Hidden manifestations of lupus in dogs

Among the pathologies of the immune system in pets, systemic lupus erythematosus in dogs is quite common. Despite its prevalence, the disease is not always correctly diagnosed by veterinarians due to certain diagnostic difficulties. From this article you will learn why dogs suffer from this disease, what are the main symptoms and causes of the pathology, and what is the therapy.

general information

Lupus erythematosus is an autoimmune disease caused by a malfunction of the immune system. Protein components of healthy cells of the body act as autoantigens - substances considered by the body as foreign. As a result, an immune response occurs - so-called antibodies are produced. These are protein compounds that can bind to cells - antigens and prevent their further reproduction. In other words, the body attacks its own cells, thereby gradually destroying itself.

Such antigen-antibody immune complexes can be found in the kidneys, synovial fluid and membranes of the joint capsules, skin, and blood vessels. Therefore, the most common targets of the disease are the skin, connective tissues, epithelium, and joints.

What factors increase the risk of lupus?

The cause of lupus is unknown in most cases. But there are a number of potential factors that can provoke the disease or contribute to its development:

• sun exposure;
• presence of infection in the body;
• taking certain types of medications (blood pressure, anticonvulsants, antibiotics);
• elderly age;
• breed.

Predisposed Breeds

Statistics show that some breeds are more likely to get lupus than others. This happens with the discoid form. But for the systemic form, the genetic factor is considered one of the most documented causes of the development of the disease.

The breeds that are most often listed as predisposed include:

• Afghan hounds;
• hounds;
• Irish Setters;
• German Shepherds;
• collie;
• Old English Sheepdogs;
• poodles;
• Shetland Sheepdogs.

Symptoms appear around 6 years of age, but can develop at any age and often relapse or go into remission throughout the animal's life.

Causes of the disease

This disease can have two forms in dogs, differing in their origin:

1. Discoid lupus erythematosus has autoimmune causes;
2. Systemic lupus erythematosus is a hereditary disease based on a genetic factor.

Both forms of the disease can have similar symptoms, so differential diagnosis is often inconclusive.

Factors that increase the risk of one or another form of the disease are:

• inflammatory processes in the body of a bacterial, fungal or viral nature;
• prolonged exposure to direct sunlight;
• use of certain medications;
• blood diseases (leukemia);
• stressful situations.

The disease is especially susceptible to older females, over the age of 5 years, both sterilized and not.

Some dog breeds are more predisposed to the disease. This can be said about German Shepherds. But there are several other breeds whose representatives quite often exhibit similar symptoms:

• collie;
• small and medium poodles;
• Afghan hounds;
• Irish setters.

Diagnosis and treatment

Autoimmune disease is quite difficult to diagnose and an accurate diagnosis requires a number of specific tests. If systemic lupus is suspected, a general blood test, biochemical examination and general urine analysis are prescribed. When making a diagnosis, it is important to accurately collect anamnesis - the onset of symptoms, the suddenness and nature of pathological changes.

Experienced doctors know that an accurate diagnosis requires testing for antinuclear bodies and double-stranded DNA antibodies. The Wasserman reaction is also carried out to test the blood for the presence of syphilis (for lupus erythematosus, the test is false positive). In some cases, samples of skin tissue or kidney structures are taken.

If at the time of contacting the veterinary clinic the dog is in serious condition, and the blood cells begin to rapidly disintegrate, the animal is hospitalized. For mild organ damage, outpatient treatment is prescribed. The purpose of the therapeutic regimen includes taking into account the form of the disease, stage of development, damage to internal organs and the age of the pet.

The animal is provided with maximum peace and comfort necessary to reduce the load on joints and bones, preventing their destruction. It is also necessary to reduce the time spent in direct sunlight by walking your pet only after sunset. The main treatment consists of the use of medications that alleviate the serious condition of the sick animal and prevent complications due to the autoimmune disease.

To reduce the immune response of the system, specific immunosuppressants and corticosteroid drugs are used. The affected areas of the skin are treated with anti-inflammatory hormonal ointments. For large areas of damage, injections of Prednisolone and vitamin E are prescribed (which allows faster restoration of damaged skin areas).

