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PurposeThis project sought to test the role of diet-related inflammation in modulating the risk of oesophageal cancer.MethodsA nationwide population-based case-control study was conducted from 1 December 1994 through 31 December 1997 in Sweden. All newly diagnosed patients with adenocarcinoma of the oesophagus or gastroesophageal junction and a randomly selected half of patients with oesophageal squamous cell carcinoma were eligible as cases. Using the Swedish Registry of the Total Population, the control group was randomly selected from the entire Swedish population and frequency-matched on age (within 10 years) and sex. The literature-derived dietary inflammatory index (DII) was developed to describe the inflammatory potential of diet. DII scores were computed based on a food frequency questionnaire. Higher DII scores indicate more pro-inflammatory diets. Odds ratios and 95 % confidence intervals (CI) were computed to assess risk associated between DII scores and oesophageal cancer using logistic regression adjusted by potential confounders.ResultsIn total, 189 oesophageal adenocarcinomas, 262 gastroesophageal junctional adenocarcinomas, 167 oesophageal squamous cell carcinomas, and 820 control subjects were recruited into the study. Significant associations with DII were observed for oesophageal squamous cell carcinoma (ORQuartile4vs1 4.35, 95 % CI 2.24, 8.43), oesophageal adenocarcinoma (ORQuartile4vs1 3.59, 95 % CI 1.87, 6.89), and gastroesophageal junctional adenocarcinoma (ORQuartile4vs1 2.04, 95 % CI 1.24, 3.36). Significant trends across quartiles of DII were observed for all subtypes of oesophageal cancer.ConclusionsDiet-related inflammation appears to be associated with an increased risk of oesophageal cancer, regardless of histological type.

ObjectiveThis study aimed to assess risk factors for developing marginal ulcer (MU) after gastric bypass (GBP) surgery for obesity.BackgroundMU is a common and potentially serious complication of GBP surgery, little is known about its etiology.MethodsThis population-based cohort study of GBP in 2006-2011 evaluated MU in relation to diabetes, hyperlipidemia, hypertension, chronic obstructive pulmonary disease (COPD), ulcer history, use of proton pump inhibitors (PPIs), aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and selective serotonin reuptake inhibitors (SSRIs). Multivariable Cox proportional hazard regression models estimated hazard ratios (HRs) and 95% confidence intervals (CIs), adjusted for confounding.ResultsAmong 20,294 GBP patients, diabetes and peptic ulcer history entailed statistically significantly increased risk of MU (HR = 1.26, 95% CI 1.03-1.55 and HR  =  2.70, 95% CI 1.81-4.03), although hyperlipidemia, hypertension, and COPD did not. PPI users had an increased HR of MU (HR  =  1.37, 95% CI 1.17-1.60). Aspirin and NSAID consumption less than or equal to median entailed decreased HRs of MU (HR  =  0.56, 95% CI 0.37-0.86 and HR  =  0.30, 95% CI 0.24-0.38), although aspirin and NSAID users more than median had an increased risk and no association with MU, respectively (HR  =  1.90, 95% CI 1.41-2.58 and HR  =  0.90, 95% CI 0.76-1.87). The use of SSRI less than or equal to median had a decreased risk of MU (HR  =  0.50, 95% CI 0.37-0.67), although use more than median entailed increased HR (HR  =  1.26, 95% CI 1.01-1.56).ConclusionsDiabetes and peptic ulcer history seem to be risk factors for MU, but not hyperlipidemia, hypertension, or COPD. Limited doses of aspirin, NSAIDs, and SSRIs might not increase the risk, although higher doses of aspirin do. The association with PPI could be due to confounding by indication.

