Contribution of H. pylori and smoking trends to US incidence of intestinal-type noncardia gastric adenocarcinoma: a microsimulation model.

Contribution of H. pylori and smoking trends to US incidence of intestinal-type noncardia gastric adenocarcinoma: a microsimulation model.
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DOI:
10.1371/journal.pmed.1001451
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发表时间:
2013
期刊:
影响因子:
15.8
通讯作者:
Goldie SJ
Goldie SJ
中科院分区:
医学1区
文献类型:
--
作者:
Yeh JM;Hur C;Schrag D;Kuntz KM;Ezzati M;Stout N;Ward Z;Goldie SJ

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Jennifer Yeh和同事研究了幽门螺杆菌和吸烟趋势对过去和未来肠道型非贲门胃腺癌发病率的影响。尽管胃癌在美国的发病率急剧下降,但它仍然是全球癌症死亡率的第二大原因。更好地了解下降的原因可以为有效的预防策略提供重要的见解。我们试图估计危险因素趋势对过去和未来肠型非贲门胃腺癌(NCGA)发病率的贡献。我们建立了一个基于人群的肠道型NCGA微观模拟模型,并将其校准为美国癌前病变和癌症的流行病学数据。该模型明确纳入了幽门螺杆菌和吸烟对疾病自然史的影响,其中出生队列特定趋势来自国家健康和营养检查调查(NHANES)和国家健康访谈调查(NHIS)。1978年至2008年间,该模型估计肠道型NCGA发病率下降了60%,从11.0 / 10万男性降至4.4 / 10万男性,与国家统计数据差异<3%。幽门螺杆菌和吸烟趋势合计占观察到的下降的47%(范围= 30%-58%)。如果没有烟草控制,发病率只会下降56%,这表明在20世纪60年代以后观察到的较低的开始吸烟率和较高的戒烟率加速了癌症发病率的相对下降7%(范围= 0%-21%)。随着风险因素趋势的持续,预计在2008年至2040年期间,发病率将进一步下降47%,其中大部分将归因于幽门螺杆菌和吸烟(81%;范围为61%-100%)。局限性包括假设所有其他影响胃癌发生的危险因素为一个因素,并限制对男性的分析。可改变的危险因素的趋势解释了美国肠道型NCGA发病率下降的重要比例,并预计将继续下去。虽然过去的控烟努力加速了胃癌发病率的下降,但充分的益处需要几十年才能实现,因此进一步减少吸烟和减少幽门螺杆菌应该是胃癌控制工作的重点。胃癌(胃癌)占全球所有癌症死亡人数的十分之一,估计每年有70万人死于这种恶性肿瘤,使其成为仅次于肺癌的全球癌症相关死亡的第二大常见原因。不幸的是,据估计,到2030年,胃癌造成的全球负担将翻一番。胃癌的预后很差,只有四分之一的胃癌患者能存活5年以上。因此,为了减少死亡,确定和减少与胃癌相关的可改变的危险因素至关重要。吸烟和幽门螺杆菌(h.p ylori)的慢性胃感染是胃癌的两个常见的可改变的危险因素,特别是一种称为肠型非贲门胃腺癌(NCGA)的胃癌,它发生在胃的远端,占美国男性胃癌病例的一半以上。幽门螺杆菌启动癌前过程,因此感染这种细菌可以使肠道型NCGA的风险增加多达6倍,而吸烟通过促进现有病变的不断发展而使癌症风险增加一倍。在过去的一个世纪里,这两个风险因素的变化(特别是在1964年美国外科医生发布了吸烟与健康报告之后)导致了美国男性胃癌发病率的急剧下降。了解潜在风险因素趋势在人群水平上对肠型NCGA健康结果的综合影响有助于预测美国未来的癌症趋势和负担。因此,在这项研究中,研究人员使用了一个数学模型来估计幽门螺杆菌和吸烟趋势对美国男性肠道型NCGA发病率下降的贡献。研究人员使用来自两个国家数据库(国家健康和营养检查调查(NHANES)和国家健康访谈调查(NHIS))数据的出生队列来开发基于人群的肠道型NCGA模型。为了确保模型预测与流行病学数据一致,研究人员将模型校准为癌症和癌前病变的数据,并使用该模型预测1978年至2040年基本情况下的人口结果(其中所有风险因素趋势都允许随时间变化)。研究人员随后评估了其他风险因素,以提供对过去和未来控制胃癌的潜在益处的见解。使用这些方法,研究人员估计,肠道型NCGA(按年龄标准化)的发病率在1978年至2008年间从每10万名男性11.0例下降到4.4例,下降了60%。当研究人员仅将幽门螺杆菌患病率和吸烟趋势纳入模型时(两者都在一段时间内急剧下降),他们发现肠道型NCGA发病率仅下降了28%(从每10万人12.7人降至9.2人),这表明幽门螺杆菌和吸烟趋势对观察到的下降负有47%的责任。研究人员发现,仅幽门螺杆菌的趋势就对癌症发病率下降的43%负有责任,而吸烟趋势只对癌症发病率下降的3%负有责任。研究人员还发现证据表明,在20世纪60年代之后,观察到的低吸烟率和高戒烟率的趋势加速了肠道型NCGA发病率下降7%。最后,研究人员发现,肠道型NCGA发病率预计在2008年至2040年间将再下降47%(每10万男性4.4至2.3例),其中幽门螺杆菌和吸烟趋势占观察到的下降的80%以上。这些发现表明,结合吸烟率的下降,1978年至2008年间美国男性肠道型NCGA癌发病率的下降几乎有一半可归因于幽门螺杆菌感染率的下降。预计到2040年,这种癌症的发病率将继续下降,幽门螺杆菌感染和吸烟的趋势占观察到的下降的80%以上,突出了风险因素随时间变化之间关系的重要性,并实现癌症发病率的长期降低。该研究受到模型中假设的限制,并且只检查了一种类型的胃癌,并排除了女性。然而,该模型研究强调,继续努力降低吸烟率和幽门螺杆菌感染率将有助于降低胃癌的发病率。请通过本摘要的在线版本http://dx.doi.org/10.1371/journal.pmed.1001451访问这些网站。国家癌症研究所提供有关胃癌的详细信息胃癌基金会为患者和专业人员提供有关胃癌的信息英国癌症研究所解释了胃癌的类型
Jennifer Yeh and colleagues examine the contribution of IHelicobacter pyloriI and smoking trends to the incidence of past and future intestinal-type noncardia gastric adenocarcinoma. Please see later in the article for the Editors' Summary Although gastric cancer has declined dramatically in the US, the disease remains the second leading cause of cancer mortality worldwide. A better understanding of reasons for the decline can provide important insights into effective preventive strategies. We sought to estimate the contribution of risk factor trends on past and future intestinal-type