退伍军人非霍奇金淋巴瘤风险与慢性免疫刺激间的种族差异
发布时间：2011-01-19 | 来源：医脉通
关键词：
非霍奇金淋巴瘤
免疫刺激
文献出处：JCO Dec 20, 2010.
期刊影响因子:17.793
美国最近研究可解释非霍奇金淋巴瘤（NHL）发病率种族差异的潜在病因。本研究在线发表在2010.12.20的《Journal Clinical Oncology》。 NHL风险差异，支持调控免疫/炎症反应基因的种族差异。
研究评价了400万多住院美国退伍军人的免疫相关状况与非霍奇金淋巴瘤风险，包括对9496例NHL患者（7999例白人患者及1497例黑人患者）进行达26年随访。应用时倚泊松回归评价有特定自身免疫性疾病、感染及过敏疾病病史的患者与无这些疾病病史的患者间的NHL风险比值比（RRs）及95%CIs，校正了达到年龄、日历年、种族、医院访问次数及纳入与退出研究的时间。
伴感染状况（尤其是胃肝、生殖及全身感染）的患者患NHL风险增高（RR， 1.2； 95% CI， 1.1 - 1.2）。伴自身免疫性疾病患者较不伴该病的患者更易患NHL，尤其是典型的可检测到自身抗体伴全身累及者（RR， 2.0；95% CI， 1.8 - 2.2）。过敏亦与风险增高相关（RR， 1.4；95% CI， 1.3 - 1.5）。虽然黑人NHL风险较白人低（RR， 0.87； 95% CI， 0.82 - 0.92，但黑人与感染相关的NHL风险稍高于白人（似然比检验， P = 0.002）且有较高的与过敏相关的NHL风险（似然比检验， P = 0.05）。种族间与自身免疫状况相关的NHL风险相当（似然比检验， P = 0.5）。
医脉通推荐英文摘要
J Clin Oncol. 2010 Dec 20. doi:10.1200/JCO.2010.30.1515
Racial Differences in Chronic Immune Stimulatory Conditions and Risk of Non-Hodgkin's Lymphoma in Veterans From the United States
Jill Koshiol, Tram Kim Lam, Gloria Gridley, David Check,
（Corresponding author: Jill Koshiol, PhD, National Cancer Institute, 6120 Executive Blvd, MSC 7248, Bethesda, MD 20892-7248）
Purpose To examine underlying etiologic factors that may explain the racial disparity in non-Hodgkin's lymphoma (NHL) incidence patterns.
Patients and Methods We assessed immune-related conditions and risk of developing NHL among more than 4 million hospitalized US veterans including 9,496 patients with NHL (7,999 white patients and 1,497 black patients) with up to 26 years of follow-up. We used time-dependent Poisson regression to estimate rate ratios (RRs) and 95% CIs for NHL risk among patients with a history of specific autoimmune diseases, infections, and allergies compared with patients without such history, adjusting for attained age, calendar year, race, number of hospital visits, and time between study entry and exit.
Results Patients with infectious conditions had an increased risk of developing NHL (RR, 1.2; 95% CI, 1.1 to 1.2), particularly for gastrohepatic, genital, and systemic infectious conditions. Patients with autoimmune disease were generally more likely to develop NHL than patients without autoimmune disease, especially for conditions that typically present with detectable autoantibodies with systemic involvement (RR, 2.0; 95% CI, 1.8 to 2.2). Allergies were also associated with increased risk (RR, 1.4; 95% CI, 1.3 to 1.5). Although the risk of NHL was lower for blacks than whites (RR, 0.87; 95% CI, 0.82 to 0.92), blacks had a slightly higher risk of NHL associated with infections than whites (likelihood ratio test, P = .002) and a tendency toward higher risk associated with allergies (likelihood ratio test, P = .05). Risks associated with autoimmune conditions were similar by race (likelihood ratio test, P = .5).
Conclusion The observed difference in NHL risk by race supports a role for race-related differences in genes regulating immune/inflammatory response.
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