A total of 6161 cases with a first episode of acute pancreatitis and 61,637 controls were included in the final analyses. Cases were all patients diagnosed as having a first episode of acute pancreatitis during the study period, defined by the diagnosis code K85 in the International Statistical Classification of Diseases, 10th Revision (ICD-10). Controls were randomly selected from the source population at risk of developing acute pancreatitis. For each case, 10 controls, matched for age, sex, and calendar period, were randomly selected from the general population. Oral glucocorticoid use was assessed from the Swedish Prescribed Drug Register. Current, recent, and former users were defined as patients who collected their glucocorticoid prescription within 30, 31 to 180, and after 180 days before the index date, respectively.
Unconditional logistic regression was performed to calculate the odds ratios (ORs) with 95% confidence intervals for the association between oral glucocorticoid use and acute pancreatitis. Multivariable adjustment was made for potential confounders including, among others, alcohol abuse, diabetes, and concomitant drug use.
The study included 6161 cases of acute pancreatitis and 61,637 controls. The risk of acute pancreatitis was increased among current users of oral glucocorticoids compared with nonusers (OR, 1.53; 95% CI, 1.27-1.84). This risk was highest 4 to 14 days after drug dispensation (OR, 1.73; 95% CI, 1.31-2.28) and attenuated thereafter. There was no association between oral glucocorticoid use and acute pancreatitis immediately after drug dispensation. There was no increased risk of acute pancreatitis among recent or former users of glucocorticoids compared with nonusers.
Current oral glucocorticoid use is associated with an increased risk of acute pancreatitis.
Little is known about how discontinuation of low-dose aspirin therapy after peptic ulcer bleeding affects patient mortality or acute cardiovascular events.
We performed a retrospective cohort study by using data from patients who received low-dose aspirin therapy and were treated for bleeding peptic ulcers between 2007 and 2010 at Karolinska University Hospital, Stockholm, Sweden. We used a multivariable Cox regression model to adjust for potential confounders and analyze associations between discontinuation of low-dose aspirin therapy at discharge, death, and acute cardiovascular events.
Of the 118 patients who received low-dose aspirin therapy, the therapy was discontinued for 47 (40%). During a median follow-up period of 2 years after hospital discharge, 44 of the 118 patients (37%) either died or developed acute cardiovascular events. Adjusting for confounders, patients with cardiovascular comorbidities who discontinued low-dose aspirin therapy had an almost 7-fold increase in risk for death or acute cardiovascular events (hazard ratio, 6.9; 95% confidence interval, 1.4-34.8) compared with patients who continued this therapy during the first 6 months of the follow-up period. A corresponding association was not observed among patients without cardiovascular comorbidities when the study began.
In patients with cardiovascular disease, discontinuation of low-dose aspirin therapy after peptic ulcer bleeding increases risk of death and acute cardiovascular events almost 7-fold.
To assess the role of exogenous estrogen in the etiology of biliary tract cancer, a nationwide population-based cohort study in Sweden was performed.
The study included all men in Sweden with prostate cancer diagnosed in 1961-2008. Due to treatment standards, patients diagnosed in 1961-1980 were considered more exposed to estrogen, while those diagnosed in 1981-2008 were regarded less exposed. Standardized incidence ratios (SIRs) with 95% confidence intervals (CIs) were calculated to estimate the risk of biliary tract cancer in cohort members compared to the corresponding Swedish male population.
After 849 307 person-years of follow-up in 203 131 prostate cancer patients, there were 41 incident gallbladder cancers and 36 cancers of the extra-hepatic bile ducts. In overall, there were no apparent differences in the risk of gallbladder cancer or bile duct cancer between patients diagnosed in 1961-1980 and patients diagnosed in 1981-2008. However, in patients diagnosed in 1961-1980, there was a statistically non-significant increased risk of gallbladder cancer (SIR 1.34; 95% CI 0.71-2.29) and extra-hepatic bile duct cancer (SIR 1.20; 95% CI 0.55-2.28)?>?5 years of follow-up after the prostate cancer diagnosis. No such association was found for patients diagnosed in 1981-2008. Sensitivity analyses excluding prostate cancer patients exposed to potential confounding factors did not change the SIRs.
Long exposure to high doses of exogenous estrogen might increase the risk of biliary tract cancer. However, any potential excess risk of bile duct cancer resulted by prolonged exposure to high doses of exogenous estrogen seems to be small.
Epidemiologic data on the role of diet in acute pancreatitis are sparse.
We examined the association of total fish consumption, as well as of consumption of fatty fish and lean fish separately, with risk of non-gallstone-related acute pancreatitis.
We used data from 2 prospective cohorts, the Cohort of Swedish Men and the Swedish Mammography Cohort, that included 39,267 men and 32,191 women who were aged 45-84 y at the start of a 13-y follow-up period (1998-2010). Fish consumption was assessed by using a food-frequency questionnaire at baseline, and cases of incident non-gallstone-related acute pancreatitis were identified by linkage to the Swedish National Patient Register. HRs were estimated by using Cox proportional hazard models.