noncardia gastric adenocarcinoma (NCGA) incidence. We developed a population-based microsimulation model of intestinal-type NCGA and calibrated it to US epidemiologic data on precancerous lesions and cancer. The model explicitly incorporated the impact of Helicobacter pylori and smoking on disease natural history, for which birth cohort-specific trends were derived from the National Health and Nutrition Examination Survey (NHANES) and National Health Interview Survey (NHIS). Between 1978 and 2008, the model estimated that intestinal-type NCGA incidence declined 60% from 11.0 to 4.4 per 100,000 men, <3% discrepancy from national statistics. H. pylori and smoking trends combined accounted for 47% (range = 30%–58%) of the observed decline. With no tobacco control, incidence would have declined only 56%, suggesting that lower smoking initiation and higher cessation rates observed after the 1960s accelerated the relative decline in cancer incidence by 7% (range = 0%–21%). With continued risk factor trends, incidence is projected to decline an additional 47% between 2008 and 2040, the majority of which will be attributable to H. pylori and smoking (81%; range = 61%–100%). Limitations include assuming all other risk factors influenced gastric carcinogenesis as one factor and restricting the analysis to men. Trends in modifiable risk factors explain a significant proportion of the decline of intestinal-type NCGA incidence in the US, and are projected to continue. Although past tobacco control efforts have hastened the decline, full benefits will take decades to be realized, and further discouragement of smoking and reduction of H. pylori should be priorities for gastric cancer control efforts. Please see later in the article for the Editors' Summary Cancer of the stomach (gastric cancer) is responsible for a tenth of all cancer deaths world-wide, with an estimated 700,000 people dying from this malignancy every year, making it the second most common cause of global cancer-related deaths after lung cancer. Unfortunately, the projected global burden of this disease estimate that deaths from gastric cancer will double by 2030. Gastric cancer has a poor prognosis with only a quarter of people with this type of cancer surviving more than five years. In order to reduce deaths, it is therefore of utmost importance to identify and reduce the modifiable risk factors associated with gastric cancer. Smoking and chronic gastric infection with the bacteria Helicobacter pylori (H. pylori), are known to be two common modifiable risk factors for gastric cancer, particularly for a type of gastric cancer called intestinal-type noncardia gastric adenocarcinoma (NCGA), which occurs at the distal end of the stomach and accounts for more than half of all cases of gastric cancer in US men. H. pylori initiates a precancerous process, and so infection with this bacteria can increase intestinal-type NCGA risk by as much as 6-fold while smoking doubles cancer risk by advancing increasing progression of existing lesions. Changes in these two risk factors over the past century (especially following the US Surgeon General's Report on Smoking and Health in 1964) have led to a dramatic decline in the rates of gastric cancer in US men. Understanding the combined effects of underlying risk factor trends on health