| 1. |
- Rota, M, et al.
(författare)
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Erratum
- 2018
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Ingår i: International journal of cancer. - : Wiley. - 1097-0215 .- 0020-7136. ; 143:8, s. E10-E10
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Tidskriftsartikel (refereegranskat)
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| 2. |
- Azodi, OS, et al.
(författare)
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Effect of type of alcoholic beverage in causing acute pancreatitis
- 2011
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Ingår i: The British journal of surgery. - : Oxford University Press (OUP). - 1365-2168 .- 0007-1323. ; 98:11, s. 1609-1616
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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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| 3. |
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| 4. |
- Burgaz, A., et al.
(författare)
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Confirmed hypertension and plasma 25(OH)D concentrations amongst elderly men
- 2011
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Ingår i: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 269:2, s. 211-218
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Tidskriftsartikel (refereegranskat)abstract
- Objectives. The results of experimental studies suggest that vitamin D deficiency activates the renin-angiotensin system and predisposes to hypertension. Results of previous epidemiological studies investigating the association between 25-hydroxyvitamin D [25(OH)D] status and hypertension have not been consistent, perhaps because of their sole reliance on office blood pressure (BP) measurements leading to some misclassification of hypertension status. No previous studies have examined the association between 25(OH)D status and confirmed hypertension assessed with both office and 24-h BP measurements. Design. In this cross-sectional study, we investigated 833 Caucasian men, aged 71 +/- 0.6 years, to determine the association between plasma 25(OH)D concentrations, measured with high-pressure liquid chromatography mass spectrometry, and the prevalence of hypertension. We used both supine office and 24-h BP measurements for classifying participants as normotensive or confirmed hypertensive; participants with inconsistent classifications were excluded. Results. In a multivariable adjusted logistic regression model, men with 25(OH)D concentrations < 37.5 nmol L-1 had a 3-fold higher prevalence of confirmed hypertension compared to those with >= 37.5 nmol L-1 25(OH)D (odds ratio = 3.3, 95% CI: 1.0-11.0). Conclusions. Our results show that low plasma 25(OH)D concentration is associated with a higher prevalence of confirmed hypertension.
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| 5. |
- Discacciati, A, et al.
(författare)
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Body mass index and incidence of localized and advanced prostate cancer--a dose-response meta-analysis of prospective studies
- 2012
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Ingår i: Annals of Oncology. - : Elsevier BV. - 0923-7534 .- 1569-8041. ; 23:7, s. 1665-71
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The relationship between obesity and risk of prostate cancer (PCa) is unclear; however, etiologic heterogeneity by subtype of PCa (localized, advanced) related to obesity was suggested. Therefore, we conducted a dose-response meta-analysis of prospective studies to assess the association between body mass index (BMI) and risk of localized and advanced PCa.MATERIALS AND METHODS: Relevant prospective studies were identified by a search of Medline and Embase databases to 03 October 2011. Twelve studies on localized PCa (1,033,009 men, 19,130 cases) and 13 on advanced PCa (1,080,790 men, 7067 cases) were identified. We carried out a dose-response meta-analysis using random-effects model.RESULTS: For localized PCa, we observed an inverse linear relationship with BMI [Ptrend<0.001, relative risk (RR): 0.94 (95% confidence interval, 95% CI, 0.91-0.97) for every 5 kg/m2 increase]; there was no evidence of heterogeneity (Pheterogeneity=0.27). For advanced PCa, we observed a linear direct relationship with BMI (Ptrend=0.001, RR: 1.09 (95% CI 1.02-1.16) for every 5 kg/m2 increase); there was weak evidence of heterogeneity (Pheterogeneity=0.08). Omitting one study that contributed substantially to the heterogeneity yielded a pooled RR of 1.07 (95% CI 1.01-1.13) for every 5 kg/m2 increase (Pheterogeneity=0.26).CONCLUSIONS: The quantitative summary of the accumulated evidence indicates that obesity may have a dual effect on PCa-a decreased risk for localized PCa and an increased risk for advanced PCa.
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| 6. |
- Discacciati, A., et al.