During a total follow-up of 860,176 person-years, 320 cases (209 cases in men and 111 cases in women) of incident non-gallstone-related acute pancreatitis were identified. We observed that total fish consumption =2.0-3.0 servings/wk was associated with a significantly decreased risk of the disease (P-nonlinearity = 0.017). In comparison with 0.9 servings/wk, multivariable-adjusted HRs were 0.86 (95% CI: 0.76, 0.96), 0.77 (95% CI: 0.62, 0.96), and 0.85 (95% CI: 0.65, 1.10) for 1.4, 2.4, and 3.5 servings/wk, respectively. In the analysis of fatty fish and lean fish, we observed that the consumption of each subtype had a similarly shaped association with risk of non-gallstone-related acute pancreatitis as that observed for total fish consumption, although neither was significant. Multivariable-adjusted HRs were 0.83 for fatty fish (95% CI: 0.65, 1.04) and 0.87 for lean fish (95% CI: 0.69, 1.11) when 0.6-2.0 servings/wk was compared with =0.5 servings/wk.
Our data suggest that the consumption of total fish (fatty fish and lean fish combined) may be associated with decreased risk of non-gallstone-related acute pancreatitis.
Obesity and type 2 diabetes--diseases linked to glucose intolerance and insulin resistance--have been positively associated with the risk of acute pancreatitis. However, it is unclear whether consumption of foods that increase postprandial glycemia and insulinemia have similar associations. We examined the association between dietary glycemic load and risk of non-gallstone-related acute pancreatitis.
We performed a prospective study of 44,791 men and 36,309 women (aged 45-84 years), without a history of acute pancreatitis, from the Cohort of Swedish Men and the Swedish Mammography Cohort. Glycemic loads were calculated from food frequency questionnaire data collected in 1997, and participants were followed for the development of non-gallstone-related acute pancreatitis through 2010 via linkage to the Swedish National Patient Register. Hazard ratios (HRs) were estimated using Cox proportional hazard models.
During a total follow-up of 967,568 person-years, there were 364 cases of incident non-gallstone-related acute pancreatitis (236 in men and 128 in women). Incidence rates, standardized for age and sex, were 49 cases per 100,000 person-years in the highest quartile of glycemic load and 33 cases per 100,000 person-years in the lowest. The multivariate-adjusted HR of non-gallstone-related acute pancreatitis was 1.60 (95% confidence interval [CI], 1.17-2.18) for the highest compared with the lowest quartile. Every 50-unit increase in glycemic load per day (~ 3 servings of white bread) had an HR of 1.38 in men (95% CI, 1.11-1.72) and women (95% CI, 1.02-1.86).
Based on a large, prospective cohort study, diets with high glycemic load are associated with an increased risk of non-gallstone-related acute pancreatitis.
The influence of hospital and surgeon volume on survival after esophageal cancer surgery deserves clarification, particularly the prognosis after the early postoperative period. The interaction between hospital and surgeon volume, and the influence of known prognostic factors need to be taken into account.
A nationwide Swedish population-based cohort study of 1,335 patients with esophageal cancer who underwent esophageal resection in 1987 to 2005, with follow-up for survival until February 2011, was conducted. The associations between annual hospital volume, annual surgeon volume, and cumulative surgeon volume and risk of mortality were calculated with multivariable parametric survival analysis, providing hazard ratios (HRs) with 95% CIs. HRs were mutually adjusted for the surgery volume variables and further adjusted for the prognostic factors age, sex, comorbidity, calendar period, tumor stage, tumor histology, and neoadjuvant therapy.
There was no independent association between annual hospital volume and overall survival, and hospital volume was not associated with short-term mortality after adjustment for hospital clustering effects. A combination of higher annual and cumulative surgeon volume reduced the mortality occurring at least 3 months after surgery (P trend
To evaluate the effect of major postoperative complications on health-related quality of life (HRQL) in 5-year survivors of esophageal cancer surgery.
This study was based on the Swedish Esophageal and Cardia Cancer register with almost complete nationwide coverage and data on esophageal cancer surgery collected prospectively between 2001 and 2005. Patients who were alive 5 years after surgery were eligible. HRQL was assessed longitudinally until 5 years after surgery by using the validated European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire C30 and OES18. Linear mixed models were used to assess the mean score difference (MD) with 95% CIs of each aspect of HRQL in patients with or without major postoperative complications. Adjustment was made for several potential confounders.
Of 153 patients who survived 5 years, 141 patients (92%) answered the 5-year HRQL questionnaires. Of these individuals, 46 patients (33%) sustained a major postoperative complication. Dyspnea (MD, 15; 95% CI, 6 to 23), fatigue (MD, 13; 95% CI, 5 to 20), and eating restrictions (MD, 10; 95% CI, 2 to 17) were clinically and statistically significantly deteriorated throughout the follow-up in patients with major postoperative complications compared with patients without major complications. Although problems with choking declined to levels comparable with patients without major postoperative complications, sleep difficulties and gastroesophageal reflux progressively worsened during follow-up.