BackgroundThe role of the metabolic syndrome in the etiology of esophageal and gastric cancer is unclear.MethodsThis was a large nationwide cohort study based on data from 11 prospective population-based cohorts in Norway with long-term follow-up, the Cohort of Norway (CONOR) and the third Nord-Trøndelag Health Study (HUNT3). The metabolic syndrome was assessed by objective anthropometric and metabolic biochemical measures and was defined by the presence of at least three of the following five factors: increased waist circumference, elevated triglycerides, low high-density lipoprotein cholesterol, hypertension and high glucose. Newly diagnosed cases of esophageal adenocarcinoma, esophageal squamous-cell carcinoma and gastric adenocarcinoma were identified from the Norwegian Cancer Registry. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazard models with adjustment for potential confounders.ResultAmong 192,903 participants followed up for an average of 10.6 years, 62 developed esophageal adenocarcinoma, 64 had esophageal squamous-cell carcinoma and 373 had gastric adenocarcinoma. The metabolic syndrome was significantly associated with an increased risk of gastric adenocarcinoma (HR 1.44, 95% CI 1.14-1.82), but not associated with esophageal adenocarcinoma (HR 1.32, 95% CI 0.77-2.26) or esophageal squamous-cell carcinoma (HR 1.08, 95% CI 0.64-1.83). Increased waist circumference was associated with an increased HR of esophageal adenocarcinoma (HR 2.48, 95% CI 1.27-4.85). No significant association was found between any single component of the metabolic syndrome and risk of esophageal squamous-cell carcinoma. High waist circumference (HR 1.71, 95% CI 1.05-2.80), hypertension (HR 2.41, 95% CI 1.44-4.03) and non-fasting glucose (HR 1.74, 95% CI 1.18-2.56) were also related to an increased risk of gastric adenocarcinoma in women, but not in men.ConclusionMetabolic syndrome was associated with an increased risk of gastric adenocarcinoma in women. Of the individual components of the metabolic syndrome, high waist circumference was positively associated with risk of esophageal adenocarcinoma. Positive associations were also observed for women between high waist circumference, hypertension, high non-fasting glucose and risk of gastric adenocarcinoma. However, further evidence is warranted due to the limited number of cases and the inability to effectively identify gastric cardia adenocarcinoma.

BackgroundAssociations between type 2 diabetes, anti-diabetic medications and pancreatic cancer are controversial. This study aims to clarify such associations with new-onset type 2 diabetes and repeated measurements of glycated haemoglobin (HbA1c) levels.MethodsA nested case-control study was initiated from the Health Improvement Network (THIN) in UK from 1996 to 2010. Information of pancreatic cancer cases was retrieved electronically from the medical records and manually validated. Control subjects were randomly selected and frequency-matched to the cases on sex, age, and calendar years. Multivariable unconditional logistic regression was performed to estimate odds ratios (OR) and 95% confidence intervals (CI), and adjusted for potential confounders.ResultsAmong 1,574,768 person-years of follow-up, 529 pancreatic cancer cases and 5000 controls were identified. Type 2 diabetes, or changed HbA1c levels (rather than HbA1c levels at diabetes diagnosis) in diabetes patients (⩾4 mmol mol(-1) compared with

BackgroundThe strong female predominance of biliary tract cancer (BTC) may be related to reproductive factors. We aimed to clarify whether parity or age at first birth influence the risk of BTC.MethodsThis was a population-based, case-control study including Swedish female and male cases of cancer of the gallbladder (GBC), extra hepatic bile ducts (EHCC), or the ampulla of Vater (AVC) between 1960 and 2008. For each case, 10 age- and sex-matched controls were randomly selected. Conditional logistic regression was used to calculate odds ratios (ORs) with 95% confidence intervals (CIs), adjusted for potential confounders.ResultsIn total, 1169 cases of GBC, 432 cases of EHCC and 295 cases of AVC were included. Multi- and nulliparous women and men had an increased risk of all tumor locations in the biliary tract compared to uniparous women and men, respectively. Whereas higher age at first birth was associated with a decreased risk of GBC in women, no such association was found in men. There were no clear differences in the risk of EHCC and AVC between women and men.ConclusionSex hormones may play a role in the etiology of GBC. The associations between reproductive factors and EHCC and AVC are similar in women and men, which do not support the sex hormone hypothesis.

Dietary lignans, quercetin and resveratrol have oestrogenic properties, and animal studies suggest that they synergistically decrease cancer risk. A protective effect of lignans on the development of oesophageal cancer in humans has recently been demonstrated, and the present study aimed to test whether these three phytochemicals synergistically decrease the risk of oesophageal cancer. Data from a Swedish nationwide population-based case-control study that recruited 181 cases of oesophageal adenocarcinoma (OAC), 158 cases of oesophageal squamous-cell carcinoma (OSCC), 255 cases of gastro-oesophageal junctional adenocarcinoma (JAC) and 806 controls were analysed. Exposure data were collected through face-to-face interviews and questionnaires. The intake of lignans, quercetin and resveratrol was assessed using a sixty-three-item FFQ. Reduced-rank regression was used to assess a dietary pattern, and a simplified dietary pattern score was categorised into quintiles on the basis of the distribution among the control subjects. Unconditional multivariable logistic regression provided OR with 95% CI, adjusted for all the potential risk factors. A dietary pattern rich in lignans, quercetin and resveratrol was mainly characterised by a high intake of tea, wine, lettuce, mixed vegetables, tomatoes, and whole-grain bread and a low intake of milk. There were dose-dependent associations between simplified dietary pattern scores and all types of oesophageal cancer (all P for trend < 0.05). On comparing the highest quintiles with the lowest, the adjusted OR were found to be 0.24 (95% CI 0.12, 0.49) for OAC, 0.31 (95% CI 0.15, 0.65) for OSCC, and 0.49 (95% CI 0.28, 0.84) for JAC. The results of the present study indicate that a dietary pattern characterised by the intake of lignans, quercetin and resveratrol may play a protective role in the development of oesophageal cancer in the Swedish population.

