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AFGHANS ARE US -HEALTH
SYSTEMIC
LUPUS ERYTHEMATOSUS
J.K. Dunn
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INTRODUCTION
Systemic lupus erythematosus (SLE) is a multisystemetic immune-mediated
disorder characterised by the presence of circulating antinuclear
antibodies (ANA). The disease has been reported in the dog and less
frequently in the cat.
In the Dog, German Shepherds, Poodles, Shetland Sheepdogs, Collies and
Beagles appear to be over represented (Scott et al 1983). The age of
onset is extremely variable ranging from less than a year to greater
than ten years. Unlike humans, where there is a definite female
predisposition for the disease, male dogs appear to be as susceptible as
females (Grimden & Johnson 1983)
PATHOGENIS
Systemic lupus erythematosus is an immune complex disorder of unknown
aetiology. Antinuclear antibodies are produced that bind to components
of the nucleus. The interaction of these antinuclear antibodies with
their respective antigens results in a type III hypersensitivity
response. Since the nuclear antigens involved are not restricted to a
specific cell type SLE is a multisystemic disease. Deposition of immune
complexes may occur in glomercular capillaries and basement membrane, in
synovial membranes and in skin at the level of the dermal epiduramal
junction. Immune complex deposition results in activation of the
complement cascade and release of potent inflammatory mediators.
Neutrils are attracted to sites of immune complex deposition resulting
in vasculitis and tissue damage. Antibodies may also be directed against
cell surface antigens on red blood cells, platelets and leucoytes and
occasionally antibodies are produced against clotting factors; a
lupus-type anticoagulant which inhibited the activation of thrombin was
recently reported i8n one dog with haemolytic anaemia, thrombocytopenia,
membrous glomerulonephritus, polyarthritis and pulmonary thromboembolism
(Stone et al 1994). Although the clinical signs were highly suggestive
of SLE this dog was ANA negative.
It has been shown that the serological abnormalities associated with
spontaneous SLE can be transmitted to normal dogs and mice by cell free
extracts suggesting the presence of an infectious agent. Indeed there is
limited evidence to support a role for C-type virus in the development
of SLE in humans and dogs.
However it is unlikely that the presence of virus alone is sufficient
to provoke clinical disease and that development of the disease requires
interaction of the virus with an aberrant immune response in a
genetically susceptible host . Dogs with SLE have decreased levels of
serum thymic factor, decreased numbers of circulating lymphoctes and
also lower total haemolytic complement levels.
Certain drugs, for example hydralazine and potentiated sulphyonamides (trimethoprim-sulphadiazine)
may induce a lupus like syndrome in dogs.
CLINICAL SIGNS
The clinical signs of SLE can be conveniently divided into major and
minor signs, the major signs representing body systems which are most
frequently involved and are therefore more suggestive of SLE (se below).
In addition affected dogs often show non-specific signs such as fever,
lethargy, anorexia and weight loss.
MAJOR SIGNS
Shifting lameness (polyarthritis)
Proteinuria (glomerulonephropathy)
Dermatopathy
Haematological abnormalities (anaemia, thrombocytopenia, leucopenia)
MINOR SIGNS
Polymyositis
Pericarditis/myocarditis
Pleuritis
Generalised lymphadenopathy
Oral ulceration
CNS signs (behaviour changes, seizures, ataxia)
Gastrointestinal signs (vomiting, diarrhoea)
The clinical signs of SLE vary considerably and reflect the systems
involved. They may mimic other diseases and have a tendency to wax and
wane. Fever is common during the acute phase of the disease. Non-septic,
non erosive polyarthritis appears to be the most common manifestation of
SLE and is characterised by shifting lameness, joint pain and
periarticular soft tissue swelling. Approximately 50% of dogs have
significant proteinura indictive of of glomular damage. The skin lesions
associated with SLE are extremely variable. The lesions are often
erythematous and /or seborrhoeic and most commonly involve the face,
ears and limba. Mucocutaneous ulceration may be evident and the very
occasional dog may present with lupus panniculitis, a condition
characterised by multiple cutaneous modules which subsequently ulcerate
and develop fistulae.
Although previous reports have suggested that immune-mediated (coombs
positive) haemolytic anaemia is commonly associated with SLE, two of the
more recent retrospective surveys have suggested that non-regenerative
anaemia may be more common occurrence.
DIAGNOSIS
Since the clinical manifestations of SLE are extremely variable opinions
vary as to which sets of clinical signs can be used as a reliable
diagnosis criteria. Several schemes have been proposed. Since neither
the major or minor clinical signs described above are truly specific for
SLE, a combination of these signs together with supportive serological
evidence is helpful in establishing a diagnosis. The following scheme
proposed by Gorman and Weirner offers a degree of flexibility and
acknowledges the fact that not every case of SLE has a positive ANA test
and that diagnosis of SLE probably includes numerous overlap syndromes
which have some of the clinical signs and/or autoantibodies which are
suggestive of the disease.
DEFINITE SLE
* positive ANA test plus two major signs
* positive ANA test plus one major and two minor signs
PROBABLE SLE
possible ANA test and one major sign
negative ANA test and two major signs
THERAPY
In one study just over 40% of SLE cases were successfully managed with
prednisolone alone and long term remission was achieved on alternate day
glucocorticoid therapy. Cases of SLE that presents with immune mediated
haemolytic anaemia, immune mediated thrombocytopenia or
glomerulonephritis are more likely to be refractory to prednisolone
alone. Combination therapy using prednisolone and azathioprine has
proved to be effective in refracatory cases or in cases in which the
maintenance dose of prednisolone produces unacceptable side effects.
Induction doses of prednisolone of 2-4 mg/kg body weight should be used
reducing to an every other day maintenance dose of 5-1mg/kg body weight.
Azathioprine can be given at a dose of 1-2mg/kg body weight daily
reducing to 1mg/kg body weight every other day (prednisolone can be
given on alternate days to the azathioprine). An attempt to stop therapy
may be made in dogs that remain disease free for 6 months. The most
common causes of dogs with SLE are renal failure and infections such as
bronchopnecumonia and scepticemia. |
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