(författare)
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Body mass index in early and middle-late adulthood and risk of localised, advanced and fatal prostate cancer : a population-based prospective study
- 2011
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Ingår i: British Journal of Cancer. - : NATURE PUBLISHING GROUP. - 0007-0920 .- 1532-1827. ; 105:7, s. 1061-1068
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The relationships between body mass index (BMI) during early and middle-late adulthood and incidence of prostate cancer (PCa) by subtype of the disease (localised, advanced) and fatal PCa is unclear. METHODS: A population-based cohort of 36 959 Swedish men aged 45-79 years was followed up from January 1998 through December 2008 for incidence of PCa (1530 localised and 554 advanced cases were diagnosed) and through December 2007 for PCa mortality (225 fatal cases). RESULTS: From a competing-risks analysis, incidence of localised PCa was observed to be inversely associated with BMI at baseline (middle-late adulthood; rate ratio (RR) for 35 kgm(-2) when compared with 22 kgm(-2) was 0.69 (95% CI 0.52 - 0.92)), but not at age 30. For fatal PCa, BMI at baseline was associated with a nonstatistically significant increased risk (RR for every five-unit increase: 1.12 (0.88 - 1.43)) and BMI at age 30 with a decreased risk (RR for every five-unit increase: 0.72 (0.51 - 1.01)). CONCLUSION: Our results indicate an inverse association between obesity during middle-late, but not early adulthood, and localised PCa. They also suggest a dual association between BMI and fatal PCa - a decreased risk among men who were obese during early adulthood and an increased risk among those who were obese during middle-late adulthood. British Journal of Cancer (2011) 105, 1061-1068. doi:10.1038/bjc.2011.319 www.bjcancer.com Published online 16 August 2011 (C) 2011 Cancer Research UK
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| 7. |
- Discacciati, A., et al.
(författare)
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Coffee consumption and risk of localized, advanced and fatal prostate cancer : a population-based prospective study
- 2013
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Ingår i: Annals of Oncology. - : Elsevier BV. - 0923-7534 .- 1569-8041. ; 24:7, s. 1912-1918
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Tidskriftsartikel (refereegranskat)abstract
- Background: The epidemiological evidence on possible relationships between coffee consumption and prostate cancer (PCa) risk by subtype of the disease (localized, advanced) and fatal PCa risk is limited.Materials and methods: A population-based cohort of 44 613 Swedish men aged 45-79 years was followed up from January 1998 through December 2010 for incidence of localized (n = 2368), advanced (n = 918) and fatal (n = 515) PCa. We assessed the associations between coffee consumption and localized, advanced and fatal PCa risk using competing-risk regressions. We examined possible effect modification by body mass index (BMI).Results: For localized PCa, each one cup increase in daily coffee consumption was associated with a 3% reduced risk [sub-hazard ratio (SHR) = 0.97, 95% confidence interval (CI) = 0.95-0.99]. For advanced and fatal PCa, we found a non-significant inverse association; each one cup increase was associated with a 2% reduced risk of advanced [SHR (95% CI) = 0.98 (0.95-1.02)] and fatal PCa [SHR (95% CI) = 0.98 (0.93-1.03)]. We observed evidence of effect modification by BMI for localized PCa (P-interaction = 0.03); the inverse association was stronger among overweight and obese men (BMI >= 25 kg/m(2)) compared with normal-weight men (BMI < 25 kg/m(2)).Conclusions: We observed a clear inverse association between coffee consumption and risk of localized PCa, especially among overweight and obese men.
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| 8. |
- Discacciati, A., et al.
(författare)
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Coffee consumption and risk of nonaggressive, aggressive and fatal prostate cancer-a dose-response meta-analysis
- 2014
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Ingår i: Annals of Oncology. - : OXFORD UNIV PRESS. - 0923-7534 .- 1569-8041. ; 25:3, s. 584-591
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Forskningsöversikt (refereegranskat)abstract
- Existing epidemiological evidence is controversial regarding the possible associations between coffee consumption and risk of prostate cancer (PCa) by aggressiveness of the disease. We conducted a random-effects dose-response meta-analysis to assess the relationships between coffee consumption and nonaggressive, aggressive and fatal PCa risk. Studies were identified by a search of Medline and Embase databases to 15 July 2013. We carried out separate analyses by grade (Gleason score: low-grade, high-grade) and stage (TNM staging system: localized, advanced) of the tumors. Nonaggressive tumors were defined as low-grade or localized, while aggressive tumors were defined as high-grade or advanced. Eight studies (three case-control and five cohort) were included in this meta-analysis. Gleason 7 tumors were classified as high-grade in one study, while in another study, Gleason 7(4 + 3) tumors were classified as high-grade and Gleason 7(3 + 4) as low-grade. In the remaining four studies, Gleason 7 tumors were excluded from the analyses or analyzed separately. The pooled relative risk (RR) for a consumption increment of 3 cups/day was 0.97 [95% confidence interval (CI) 0.92-1.03] for low-grade PCa (n = 6), 0.97 (95% CI 0.94-0.99) for localized PCa (n = 6), 0.89 (95% CI 0.78-1.00) for high-grade PCa (n = 6), 0.95 (95% CI 0.85-1.06) for advanced PCa (n = 6) and 0.89 (95% CI 0.82-0.97) for fatal PCa (n = 4). No evidence of publication bias was observed. Heterogeneity was absent or marginal (I-2 range = 0-26%), with the only exception of the analysis on advanced PCa, where moderate heterogeneity was observed (I-2 = 60%). When restricting the analyses only to those studies that defined high-grade tumors as Gleason 8-10, the inverse association became slightly stronger [RR: 0.84 (95% CI 0.72-0.98); n = 4]. Results from this dose-response meta-analysis suggest that coffee consumption may be inversely associated with the risk of fatal PCa. No clear evidence of an association with PCa incidence was observed.
