Longitudinal fluctuation of anti-lipoprotein lipase antibody is related with disease activity in systemic lupus erythematosus patients without anti-dsDNA antibodies
Longitudinal fluctuation of anti-lipoprotein lipase antibody is related with disease activity in systemic lupus erythematosus patients without anti-dsDNA antibodies
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DOI：
10.1590/s0482-50042009000100005
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发表时间：
2009-02-01
影响因子：
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通讯作者：
Bonfá, Eloísa
中科院分区：
文献类型：
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作者：
Carvalho, Jozélio Freire de;Viana, Vilma Santos Trindade;Bonfá, Eloísa
简介：系统性红斑狼疮 (SLE) 的特点是临床发作和缓解期，随后出现血清特异性自身抗体（例如抗 dsDNA）的改变，这种抗体出现在 40% 的病例中，并且与肾脏受累密切相关。最近，有关于 SLE 中抗脂蛋白脂肪酶抗体（抗 LPL）的两个亚群的描述：具有和不具有抗 dsDNA 活性。没有分析这些抗体与 SLE 炎症活性之间可能的关系。目的：纵向评估抗 dsDNA 抗体持续阴性的患者中抗 LPL 与狼疮活动性之间的关联。患者和方法：选择 5 名 SLE 患者，通过 ELISA 和使用 critithia luciliae 进行间接免疫荧光检测，抗 dsDNA 持续呈阴性，并且通过 ELISA 检测抗 LPL 滴度高（> 5 SD），并随访至少 2 年。结果：病例1：24岁男性，2001年患SLE，表现为肺泡出血、蛋白尿、全身性高血压、颧骨皮疹、口腔溃疡、多发性关节炎，ANA阳性，SLEDAI=16，抗-LPL=144U。他接受了静脉注射（IV）甲基泼尼松龙治疗，随后接受泼尼松治疗，并取得了良好的反应。 SLEDAI=0，抗LPL下降至109U。 2002年4月新的肾耀斑，SLEDAI=10，抗LPL（150U）新增量。开始静脉注射环磷酰胺和甲泼尼龙，病情缓解，SLEDAI=0，抗-LPL（77U）下降，直至2003年转阴。病例2：32岁女性，1997年患SLE。2001年9月开始出现皮肤血管炎、发热、皮疹，SLEDAI=10，抗-LPL=80U。 2002年1月，她出现肾脏受累和全身性高血压，SLEDAI=8，抗-LPL=25U。她接受了皮质类固醇和环磷酰胺治疗，情况有所改善。 2003年，她无症状，SLEDAI=2，抗LPL=12U。病例3：一名39岁男性，自1997年起患有SLE。在使用氯喹的情况下，他病情稳定，3年无疾病活动，所有研究期间SLEDAI = 0，抗LPL滴度无波动：85U（2001），100U（2002）e 86U（2003）。病例4：一名58岁女性自1996年以来患有SLE。她自2001年8月以来一直处于缓解状态，在整个研究期间SLEDAI = 0。抗-LPL 滴度没有显着变化：71U (2001)、42U (2002) e 61U (2003)。病例5：一名55岁女性，自1989年起患有SLE。自2000年使用氯喹以来，她的情况稳定，SLEDAI = 0，抗LPL滴度无变化：71U（1999），92U（2001），71U（2002）e 90U（2003）。结论：对入选患者的纵向评估显示，抗LPL滴度波动与SLEDAI评分呈正相关。这些发现表明，这种变异可能是没有抗 dsDNA 抗体的患者狼疮活动的新标志。
INTRODUCTION: Systemic lupus erythematosus (SLE) is characterized by periods of clinical flares and remission that are followed by alterations of sera specific autoantibodies such as anti-dsDNA, present in 40% of the cases and strongly associated with renal involvement. Recently, there was a description of two subpopulations of anti-lipoprotein lipase antibodies (anti-LPL) in SLE: with and without anti-dsDNA activity. A possible relationship between these antibodies with inflammatory activity of SLE was not analyzed. OBJECTIVES: To evaluate longitudinally the association between anti-LPL with lupus activity in patients persistently negatives for anti-dsDNA antibodies. PATIENTS AND METHODS: Five SLE patients with persistently negative anti-dsDNA measured by ELISA and indirect immunofluorescence using crithidia luciliae and high titers of anti-LPL by ELISA (> 5 SD) were selected and followed for at least 2 years. RESULTS: Case 1: A 24-year-old male with SLE since 2001, presented with alveolar hemorrhage, proteinuria, systemic hypertension, malar rash, oral ulcers, polyarthritis, positive ANA, SLEDAI=16 and anti-LPL=144U. He was treated with intravenous (IV) methylprednisolone followed by prednisone and had an excellent response. SLEDAI=0, anti-LPL decreased to 109U. New renal flare in April 2002, SLEDAI=10 and a new increment of anti-LPL (150U). IV Cyclophosphamide and methylprednisolone were started and he achieved remission, SLEDAI=0 and a decrease of anti-LPL (77U) until become negative in 2003. Case 2: A 32-year-old female had SLE since 1997. In September 2001 began cutaneous vasculitis, fever and rash, SLEDAI=10, anti-LPL=80U. In January 2002, she had renal involvement and systemic hypertension, SLEDAI=8 and anti-LPL= 25U. She received corticosteroid and cyclophosphamide and improved. In 2003, she was asymptomatic, SLEDAI=2 and anti-LPL=12U. Case 3: A 39-year-old male has SLE since 1997. He was stable, under chloroquine use, without disease activity for 3 years, SLEDAI=0 in all period studied and no fluctuation of anti-LPL titers: 85U (2001),100U (2002) e 86U (2003). Case 4: A 58-year-old female had SLE since 1996. She was in remission since August 2001 with a SLEDAI=0 during all this study. Anti-LPL titers did not significantly change: 71U (2001), 42U (2002) e 61U (2003). Case 5: A 55-year-old female had SLE since 1989. She was stable since 2000 using chloroquine, SLEDAI=0, and anti-LPL titers without variations: 71U (1999), 92U (2001), 71U (2002) e 90U (2003). CONCLUSION: The longitudinal evaluation of the selected patients showed a positive correlation between the fluctuations of the titers of anti-LPL with the SLEDAI score. These findings suggest that this variation may be a new marker for lupus activity in patients without anti-dsDNA antibodies.