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1.
  • Azodi, OS, et al. (författare)
  • Effect of type of alcoholic beverage in causing acute pancreatitis
  • 2011
  • Ingår i: The British journal of surgery. - : Oxford University Press (OUP). - 1365-2168 .- 0007-1323. ; 98:11, s. 1609-1616
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundThe effect of different alcoholic beverages and drinking behaviour on the risk of acute pancreatitis has rarely been studied. The aim of this study was to investigate the effect of different types of alcoholic beverage in causing acute pancreatitis.MethodsA follow-up study was conducted, using the Swedish Mammography Cohort and Cohort of Swedish Men, to study the association between consumption of spirits, wine and beer and the risk of acute pancreatitis. No patient with a history of chronic pancreatitis was included and those who developed pancreatic cancer during follow-up were excluded. Multivariable Cox proportional hazards models were used to estimate rate ratios.ResultsIn total, 84 601 individuals, aged 46-84 years, were followed for a median of 10 years, of whom 513 developed acute pancreatitis. There was a dose–response association between the amount of spirits consumed on a single occasion and the risk of acute pancreatitis. After multivariable adjustments, there was a 52 per cent (risk ratio 1·52, 95 per cent confidence interval 1·12 to 2·06) increased risk of acute pancreatitis for every increment of five standard drinks of spirits consumed on a single occasion. The association weakened slightly when those with gallstone-related pancreatitis were excluded. There was no association between consumption of wine or beer, frequency of alcoholic beverage consumption including spirits, or average total monthly consumption of alcohol (ethanol) and the risk of acute pancreatitis.ConclusionThe risk of acute pancreatitis was associated with the amount of spirits consumed on a single occasion but not with wine or beer consumption.
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2.
  • Hjern, F., et al. (författare)
  • Cohort study of corticosteroid use and risk of hospital admission for diverticular disease
  • 2015
  • Ingår i: British Journal of Surgery. - : WILEY-BLACKWELL. - 0007-1323 .- 1365-2168. ; 102:1, s. 119-124
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Medication has been suggested as a potential risk factor for diverticular disease. The objective of this study was to investigate the association between the intake of corticosteroids, indometacin or aspirin and diverticular disease. Method: This was a prospective population-based cohort study of middle-aged women in the Swedish Mammography Cohort. Use of corticosteroids (oral or inhaled), indometacin or aspirin in 1997 was determined from questionnaires. Cases of diverticular disease were identified from the Swedish national registers until the end of 2010. The relative risk (RR) of diverticular disease requiring hospital admission according to the use of medication was estimated using Cox proportional hazards models, adjusted for age, body mass index, physical activity, fibre intake, diabetes, hypertension, alcohol, smoking and education. Results: A total of 36 586 middle-aged women in the Swedish Mammography Cohort were included, of whom 674 (18 per cent) were hospitalized with diverticular disease at least once. Some 72 per cent of women reported intake of oral corticosteroids and 85 per cent use of inhaled corticosteroids. In multivariable analysis, women who reported oral corticosteroid intake had a 37 per cent (RR 137, 95 per cent c.i. 106 to 178; P=0012) increased risk of diverticular disease compared with those who reported no intake at all. Use of inhaled corticosteroids was associated with an even more pronounced increase in risk of 71 per cent (RR 171, 136 to 214; P<0001). There was a significant dose-response relationship, with the risk increasing with longer duration of inhaled corticosteroids (P for trend<0001). Use of indometacin (25 per cent of women) or aspirin (442 per cent) did not influence the risk. Conclusion: There was a significant relationship between corticosteroids (especially inhaled) and diverticular disease requiring hospital admission.
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3.
