Viktor Oskarsson

Vegetables, fruit and risk of non-gallstone-related acute pancreatitis: a population-based prospective cohort study

Objective To examine the association of vegetable and fruit consumption with the risk of non-gallstone-related acute pancreatitis. Design A population-based prospective cohort of 80 019 women and men, aged 46–84 years, completed a food-frequency questionnaire at baseline and was followed up for incidence of non-gallstone-related acute pancreatitis from 1 January 1998 to 31 December 2009. Participants were categorised into quintiles according to consumption of vegetables and consumption of fruit. Cox proportional hazards models were used to estimate RRs and 95% CIs. Results In total, 320 incident cases (216 men and 104 women) with non-gallstone-related acute pancreatitis were identified during 12 years of follow-up (891 136 person-years). After adjustment for potential confounders, the authors observed a significant inverse linear dose–response association between vegetable consumption and risk of non-gallstone-related acute pancreatitis; every two additional servings per day were associated with 17% risk reduction (RR=0.83; 95% CI 0.70 to 0.98; p=0.03). Among participants consuming >1 drink of alcohol per day and among those with body mass index ≥25 kg/m2, the RR for the highest compared with the lowest quintile of vegetable consumption was 0.29 (95% CI 0.13 to 0.67) and 0.49 (95% CI 0.29 to 0.85), respectively. Fruit consumption was not significantly associated with the risk of non-gallstone-related acute pancreatitis; the RR comparing extreme quintiles of consumption was 1.20 (95% CI 0.81 to 1.78). Conclusions Vegetable consumption, but not fruit consumption, may play a role in the prevention of non-gallstone-related acute pancreatitis.

Fish consumption and risk of non–gallstone-related acute pancreatitis: a prospective cohort study

BACKGROUND Epidemiologic data on the role of diet in acute pancreatitis are sparse. OBJECTIVE 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. DESIGN 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. RESULTS 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. CONCLUSION 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.

High Dietary Glycemic Load Increases the Risk of Non–Gallstone-Related Acute Pancreatitis: A Prospective Cohort Study

BACKGROUND & AIMS 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. METHODS 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. RESULTS 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). CONCLUSIONS Based on a large, prospective cohort study, diets with high glycemic load are associated with an increased risk of non-gallstone-related acute pancreatitis.

Postmenopausal hormone replacement therapy and risk of cholecystectomy: a prospective cohort study

Abstract Objective. Our aim of this study was to examine the association between the use of postmenopausal HRT and risk of cholecystectomy in Sweden, where the most common regimen of HRT (oral oestradiol in combination with testosterone-like progestin) has been different from those investigated in previous studies. Material and methods. We performed a prospective study of 27 892 postmenopausal women (aged 48–83 years) from the population-based Swedish Mammography Cohort. Use of HRT was assessed by a self-reported questionnaire at baseline in 1997, and the cohort was followed up through 2011 for procedures of cholecystectomy by linkage to the Swedish Patient Register. Cox proportional hazard models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI). Results. During 362 728 person-years of follow-up (median 14 years), 995 cases of cholecystectomy were recorded. After adjustment for potential confounders, the HR of cholecystectomy was 1.52 (95% CI, 1.33–1.74) among ever users of HRT compared with never users. The risk did not differ by current or past use (p = 0.38) or duration of use (p = 0.65), but it did differ by indication of use (p = 0.006). Women who used HRT for systemic symptoms had a higher risk of cholecystectomy than those who used it for local symptoms (HR, 1.62; 95% CI, 1.41–1.87 vs HR, 1.21; 95% CI, 0.97–1.50). Conclusions. This prospective study of postmenopausal women adds to the evidence that use of HRT may increase the risk of cholecystectomy.

Postmenopausal hormone replacement therapy and risk of acute pancreatitis: a prospective cohort study

Background: Several case reports have suggested that women’s use of exogenous sex hormones is associated with acute pancreatitis; however, relevant epidemiologic data are sparse. We examined the association between postmenopausal hormone replacement therapy and risk of acute pancreatitis. Methods: We conducted a prospective study involving 31 494 postmenopausal women (aged 48–83 yr) from the population-based Swedish Mammography Cohort. Participants completed a baseline questionnaire in 1997 assessing their use of hormone replacement therapy. We linked the cohort to the hospital-based Swedish National Patient Register to determine hospital admissions for acute pancreatitis through 2010. Relative risks (RRs) were calculated using Cox proportional hazard models. Results: Over a total follow-up of 389 456 person-years, we identified 237 cases of incident acute pancreatitis. The age-standardized incidence rates per 100 000 person-years were 71 cases among women who had ever used hormone replacement therapy and 52 cases among women who had never used such hormones. Among ever users of hormone replacement therapy, the multivariable-adjusted RR of acute pancreatitis was 1.57 (95% confidence interval [CI] 1.20–2.05) compared with never users. The risk did not differ by current or past use, but it seemed to be higher among women who used systemic therapy (RR 1.92, 95% CI 1.38–2.66) and among those with duration of therapy of more than 10 years (RR 1.87, 95% CI 1.11–3.17). Interpretation: Use of postmenopausal hormone replacement therapy was associated with increased risk of acute pancreatitis. Physicians should consider this potential increase in risk when prescribing such therapy.