The occurrence of postoperative complications exerts a long-lasting negative effect on HRQL in patients who survive 5 years after esophagectomy for cancer.
The trade-off between the benefits of surgery for gallstone disease for a large population and the risk of lethal outcome in a small minority requires knowledge of the overall mortality.
Between 2007 and 2010, 47?912 cholecystectomies for gallstone disease were registered in the Swedish Register for Cholecystectomy and endoscopic retrograde cholangiopancreatography (ERCP) (GallRiks). By linkage to the Swedish Death Register, the 30-day mortality after surgery was determined. The age- and sex-standardized mortality ratio (SMR) was estimated by dividing the observed mortality with the expected mortality rate in the Swedish general population 2007. The Charlson Comorbidity Index (CCI) was estimated by International Classification of Diseases (ICD) codes retrieved from the National Patient Register.
Within 30 days after surgery, 72 (0.15%) patients died. The 30-day mortality was close [SMR = 2.58; 95% confidence interval (CI): 2.02-3.25] to that of the Swedish general population. In multivariable logistic regression analysis, predictors of 30-day mortality were age >70 years [odds ratio (OR) 7.04, CI: 2.23-22.26], CCI > 2 (OR 1.93, CI: 1.06-3.51), American Society of Anesthesiologists (ASA) > 2 (OR 13.28, CI: 4.64-38.02), acute surgery (OR 10.05, CI:2.41-41.95), open surgical approach (OR 2.20, CI: 1.55-4.69) and peri-operative complications (OR 3.27, CI: 1.74-6.15).
Mortality after cholecystectomy is low. Co-morbidity and peri-operative complications may, however, increase mortality substantially. The increased mortality risk associated with open cholecystectomy could be explained by confounding factors influencing the decision to perform open surgery.
Cites: Lancet. 2000 Nov 11;356(9242):1632-711089821
Cites: Am J Gastroenterol. 2002 Feb;97(2):334-4011866270
An incident episode of acute pancreatitis is often followed by recurrent attacks and/or progression to chronic pancreatitis, especially if the etiology is non-gallstone-related. We examined whether overall diet quality influences the natural history of non-gallstone-related acute pancreatitis.
Three hundred and eighty-six individuals (born 1914-1952) were included in a prospective study, all of whom had an incident diagnosis of non-gallstone-related acute pancreatitis in the Swedish National Patient Register between 1998 and 2013. Participants were already enrolled in two population-based cohorts and had completed a food frequency questionnaire in 1997. Overall diet quality was calculated using a recommended food score (RFS), which was based on 25 food items. Post-diagnosis follow-up was conducted throughout 2014 for recurrence of acute pancreatitis and/or progression to chronic pancreatic disease (including cancer). Hazard ratios were estimated using Cox models.
During 1859 person-years of follow-up, 23.3% of the study population (n = 90) developed recurrent or progressive pancreatic disease. An inverse association was observed between the RFS and risk of recurrent and progressive pancreatic disease after adjustment for age and sex (hazard ratio for each 2-unit increase 0.90, 95% confidence interval 0.81-1.01) (P overall association = 0.06). However, the association became weaker and was not statistically significant after adjustment for other potential confounders, including alcohol drinking and cigarette smoking (P overall association = 0.27).
In this prospective study of individuals with non-gallstone-related acute pancreatitis, there was no clear association between overall diet quality and risk of recurrent and progressive pancreatic disease.
Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. Department of Surgery, Eskilstuna County Hospital, Eskilstuna, Sweden. Center for Clinical Research Sörmland, Uppsala University, Uppsala, Sweden. Unit of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Surgery, Västerås County Hospital, Västerås, Sweden.
Acute pancreatitis is linked to pancreatic cancer, but the direction of this association is not fully elaborated.
This was a population-based cohort study including all Swedish residents diagnosed with a first-time episode of acute pancreatitis between 1997 and 2013 and corresponding matched pancreatitis-free individuals from the general population. Hazard ratios for the association between acute pancreatitis and pancreatic cancer were estimated using multivariable Cox regression models.
Overall, 49,749 individuals with acute pancreatitis and 138,750 matched individuals without acute pancreatitis were followed up for 1,192,134 person-years (median 5.3 years). A total of 769 individuals developed pancreatic cancer, of whom 536 (69.7%) had a history of acute pancreatitis. The risk of pancreatic cancer was substantially increased during the first few years after a diagnosis of acute pancreatitis but declined gradually over time, reaching a level comparable to the pancreatitis-free population after >10 years of follow-up. In those with non-gallstone-related acute pancreatitis, the risk of pancreatic cancer declined to a level comparable to the pancreatitis-free population only when follow-up time was censored for a second episode of acute pancreatitis or a diagnosis of chronic pancreatitis. Increasing number of recurrent episodes of acute pancreatitis was associated with increased risk of pancreatic cancer.
These findings imply a delay in the diagnosis of pre-existing pancreatic cancer, if clinically presented as acute pancreatitis. Any association between non-gallstone-related acute pancreatitis and pancreatic cancer in the long-term (>10 years) could be mediated through recurrent acute pancreatitis or chronic pancreatitis.