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Biomedical subjects

G Jensen

Publications and source records attributed to G Jensen.

At least 37 records · Page 2Linked to original sources

Experimental discordant hepatic xenotransplantation in the recipient with liver failure: implications for clinical bridging trials.

BACKGROUND: Clinical xenotransplantation might start with bridge-to-bridge trials. Situations where hyperacute rejection is avoided would provide opportunities for the initiation of bridging trials. Patients with liver failure have a diminished capacity to initiate antibody and complement-induced injury of xenogeneic endothelium. Hyperacute rejection of a liver xenograft manifests as a coagulopathy. We examined the ability of a recipient with liver failure to hyperacutely reject a liver xenograft in the dog-to-pig model in the immediate postoperative period. STUDY DESIGN: Liver failure in pigs was induced with galactosamine. Canine livers were transplanted into pigs with liver failure and into healthy pigs. The postoperative course was monitored for 1 hour for histologic changes in the xenograft, changes in platelet counts, and whole blood clotting with Sonoclot analysis. In vitro assays with pig serum and canine hepatic sinusoidal endothelial cells were used to assess the effect of liver failure on serum cytotoxicity and xenoreactive antibody levels. RESULTS: All untreated pig recipients of liver xenografts died from a coagulopathy. Recipients with liver failure manifested no signs of coagulopathy, and had minimal change in platelet counts or Sonoclot (Sienco Inc., Morrison, CO) tracings. Liver xenograft biopsies from recipients with liver failure showed no evidence of the tissue injury that characterized the biopsies of control recipients. Serum from pigs was less cytotoxic to the canine hepatic sinusoidal endothelium after induction of liver failure. The xenoreactive antibody levels and repertoire were similar in the pig serum before and after liver failure was induced. CH50 (total complement) levels were diminished in pigs after the induction of liver failure. CONCLUSIONS: Liver xenotransplantation used in bridging trials in recipients with liver failure might not face the barrier of hyperacute rejection.

Animals↗

Evaluation of duplex ultrasound and captopril renography for detection of renovascular hypertension.

BACKGROUND: Renovascular hypertension is the most common form of curable secondary hypertension and, if untreated, may lead to end-stage kidney disease. Given that renal function and hypertension may improve after renal angioplasty, it is pertinent to identify patients with renal artery stenosis. The aim of the present study was to evaluate both duplex ultrasound and captopril renography for detection of renal artery stenosis among hypertensive patients. METHODS: To avoid selection bias, all patients referred to our center for evaluation of renovascular hypertension were asked to participate in the study. Patients were examined by intra-renal duplex ultrasound (N = 121), measuring pulsatility index and acceleration of the blood flow during early systole. In 98 patients, 99mTc-DTPA captopril renography was performed in conjunction with duplex ultrasound. Renal angiography was performed in all patients regardless of the results of the noninvasive tests. RESULTS: The prevalence of renal artery stenosis was 19%. In the 98 patients examined by both duplex ultrasound and captopril renography, sensitivity and positive predictive values for detection of a renal artery stenosis of 50% degree or more were 84 and 76%, respectively, for duplex ultrasound, whereas captopril renography was associated with a sensitivity and positive predictive value of 68% for both (P = NS). Specificity and negative predictive values were 94 and 96%, respectively, for duplex ultrasound, whereas the corresponding values for captopril renography were 92% for both (P = NS). Specificity and negative predictive values were 94 and 96%, respectively, for duplex ultrasound, whereas the corresponding values for captopril renography were 92% for both (P = NS). CONCLUSIONS: Both duplex ultrasound and captopril renography are associated with high specificity and negative predictive values for detection of renal artery stenosis. Sensitivity and positive predictive values are at least as good for duplex ultrasound compared with captopril renography. Given that duplex ultrasound is easier to perform and more cost effective, we propose that it should be the method of first choice when screening for renal artery stenosis in a hypertensive population.

Angiotensin-Converting Enzyme Inhibitors↗

Elevated urinary albumin excretion is not linked to the angiotensin I-converting enzyme gene polymorphism in clinically healthy subjects.