BackgroundIt is unclear whether concomitant use of clopidogrel and proton-pump inhibitors (PPIs) increases the risk of recurrence of cardiovascular disease or death in patients at high risk of upper gastrointestinal (GI) bleeding.MethodsBased on the Swedish Patient Register, a cohort of cardiovascular disease (including acute myocardial infarction, stroke and angina, from 2006 to 2008) was selected from a population with any diagnosis of upper GI bleeding. Data on drug prescription was retrieved from the Prescribed Drug Register. Patients entered into the cohort after their first discharge for cardiovascular disease and were followed up to death, recurrence of cardiovascular disease, or 90 days. A Cox regression model was conducted and hazard ratios (HRs) with 95% confidence intervals (CIs) were estimated to evaluate the risks among users of different drug prescriptions.ResultsPatients who were current users of only PPIs (HR 2.02, 95% CI 1.19-3.44), only clopidogrel (HR 1.14, 95% CI 0.53-2.45) and nonusers of both (HR 2.36, 95% CI 1.39-4.00) were at a higher risk of death compared with patients with a concomitant use. Results were similar among 1779 patients who had any history of upper GI bleeding (HR 2.05, 95% CI 1.18-3.54; HR 1.25, 95% CI 0.57-2.72; HR 2.30, 95% CI 1.33-3.98, respectively).ConclusionAmong patients at high risk of upper GI bleeding, those with a concomitant use of PPIs and clopidogrel were at a decreased risk of mortality, and possibly also a decreased risk of recurrence of cardiovascular disease.

BackgroundSex hormones may be associated with colorectal adenocarcinoma, although the association of pregnancy history and risk of colorectal cancer is not consistent.MethodsWe conducted a population-based nested case-control study of persons born between 1932 and 2008 who are in the Swedish Multi-Generation Register. In total, 12,915 women and 15,519 men with colorectal adenocarcinoma were identified during follow-up in the Swedish Cancer Register; 10 age- and sex-matched controls were selected for each case. Number of children and age at first and last birth were analyzed in relation to the risk of colorectal adenocarcinoma, using conditional logistic regression, to estimate odds ratios (ORs) and 95% confidence intervals (CIs).ResultsCompared with women without children, women with 1 or 2 children had an OR of 1.02 (95% CI = 0.93-1.13) of developing adenocarcinoma in the proximal colon; those with 3 or 4 children, 1.18 (1.06-1.32); and those with ≥5 children, 1.30 (1.05-1.61) (test for trend P < 0.01). The corresponding associations in men were 0.92 (0.84-1.00), 1.02 (0.92-1.13), and 0.97 (0.78-1.20), respectively (test for trend P = 0.13).ConclusionsHigher parity in women was associated with the risk of adenocarcinoma of the proximal colon, although not the distal colon or rectum. A similar risk with family size was not seen for fathers. Still, the influence of lifestyle factors cannot be ruled out.

OBJECTIVE: To compare radical surgery with a minimal approach for peptic ulcer bleeding in relation to survival. DESIGN: A Swedish nationwide population-based cohort study from 1987-2008 compared survival after minimal surgery and definitive surgery. The cohort was also stratified into calendar year before and after the year 2000 for subgroup analyses. Data were collected from the Swedish Patient Register. The two surgical groups were matched based on the propensity score to mimic a randomized trial design. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox regression models adjusted for potential confounders. RESULTS: 4,163 patients were included. There were no differences in survival in patients who underwent definitive surgical procedures compared to those who underwent minimal surgery for a bleeding peptic ulcer during the full study period. Using minimal surgery group as the reference, the HRs for death in the definitive surgery group within 30 days, 90 days, 1 year, and 5 years were 0.87 (95% CI 0.72-1.05), 0.93 (0.80-1.09), 1.00 (95% CI 0.87-1.14), and 1.05 (95% CI 0.95-1.16), respectively. The corresponding HRs during the calendar period after the year 2000 were 1.05 (95% CI 0.65-1.69), 1.18 (95% CI 0.81-1.73), 1.17 (0.84-1.62), and 1.27 (95% CI 0.99-1.63), respectively. CONCLUSION: This study found no worse overall survival after minimal surgery compared to more extensive surgery for refractory peptic ulcer bleeding, and indicated better long-term survival in the minimal surgery group during the more recent study period. A minimal approach is probably sufficient in most cases.

