【正文】 s manifestations and disease severity. ? Diet: No dietbased treatment of SLE has been proven effective. ? Activity: Patients should be reminded that activity may need to be modified as tolerated. ? stress such as physical illness may precipitate SLE flares. ? persons with SLE should wear sunscreen and protective clothing or avoid sun exposure to limit photosensitive rash or disease flares. ? Fever, skin, musculoskeletal, and serositis represent milder disease manifestations. These are often controlled with lowpotency medications, such as hydroxychloroquine and NSAIDS. Lowtomoderate–dose steroids and methotrexate are necessary for acute flares. Medication ? CNS involvement and renal disease must be recognized as more severe disease manifestations require highdose steroids and other immunosuppression agents such as cyclophosphamide, azathioprine, or mycophenolate. Traditionally, class IV diffuse proliferative lupus nephritis has been treated with aggressive cyclophosphamide induction therapy. Newer lupus nephritis literature has shown that mycophenolate is a safe maintenance agent and is potentially an induction agent. ? Acute emergencies in SLE include severe neurologic involvement, systemic vasculitis, profound thrombocytopenia with a TTPlike syndrome, rapidly progressive glomerulonephritis, or diffuse alveolar hemorrhage. ? Rare serious manifestations such as TTP, diffuse alveolar hemorrhage, or profound steroidrefractory thrombocytopenia may require large dosage of intravenous Methylprednisolone, plasma exchange or intravenous immunoglobulin (IVIG) ? New investigations are in progress to look at the role of rituximab and other Bcell–targeted therapies in SLE. ? Preventative care measures are necessary to minimize the risks of steroidinduced osteoporosis and accelerated atherosclerotic disease. – The ACR Guidelines for the prevention of glucocorticoidinduced osteoporosis suggest traditional steps and the consideration of prophylactic bisphosphonate therapy. – Recently, numerous authors have also advocated drafting cardiovascular prevention guidelines that equate SLE as a CAD riskequivalent similar to diabetes mellitus. Drug Category ? Nonsteroidal antiinflammatory drugs (NSAIDs) These agents provide symptomatic relief for arthralgias, fever, and mild serositis. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis NSAIDs may cause elevated liver function test results in patients with active SLE. Additionally, conitant administration with prednisone may increase risk of GI ulceration. Ibuprofen (Advil, Motrin, Ibuprin) for patients with mildtomoderate pain. ? Antimalarials The mechanism of action of antimalarials in SLE is unknown, but they do not cause generalized immunosuppression. They are useful to prevent and treat lupus skin rashes, constitutional symptoms, arthralgias, and arthritis. They also help to prevent lupus flares and have been associated with reduced morbidity and mortality in SLE. Hydroxychloroquine (Plaquenil) Inhibits chemotaxis of eosinophils and lootion of neutrophils and impairs plementdependent antigenantibody reactions. Hydroxychloroquine sulfate 200 mg is equivalent to 155 mg hydroxychloroquine base and 250 mg chloroquine phosphate. 200 mg PO qd/bid。 perinuclear antineutrophil cytoplasmic antibody [pANCA]–positive in minocyclineinduced DIL) Other laboratory tests include the following – Inflammatory markers: Erythrocyte sedimentation rate (ESR) or Creactive protein (CRP) levels may be elevated in any inflammatory condition, including SLE。 level variable based on disease activity – AntiSm Most specific antibody for SLE。 this and hypoplementemia may predispose persons with SLE ? Thrombocytopenia may be mild or part of a thrombotic thrombocytopenic purpura (TTP)–like syndrome. ? Anemia is occasionally overlooked in young menstruating women. Other ? History of recurrent early miscarriages or a single late pregnancy loss may be clues to lupus, or isolated antiphospholipid antibody syndrome. ? Family history of autoimmune disease should also raise further suspicion of SLE. Lab Studies The following are autoantibody tests used in SLE diagnosis: ANA Screening test。 sensitivity 95%。 only 3040% sensitivity – AntiSSA (Ro) or AntiSSB (La) Present in 15% of patients with SLE and other connective tissue diseases such as Sj246。 CRP levels change more acutely, and ESR lags behind disease changes. – Complement levels: C3 and C4 levels are often depressed in patients with active SLE because of consumption by immune plex–induced inflammation. In addition, some patients have congenital plement deficiency that predisposes them to SLE. – Complete blood count: Including differential diagnoses, CBC count may help to screen for leucopenia, lymphopenia, anemia, and thrombocytopenia. – Urinalysis/urine protein: Screening tests are used to evaluate for proteinuria ( g/d), hematuria, casts, or pyuria. – Creatinine: Creatinine evaluation is useful to monitor kidney disease activity. – Liver function tests: These may be mildly elevated in acute SLE or in response to therapies such as azathioprine or nonsteroidal antiinflammatory drugs (NSAIDS). – Creatinine kinase: Creatinine kinase levels may be elevated in myositis or overlap syndromes. Imaging Studies ? Joint radi