Treatment of systemic lupus erythematosus boils down to monitoring the pet’s condition, as well as eliminating the main symptoms. Animals with lupus can live for many years, but the sooner the owner contacts a qualified doctor when characteristic signs appear, the more effective the therapy will be.

Main symptoms

The main symptoms of lupus erythematosus manifest themselves in the organ and system whose tissues are most damaged and where immune complexes are localized. The disease usually affects the skin, musculoskeletal and endocrine systems, kidneys, and lymph nodes. Let's consider how the disease manifests itself in each case.

Skin and connective tissue

The cutaneous manifestations of systemic lupus erythematosus in dogs resemble those of discoid erythematous lupus. Most often, they are bilateral. These are ulcers on the skin or mucous membranes, redness, erythema, depigmentation, erosion, scales, hair loss. Primarily, they are localized around the nose, mouth, eyes or anus.

When connective tissue is damaged, all organs where there is connective tissue are gradually involved in the pathological process - the membranes of the heart, the gastrointestinal tract, the nervous system, joints.

Musculoskeletal system

The musculoskeletal system is affected by systemic lupus erythematosus. In this case, immune complexes are localized in synovial membranes and on the inner surfaces of joints.

Damage to paired joints is noted: they become enlarged, painful, and hyperemic. Deformation of the joints leads to an unnatural position of the legs. Later muscle pain occurs.

Kidneys and liver

This is the most dangerous form of the disease, in which there is a systematic threat to life, since the entire body is involved in the process. With this form of the disease, hepatonephromegaly (pathological enlargement of the liver and kidneys) may be observed. The hematopoietic system suffers because blood cells - red blood cells, platelets and leukocytes - become autoantigens. The lymph nodes become enlarged and painful. The destructive effect of lymphocytes can be directed at any organ or system.

Lupus erythematosus in most dogs is acute in nature, but sometimes takes a chronic course. The disease is preceded by nosebleeds, followed by redness on the skin. An attentive owner should not ignore these alarming symptoms. Timely measures taken will help ease the course of the disease.

In the initial stages, short-term remissions may be observed, but then the course of the disease becomes systemic.

Symptoms

The onset of the disease often goes unnoticed; canine lupus erythematosus is characterized by a clear clinical picture in advanced cases; symptoms depend on the location of the immune complexes:

• Nosebleeds:
• Lethargy, fatigue:
• Increase in general body temperature;
• Nosebleeds;
• Lameness;
• Swelling and tenderness of joints and muscles;
• Large ulcerative red skin lesions;
• Baldness;
• Epileptic seizures;
• Enlargement and pain of the liver, kidneys, lymph nodes.

Symptoms may be similar to other dog diseases; when the first signs of illness appear, the animal must be urgently taken to a specialist.

Diagnosis of the disease

Lupus erythematosus is a disease that is difficult to diagnose. When making a diagnosis, data from an external examination, anamnesis and the results of an extended biochemical analysis of blood and urine are used. It is very important for the owner to know when the pet’s first warning signs appeared, what preceded their occurrence, and how quickly the symptoms developed.

The main criteria for making a diagnosis are:

• presence of photodermatitis;
• skin rashes;
• symmetrical joint damage;
• presence of seizures;
• changes in behavior;
• decreased content of blood particles (leukopenia, thrombocytopenia, lymphopenia);
• kidney dysfunction.

Discoid lupus erythematosus

Discoid lupus erythematosus in dogs is a rare autoimmune skin disease without systemic manifestations. There is no age or gender predisposition. Shepherd dogs and collies are most susceptible to this disease.

Symptoms of this type of lupus in dogs most often appear in the nose area. Early signs of depigmentation and disruption of the normal tissue structure are noted, then erosions, ulcers and crusts form on the skin. Less commonly, the area of ​​the ears, lips and oral cavity is affected. Deep ulcers may begin to bleed over time.

In most cases, this lupus in dogs is caused by excessive ultraviolet radiation. It occurs most severely in the summer and in areas with a warm climate.