An elevated urinary albumin excretion (UAE) in non-diabetic subjects without renal or cardiovascular disease has been shown to be predictive of ischaemic heart disease. An insertion (I)/deletion (D) polymorphism in the angiotensin I-converting enzyme (ACE) gene has been identified and the D allele may be associated with cardiovascular disease. The aim of this study was to find a potential linkage between this polymorphism and elevated UAE. For studies of UAE and cardiovascular pathophysiology, a highly selected population sample has been identified comprising all clinically healthy subjects aged 40-65 years with elevated UAE in a dipstick negative urinary sample (n = 27) from The Copenhagen City Heart Study. Neither the ACE genotype distribution (p = 0.12) nor the D and I allele frequencies (p = 0.69) differed significantly between subjects with elevated UAE and a matched normoalbuminuric control group (n = 46). Elevated UAE in clinically healthy subjects is not linked to the ACE gene polymorphism.

Albuminuria↗

Temporal changes in clinic and ambulatory blood pressure during cyclic post-menopausal hormone replacement therapy.

OBJECTIVE: Post-menopausal hormone replacement (HRT) might protect against cardiovascular disease, possibly by arterial vasodilation and reduced blood pressure. Progestogens are needed to avoid endometrial disease but vascular effects are controversial. The objective was to assess temporal changes in blood pressure (BP) by two measurement techniques during a cyclic hormone replacement regimen. DESIGN AND METHODS: Sixteen healthy and normotensive post-menopausal women (age 55 +/- 3 years) were studied in a placebo-controlled, randomized crossover study, and were randomized to 17beta-oestradiol plus cyclic norethisterone acetate (NETA) or placebo in two 12-week periods separated by a 3-month washout Clinic blood pressure was measured sitting by the same observer with a mercury manometer at four visits in each period. Twenty-four hour ambulatory blood pressure was measured at baseline and in the ninth weeks of treatment in both periods. RESULTS: Clinic systolic and diastolic BP were reduced after 10 days of oestradiol (-5.1 and -3.2 mmHg respectively, P < or = 0.05). After 9 weeks of cyclic HRT, prior to progestogen addition, clinic BP returned to baseline. During addition of NETA, diastolic blood pressure was again reduced (-3.6 mmHg, P= 0.037). Mean 24 h ambulatory systolic and diastolic blood pressures were significantly lower than clinic measurements (-15.7 and -5.9 mmHg, P < 0.001) but were unaffected by HRT. CONCLUSIONS: Clinic blood pressure is reduced during a cyclic HRT regimen but the reduction varies with the HRT regimen, which might explain the diversity in previous BP findings during HRT. Norethisterone acetate might possess additive blood pressure-lowering effects in postmenopausal women.

Blood Pressure↗

Disease associated balanced chromosome rearrangements: a resource for large scale genotype-phenotype delineation in man.

Disease associated balanced chromosomal rearrangements (DBCRs), which truncate, delete, or otherwise inactivate specific genes, have been instrumental for positional cloning of many disease genes. A network of cytogenetic laboratories, Mendelian Cytogenetics Network (MCN), has been established to facilitate the identification and mapping of DBCRs. To get an estimate of the potential of this approach, we surveyed all cytogenetic archives in Denmark and southern Sweden, with a population of approximately 6.6 million. The nine laboratories have performed 71 739 postnatal cytogenetic tests. Excluding Robertsonian translocations and chromosome 9 inversions, we identified 216 DBCRs ( approximately 0.3%), including a minimum estimate of 114 de novo reciprocal translocations (0.16%) and eight de novo inversions (0.01%). Altogether, this is six times more frequent than in the general population, suggesting a causal relationship with the traits involved in most of these cases. Of the identified cases, only 25 (12%) have been published, including 12 cases with known syndromes and 13 cases with unspecified mental retardation/congenital malformations. The remaining DBCRs were associated with a plethora of traits including mental retardation, dysmorphic features, major congenital malformations, autism, and male and female infertility. Several of the unpublished DBCRs defined candidate breakpoints for nail-patella, Prader-Willi, and Schmidt syndromes, ataxia, and ulna aplasia. The implication of the survey is apparent when compared with MCN; altogether, the 292 participating laboratories have performed >2.5 million postnatal analyses, with an estimated approximately 7500 DBCRs stored in their archives, of which more than half might be causative mutations. In addition, an estimated 450-500 novel cases should be detected each year. Our data illustrate that DBCRs and MCN are resources for large scale establishment of phenotype-genotype relationships in man.

Chromosome Aberrations↗

Differentiated response of the sympathetic nervous system to angiotensin-converting enzyme inhibition in hypertension.

