Abstract：
OBJECTIVE: Fibroids are hormonally dependent uterine tumors. The literature on adiposity and fibroid prevalence is inconsistent. Previous work usually combined all those with body mass indexes (BMIs) ≥30kg/m2 into a single category and relied on clinically diagnosed fibroids which misclassifies the many women with undiagnosed fibroids. We used a prospective cohort design with periodic ultrasound screening to investigate associations between repeated measures of BMI and fibroid incidence and growth assessed at each follow-up ultrasound.
METHODS: The Study of Environment, Lifestyle & Fibroids (SELF) followed 1,693 Black/African American women, ages 23-35 from Detroit, Michigan with ultrasound every 20 months for 5 years. Measured height and repeated weight measures were used to calculate BMI. Fibroid incidence was modeled using Cox models among those who were fibroid-free at the enrollment ultrasound. Fibroid growth was estimated for individual fibroids matched across visits as the difference in log-volume between visits and was modeled using linear mixed models. All models used time-varying BMI and adjusted for time-varying covariates.
RESULTS: Compared to BMI <25kg/m2 those with BMI 30-<35kg/m2 had increased fibroid incidence (adjusted hazard ratio (aHR) 1.37, (95% Confidence Interval (CI): 0.96-1.94)), those with BMI ≥40kg/m2 had reduced incidence (aHR 0.61, (95% CI: 0.41-0.90)). Fibroid growth had mostly small magnitude associations with BMI.
CONCLUSIONS: BMI has a non-linear association with fibroid incidence that could be driven by effects of BMI on inflammation and reproductive hormones. More detailed measures of visceral and subcutaneous adiposity and their effects on hormones, DNA damage, and cell death are needed.
METHODS: The Study of Environment, Lifestyle & Fibroids (SELF) followed 1,693 Black/African American women, ages 23-35 from Detroit, Michigan with ultrasound every 20 months for 5 years. Measured height and repeated weight measures were used to calculate BMI. Fibroid incidence was modeled using Cox models among those who were fibroid-free at the enrollment ultrasound. Fibroid growth was estimated for individual fibroids matched across visits as the difference in log-volume between visits and was modeled using linear mixed models. All models used time-varying BMI and adjusted for time-varying covariates.
RESULTS: Compared to BMI <25kg/m2 those with BMI 30-<35kg/m2 had increased fibroid incidence (adjusted hazard ratio (aHR) 1.37, (95% Confidence Interval (CI): 0.96-1.94)), those with BMI ≥40kg/m2 had reduced incidence (aHR 0.61, (95% CI: 0.41-0.90)). Fibroid growth had mostly small magnitude associations with BMI.
CONCLUSIONS: BMI has a non-linear association with fibroid incidence that could be driven by effects of BMI on inflammation and reproductive hormones. More detailed measures of visceral and subcutaneous adiposity and their effects on hormones, DNA damage, and cell death are needed.
摘要：
目的：子宫肌瘤是激素依赖性子宫肿瘤。关于肥胖和肌瘤患病率的文献不一致。以前的工作通常将所有体重指数（BMIs）≥30kg/m2的人合并为一个类别，并依赖于临床诊断的肌瘤，这些肌瘤错误地将许多未确诊的肌瘤妇女分类。我们使用前瞻性队列设计与定期超声筛查，以调查BMI的重复测量与每次随访超声评估的肌瘤发生率和生长之间的关联。
方法：环境研究，生活方式和纤维（SELF）跟随1,693名黑人/非裔美国女性，来自底特律的23-35岁，密歇根州每20个月进行一次超声检查，持续5年。测量的身高和重复的体重测量用于计算BMI。在注册超声检查中无纤维瘤的患者中，使用Cox模型对纤维瘤发生率进行建模。估计在每次就诊之间匹配的个体肌瘤的纤维瘤生长作为就诊之间的对数体积差异,并使用线性混合模型进行建模。所有模型均使用随时间变化的BMI，并针对随时间变化的协变量进行了调整。
结果：与BMI<25kg/m2相比，BMI为30-<35kg/m2的患者的肌瘤发病率增加（调整后的危险比（aHR）1.37，（95％置信区间（CI）：0.96-1.94）），BMI≥40kg/m2的患者的发病率降低(aHR0.61,(95%CI:0.41~0.90)).纤维生长与BMI之间的关联大多很小。
结论：BMI与纤维瘤发病率存在非线性关联，这可能是由BMI对炎症和生殖激素的影响所驱动。内脏和皮下脂肪及其对激素的影响的更详细的措施，DNA损伤,需要细胞死亡。
方法：环境研究，生活方式和纤维（SELF）跟随1,693名黑人/非裔美国女性，来自底特律的23-35岁，密歇根州每20个月进行一次超声检查，持续5年。测量的身高和重复的体重测量用于计算BMI。在注册超声检查中无纤维瘤的患者中，使用Cox模型对纤维瘤发生率进行建模。估计在每次就诊之间匹配的个体肌瘤的纤维瘤生长作为就诊之间的对数体积差异,并使用线性混合模型进行建模。所有模型均使用随时间变化的BMI，并针对随时间变化的协变量进行了调整。
结果：与BMI<25kg/m2相比，BMI为30-<35kg/m2的患者的肌瘤发病率增加（调整后的危险比（aHR）1.37，（95％置信区间（CI）：0.96-1.94）），BMI≥40kg/m2的患者的发病率降低(aHR0.61,(95%CI:0.41~0.90)).纤维生长与BMI之间的关联大多很小。
结论：BMI与纤维瘤发病率存在非线性关联，这可能是由BMI对炎症和生殖激素的影响所驱动。内脏和皮下脂肪及其对激素的影响的更详细的措施，DNA损伤,需要细胞死亡。