When making a diagnosis, it is important to exclude nasal dermatitis caused by solar radiation, erythematous pemphigus foliaceus, and demodicosis.

For a more accurate diagnosis, laboratory tests are recommended. A skin biopsy can accurately identify discoid lupus erythematosus.

The prognosis for treatment of this type of lupus in dogs is favorable. Avoid exposing your animal to the sun from 8 a.m. to 5 p.m. If necessary, use topical sun protection.

Local steroid drugs are indicated.

Prednisolone should be used at a dosage of 2-4 mg/kg once a day orally, gradually reducing to the minimum effective dose. After the animal's condition improves, it is recommended to give prednisolone every other day. In addition, tetracycline is prescribed at a dosage of 250 mg 3 times a day. The duration of treatment is 2-3 weeks. Vitamin E is also prescribed.

In severe cases, prednisolone is used at a dosage of 4-6 mg/kg orally once a day, azathioprine at a dosage of 1-2 mg/kg orally once a day.

It should be noted that both drugs must be given only together to achieve an effect, and then the dose of the drugs can be reduced to the minimum effective, prescribing them every other day. Azathioprine, if necessary, can be replaced by chlorambucil, which should be given at a dosage of 0.2 mg/kg orally once a day.

Therapeutic techniques

There is no complete cure for the disease. Treatment can reduce autoimmune aggression and improve the general condition of the patient. The technique is chosen by the doctor depending on which organs and systems are involved in the pathological process. In advanced cases, the dog is placed in a hospital, and in milder cases, treatment is carried out on an outpatient basis.

Glucocorticosteroids (Prednisolone) are used to treat lupus erythematosus. The dose is selected individually, taking into account the patient’s age and the nature of the disease. In case of external manifestations, hormonal ointments are used. There are situations when lifelong use of hormonal therapy is prescribed.

Discoid lupus can be successfully treated with immune modulating drugs (Levamisole).

A sick dog must have a special lifestyle:

• It is worth sharply limiting your dog's exposure to the sun. To do this, you can walk her only in the early morning or evening, when solar activity drops.
• If the joints are affected, then you should not load them. To do this, it is recommended to limit the animal’s movements. The dog should be kept in a cramped space - in a cage or in a small room.
• To relieve the load on the kidneys, the dog needs a special diet with a limited protein content.

Publications in the media

Systemic lupus erythematosus (SLE, lupus erythematosus systemicus) is a systemic inflammatory disease of unknown etiology, pathogenetically associated with the production of autoantibodies and immune complexes that cause immunoinflammatory tissue damage and dysfunction of internal organs. Statistical data. Frequency: 0.02–0.05% of the population. The predominant age is 20–40 years. The predominant sex is female (10–20:1).

Etiology

• Environmental factors. There is an opinion that viruses, toxic substances and drugs can cause the development of SLE, but no convincing evidence has been obtained. In some cases, antibodies to the Epstein–Barr virus are detected in patients with SLE; the phenomenon of “molecular mimicry” of lupus autoantigens and viral proteins (Sm) is known. The ability of bacterial proteins to stimulate the synthesis of ANAT is known. UVR stimulates cell apoptosis with the appearance of autoantigens on their membrane.

• Hormonal influences. SLE occurs primarily in women of childbearing age, but hormonal factors may have a greater influence on the manifestations of the disease than on its occurrence. It was revealed that estrogens stimulate the synthesis of Th2 cytokines (IL-4, IL-6, IL-10).

Genetic features. The role of genetic factors is confirmed by the high concordance for SLE in monozygotic, but not in dizygotic twins, the connection of SLE with hereditary deficiency of individual complement components (C1q, C4, C2), the increased frequency of HLA-DR2 and HLA-DR3 Ag in patients with SLE in relation to the general populations, polymorphism of FcgRII receptor genes involved in the elimination of immune complexes.

Pathogenesis. SLE is characterized by a variety of immunoregulatory disorders. Polyclonal activation of B lymphocytes is observed against the background of hyperproduction of Th2-type cytokines (IL-4, IL-6, IL-10). Various cellular components act as autoantigens, primarily DNA and nucleoprotein complexes. They acquire a high degree of immunogenicity against the background of a defect in lymphocyte apoptosis, which promotes the accumulation of autoantigens on the surface of “apoptotic” cells.

