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THE LANCET 3 Coniff RF, Shapiro JA, Seaton TB.

Long-term efficacy and safety of acarbose in the treatment of obese subjects with non-insulindependent diabetes mellitus. Arch Intern Med 1994; 154: 244248. Andrade RJ, Lucena MI, Rodrguez-Mendizbal M. Hepatic injury caused by acarbose. Ann Intern Med 1996; 124: 931. Lee WM. Drug-induced hepatotoxicity. N Engl J Med 1995; 333: 111827.

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Department of Internal Medicine, Hospital of Laredo, 39770 Laredo, Cantabria, Spain (M Carrascosa)

Antioxidant flavonols and coronary heart disease risk


Michal G L Hertog, Edith J M Feskens, Daan Kromhout

In 1993, we reported that the intake of antioxidant flavonols (mainly quercetin) predicted a reduced rate of coronaryheart-disease (CHD) mortality in elderly men who were followed-up for 5 years.1 We have completed 10 years of follow-up of the Zutphen Elderly Study and report the recalculated relative-risk estimates. The statistical analysis was repeated as previously described;1 we excluded one man because his cause of death was unknown. In brief, flavonol intake was recorded by trained dieticians who used a cross-check dietary history method to record 804 men aged 6584 years. The men were followed up for 10 years.1 Relative risks of CHD and allcause mortality and of a first myocardial infarction were analysed for tertiles of flavonol intake by a Cox proportional hazards model. During 10 years of follow-up 90 men died from CHD and 373 died from all-causes. Of the 692 men without a history of CHD at baseline, 92 had a first myocardial infarction, which was fatal in 57 men. In the crude analysis, flavonol intake at baseline was inversely associated with CHD mortality (table). After adjustment for age, smoking, baseline history of CHD, serum total cholesterol and high-density-lipoprotein, systolic blood pressure, body-mass index, physical activity, and intake of energy and saturated fat, the relative risk of a coronary event among men in the highest tertile of flavonoid intake was 047 (95% CI 027082). The exclusion of 112
Daily flavonoid intake (mg) 0190 191299 >299 268 21 99 049 (029083) 0007 047 (027082) 0006 p for trend

men who had a history of CHD at baseline did not change the relative-risk estimates (from lowest to highest tertile: 100, 069 [038126] and 046 [023092]), p for trend=0025). Flavonol intake was also inversely associated with all-cause mortality (adjusted p for trend=0010). Flavonol intake predicted a reduced rate of first myocardial infarction, although after adjustment this association was not significant (p for trend=0078). These results strengthen our initial findings1 and also show a dose-response relationship between flavonol intake to the risk of CHD mortality and a first myocardial infarction. Current epidemiological evidence suggests that antioxidant flavonols have a protective effect on the risk of death from coronary heart disease,14 but is not conclusive.2,4 Flavonols inhibit oxidation and cytotoxicity of low-densitylipoproteins, and affect haemostasis in vitro; however, studies of the effects of wine and tea, two important dietary sources of flavonols, yielded inconclusive or contradictory findings.5 Thus, the possibility that dietary flavonols reduce the risk of coronary heart disease remains open.
1 Hertog MGL, Feskens EJM, Hollman PCH, Katan MB, Kromhout D. Dietary antioxidant flavonols and risk of coronary heart disease: the Zutphen Elderly Study. Lancet 1993; 342: 100711. Rimm ER, Katan MB, Ascherio A, Stampfer M, Willett W. Relation between intake of flavonols and risk for coronary heart disease in male health professionals. Ann Intern Med 1996; 125: 38489. Knekt P, Jrvinen R, Reunanen A, Maatela J. Flavonoid intake and coronary mortality in Finland: a cohort study. BMJ 1996; 312: 47881. Hertog MGL, Sweetnam PM, Fehily AM, Elwood PC, Kromhout D. Antioxidant flavonols and ischaemic heart disease in a Welsh population of men: the Caerphilly Study. Am J Clin Nutr (in press). Hertog MGL, Katan MB. Quercetin in foods, cardiovascular disease and cancer. In: Rice-Evans C, Packer L, eds. Flavonoids in health disease. New York: Marcel Dekker Inc (in press).

Department of Chronic Diseases and Environmental Epidemiology and Division of Public Health Research, National Institute of Public Health and the Environment, PO Box 1, NL-3720 BA Bilthoven, Netherlands (E Feskens)

Increase in pneumococcal bacteraemia in Sweden


Johan Giesecke, Hans Fredlund

Mortality from coronary heart disease (n=804) Number of men 268 268 Deaths 39 30 Mortality rate 204 145 (per 1000 person-years) Crude relative risk 100 071 (044114) (95% CI) Relative risk adjusted for 100 058 (035095) age, diet, and risk factors*

Incidence of fatal and non-fatal first myocardial infarction (n=692) Number of men 230 231 231 Deaths 37 32 23 Incidence rate 176 148 104 (per 1000 person-years) Crude relative risk 100 084 (053135) 059 (035100) 0049 (95% CI) Relative risk adjusted for 100 089 (055144) 062 (0236105) 0078 age, diet, and risk factors* *Intake of total energy, saturated fatty acids, physical activity, body-mass index, smoking, serum total and high-density-lipoprotein cholesterol, and systolic blood pressure. History of myocardial infarction in 1985 included as additoinal covariate. Only men with no history of myocardial infarction at baseline.

Relative risk of mortality from coronary heart disease and occurrence of myocardial infarction during 10 years of followup by tertile of flavonoid intake (Zutphen Elderly Study)

An unexplained increase in the incidence of invasive pneumococcal disease has been reported from the UK1 and Norway,2 and also in Finnish children vaccinated against Haemophilus influenzae type b (Hib).3,4 However, the Norwegian study found a protective effect against pneumococcal septicaemia from Hib vaccination in small children. We therefore analysed the Swedish surveillance data for time and age trends. Since July, 1988, all blood and cerebrospinal fluid cultures positive for Streptococcal pneumoniae are routinely reported from the microbiological laboratories to the Swedish Institute for Infectious Disease Control. These analyses are done by 30 laboratories across the country. The date of birth and sex of the patient are also recorded. Serotyping is not routinely done. Because the laboratories joined the reporting scheme at different times, we restricted our analysis to the period from 1990. Between 1990 and 1995, the annual number of reported isolates of pneumococci from samples of blood or cerebrospinal fluid increased from 449 to 1155 (160%) (figure). The entire increase was in the number of positiveblood cultures, whereas there was virtually no change in the number of positive cerebrospinal-fluid cultures.

Vol 349 March 8, 1997

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