Background: The differentiation of specific, long-term health-related quality of life (HRQL) trajectories among esophageal cancer survivors remains unclear. The authors aimed to identify potentially distinctly different HRQL-trajectories and uncover the underlying factors of such trajectories in patients having undergone surgery (esophagectomy) for esophageal cancer. Materials and methods: This nationwide, prospective, and longitudinal cohort study included 420 patients who underwent curative treatment for esophageal cancer, including esophageal cancer surgery, in Sweden from 2001to 2005. The main outcome was HRQL summary score trajectories, measured by the well-validated EORTC QLQ-C30 questionnaire at 6 months, 3, 5, 10, and 15 years after esophagectomy, and analyzed using growth mixture models. Potentially underlying factors for these trajectories (age, sex, education, proxy baseline HRQL, comorbidity, tumor histology, chemo(radio)therapy, pathological tumor stage, and postoperative complications) were analyzed using weighted logistic regression providing odds ratios (OR) with 95% CI. Results: Four distinct HRQL summary score trajectories were identified: Persistently good, improving, deteriorating, and persistently poor. The odds of belonging to a persistently poor trajectory were decreased by longer education ( >12 years versus <9 years: OR 0.18, 95% CI: 0.05-0.66) and adenocarcinoma histology (adenocarcinoma versus squamous cell carcinoma: OR 0.37, 95% CI: 0.16-0.85), and increased by more advanced pathological tumor stage (III-IV versus 0-I: OR 2.82, 95% CI: 1.08-7.41) and postoperative complications (OR 2.94, 95% CI: 1.36-6.36). Conclusion: Distinct trajectories with persistently poor or deteriorating HRQL were identified after curative treatment for esophageal cancer. Education, tumor histology, pathological tumor stage, and postoperative complications might influence HRQL trajectories. The resultsmay contribute to amore tailored follow-up with timely and targeted interventions. Future research remains to confirm these findings. [ABSTRACT FROM AUTHOR]

ObjectiveThe purpose was to determine whether obesity surgery is associated with a long-term increased risk of colorectal cancer.BackgroundLong-term cancer risk after obesity surgery is not well characterized. Preliminary epidemiological observations and human tissue biomarker studies recently suggested an increased risk of colorectal cancer after obesity surgery.MethodsA nationwide retrospective register-based cohort study in Sweden was conducted in 1980-2009. The long-term risk of colorectal cancer in patients who underwent obesity surgery, and in an obese no surgery cohort, was compared with that of the age-, sex- and calendar year-matched general background population between 1980 and 2009. Obese individuals were stratified into an obesity surgery cohort and an obese no surgery cohort. The standardized incidence ratio (SIR), with 95% confidence interval (CI), was calculated.ResultsOf 77,111 obese patients, 15,095 constituted the obesity surgery cohort and 62,016 constituted the obese no surgery cohort. In the obesity surgery cohort, we observed 70 patients with colorectal cancer, rendering an overall SIR of 1.60 (95% CI 1.25-2.02). The SIR for colorectal cancer increased with length of time after surgery, with a SIR of 2.00 (95% CI 1.48-2.64) after 10 years or more. In contrast, the overall SIR in the obese no surgery cohort (containing 373 colorectal cancers) was 1.26 (95% CI 1.14-1.40) and remained stable with increasing follow-up time.ConclusionsObesity surgery seems to be associated with an increased risk of colorectal cancer over time. These findings would prompt evaluation of colonoscopy surveillance for the increasingly large population who undergo obesity surgery.

BackgroundNon-steroidal anti-inflammatory drugs (NSAIDs) and proton pump inhibitors (PPIs) are regarded as two types of drugs that respectively increase and decrease the risk of peptic ulcer bleeding. However, their relation to occurrence, recurrence and death of bleeding in the population level is not clear.Study objectiveTo clarify recent calendar-time correlations between sales of NSAIDs and PPIs and the occurrence of peptic ulcer bleeding, re-bleeding and death.DesignEcological study.ResultsThe time trend of peptic ulcer bleeding did not correlate with PPI sales but did correlate with NSAIDs in mem (R(male)=0.6571, P(male)=0.05). Sales of PPIs (inverse) and NSAIDs correlated with re-bleeding in women (R(male)=-0.8754, P(male)=0.002 and R(female)=0.7161, P(female)=0.03, respectively), but not in men. An inverse correlation between PPI sales and 30-day death after bleeding was found (R(male)=-0.9392, P(male)=0.0002 and R(female)=-0.8561, P(female)=0.003), and NSAID sales were found to correlate with increased death after bleeding ((R(male)=0.7278, P(male)=0.03, R(female)=0.7858, P(female)=0.01).ConclusionsThe sales of NSAIDs and PPIs correlate with recurrence of peptic ulcer bleeding in women and death after peptic ulcer bleeding in both genders in the population level.