Hepatoblastoma and low birth weight
Hepatoblastoma and low birth weight
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肝母细胞瘤和低出生体重
作者：
L. Spector;J. Feusner;J. Ross
先前注意到的肝母细胞瘤（HB）发病率升高的可能性受到出生体重< 2500 g的HB病例不成比例的影响，目前尚未正式分析。因此，我们希望向您的读者提供美国HB发病率增长率的最新估计，并告知他们其与低出生比例（%LBW: 1,500 - 2,500 g），特别是极低出生体重（%VLBW:<1,500 g）上升的关系。来自监测、流行病学和最终结果（SEER）项目[3]的HB发病率数据使用泊松回归进行分析。在所有5岁以下儿童中，每百万儿童年的HB发病率从1975-1979年的2.59 （95% CI: 1.70-3.93）上升到1995-1999年的5.27 (95% CI: 4.03-6.88)，每年的发病率显著上升3.87% （95% CI: 1.72-6.06）。1-4岁儿童的HB发病率（每年5.26%;95% CI: 2.35-8.25）比婴儿的发病率（每年2.24%;95% CI: 0.10-5.54）增加得更快。这些对HB发病率变化的估计较低，但比早期的估计更精确。然后，我们将1981-1999年出生第一年的HB率与同一日历年的出生体重数据[4]，以及1983-1999年1-4岁的HB率与之前两个日历年（即1981-1997年）的出生体重数据[4]联系起来。lbw和VLBW出生率每增加1%，前者的比率分别为1.51 （95% CI: 0.65-3.53;P1⁄4 0.34）和4.63 (95% CI: 0.30 - 71.08; P1⁄4 0.27)，后者的比率分别为2.21 （95% CI: 0.96-5.10;P1⁄4 0.06）和9.96 （95% CI: 0.62-160;P1⁄4 0.10）。这些数据表明，HB率的上升与低出生体重百分比的上升是一致的，特别是低出生体重百分比的上升，但是，由于是生态的，它们不能被认为是因果关系。这些发现对hb病因学有一定的启示。体重本身更可能是其他暴露的标志，而不是风险因素。LBW儿童的HB可能是早产儿治疗和婴儿基因决定的耐受治疗能力的结果。产后癌变可能提示诊断HB时年龄较大。因此值得注意的是，合并LBW的HB患者似乎比出生体重正常的患者诊断年龄更大，并且在本分析中，HB的发病率在1-4岁的儿童中增长最快。此外，我们发现最强的生态关联是VLBW与大一点的儿童HB之间的关系，因为这类婴儿的体型极小，器官不成熟，治疗可能更积极。设计一项结构良好的病例对照研究将非常重要，该研究可以确定早产治疗的强度和持续时间是否是LBW儿童发生HB的危险因素。
The possibility that the previously noted rise in hepatoblastoma (HB) incidence [1] was influenced by the disproportionate number ofHB caseswith birthweight <2,500 g [2] has not been formally analyzed. We, therefore, wish to provide your readers an updated estimate of the rate of increase of HB incidence in the United States and to apprise them of its association with a rise in the proportion of births that are low (%LBW: 1,500–2,500 g) and especially very low birth weight (%VLBW:<1,500 g). Data on HB incidence from the Surveillance, Epidemiology, and End Results (SEER) program [3] were analyzed using Poisson regression. The rate of HB per million child-years among all children <5 years old rose from 2.59 (95% CI: 1.70–3.93) in 1975–1979 to 5.27 (95% CI: 4.03–6.88) in 1995–1999, representing a significant 3.87% (95% CI: 1.72–6.06) rise in incidence per annum. The rate of HB among children 1–4 years of age increased more rapidly (5.26% per annum; 95% CI: 2.35–8.25), than did the rate among infants (2.24% per annum; 95% CI: 0.10–5.54). These estimates of the change in incidence of HB are lower, but more precise, than earlier estimates [1]. We then related the rate of HB in the first year of life in 1981–1999 to birth weight figures [4] for the same calendar year and the rate of HB at 1–4 years of age in 1983–1999 to birth weight figures [4] for two calendar years prior (i.e., 1981–1997). The rate ratios were 1.51 (95% CI: 0.65–3.53; P1⁄4 0.34) and 4.63 (95% CI: 0.30– 71.08; P1⁄4 0.27) for a 1% rise in LBWand VLBW births, respectively, for the former analysis and 2.21 (95% CI: 0.96–5.10;P1⁄4 0.06) and 9.96 (95%: 0.62–160;P1⁄4 0.10) for the latter. These data suggest that the rise in the rate of HB was consistent with the rise in the %LBW and especially %VLBW births, but, being ecologic, they cannot be considered causal. These findings have some implications forHB etiology. LBW per se is more likely a marker for other exposures rather than a risk factor. HB among LBW children may be a consequence of treatment for prematurity and infants’ genetically determined ability to tolerate treatment. Postnatal carcinogenesis might suggest an older age at diagnosis of HB. Thus it is worth noting that HB patients with LBW appear to be diagnosed at older ages than do patients with normal birth weight [5], and in the present analysis the rate of HB is increasing most rapidly among 1–4 year olds. Moreover, the strongest ecologic association we found was between VLBW, for which treatment might more aggressive given such infants’ extremely small body size and organ immaturity, and HB in older children. It will be important to design a well-constructed case-control study that can determine whether the intensity and duration of treatment for prematurity is a risk factor for HB among children with LBW.