / kg m.c. every 24 hours, the dose is then reduced to half and given every 48 hours).

Removal of other claws affected by changes under general anesthesia and loose bandaging of the paws for 48 hours after the procedure.

Sometimes long-term antibiotic therapy (most often doxycycline or cefalexin), analgesic treatment, local disinfectant treatment helps,

Important in this disease is a hypoallergenic diet or food with a selected source of protein, high in essential fatty acids.

In local therapy, the use of tacrolismus on the claw bed is recommended.

Treatment should be carried out for at least 8 weeks.

In the presence of bacterial infections, it is necessary to use antibiotics (amoxicillin with clavulanic acid or cephalexin).

Usually, claws that have not come off and are not painful will grow back, but most often they are deformed and require proper care for the rest of the animal's life.


Dog's lupus (regardless of its form) is a chronic disease that requires constant monitoring, regular examinations and - as a rule - lifelong treatment.

After the diagnosis is made, more frequent visits to the doctor are necessary in order to determine the appropriate therapeutic program and doses of drugs. Following remission, checks may be less frequent.

Unfortunately, a complete cure for lupus is currently not possible.

There are cases of spontaneous remissions, but they are extremely rare.

It should be remembered that this disease can have a very different course, and thus affects both the quality of life of the dog and its guardians, but - with proper treatment and following general recommendations - many dogs function completely normally.

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