Letter: coffee consumption and gallstone disease - a cautionary note on the assignment of exposure values in dose-response meta-analyses.

SIRS, We read with interest the dose–response meta-analysis by Zhang et al., where the authors reported a nonlinear inverse association between coffee consumption and risk of gallstone disease (Pnon-linearity <0.05). 1 This analysis was based on four prospective cohort studies that presented results for several categories of coffee consumption. According to common practice, Zhang et al. assigned the mid-point of each category as a proxy for the exposure level. For the highest open-ended category, however, the mid-point was set at 1.5 times the lower boundary, which is quite unusual and may lead to too high values of coffee consumption (up to 9 cups/ day). In this letter, we would like to discuss the consequences of that exposure assignment and, by doing so, draw attention to the importance of sensitivity analyses in dose–response meta-analyses. Data were reanalysed using different methods of exposure assignment. In addition to that of Zhang et al. (which referred to a meta-analysis on egg consumption), we used a method proposed in two recent meta-analyses on coffee consumption. 6 This method is different in only one respect; it assumes that the highest openended category has the same amplitude as the preceding one, which may lead to more reasonable values of coffee consumption (up to 6.5 cups/day). For comparison, we obtained the actual median values directly from the authors of the original studies (up to 7 cups/day). Statistical analyses were conducted with the R package dosresmeta. Compared to the median values, Zhang et al.’s midpoints overestimated the coffee consumption in the highest categories by at least 22%. In contrast, the alternative mid-points were much closer to the median values ( 8%). As expected, we observed a non-linear inverse association between coffee consumption and risk of gallstone disease when using Zhang et al.’s mid-points (Pnon-linearity <0.05) (Figure 1). However, there was no evidence of a nonlinear association when using the other methods of exposure assignment, neither the alternative mid-points (Pnon-linearity = 0.60) nor the median values (Pnon-linearity = 0.69). Furthermore, using either of these two methods, the inverse association was stronger than that reported by Zhang et al. For example, the hazard ratio (95% confidence interval) for 6 cups/day vs. 0 cups/day was 0.66 (0.51–0.85) when we used the median values [previously reported to be 0.75 (0.64–0.88)]. The issues we have discussed in this letter do not change Zhang et al.’s conclusion that coffee consumption is related to a decreased risk of gallstone disease. However, they do change the interpretation of the dose– response results, that is, the shape and magnitude of the exposure-disease association (which is highly relevant given the widespread consumption of coffee and the high incidence of gallstones). More broadly, this letter exemplifies the general importance of exposure assignment in dose–response meta-analyses. Whenever possible, we encourage metaanalysts to retrieve information on the exposure distribution directly from the original authors. We also recommend that sensitivity analyses are routinely performed to examine whether the assigned exposure values have a strong influence on the dose–response results.

A prospective cohort study on the association between coffee drinking and risk of non-gallstone-related acute pancreatitis.

Only one previous study has examined the association between coffee consumption and risk of acute pancreatitis, and it found a reduced risk for alcohol-related episodes among high consumers of coffee. Therefore, we examined (1) the association between coffee consumption and risk of non-gallstone-related acute pancreatitis and (2) whether this association was modified by alcohol intake. Data were obtained from two prospective cohorts, the Cohort of Swedish Men and the Swedish Mammography Cohort, including 76 731 men and women (born 1914-1952). Coffee consumption was assessed at baseline with a FFQ, and the cohorts were followed up between 1998 and 2012 via linkage to national health registries. Hazard ratios were estimated using Cox models, with adjustment for potential confounding factors. During 1 035 881 person-years of total follow-up, 383 cases (246 in men and 137 in women) of incident non-gallstone-related acute pancreatitis were identified. Overall, and irrespective of whether a categorical or a continuous exposure model was used, we observed no association between coffee consumption and risk of non-gallstone-related acute pancreatitis (e.g. the multivariable-adjusted hazard ratio for each 1 cup/d increase in coffee consumption was 0·97; 95 % CI 0·92, 1·03). There was no evidence of effect modification by alcohol intake (P interaction=0·77). In conclusion, coffee consumption was not associated with risk of non-gallstone-related acute pancreatitis in this large prospective cohort study. Because of the limited number of epidemiological studies and their conflicting results, further research is needed to elucidate this potential association.

Polypharmacy and risk of acute pancreatitis.

Drug‐induced pancreatitis is receiving increased medical and epidemiological attention. However, as no study has examined the role of polypharmacy per se in the development of acute pancreatitis, we examined the association between polypharmacy and risk of acute pancreatitis.

Pancreatic Cancer Following Acute Pancreatitis: A Population-based Matched Cohort Study

BACKGROUND: Acute pancreatitis is linked to pancreatic cancer, but the direction of this association is not fully elaborated. METHODS: 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. RESULTS: 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. CONCLUSION: 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.