Hypertension with renal artery stenosis is associated with both an activated renin-angiotensin system and elevated sympathetic activity. Therefore, in this condition it may be favorable to use a therapeutic modality that does not reflexly increase heart rate, renin secretion, and sympathetic nervous activity. The purpose of the present study was to assess overall, renal, and muscle sympathetic activity after short-term administration of an angiotensin-converting enzyme inhibitor (enalaprilat) and a nonspecific vasodilator (dihydralazine) to hypertensive patients with renal artery stenosis. Forty-eight patients undergoing a clinical investigation for renovascular hypertension were included in the study. An isotope dilution technique for assessing norepinephrine spillover was used to estimate overall and bilateral renal sympathetic nerve activity. In 11 patients simultaneous intraneural recordings of efferent muscle sympathetic nerve activity were performed. Thirty minutes after dihydralazine administration, mean arterial pressure fell by 15%, whereas plasma angiotensin II, muscle sympathetic nerve activity, heart rate, and total body norepinephrine spillover increased (P<0.05 for all). In contrast, after enalaprilat administration a fall in arterial pressure similar to that for dihydralazine was followed by decreased angiotensin II levels and unchanged muscle sympathetic nerve activity, heart rate, and total body norepinephrine spillover, whereas renal norepinephrine spillover increased by 44% (P<0.05). Acute blood pressure reduction by an angiotensin-converting enzyme inhibitor provokes a differentiated sympathetic response in patients with hypertension and renal artery stenosis, inasmuch that overall and muscle sympathetic reflex activation are blunted, whereas the reflex renal sympathetic response to blood pressure reduction is preserved.

Angiotensin II↗

Elevated circulating leptin levels in arterial hypertension: relationship to arteriovenous overflow and extraction of leptin.

Leptin, a peptide hormone produced mainly in fat cells, appears to be important for the regulation of metabolism, insulin secretion/sensitivity and body weight. Recently, elevated plasma leptin levels have been reported in patients with arterial hypertension. Because a change in circulating leptin concentrations in such patients could be caused by altered rates of production or disposal, or both, the aim of the present study was to identify regions of leptin overflow into the bloodstream and of leptin extraction. Patients with arterial hypertension (n=12) and normotensive controls (n=20) were studied during catheterization with elective blood sampling from different vascular beds (artery, and renal, hepatic, iliac and cubital veins). Plasma leptin was determined by a radioimmunoassay. Patients with hypertension had significantly elevated levels of circulating leptin (12.8 ng/l, compared with 4.1 ng/l in the controls; P<0.001), and this was also the case when adjusted for body mass index (BMI) [0.435 and 0.167 ng/l per unit BMI (kg/m(2)) respectively; P<0.001]. Circulating leptin was directly related to arterial blood pressure (r=0.38-0.62, P</=0.05-0.005) and immunoreactive insulin (r=0.51, P<0.62), but not to plasma renin activity. A significant renal extraction ratio for leptin was seen in the hypertensive patients, but this was not significantly lower than that in the controls (0.09 compared with 0. 16; P=0.1). The hypertensive patients had a significantly higher hepatic venous/arterial leptin ratio than the controls (1.02 compared with 0.93; P<0.02), and this ratio was correlated directly with the BMI (r=0.38, P=0.05) and immunoreactive insulin (r=0.43, P<0.05). In both hypertensive patients and controls there was a significant spillover of leptin into the iliac vein, but not into the cubital vein. In conclusion, the high concentration of circulating leptin in patients with arterial hypertension is probably caused by increased release of leptin from abdominal (especially mesenteric and omental) and gluteal adipose tissue stores, and renal extraction is slightly reduced. Leptin kinetics in arterial hypertension require further investigation.

Adult↗

[Beta-blockade--a new therapeutic modality in chronic heart insufficiency].

Heart failure due to decreased left ventricular function is a condition with a considerable morbidity and mortality. Until recently beta-blocker treatment has been considered contraindicated in this condition. During the last 20 years a number of investigations have pointed to a possible positive effect of beta-blocker treatment in chronic heart failure and recently several major randomized trials have shown a significantly increased survival during beta-blocker treatment. This review summarizes the background for the use of beta-blocker treatment in chronic heart failure patients.

Adrenergic beta-Antagonists↗

Extrapyramidal side effects during chronic combined dopamine D1 and D2 antagonist treatment in Cebus apella monkeys.