Systemic immune inflammation can develop in various ways. It can be initiated by the deposition of CEC in tissues, the formation of immune complexes in situ, and also during cytokine-dependent effector reactions. Cytokines (primarily IL-1, TNF-a) are associated with increased procoagulant properties, overexpression of intercellular adhesion molecules, and activation of leukocytes. Thus, the endothelium becomes a target even in areas free of immune complexes.

Classification by V.A. Nasonova (1972-1986) • Variant of the course •• Acute course is characterized by a sudden onset with a sharp increase in body temperature, rapid damage to internal organs, including the kidneys, as well as significant immunological activity (high ANAT titers) •• Subacute course is characterized by periodically occurring exacerbations of the disease, not expressed to the same extent as in the acute course, and the development of kidney damage during the first year of the disease •• The chronic course is characterized by a long-term predominance of one or more symptoms (discoid skin lesions, polyarthritis, thrombocytopenia, Raynaud's phenomenon, slight proteinuria, epileptiform seizures). A chronic course is especially characteristic when SLE is combined with APS • SLE activity In Russia, a division into 3 degrees of activity is traditionally used •• I degree: normal body temperature, slight weight loss, discoid lesions on the skin, adhesive pericarditis and pleurisy, cardiosclerosis, urinary syndrome, Hb 120 g/l or more, g-globulins - 20–23%, LE cells are single or absent, ANAT titer - 1:32, type of luminescence - homogeneous •• II degree: body temperature less than 38 ° C, moderate weight loss, erythema on the skin , dry pericarditis and pleurisy, moderate myocarditis, nephritic syndrome, Hb 110-100 g/l, g-globulins - 24-30%, LE cells - 1-4 per 1000 leukocytes, ANAT titer - 1:64, type of luminescence - homogeneous and peripheral •• III degree: body temperature 38 °C and above, severe weight loss, “butterflies” on the face, capillaritis, effusion pericarditis and pleurisy, severe myocarditis, nephrotic syndrome, Hb less than 100 g/l, g-globulins - 30– 35%, LE cells - 5 or more per 1000 leukocytes, ANAT titer - 1:128, type of luminescence - peripheral.

Clinical picture

• Skin lesions •• Discoid lesions - coin-shaped lesions with hyperemic edges, central atrophy and depigmentation •• Erythematous butterfly dermatitis of the nose and cheekbones (erythema on the cheeks and dorsum of the nose) •• Photosensitivity - skin rashes as a result unusual reaction to sunlight •• Subacute cutaneous lupus - lesions on the face, chest, neck, limbs with polycyclic contours, with telangiectasia, sometimes psoriasis-like •• Alopecia (generalized or focal) •• Panniculitis •• Urticaria •• Periungual microinfarcts caused by vasculitis • • Livedo reticularis (tree-like pattern on the skin of the lower extremities as part of APS).

• Damage to mucous membranes: cheilitis, erosion.

• Joint damage •• Arthralgia •• Symmetrical non-erosive arthritis without deformities, most often localized in the small joints of the hand, wrist and knee joints •• Arthropathy (Jaccoud's syndrome) with persistent deformities occurs due to the involvement of ligaments and tendons, and not due to erosive arthritis •• Aseptic necrosis.

• Muscle involvement •• Myalgias •• Proximal muscle weakness resembling polymyositis •• Steroid myopathy.

• Lung damage •• Pleurisy - pleural friction noise, effusion and significant limitation of diaphragm mobility •• Pneumonitis - shortness of breath, pain during breathing, on auscultation - moist rales in the lower parts of the lungs, on the radiograph - high standing diaphragm, disc-shaped atelectasis •• Pulmonary hypertension with recurrent pulmonary embolism.

• Heart damage •• Pericarditis, usually adhesive •• Liebman-Sachs endocarditis may be accompanied by embolism and infection (develops as part of APS) •• Myocarditis with conduction disturbances, arrhythmias and sometimes heart failure •• In acute SLE, coronary vasculitis is possible vessels, however, the main cause of MI in patients with SLE is atherosclerosis due to long-term GC therapy for nephrotic syndrome or APS.