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| 9. |
- Sadr-Azodi, O., et al.
(författare)
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Abdominal and Total Adiposity and The Risk of Acute Pancreatitis : A Population-Based Prospective Cohort Study
- 2013
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Ingår i: American Journal of Gastroenterology. - : NATURE PUBLISHING GROUP. - 0002-9270 .- 1572-0241. ; 108:1, s. 133-139
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: Previous research has indicated that obesity may be linked to the severity of acute pancreatitis. However, the association between abdominal and total adiposity as risk factors in the development of acute pancreatitis in a general population has not been studied. METHODS: A follow-up study was conducted, using the Swedish Mammography Cohort and the Cohort of Swedish Men, to examine the association between waist circumference and body mass index (BMI) and the risk of first-time acute pancreatitis. Severe acute pancreatitis was defined as hospital stay of >14 days, in-hospital death, or mortality within 30 days of discharge. Cox proportional hazards models were used to estimate rate ratios (RRs) with 95% confidence intervals (CIs), adjusted for confounders. RESULTS: In total, 68,158 individuals, aged 46-84 years, were studied for a median of 12 years. During this time, 424 persons developed first-time acute pancreatitis. The risk of acute pancreatitis among those with a waist circumference of >105 cm was twofold increased (RR = 2.37; 95 % CI: 1.50-3.74) compared with individuals with a waist circumference of 75.1-85.0 cm, when adjusted for confounders. This association was seen in patients with non-gallstone-related and gallstone-related acute pancreatitis. The results remained unchanged when stratifying the analyses with regards to sex or the severity of acute pancreatitis. There was no association between BMI and the risk of acute pancreatitis. CONCLUSIONS: Abdominal adiposity, but not total adiposity, is an independent risk factor for the development of acute pancreatitis. Am J Gastroenterol 2013; 108:133-139; doi:10.1038/ajg.2012.381; published online 13 November 2012
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| 10. |
- Sadr-Azodi, O., et al.
(författare)
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Cigarette smoking, smoking cessation and acute pancreatitis : a prospective population-based study
- 2012
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Ingår i: Gut. - : BMJ PUBLISHING GROUP. - 0017-5749 .- 1468-3288. ; 61:2, s. 262-267
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Tidskriftsartikel (refereegranskat)abstract
- Background Several studies have shown that smoking increases the risk of chronic pancreatitis. However, the impact of smoking on the development of acute pancreatitis has not been fully studied. Objective To clarify the association between cigarette smoking, smoking cessation and the risk of acute pancreatitis. Design A follow-up study was conducted of 84 667 Swedish women and men, aged 46-84, during 12 years to study the association between smoking status, smoking intensity and duration, duration of smoking cessation and the risk of acute pancreatitis. Only those with the first event of the disease and no previous history of acute pancreatitis were included. Cox proportional hazards models were used to estimate rate ratios (RRs) with 95% CI for different smoking-related variables, adjusted for age, gender, body mass index, diabetes, educational level and alcohol consumption. Results In total, 307 cases with non-gallstone-related and 234 cases with gallstone-related acute pancreatitis were identified. The risk of non-gallstone-related acute pancreatitis was more than double (RR 2.29; 95% CI 1.63 to 3.22, p<0.01) among current smokers with >= 20 pack-years of smoking as compared with never-smokers. The corresponding risk among individuals with >= 400 g monthly consumption of alcohol was increased more than fourfold (RR=4.12; 95% CI 1.98 to 8.60, p<0.01). The duration of smoking rather than smoking intensity increased the risk of non-gallstone-related acute pancreatitis. After two decades of smoking cessation the risk of non-gallstone-related acute pancreatitis was reduced to a level comparable to that of non-smokers. There was no association between smoking and gallstone-related acute pancreatitis. Conclusion Smoking is an important risk factor for non-gallstone-related acute pancreatitis. Early smoking cessation should be recommended as a part of the clinical management of patients with acute pancreatitis.
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