Sève Pascal, Ferry Tristan, Koenig Martial, Cathebras Pascal, Rousset Hugues, Broussolle Christiane
Department of Internal Medicine, Hôtel-Dieu, Hospices Civils de Lyon, Université Claude Bernard Lyon I, France.
Semin Arthritis Rheum. 2005 Feb;34(4):642-8. doi: 10.1016/j.semarthrit.2004.07.008.
To describe 2 cases of parvovirus B19 (B19) infection mimicking systemic lupus erythematosus (SLE) and to identify all cases of SLE imitated by and/or associated with B19 in the medical literature.
A computer-assisted (PubMed) search of the medical literature from 1975 to 2003 was performed using the following key words: parvovirus, B19, SLE, lupus, antibodies, auto-immunity.
Thirty-eight patients were identified: 35 women, 3 men; mean age = 28.8 years. Clinical manifestations were as follows: fever (24 patients); articular involvement (36 patients); cutaneous lesions (28 patients); lymphadenopathy (9 patients); hepato- and/or splenomegaly (6 patients); serositis (6 patients); renal involvement (4 patients); cerebral impairment (10 patients). Cytopenia was observed in 23 cases. Antinuclear antibodies were detected in 34 patients, anti-double-stranded DNA antibodies in 20 patients, anti-Sm antibodies in 4 patients, antinuclear ribonucleoprotein antibodies in 5 patients, anti-Ro-SSA antibodies in 4 patients, anti-La-SSB antibodies in 4 patients, and anticardiolipin and/or anti-beta2-glycoprotein I antibodies in 8 patients. Hypocomplementemia was found in 15 of 26 patients. In 19 cases, the B19 infection had a self-limiting course. In 6 cases, B19 infection occurred in a context of previously established SLE, simulating SLE exacerbation. In 6 observations, symptoms persisted several months after the viral infection. In 7 cases, the exact relationship between SLE and B19 could not be determined.
B19 infection may present a clinical and serological tableau making it difficult to distinguish between a viral infection and the first episode of SLE. Although B19 may modulate the clinical and biological features of rheumatic disease, studies in large series do not support a causative role for B19 in the pathogenesis of SLE.
描述2例酷似系统性红斑狼疮(SLE)的细小病毒B19(B19)感染病例,并在医学文献中识别所有由B19模仿和/或与之相关的SLE病例。
使用以下关键词对1975年至2003年的医学文献进行计算机辅助(PubMed)检索:细小病毒、B19、SLE、狼疮、抗体、自身免疫。
共识别出38例患者:35名女性,3名男性;平均年龄=28.8岁。临床表现如下:发热(24例);关节受累(36例);皮肤病变(28例);淋巴结病(9例);肝和/或脾肿大(6例);浆膜炎(6例);肾脏受累(4例);脑功能障碍(10例)。23例观察到血细胞减少。34例患者检测到抗核抗体,20例患者检测到抗双链DNA抗体,4例患者检测到抗Sm抗体,5例患者检测到抗核核糖核蛋白抗体,4例患者检测到抗Ro-SSA抗体,4例患者检测到抗La-SSB抗体,8例患者检测到抗心磷脂和/或抗β2糖蛋白I抗体。26例患者中有15例发现补体低下。19例中,B19感染呈自限性病程。6例中,B19感染发生在先前确诊的SLE背景下,模拟SLE病情加重。6例观察中,病毒感染后症状持续数月。7例中,SLE与B19的确切关系无法确定。
B19感染可能呈现出一种临床和血清学表现,使得难以区分病毒感染和SLE的首发发作。虽然B19可能调节风湿性疾病的临床和生物学特征,但大型系列研究不支持B19在SLE发病机制中起致病作用。