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类风湿关节炎肝脏受累的频率及发病机制研究。

Studies on the frequency and pathogenesis of liver involvement in rheumatoid arthritis.

作者信息

Fernandes L, Sullivan S, McFarlane I G, Wojcicka B M, Warnes T W, Eddleston A L, Hamilton E B, Williams R

出版信息

Ann Rheum Dis. 1979 Dec;38(6):501-6. doi: 10.1136/ard.38.6.501.

Abstract

A systematic prospective survey of 100 outpatients with rheumatoid arthritis revealed that 45 had biochemical evidence of liver disease. In most cases this was due to increases in total serum alkaline phosphatase (ALP) and/or gammaglutamyl transpeptidase (GGT). Examination of serum ALP isoenzyme profiles in 50 of the patients showed that the liver isoenzyme was the sole or major component in 44 patients, including many with normal total ALP levels. 18% had raised serum liver ALP together with raised GGT, suggestive of an underlying hepatobiliary lesion. No correlation could be detected between raised serum levels of liver enzymes and the age or sex of the patient, duration or severity of arthritis, and drug or alcohol history. However, there was a significant correlation between raised serum ALP and lacrimal or salivary gland dysfunction. It is suggested that immunological mechanisms may be involved in the development of hepatic abnormalities in rheumatoid arthritis.

摘要

对100例类风湿性关节炎门诊患者进行的一项系统性前瞻性调查显示,45例有肝病的生化证据。在大多数情况下,这是由于血清总碱性磷酸酶(ALP)和/或γ-谷氨酰转肽酶(GGT)升高所致。对其中50例患者的血清ALP同工酶谱进行检查发现,在44例患者中肝脏同工酶是唯一或主要成分,其中包括许多总ALP水平正常的患者。18%的患者血清肝脏ALP升高同时GGT也升高,提示存在潜在的肝胆病变。未发现血清肝酶升高与患者的年龄、性别、关节炎病程或严重程度以及药物或饮酒史之间存在相关性。然而,血清ALP升高与泪腺或唾液腺功能障碍之间存在显著相关性。提示免疫机制可能参与类风湿性关节炎肝脏异常的发生。

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本文引用的文献

1
The liver in rheumatoid arthritis.类风湿关节炎中的肝脏
Ann Rheum Dis. 1955 Jun;14(2):162-9. doi: 10.1136/ard.14.2.162.
5
Serum biochemical values in rheumatoid disease.类风湿病中的血清生化值。
Ann Rheum Dis. 1971 Mar;30(2):166-70. doi: 10.1136/ard.30.2.166.
6
"Sicca complex" in liver disease.肝脏疾病中的“干燥综合征”。
Br Med J. 1970 Nov 7;4(5731):340-2. doi: 10.1136/bmj.4.5731.340.
8
Cellular hypersensitivity in Sjögren's syndrome.
Acta Med Scand. 1968 Oct;184(4):319-22. doi: 10.1111/j.0954-6820.1968.tb02465.x.

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