Previous studies in non-human primates have shown that tolerance to dystonia occurs during chronic dopamine D1 (D1) but not D2 antagonism and induction/aggravation of oral dyskinesia (TD) during D2 but not D1 antagonism. We were therefore interested in determining the effects of combined chronic D1 + D2 antagonism on dystonia and dyskinesia. To this intent, 8 male Cebus apella monkeys were treated 10 weeks with gradually increasing doses of D1 antagonist (NNC 112) + a D2 antagonist (raclopride), followed by 2 weeks of treatment with the D2 antagonist alone. Due to previous neuroleptic exposure, 5 monkeys had TD and all were sensitized to dystonia. During the combined antagonist treatment, tolerance to dystonia occurred; the tolerance disappearing upon discontinuation of the D1 antagonist and continuation of the D2 antagonist alone. Parallel to these results, improvement of TD was seen during the combined antagonist treatment with worsening during the D2 antagonist alone. Both the combined antagonists and the D2 antagonist alone resulted in moderate/severe bradykinesia, with no tolerance. These findings indicate that supplementation of traditional D2 antagonism with a D1 antagonist would lessen the risk of dystonia and allow alleviation of preexisting TD, though parkinsonian side effects might still occur. The findings further indicate that separate dopaminergic mechanisms control dystonia/dyskinesia and parkinsonism.

Animals↗

ST-segment deviation during 24-hour ambulatory electrocardiographic monitoring and exercise stress test in healthy male subjects 51 to 75 years of age: the Copenhagen City Heart Study.

BACKGROUND: Although ST-segment deviation has been evaluated and used during many years both on continuous electrocardiographic Holter monitoring and during exercise stress testing, considerable controversy still remains concerning the prevalence and diagnostic significance of fortuitously discovered ST-segment deviation in asymptomatic healthy persons. METHODS AND RESULTS: The occurrence of ST-segment deviation was studied in a population of 63 clinically healthy male subjects 51 to 75 years of age, with the use of 24-hour Holter monitoring and exercise stress testing. The subjects were recruited from the Copenhagen City Heart Study and were without cardiovascular risk factors, chronic diseases, or medication and without cardiovascular events during 5 to 12 years before and 3 to 5 years after admission. The specificity, that is, the probability of displaying a negative test result in healthy subjects without disease, was 1.0 when using as criterion for significant ST-segment deviation a horizontal or descending ST-segment depression of >0.20 mV or ST-segment elevation >/=0.15 mV during Holter monitoring, and acceptable, for example, 0.95, when using as criterion a horizontal or descending ST-segment depression of >/=0.15 mV during Holter monitoring or at the exercise test, respectively. Furthermore, the specificity was 0.95 when a horizontal or downsloping ST-segment depression of 0.1 mV was displayed in both the Holter and exercise electrocardiographic recording system. CONCLUSIONS: Thus in asymptomatic persons, the usual criterion for significant ST-segment depression of 0.1 mV can be applied when occurring in both electrocardiographic recording systems. However, if one test alone is used, the criterion of significant ST-segment depression should be 0.15 mV. Absence of ST-segment deviation during Holter monitoring and exercise stress testing, indicated with a specificity of 1.0 or 0.95 according to choice of criterion, implies that the person is in a healthy state.

Aged↗

Increased cardiovascular mortality in hypertensive patients with renal artery stenosis. Relation to sympathetic activation, renal function and treatment regimens.

BACKGROUND: Previous studies in hypertensive patients with renovascular disease have shown both elevated sympathetic nerve activity and increased cardiovascular mortality. OBJECTIVE: The aim of the present study was to assess long-term survival in hypertensive patients with renal artery stenosis in relation to sympathetic activation, renal function and treatment regimens. SUBJECTS AND METHODS: A total of 169 consecutive patients aged 54 +/- 1 years with hypertension underwent a clinical investigation for renovascular hypertension including renal angiography and measurement of bilateral renal renin secretion. In 107 of these patients, arterial plasma concentrations of noradrenaline were measured. The mean follow-up time was 7.1 +/- 0.3 years and survival data were available in all patients up to May 1997. For comparison, healthy age-matched normotensive controls were examined. RESULTS: Arterial noradrenaline concentrations were threefold elevated in hypertensive patients with renal artery stenosis compared to healthy controls (P < 0.01). During the follow-up time, 44 patients died. Cardiovascular mortality accounted for 75% of all deaths. The risk ratio for overall mortality in hypertensive patients with renal artery stenosis compared to the normal population of Sweden, matched for age, was 3.3 (2.4-4.4), whereas the risk ratio for cardiovascular mortality was 5.7 (3.9-8.0). The arterial plasma concentration of noradrenaline was 3.11 +/- 0.30 pmol/ml in patients who died compared to 3.84 +/- 0.26 pmol/ml in survivors. Reduced renal function and age were independent predictors of death. Survival did not differ between patients undergoing intervention with either renal angioplasty or surgical reconstruction for renal artery stenosis and patients not undergoing intervention. CONCLUSIONS: Although sympathetic nerve activity is elevated in hypertensive patients with renal artery stenosis, our results do not suggest that this adrenergic over-activity is directly linked to the observed high cardiovascular mortality. Mortality in hypertensive patients with renovascular disease remains high whether an interventional treatment is performed or not, possibly due to the concomitant coronary disease.

