Chronic immune stimulation and subsequent Waldenström macroglobulinemia.

Chronic immune stimulation and subsequent Waldenström macroglobulinemia.
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慢性免疫刺激和随后的华氏巨球蛋白血症。

DOI:
10.1001/archinternmed.2008.4
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发表时间:
2008-09-22
影响因子:
--
通讯作者:
Landgren, Ola
Landgren, Ola
中科院分区:
其他
文献类型:
--
作者:
Koshiol, Jill;Gridley, Gloria;Engels, Eric A.;McMaster, Mary L.;Landgren, Ola

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某些自身免疫性疾病和感染性疾病与非霍奇金淋巴瘤 (NHL) 亚型风险增加相关。之前的一些研究表明,慢性炎症可能特别会增加独特的 NHL 亚型华氏巨球蛋白血症 (WM) 的风险。我们评估了 400 万美国退伍军人与各种慢性免疫刺激疾病相关的 WM 风险。我们发现了 361 例 WM 病例,并进行了长达 27 年的随访。使用时间依赖性泊松回归,我们估计了与自身免疫性疾病史相关的 WM 风险的比率 (RR) 和 95% 置信区间 (CI),这些疾病通常有自身抗体(系统或器官受累)或没有自身抗体、感染和过敏。所有模型均根据达到的年龄、日历年、种族、医院就诊次数以及研究进入和退出之间的延迟进行调整。 WM 的年龄标准化发病率为 0.34/10 万人年。患有任何既往自身免疫性疾病(RR,2.2;95% CI,1.7-3.0)、自身抗体有全身受累(RR,2.50;95% CI,1.55-4.02)、自身抗体有器官受累(RR,2.30;95% CI,1.57-3.37)的个体,WM 风险较高。肝炎(RR,3.39;95% CI,1.38-8.30)、人类免疫缺陷病毒(HIV)(RR,12.05;95% CI,2.83-51.46)和立克次体病(RR,3.35;95% CI,1.38-8.14)也增加了 WM 的风险。迄今为止,我们发现有自身免疫性疾病个人病史并携带自身抗体的人,患 WM 的风险增加 2 至 3 倍,并且患肝炎、艾滋病毒和立克次体病的风险显着增加。我们的研究结果为迄今未知的 WM 病因学提供了新的见解。
Certain autoimmune and infectious conditions are associated with increased risks of subtypes of non-Hodgkin’s lymphomas (NHL). A few prior studies suggest that chronic inflammation may particularly elevate risk for the distinct NHL subtype Waldenström’s macroglobulinemia (WM). We assessed WM risk in relation to a wide range of chronic immune stimulatory conditions among 4 million U.S. veterans. We identified 361 WM cases with up to 27 years of follow-up. Using time-dependent Poisson regression we estimated rate ratios (RR) and 95% confidence intervals (CI) for WM risk in relation to history of autoimmune diseases that typically have autoantibodies (with systematic or organ involvement) or do not have autoantibodies, infections, and allergies. All models were adjusted for attained age, calendar-year, race, number of hospital visits, and latency between study entry and exit. The age-standardized incidence of WM was 0.34/100,000 person-years. WM risk was elevated among individuals with any prior autoimmune condition (RR, 2.2; 95% CI, 1.7–3.0), autoantibodies with systemic involvement (RR, 2.50; 95% CI, 1.55–4.02), autoantibodies with organ involvement (RR, 2.30; 95% CI, 1.57–3.37). Risks for WM were also increased with hepatitis (RR, 3.39; 95% CI, 1.38–8.30), human immunodeficiency virus (HIV) (RR, 12.05; 95% CI, 2.83–51.46), and rickettsiosis (RR, 3.35; 95% CI, 1.38–8.14) In the largest investigation of WM risk factors to date, we found 2- to 3-fold elevated risk of WM among persons with a personal history of autoimmune diseases with autoantibodies and notably elevated risks for hepatitis, HIV, and rickettsiosis. Our findings provide novel insights into the as yet unknown etiology of WM.
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