  • Hjern, F., et al. (författare)
  • Smoking and the risk of diverticular disease in women
  • 2011
  • Ingår i: British Journal of Surgery. - : WILEY-BLACKWELL. - 0007-1323 .- 1365-2168. ; 98:7, s. 997-1002
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The relationship between smoking and the risk of diverticular disease is unclear. An observational cohort study was undertaken to investigate the association between smoking and diverticular disease. Methods: Women in the Swedish Mammography Cohort born between 1914 and 1948 were followed from 1997 to 2008. Information on smoking and other lifestyle factors was collected through questionnaires. Patients with symptomatic diverticular disease were identified from Swedish national registers. Relative risks (RRs) of symptomatic diverticular disease (resulting in hospital admission or death) according to smoking status were estimated using Cox proportional hazards models. Results: Of 35 809 women included in the study, 561 (1.6 per cent) had symptomatic diverticular disease. In multivariable analysis, current smokers had an increased risk of symptomatic diverticular disease compared with non-smokers after adjustment for age, intake of dietary fibre, diabetes, hypertension, use of acetylsalicylic acid, non-steroidal anti-inflammatory drugs or steroid medication, alcohol consumption, body mass index, physical activity and level of education (RR 1.23, 95 per cent confidence interval 0.99 to 1.52). Past smokers also had an increased risk (RR 1.26, 1.02 to 1.56). Smokers had a higher risk of developing a diverticular perforation/abscess than non-smokers (RR 1.89, 1.15 to 3.10). Conclusion: Smoking is associated with symptomatic diverticular disease.
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5.
  • Stackelberg, O, et al. (författare)
  • Obesity and abdominal aortic aneurysm
  • 2013
  • Ingår i: British Journal of Surgery. - : Oxford University Press (OUP). - 0007-1323 .- 1365-2168. ; 100:3, s. 360-366
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The relationship between obesity and abdominal aortic aneurysm (AAA) is unclear. An observational cohort study was undertaken to examine the associations between waist circumference as a measure of abdominal adiposity, and between body mass index (BMI) as a measure of total adiposity, and risk of AAA. METHODS: Data were used from the population-based Swedish Mammography Cohort and the Cohort of Swedish Men, involving 63 655 men and women, aged 46-84 years. Between 1998 and 2009, 597 patients with incident AAA defined by relevant clinical events were identified by linkage to the Swedish Inpatient Register and the Swedish Vascular Registry. Cox proportional hazards models were used to estimate relative risks (RRs) with 95 per cent confidence intervals. RESULTS: In multivariable analysis, individuals with an increased waist circumference had a 30 per cent higher risk of AAA (RR 1·30, 95 per cent confidence interval 1·05 to 1·60) compared with those with a normal waist circumference. The risk of AAA increased by 15 per cent (RR 1·15, 1·05 to 1·26) per 5-cm increment of waist circumference up to the level 100 cm for men and 88 cm for women. There was no association between BMI and risk of AAA. CONCLUSION: Abdominal, but not total, adiposity was associated with an increased risk of incident AAA. A threshold was observed at a waist circumference of 100 cm for men and 88 cm for women.
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6.
  • Stackelberg, O., et al. (författare)
  • Sex differences in the association between smoking and abdominal aortic aneurysm
  • 2014
  • Ingår i: British Journal of Surgery. - : Oxford University Press (OUP). - 0007-1323 .- 1365-2168. ; 101:10, s. 1230-1237
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: It is unclear whether recommendations about ultrasound screening programmes for abdominal aortic aneurysm (AAA) among men should be extended to include women who smoke. The aim was to examine sex-specific dose-response associations between AAA risk and smoking status, pack-years smoked and time since smoking cessation. Methods: Women in the Swedish Mammography Cohort and men in the Cohort of Swedish Men were followed up from 1998 to 2011. AAA was identified through linkage of the cohorts to the Swedish Inpatient Register and the Swedish National Register for Vascular Surgery (Swedvasc), and not through general ultrasound screening. Associations were estimated with Cox proportional hazards models. Results: The cohorts included 35 550 women and 42 596 men, aged 46-84 years. During follow-up, AAA was identified in 199 women and 958 men. The incidence of AAA per 100 000 person-years was 76 among men who never smoked and 136 among women who currently smoke. Regarding AAA risk, women were more sensitive to current smoking (P-interaction = 0.002). Compared with never smokers, the hazard ratio (HR) for AAA in current smokers with more than 20 pack-years was 10.97 (95 per cent confidence interval 7.41 to 16.26) among women and 6 55 (5 36 to 7 99) among men. Following smoking cessation, women had a more rapid decline in excess risk (P-interaction < 0 001). The risk was halved after 11 years (HR 0.51, 0.32 to 0.81) among women and after 23 years (HR 0.50, 0.42 to 0.60) among men. Conclusion: There were sex differences in the associations between smoking status and AAA risk. These data support further investigation of targeted AAA screening among women who smoke.
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