• Kidney damage (morphological types and clinical manifestations, see Lupus nephritis).

• Damage to the gastrointestinal tract •• Esophageal motility disorders •• NSAID-associated gastropathy •• Budd-Chiari syndrome within APS •• Thrombosis of mesenteric vessels (with APS).

• Damage to the central nervous system •• Headache resembling migraine, not relieved by analgesics (more often with APS) •• Epileptiform seizures •• Ischemic strokes (rare) •• Neuropathy of the cranial nerves, more often the optic nerve •• Guillain-Barre syndrome (rarely) ) •• Multiple mononeuritis (rare) •• Chorea (in APS) •• Transverse myelitis •• Acute psychosis (may be a manifestation of SLE or, less commonly, a side effect of steroids) •• Organic brain syndrome (impaired mental functions) •• Mood disorders (euphoria, less often depression).

• Sjögren's syndrome • Raynaud's syndrome • APS • Lymphadenopathy, splenomegaly.

Clinical and immunological forms of SLE

• SLE in elderly patients: skin, joint syndromes and kidney damage occur less frequently; Sjögren's syndrome, lung damage, and peripheral neuropathies often develop. Abs to RNA polymerase are often detected • Neonatal SLE in children born to mothers with SLE: erythematous rash, complete AV block, hemolytic anemia; serological marker - AT to RNA polymerase • Subacute cutaneous lupus erythematosus is characterized by severe dermatitis caused by photosensitivity. Occurs more often in men. Polyarthritis and serositis are characteristic; detect antibodies to RNA polymerase (Ro-Ag) and the protein that is part of RNA (La-Ag) • Seronegative SLE (absent ANAT) is clinically close to subacute cutaneous, kidney damage rarely occurs.

Laboratory data

• CBC •• Hemolytic anemia, reticulocytosis, positive Coombs test. Hypochromic anemia as a result of chronic inflammation or a side effect of a drug •• Leukopenia (as a result of the activity of SLE or a side effect of a drug) •• An increase in the content of CRP is not typical •• ESR correlates with the activity of the process.

• ANAT is detected in 95% of SLE cases. To detect autoantibodies to nuclear and cytoplasmic Ags, enzyme immunoassay, radioimmunological methods, and immunoblotting are used •• Antibodies to double-stranded DNA are specific for SLE •• Antibodies to histones are more typical for drug-induced lupus •• Abs to small nuclear ribonucleoproteins (ABs to Sm, ABs to Ro/ Ss-A, antibodies to La/SS-B) are often found in chronic SLE.

• The discovery of LE cells (leukocytes that have phagocytosed nuclear material) in the blood is of historical significance from a modern perspective.

• In APS associated with SLE, antibodies to phospholipids and a false-positive von Wassermann reaction are detected (see Antiphospholipid syndrome).

Instrumental data. Special research methods are carried out - kidney biopsy, x-ray examination of the chest organs, CT and MRI of the brain, echocardiography to identify valve pathology in endocarditis. Examination of synovial fluid: leukocytes no more than 2.0´109/l, neutrophils less than 50%.

American Rheumatology Association Diagnostic Criteria

The diagnosis of SLE is considered reliable if 4 or more criteria are present (sensitivity - 96%, specificity - 96%).

• Malar rash: fixed erythema (flat or raised) on the malar prominences, tending to extend to the nasolabial area.

• Discoid rash: erythematous, raised plaques with adherent skin scales and follicular plugs; Old lesions may have atrophic scars.

• Photodermatitis: a skin rash that occurs as a result of an unusual reaction to sunlight (history or medical observation).

• Oral ulcers: ulcerations of the mouth or nasopharynx, usually painless (registered by physician).

• Arthritis: non-erosive arthritis affecting 2 or more peripheral joints, characterized by tenderness, swelling and effusion.

