전신 홍반 루푸스의 검사실 소견과 신장 병리 (Laboratory findings and renal pathology in systemic lupus erythematosus)

서지정보

· 발행기관 : 대한내과학회
· 수록지 정보 : 대한내과학회지 / 78권 / 4호 / 416 ~ 424페이지
· 저자명 : 이상원

초록

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease of unknown cause. SLE can involve various major organs including heart, lung, kidney, nervous system and bone marrow. Abnormality in immune system producing various autoantibodies is one of the marked features of this disease. Although most diagnostic items primarily depends on clinical symptoms, four of them are the results of laboratory tests; hematologic abnormalities, antinuclear antibody (ANA), immunologic abnormalities and urinalysis. Most patients with SLE have anemia during the disease course. Anemia with chronic disease is the most common in SLE, followed by immune mediated hemolytic anemia and iron deficiency anemia. Fifteen percent of SLE patients have leukopenia and 20% of them have lymphopenia. Leukopenia in SLE is mostly associated with immune mechanism, drugs, bone marrow dysfunction and hyperspenism. Thrombocytopenia in SLE is induced by immune-mediated destruction of platelet, aggregation of platelet in hemolytic anemia, decreased production of platelet by immunosuppressant and concurrent antiphospholipid syndrome. ANA is the most typical blood test in SLE and can be useful screening test. ANA can be also detected in healthy people and patients with other rheumatic and non-rheumatic diseases. Anti-ds DNA Ab and anti-Sm Ab are specific autoantibodies for SLE and are associated clinical manifestations. Anti-ds DNA Ab is well correlated with disease activity of SLE. Lupus nephritis can be classified into six patterns by light microscopy, immunofluorescence and electron microscopy. Class III and IV represent focal and diffuse glomerulonephritis and relatively poor prognosis. Thus patients having these classes of glomerulonephritis need intensive immunosuppressive treatment. The risk of development of lupus nephritis increases in male and younger patients. In SLE patients with end stage renal disease, SLE activity is usually low.

영어초록

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease of unknown cause. SLE can involve various major organs including heart, lung, kidney, nervous system and bone marrow. Abnormality in immune system producing various autoantibodies is one of the marked features of this disease. Although most diagnostic items primarily depends on clinical symptoms, four of them are the results of laboratory tests; hematologic abnormalities, antinuclear antibody (ANA), immunologic abnormalities and urinalysis. Most patients with SLE have anemia during the disease course. Anemia with chronic disease is the most common in SLE, followed by immune mediated hemolytic anemia and iron deficiency anemia. Fifteen percent of SLE patients have leukopenia and 20% of them have lymphopenia. Leukopenia in SLE is mostly associated with immune mechanism, drugs, bone marrow dysfunction and hyperspenism. Thrombocytopenia in SLE is induced by immune-mediated destruction of platelet, aggregation of platelet in hemolytic anemia, decreased production of platelet by immunosuppressant and concurrent antiphospholipid syndrome. ANA is the most typical blood test in SLE and can be useful screening test. ANA can be also detected in healthy people and patients with other rheumatic and non-rheumatic diseases. Anti-ds DNA Ab and anti-Sm Ab are specific autoantibodies for SLE and are associated clinical manifestations. Anti-ds DNA Ab is well correlated with disease activity of SLE. Lupus nephritis can be classified into six patterns by light microscopy, immunofluorescence and electron microscopy. Class III and IV represent focal and diffuse glomerulonephritis and relatively poor prognosis. Thus patients having these classes of glomerulonephritis need intensive immunosuppressive treatment. The risk of development of lupus nephritis increases in male and younger patients. In SLE patients with end stage renal disease, SLE activity is usually low.

참고자료

· 없음