Angiography↗

Familial predisposition and susceptibility to the effect of other risk factors for myocardial infarction.

STUDY OBJECTIVES: To assess if familial predisposition to myocardial infarction (MI) is an indicator of increased susceptibility to the effect of other established risk factors. The study assessed whether a family history of MI modifies the effect of arterial blood pressure, plasma cholesterol, high and low density lipoprotein cholesterol, % triglycerides, diabetes mellitus, body mass index, height, smoking habits, alcohol intake, physical activity level, and educational level on the incidence of MI. DESIGN: Prospective population based cohort study of cardiovascular risk and risk factors with follow up of MI by record linkage with the Cause of Death Register and The National Hospital Discharge Register until 1994. SETTING: The Copenhagen Centre for Prospective Population Studies, where data from three Danish studies are integrated. PARTICIPANTS: Subjects were 24,664 people aged 20-93, examined between 1976 and 1987. MAIN RESULTS: A total of 1763 new cases of MI occurred during 293,559 person years of observation. All risk factors, including family history of MI reported by 4012 subjects, were, as expected, associated with incidence of MI. With a few inconsistent exceptions we found no significant interactions between family history of MI and cardiovascular risk factors in their effect on MI. CONCLUSIONS: The familial predisposition to MI does not consistently modify the effect of other risk factors on the risk of MI. However, subjects with a family history of MI may still be regarded as an appropriate target group for screening for cardiovascular risk and intervention against other risk factors.

Adult↗

Mutations in the lipoprotein lipase gene associated with ischemic heart disease in men. The Copenhagen city heart study.

The aim of this study was to test the hypothesis that the Asp9Asn substitution and the T(-93)-->G mutation in the promoter of the lipoprotein lipase gene affect plasma lipid levels and thereby the risk of ischemic heart disease (IHD). We genotyped 9033 men and women from a general population sample and 940 patients with IHD. The frequency of both the G allele and the Asn9 allele in the general population sample was approximately 0.015 for both men and women. These 2 mutations appeared together in 95% of carriers. The average triglyceride-raising effect associated with double heterozygosity for the T(-93)-->G mutation and the Asp9Asn substitution was 0.28 mmol/L (P=0.004) and 0.16 mmol/L (P=0.10) in men and women, respectively. On logistic regression analysis allowing for age, the risk of IHD for double heterozygous men and women was increased 90% (95% confidence interval [CI], 20% to 200%) and 30% (95% CI, -40% to 170%), respectively, compared with noncarriers. When, in addition, other conventional cardiovascular risk factors were allowed for, the risk of IHD for double heterozygous men and women was increased 70% (95% CI, 0% to 190%) and 20% (95% CI, -50% to 180%), respectively. Of the overall risk of IHD in men in the general population, the fraction attributable to double heterozygosity was 3%, similar to the 5% attributable to diabetes mellitus. These results demonstrate that the Asp9Asn substitution is in linkage disequilibrium with the T(-93)-->G mutation and that the double-heterozygous carrier status is associated with elevated plasma triglycerides and an increased risk of IHD in men.

Adult↗

Clinical and economic effectiveness of an inpatient anticoagulation service.

We conducted a prospective cohort study to evaluate clinical and economic end points achieved by a pharmacist-managed anticoagulation service compared with usual care (50 patients/group). The primary therapeutic end point was the time between starting heparin therapy and surpassing the activated partial thromboplastin time therapeutic threshold. The primary economic end point was the direct variable cost of hospitalization from admission to discharge. No significant differences between groups were noted for the primary therapeutic end point. Total hospital costs were significantly lower for patients receiving pharmacist-managed care than for those receiving usual care ($1594 and $2014, respectively, 1997 dollars, p=0.04). Earlier start of warfarin (p=0.05) and shorter hospital stay (5 and 7 days, p=0.05) were associated with the pharmacist-managed group.

Anticoagulants↗

Endothelial haemostatic factors are associated with progression of urinary albumin excretion in clinically healthy subjects: a 4-year prospective study.

