Halliday M L, Coates R A, Rankin J G
Department of Preventive Medicine and Biostatistics, University of Toronto, Canada.
Int J Epidemiol. 1991 Mar;20(1):199-208. doi: 10.1093/ije/20.1.199.
Cirrhosis mortality death rates in Ontario for ages 20 and over declined from a high of 9.3 per 100,000 in 1911 to a low of 5.6 per 100,000 in 1919 (p less than 0.001) and after a 17-year period of relative stability, rose steadily to a high of 19.7 per 100,000 in 1975 (p less than 0.0001) and then declined to 13.3 per 100,000 in 1986 (p less than 0.001). Rates were consistently higher for men than for women and the male to female ratio of the rates increased from a low of 1.3 in 1933 to a high of 2.5 in 1986. The rate of increase in the rates for both men and women, and the rate of decline after the mid 1970s was most noted in the younger ages. Differences in trend could not be related to changes in disease classification, method of recording deaths, changes in diagnostic habits such as introduction of needle liver biopsy or to method of standardizing the rates. There was a positive and significant correlation between per capita alcohol consumption and rates of cirrhosis in Ontario from 1932 to 1975. However, while cirrhosis rates declined markedly from 1976 to 1986, alcohol consumption remained stable from 1976 to 1980 and declined only slightly from 1981 to 1986. A possible explanation for lack of correlation between alcohol consumption and the cirrhosis rates from 1976 to 1986 could be that the balance of force favoured recovery i.e. those people who already had cirrhosis who decreased (or stopped) their consumption of alcohol, did not die. Correlations with lagged alcohol consumption could not explain all the changes in the cirrhosis rates. Although cirrhosis rates consistently increased with increasing age from 35 to 85, our results showed that succeeding generations were developing cirrhosis at successively younger ages after the age of 35. Possible explanations for this cohort effect are increased survival from infectious diseases in infancy and childhood, increase in hepatitis B infection, excessive drinking habits being established at younger ages or a change in the pathogenesis of the disease.
安大略省20岁及以上人群的肝硬化死亡率从1911年每10万人9.3的高位降至1919年每10万人5.6的低位(p<0.001),在经历了17年的相对稳定期后,稳步上升至1975年每10万人19.7的高位(p<0.0001),随后又降至1986年每10万人13.3(p<0.001)。男性的死亡率始终高于女性,死亡率的男女比例从1933年的1.3的低位升至1986年的2.5的高位。男性和女性死亡率的上升速度以及20世纪70年代中期以后的下降速度在较年轻年龄段最为明显。趋势差异与疾病分类的变化、死亡记录方法、诊断习惯的改变(如肝穿刺活检的引入)或标准化率的方法无关。1932年至1975年,安大略省人均酒精消费量与肝硬化发病率之间存在正相关且显著相关。然而,虽然1976年至1986年肝硬化发病率显著下降,但1976年至1980年酒精消费量保持稳定,1981年至1986年才略有下降。1976年至1986年酒精消费与肝硬化发病率缺乏相关性的一个可能解释是,力量平衡有利于康复,即那些已经患有肝硬化但减少(或停止)饮酒的人没有死亡。与滞后酒精消费的相关性无法解释肝硬化发病率的所有变化。尽管从35岁到85岁,肝硬化发病率随年龄增长而持续上升,但我们的结果表明,35岁以后,后代患肝硬化的年龄越来越小。这种队列效应的可能解释是婴儿期和儿童期传染病存活率的提高、乙型肝炎感染的增加、在较年轻年龄养成的过度饮酒习惯或疾病发病机制的改变。