Acute or insidious in its onset, it is chronic, remitting and relapsing, often febrile illness, characterized principally by injury to skin, joints, kidney and serosal membrane

Acute or insidious in its onset, it is chronic, remitting and relapsing, often febrile illness, characterized principally by injury to skin, joints, kidney and serosal membrane

remitting and relapsing. kidney and serosal membrane . often febrile illness. characterized principally by injury to skin.Definition Acute or insidious in its onset. joints. it is chronic.

characterized principally by injury to skin. kidney and serosal membrane .Definition Acute or insidious in its onset. it is chronic. joints. often febrile illness. remitting and relapsing.

joints. remitting and relapsing. it is chronic. often febrile illness. kidney and serosal membrane . characterized principally by injury to skin.Definition Acute or insidious in its onset.

sparing nasolabial folds 2. Malar rash: Fixed erythema over malar areas.5g/24hour or 3+ or B) cellular casts 8. Haematological disorder: A) haemolytic anaemia or B) leucopenia or C) thrombocytopenia 10. Photosensitivity: Skin rash after exposure to sunlight. e. Arthritis:Tenderness. Oral ulcers: Oral or nasopharyngeal. 11. history or physical exam 4.Criteria of the ARA for the classification of SLE 1.g. Neurological disorder: A) seizures or B) psychiatric disorder (having excluded other causes. swelling. drigs) 9. Immunologic disorder: A) positive LE cells or B) raised anti-native DNA antibdy binding or C) anti-Sm antibody or D) false positive serological test for syphilis. by physical exam 5. Discoid rash: Erythematous raised patches with keratotic scaling and follicular plugging 3. Positive antinuclear antibody: . Renal disorder A) proteinuria>0. Serositis: A) pleuritis or B) pericarditis 7. painless. effusion in 2 or more peripheral joints 6.

It may be a flat or a raised rash. . It is present over the cheeks below the eyes and across the bridge of the nose. Malar rash This is a "butterfly-shaped" red rash.1. The rashes are made worse by sun exposure.

. Atrophic scarring may occur in older lesions.2. raised patches with scaling of the overlying skin. Discoid lupus These are red.

Photosensitivity 4. Oral Ulcers Painless sores in the nose or mouth. .3.

5. swelling and effusion. Characterized by tenderness. Arthritis • • • Nonerrosive arthritis. . Involve two or more pripheral joints.

5 gm/dl or > 3.6. if quantitation not • Cellular casts performed . Renal disorders It includes • Persistent proteinuria > 0.

7. Serositis It can be in two forms. • • Pleuritis Pericarditis .

• Pleuritis History of pleuritic pain or rub heard by a physician or evidence of pleural effusion. .

• Pericarditis Documented by ECG or rub or evidence of pericardial effusion. .

9.5*109/L) Thrombocytopenia (<100*109/L) .8. Neurological disorders It include seizures and psychosis in the absence of offending drug and known metabolic derangements. Hematologic disorders • • • • It includes Hemolytic anemia Leukocytopenia (<4.0*109/L) Lymphopenia (<1.

Immunological disorders It includes the presence of • Anti DNA antibody • Anti Sm antibody • Anti phospholipid antibody 11.Antinuclear antibody .10.

anti-platelet antibodies . antierythrocyte antibodies. anti-dsDNA. anti-RNP. anti-neurone antibodies. anti-SSB • Cells surface antigens lymphocytotoxic antibodies. anti-Sm. antibodies to extracellular nuclear antigen (ENA. anti-Jo1) • Cytoplasmic components anti-SSA.Autoantibodies in SLE Targets of autoantibodies are • Nuclear components ANA.

1.Anti-nuclear antibodies They are directed against nuclear antigens and are divided into four categories. Against non histone proteins bound to RNA 4. Against histone 3. Against DNA 2. Against nucleolar antigens .

• Four type of patterns are detected. .Detection of Antinuclear Antibodies • It is done by indirect immunoflourescence technique.

histones. and occasionally DNA. .1. Homogenous pattern This reflects antibodies to chromatin.

. Rim (peripheral ) pattern This indicates antibodies to DNA.2.

. SS-A and SS-B reactive antigens.3. • Examples: Sm antigen. Speckled pattern • This is most commonly observed and least specific pattern. It shows presence of antibodies to non-DNA nuclear constituents.

Nucleolar pattern It represents antibodies to RNA. .4.

annexin V. fetal loss and thrombocytopenia. B2-glycoprotein I.  Antiphospholipid antibody: • are present in 40-50% of lupus patients. • Some of these antibodies are termed as lupus anticoagulant. • These proteins include prothrombin. protein S and protein C. • are directed aginst epitopes of plasma proteins. .Secondary Antiphospholipid syndrome  It is characterized by recurrent arterial and /or venous thrombosis. High titer of Antiphospholipid antibody can be found in APS patients.

2.Etiology of SLE • 1. Three factors are involved in SLE. Genetic Factors Immunological factors Encironmental factors . 3.

• Family members have an increased risk of developing SLE. and up to 20% of clinically unaffected first-degree relatives may reveal autoantibodies. . particularly at the HLA-DQ locus. • there is a positive association between SLE and class II HLA genes.Genetic factors • There is a high rate of concordance in monozygotic twins (25%) versus dizygotic twins (1% to 3%). • Some lupus patients (about 6%) have inherited deficiencies of complement components.

Escape tolerance of CD4+ helper T cells. Increased production of Autonuclear antibodies by B cells.Immunological factors • • • • Defective elimination of self reactive B cells. . Exposure to type 1 interferons.

• Sex hormones also seem to exert an important influence on the occurrence of SLE. leading to an increased burden of nuclear fragments.g.. • An example of nongenetic (e. • UV radiation causes apoptosis of host cells. including procainamide and hydralazine. .Environmental factors • Ultraviolet (UV) radiation (sun exposure) exacerbates the lesions of SLE. environmental) variables in initiating SLE is the occurrence of a lupus-like syndrome in patients receiving certain drugs. with clinical features of SLE appearing in 15% to 20% of them. • Most patients treated with procainamide for more than 6 months develop ANAs.

Sign up to vote on this title
UsefulNot useful