outcomes for intestinal-type NCGA at the population level can help to predict future cancer trends and burden in the US. So in this study, the researchers used a mathematical model to estimate the contribution of H. pylori and smoking trends on the decline in intestinal-type NCGA incidence in US men. The researchers used birth cohorts derived from data in two national databases, the National Health and Nutrition Examination Survey (NHANES) and National Health Interview Survey (NHIS) to develop a population-based model of intestinal-type NCGA. To ensure model predictions were consistent with epidemiologic data, the researchers calibrated the model to data on cancer and precancerous lesions and using the model, projected population outcomes between 1978 and 2040 for a base-case scenario (in which all risk factor trends were allowed to vary over time). The researchers then evaluated alternative risk factors scenarios to provide insights on the potential benefit of past and future efforts to control gastric cancer. Using these methods, the researchers estimated that the incidence of intestinal-type NCGA (standardized by age) fell from 11.0 to 4.4 per 100,000 men between 1978 and 2008, a drop of 60%. When the researchers incorporated only H. pylori prevalence and smoking trends into the model (both of which fell dramatically over the time period) they found that intestinal-type NCGA incidence fell by only 28% (from 12.7 to 9.2 per 100,000 men), suggesting that H. pylori and smoking trends are responsible for 47% of the observed decline. The researchers found that H. pylori trends alone were responsible for 43% of the decrease in cancer but smoking trends were responsible for only a 3% drop. The researchers also found evidence that after the 1960s, observed trends in lower smoking initiation and higher cessation accelerated the decline in intestinal-type NCGA incidence by 7%. Finally, the researchers found that intestinal-type NCGA incidence is projected to decline an additional 47% between 2008 and 2040 (4.4 to 2.3 per 100,000 men) with H. pylori and smoking trends accounting for more than 80% of the observed fall. These findings suggest that, combined with a fall in smoking rates, almost half of the observed fall in rates of intestinal-type NCGA cancer in US men between 1978 and 2008 was attributable to the decline in infection rates of H. pylori. Rates for this cancer are projected to continue to fall by 2040, with trends for both H. pylori infection and smoking accounting for more than 80% of the observed fall, highlighting the importance of the relationship between risk factors changes over time and achieving long-term reduction in cancer rates. This study is limited by the assumptions made in the model and in that it only examined one type of gastric cancer and excluded women. Nevertheless, this modeling study highlights that continued efforts to reduce rates of smoking and H. pylori infection will help to reduce rates of gastric cancer. Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001451. The National Cancer Institute gives detailed information about gastric cancer The Gastric Cancer Foundation has information on gastric cancer for patients and professionals Cancer Research UK explains types of gastric cancer
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