A slightly elevated urinary albumin excretion rate (UAER), above 5-10 microgram/min, is a predictor of atherosclerotic cardiovascular disease. Endothelial dysfunction is an important early feature of atherosclerosis. The plasma concentration of von Willebrand factor (vWF), a potential marker of endothelial dysfunction, predicts a subsequent increase of UAER in patients with diabetes. The aim of this study is to test the hypothesis that high concentrations of vWF as well as other haemostatic factors predict progression of UAER in clinically healthy subjects. UAER was measured together with selected markers of haemostatic function-vWF, tissue plasminogen activator (tPA), plasminogen activator inhibitor, factor VII and fibrinogen-in healthy volunteers aged 40-65 years. After a mean follow-up of 4.1 years, 64 of 74 agreed to a re-examination including re-measurement of UAER. Baseline vWF and tPA were both positively correlated to the change in UAER during follow-up (r=0.26, P=0.04 and r=0.40, P=0.001 respectively). The mean UAER increased significantly by 7.6 microgram/min and 7.5 microgram/min respectively in subjects with vWF and tPA above the medians at baseline (P=0.01 and P=0.003 respectively), whereas no changes in UAER were seen in subjects with vWF and tPA below the medians. Subjects with high tPA were also characterized by an excess of other cardiovascular risk factors at baseline. No significant differences in these risk factors were present between subjects with high or low vWF. High plasma concentrations of vWF and tPA are associated with progression of UAER in clinically healthy subjects. Both vWF and tPA are secreted by endothelial cells and the results suggest that endothelial dysfunction leads to progression of UAER.

Adult↗

A 15-year follow-up study of ventilatory function in adults with asthma.

BACKGROUND: Although the prevalence of asthma and morbidity related to asthma are increasing, little is known about the natural history of lung function in adults with this disease. METHODS: We used data from a longitudinal epidemiologic study of the general population in a Danish city, the Copenhagen City Heart Study, to analyze changes over time in the forced expiratory volume in one second (FEV1) in adults with self-reported asthma and adults without asthma. The study was conducted between 1976 and 1994; for each patient, three measurements of lung function were obtained over a 15-year period. The final data set consisted of measurements from 17,506 subjects (8136 men and 9370 women), of whom 1095 had asthma. RESULTS: Among subjects who participated in all three evaluations, the unadjusted decline in FEV1 among subjects with asthma was 38 ml per year, as compared with 22 ml per year in those without asthma. The decline in FEV1 normalized for height (FEV1 divided by the square of the height in meters) was greater among the subjects with asthma than among those without the disease (P<0.001). Among both men and women, and among both smokers and nonsmokers, subjects with asthma had greater declines in FEV1 over time than those without asthma (P<0.001). At the age of 60 years, a 175-cm-tall nonsmoking man without asthma had an average FEV1 of 3.05 liters, as compared with 1.99 liters for a man of similar age and height who smoked and had asthma. CONCLUSIONS: In a sample of the general population, people who identified themselves as having asthma had substantially greater declines in FEV1 over time than those who did not.

Adult↗

Population based cohort study of the association between alcohol intake and cancer of the upper digestive tract.

OBJECTIVE: To examine the relation between different types of alcoholic drinks and upper digestive tract cancers (oropharyngeal and oesophageal). DESIGN: Population based study with baseline assessment of intake of beer, wine, and spirits, smoking habits, educational level, and 2-19 years' follow up on risk of upper digestive tract cancer. SETTING: Denmark. SUBJECTS: 15 117 men and 13 063 women aged 20 to 98 years. MAIN OUTCOME MEASURE: Number and time of identification of incident upper digestive tract cancer during follow up. RESULTS: During a mean follow up of 13.5 years, 156 subjects developed upper digestive tract cancer. Compared with non-drinkers (drinkers of <1 drink/week), subjects who drank 7-21 beers or spirits a week but no wine were at a risk of 3.0 (95% confidence interval 1.5 to 6.1), whereas those who had the same total alcohol intake but with wine as >=30% of their intake had a risk of 0.5 (0.2 to 1.4). Drinkers of >21 beers and spirits but no wine had a relative risk of 5.2 (2.7 to 10.2) compared with non-drinkers, whereas those who drank the same amount, but included wine in their alcohol intake, had a relative risk of 1.7 (0.6 to 4. 4). CONCLUSION: A moderate intake of wine probably does not increase the risk of upper digestive tract cancer, whereas a moderate intake of beer or spirits increases the risk considerably.

Adult↗