• Serositis: •• Pleurisy: history of pleural pain or pleural friction rub or the presence of pleural effusion •• Pericarditis, confirmed by echocardiography or physically when the doctor listens to a pericardial friction rub.

• Kidney damage: persistent proteinuria >0.5 g/day or cellular casts in the urine (erythrocyte, hyaline, granular).

• CNS involvement •• Seizures: in the absence of medications or metabolic disorders (uremia, ketoacidosis, electrolyte imbalance) •• Psychosis: in the absence of medications or electrolyte disorders.

• Hematological disorders: leukopenia <4.0´109/l (registered 2 or more times) or lymphopenia <1.5´109/l (registered 2 or more times) or thrombocytopenia <100´109/l (not related to taking drugs)

• Immunological disorders: •• Anti-DNA: antibodies to native DNA in increased titer, or •• Anti-Sm: presence of antibodies to nuclear Sm-Ag, or •• Detection of antiphospholipid antibodies, lupus anticoagulant, false-positive von Wasserman reaction for as long as minimum 6 months with confirmed absence of syphilis using the Treponema pallidum immobilization test and the fluorescent adsorption test of treponemal antibodies

• ANAT: increase in the titer of ANAT detected by indirect immunofluorescence or a similar method during any period of the disease in the absence of taking medications that cause lupus-like syndrome

TREATMENT

General tactics • The basis of treatment is GCs (from high doses in the active phase they move very slowly to maintenance doses, continuing treatment even during remission) • For active lupus nephritis, generalized vasculitis, high general disease activity, resistance to GCs, cytostatic immunosuppressants are prescribed.

Regimen and diet • Insolation is contraindicated for patients • The diet must be low in fat, high in polyunsaturated fatty acids, calcium and vitamin D • Contraception is important, but oral contraceptives with a high estrogen content are contraindicated.

Drug treatment

• GK •• Prednisolone 1 mg/kg/day orally until the onset of clinical effect (4–6 weeks), then slowly (no more than 5% of the initial dose per week) reducing the dose to a maintenance dose (5–7.5 mg/day) . For glomerulonephritis, acute cerebral disorders, hemolytic crisis, the dose is increased to 80–100 mg/day •• Pulse therapy with methylprednisolone is carried out for the following indications: rapidly progressive glomerulonephritis, young age, high immunological activity. NB: Pulse therapy is not a “therapy of despair”, but an integral part of an intensive care program. In addition to “classical” pulse therapy (methylprednisolone 15–20 mg/kg body weight IV daily for 3 consecutive days), pulse therapy is re-prescribed at intervals of several weeks. Pulse therapy can be enhanced with cyclophosphamide 1 g IV on the 2nd day of treatment. In prognostically unfavorable and treatment-resistant cases, synchronous intensive therapy programs are developed, where pulse therapy with methylprednisolone and cyclophosphamide is preceded by a plasmapheresis procedure. After pulse therapy, the dose of prednisolone should be reduced slowly.

• Immunosuppressants •• Cyclophosphamide: with the development of proliferative and membranous lupus nephritis and severe damage to the central nervous system, 0.5–1 g/m2 IV monthly for 6–12 months, then every 3 months for 2 years •• Azathioprine: in as part of the maintenance therapy of lupus nephritis, with resistance of hemolytic anemia and thrombocytopenia to treatment with GCs (1–4 mg/kg/day orally) •• Methotrexate: enhances the effect of GCs in relation to arthritis, myositis, neuropsychiatric manifestations (15 mg per week) •• Mycophenolate mofetil (1.5–2 g/day): a positive effect is noted in lupus glomerulonephritis refractory to treatment. Side effects characteristic of cytostatics develop less frequently •• Cyclosporine: effective for thrombocytopenia, anemia, leukopenia, skin manifestations of SLE, treatment-refractory arthritis and polyserositis, APS (2.5–4 mg/kg/day).

• Aminoquinoline derivatives •• Prescribed for skin and joint manifestations of SLE. Hydroxychloroquine from 400 mg/day for 3–4 months, then 200 mg/day.

• NSAIDs •• The need for NSAIDs in SLE does not occur as often as in other arthritis. Be aware of the atypical side effects of NSAIDs in SLE (eg, aseptic meningitis with ibuprofen or sulindac).

