Tobacco smoking and regression of low-grade cervical abnormalities
Tobacco smoking and regression of low-grade cervical abnormalities
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DOI：
10.1111/j.1349-7006.2010.01642.x
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发表时间：
2010-09-01
期刊：
影响因子：
5.7
通讯作者：
Yoshikawa, Hiroyuki
中科院分区：
文献类型：
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作者：
Matsumoto, Koji;Oki, Akinori;Yoshikawa, Hiroyuki
由于缺乏前瞻性数据，吸烟在宫颈多阶段癌变中的作用尚未完全了解。为了评估吸烟与宫颈前病变自然消退之间的关系，共516例低度鳞状上皮内病变（LSIL）妇女每4个月进行一次细胞学和阴道镜检查。2年内LSIL消退的概率与吸烟行为相关，消退定义为至少连续两次阴性巴氏涂片和正常阴道镜检查。妇女的年龄，初始活检结果，和人乳头瘤病毒（HPV）基因型被纳入多变量模型进行调整。我们的研究对象包括258名从不吸烟者和258名吸烟者（179名当前吸烟者和79名既往吸烟者）。在平均39.8个月的随访时间内，320个病变恢复到正常细胞学。吸烟者2年内的消退概率显著低于从不吸烟者（55.0% vs 68.8%，P = 0.004）。LSIL持续存在的风险随着吸烟强度和持续时间以及开始吸烟时年龄的增加而增加（分别为P = 0.003，P < 0.001和P = 0.03）。吸烟者持续性HPV感染的风险是从不吸烟者的两倍（比值比，2.50; 95%置信区间，1.30-4.81; P = 0.006）。在年轻女性中，从童年开始被动吸烟降低了2年内消退的概率（56.7% vs 85.9%，P < 0.001）。对广泛的宫颈癌风险因素进行进一步调整并没有改变研究结果。总之，吸烟可能会干扰宫颈前病变的消退。儿童时期接触二手烟可能会增加年轻女性持续性宫颈异常的风险。（Cancer Sci 2010）。
The role of tobacco smoking in the multistage carcinogenesis at the cervix is not fully understood because of a paucity of prospective data. To assess the relationship between smoking and spontaneous regression of cervical precursor lesions, a total of 516 women with low-grade squamous intraepithelial lesion (LSIL) were monitored by cytology and colposcopy every 4 months. Probability of LSIL regression within 2 years was analyzed in relation to smoking behaviors, with regression defined as at least two consecutive negative Pap smears and normal colposcopy. Women's age, initial biopsy results, and human papillomavirus (HPV) genotypes were included in the multivariate models for adjustments. Our study subjects included 258 never-smokers and 258 smokers (179 current and 79 former smokers). During a mean follow-up time of 39.8 months, 320 lesions regressed to normal cytology. Probability of regression within 2 years was significantly lower in smokers than in never-smokers (55.0% vs 68.8%, P = 0.004). The risk of LSIL persistence increased with smoking intensity and duration and with younger age at starting smoking (P = 0.003, P < 0.001, and P = 0.03, respectively). Smokers had twice as high a risk of persistent HPV infection compared to never-smokers (odds ratio, 2.50; 95% confidence interval, 1.30-4.81; P = 0.006). In young women, passive smoking since childhood reduced probability of regression within 2 years (56.7% vs 85.9%, P < 0.001). Further adjustments for a wide range of cervical cancer risk factors did not change the findings. In conclusion, tobacco smoking may interfere with regression of cervical precursor lesions. Childhood exposure to second-hand smoke may increase a risk of persistent cervical abnormalities among young women. (Cancer Sci 2010).