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- 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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- 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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- 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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- Threadgold, J, et al.
(författare)
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The N34S mutation of SPINK1 (PSTI) is associated with a familial pattern of idiopathic chronic pancreatitis but does not cause the disease
- 2002
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Ingår i: Gut. - : BMJ. - 1468-3288 .- 0017-5749. ; 50:5, s. 675-681
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Tidskriftsartikel (refereegranskat)abstract
- Background: Mutations in the PRSS1 gene explain most occurrences of hereditary pancreatitis (HP) but many HP families have no PRSS1 mutation. Recently, an association between the mutation N34S in the pancreatic secretary trypsin inhibitor (SPINK1 or PSTI) gene and idiopathic chronic pancreatitis (ICP) was reported. It is unclear whether the N34S mutation is a cause of pancreatitis per se, whether it modifies the disease, or whether it is a marker of the disease. Patients and methods: A total of 327 individuals from 217 families affected by pancreatitis were tested: 152 from families with HP, 108 from families with ICP, and 67 with alcohol related CP (ACP). Seven patients with ICP had a family history of pancreatitis but no evidence of autosomal dominant disease (f-ICP) compared with 87 patients with true ICP (t-ICP). Two hundred controls were also tested for the N34S mutation. The findings were related to clinical outcome. Results: The N34S mutation was carried by five controls (2.5%; allele frequency 1.25%), 11/87 (13%) t-ICP patients (p=0.0013 v controls), and 6/7 (86%) affected (p<0.0001 v controls) and 1/9 (11%) unaffected f-ICP cases. N34S was found in 4/108 affected HP patients (p=0.724 v controls), in, 3/27 (11%) with wild-type and in 1/81 (1%) with mutant PRSS1, and 4/67 ACP patients (all p>0.05 v controls). The presence of the N34S mutation was not associated with early disease onset or disease severity. Conclusions: The prevalence of the N34S mutation was increased in patients with ICP and was greatest in f-ICP cases. Segregation of the N34S mutation in families with pancreatitis is unexplained and points to a complex association between N34S and another putative pancreatitis related gene.
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