• Monoclonal antibodies •• “Biological agents”: monoclonal antibodies to IL-10 in preliminary studies showed a positive effect on skin lesions, kidneys, arthritis, serositis, refractory to GC therapy.

• Immunoglobulin •• For treatment-resistant SLE, severe thrombocytopenia - immunoglobulin 0.4 g/kg/day IV for 5 days. Not indicated for lupus nephritis.

Non-drug therapy. If kidney function is impaired, hemodialysis is performed.

Surgery. Autologous stem cell transplantation has been proposed for the treatment of refractory and severe SLE.

Features in pregnant women • Frequent spontaneous miscarriages indicate the presence of APS (observed in 30–50% of patients with SLE) • Exacerbations of SLE often occur in the first trimester of pregnancy and in the first 6 weeks after birth; the latter is explained by hyperprolactinemia, therefore lactation in patients with SLE is not desirable • The optimal conditions for the course of pregnancy are considered to be the absence of functional failure of organs and systems and pathology of the central nervous system in the anamnesis, achieving remission while maintaining a maintenance dose of GC • Cyclosporine A has the least teratogenic effect among cytostatics • If proteinuria occurs in the first trimester of pregnancy it is necessary to terminate it • The method of choice for delivery is caesarean section.

Features in children • Neonatal SLE develops rarely (less than 1% of children born to mothers with SLE).

Features in old age. If SLE develops after the age of 50 years, it is necessary to exclude paraneoplastic syndromes.

Forecast. In the first years of the disease, mortality is caused by the activity of glomerulonephritis and intercurrent infections; subsequently, atherosclerosis plays an important role. The prognosis for life expectancy is significantly reduced in the presence of APS.

ICD-10 • M32 Systemic lupus erythematosus

Application. Misher cheilitis (granulomatous cheilitis) is a disease of unknown etiology, characterized by persistent inflammatory thickening of the lips with the formation in the thickness of their skin of small, sharply demarcated granulomas, consisting of epithelioid cells, lymphocytes and a small number of giant cells. ICD-10. K13.4 Granuloma and granuloma-like lesions of the oral mucosa

Prevention and surveillance

The main preventive measure is the exclusion of animals with hereditary forms of the disease from the breeding program to prevent the spread of genetic disorders to offspring.

Animals predisposed to the disease should not be allowed outside at times when ultraviolet radiation is especially active. Sunlight is a strong predisposing factor for the disease. The dog's diet should be rich in protein, minerals and vitamins.

Sick animals require constant monitoring, since the treatment method involves long-term suppression of the immune system. During the period of active treatment, the animal is brought for a veterinary examination every 7 days. The frequency of further visits is determined by the attending physician.

How to care for a sick dog

In addition to medications, your doctor may recommend additional treatments. Among them:

1. Switch to a diet of natural foods that have not been processed with chemicals or preservatives.
2. Additional anti-inflammatory foods such as turmeric. It has anti-inflammatory properties, but is also rich in Omega-3 acids, vitamin E, selenium and vitamin C.
3. Probiotics will also be helpful.
4. It is recommended not to expose the dog to stress and to avoid any situations that make the animal nervous.

Do not forget that ultraviolet light, which contributes to the development of discoid lupus, will always be contraindicated for your animal. And you need to control the time he spends in the sun. Walking is recommended early in the morning or late in the evening. For animals kept in an enclosure, it must be completely shaded.

Did you know? No two cases of lupus present exactly the same way. This is a feature of autoimmune diseases.

The prognosis for the discoid form is usually good. Most dogs can control lupus with appropriate follow-up care and ongoing therapy. Signs can wax and wane, so you should always be prepared to deal with the next flare-up throughout your pet’s life.

The prognosis for recovery for animals with a systemic form of the disease is very cautious. It is difficult to treat, can progress and behave unpredictably. Therefore, long-term treatment is prescribed to animals with this form of lupus. But with prolonged suppression of the immune system, serious side effects can develop. This makes the prognosis for recovery very doubtful.