Objective To accurately measure the incidence of gastric cancer among patients with gastric precancerous lesions, and to quantify the excess incidence in comparison with people with normal mucosa on endoscopy and a general population. Design Population based cohort study. Setting Population of Sweden using data from its national disease registers. Participants 405 172 patients who had gastric biopsy samples taken for non-malignant indications between 1979 and 2011. Main outcome measures Incidence of gastric cancer, reported separately for patients with different mucosal changes in biopsy samples. Standardised incidence ratios provided estimation of the relative risk, using the general Swedish population as reference; and hazard ratios were derived from Cox regression modelling for internal comparisons with patients with normal gastric mucosa. Results After excluding the first two years of follow-up, 1599 cases of gastric cancer were identified. The annual crude incidence of gastric cancer was 20×10⁻⁵ for those in the normal mucosa group (standardised incidence ratio 1.0), 42×10⁻⁵ for those with minor changes (1.5), 59×10⁻⁵ for the gastritis group (1.8), 100×10⁻⁵ for the atrophic gastritis group (2.8), 129×10⁻⁵ for the intestinal metaplasia group (3.4), and 263×10⁻⁵ for the dysplasia group (6.5). Cox regression modelling confirmed that excess risks increased monotonically with progressive severity of gastric lesions, with the highest hazard ratio of 10.9 (dysplasia versus normal mucosa, 95% confidence interval 7.7 to 15.4). The increased incidence was stable throughout the follow-up period, and the gaps between cumulative incidence curves grew continuously. Conclusions Among patients who undergo gastroscopy with biopsy for clinical indications, approximately 1 in 256 with normal mucosa, 1 in 85 with gastritis, 1 in 50 with atrophic gastritis, 1 in 39 with intestinal metaplasia, and 1 in 19 with dysplasia will develop gastric cancer within 20 years. These numbers, along with cost-benefit analyses, should guide future surveillance policies for these particular patient groups.

Background: The poor survival of patients with gastroesophageal cancers may improve if additional esophageal precursor lesions to Barrett’s esophagus and squamous dysplasia are identified. We estimated the risk for gastroesophageal cancers among patients with various histopathological abnormalities in the esophagus, including Barrett’s esophagus, subdivided by histopathological types. Methods: Histopathology data from esophageal biopsies obtained 1979–2014 were linked with several national population-based registers in Sweden. Patients were followed from 2 years after the first biopsy date until cancer, death, emigration, esophagectomy/gastrectomy or end of follow-up, 31st of December 2016, whichever came first. We estimated standardized incidence ratios (SIRs) as measures of relative risk with the Swedish general population as reference. Results: In total 367 esophageal adenocarcinoma (EAC) cases were ascertained during 831,394 person-years of follow-up. The incidence rate (IR) for EAC was 0.1 per 1000 person-years for normal morphology, 0.2–0.5 for inflammatory changes, and 0.8–2.9 for metaplasia. The IR was 1.0 per 1000 person-years (95% confidence interval 0.7–1.3) among patients with non-dysplastic intestinal metaplasia, 0.9 (0.8–1.1) in non-dysplastic gastric/glandular metaplasia and 2.9 (2.0–4.2) among columnar metaplasia patients with low-grade dysplasia. The SIRs were 11.7 (95% confidence interval 8.6–15.5), 12.0 (10.0–14.2) and 30.2 (20.5–42.8), respectively. The SIRs for gastric cardia adenocarcinoma (GCA) were moderately elevated. Conclusions: For the first time, we demonstrate that patients with esophageal inflammatory and other metaplastic abnormalities than Barrett’s esophagus have an increased risk of EAC and GCA compared to the general population. Moreover, patients with different histopathologic subtypes of Barrett’s esophagus have a comparable risk for EAC.

Purpose: The survival of esophageal and gastric cancer patients treated with chemotherapy is rarely assessed outside of clinical trials. Therefore, we compared the effectiveness of various curative or palliative chemotherapy regimens on the survival of esophageal and gastric cancer patients in a “real world” clinical setting. Methods: We identified a cohort of 966 incident esophageal and gastric cancer patients in Stockholm/Gotland County (a low-risk Western population) during 2008–2013. Patients who received chemotherapy with curative intention (n = 279) and palliative intention (n = 182) were analyzed separately. Using Cox proportional hazards regression models, we estimated hazard ratios (HRs) with 95% confidence intervals (CIs) and adjusted for the potential confounding factors: age, sex, TNM stage, radiotherapy, comorbidity, marital status, education, income, and country of birth. Results: In esophageal cancer patients with curative treatment intention, we observed a higher hazard for death among patients who received carboplatin-fluorouracil compared to patients who received cisplatin-fluorouracil, corresponding to a HR of 2.18 (95% CI 1.09–4.37). Conversely, in patients with cancer in the gastroesophageal junction who had a curative treatment intention at diagnosis, we observed a reduced hazard for death among those who received fluorouracil-oxaliplatin, compared to patients who received cisplatin-fluorouracil (HR 0.28; 95% CI 0.08–0.96). Conclusion: Among patients with esophageal cancer who received treatment with curative intention, cisplatin-fluorouracil was associated with better survival compared to carboplatin-fluorouracil, while patients with gastroesophageal junction cancer who were treated with cisplatin-fluorouracil had worse survival compared to fluorouracil-oxaliplatin.

Background: Higher socioeconomic status (SES) among people with migraine has been associated with an increased use of triptans, but it is undetermined whether high SES is also associated with dispensation of monoclonal antibodies against calcitonin gene-related peptide (CGRPi), a prophylactic treatment against migraine episodes. Our hypothesis was that higher SES is associated with CGRPi dispensation, although the association is expected to be attenuated in a country that generally allows for reimbursement of CGRPi costs. Methods: In this register-based nested case-control study, the association between SES, categorized into three levels (low, middle and high) and the outcome of a first dispensation of a CGRPi was assessed among people with a migraine diagnosis in Region Stockholm, using univariable and multivariable logistic regression models. Results: Of 52,996 individuals in the study population, 3.2% (n = 1674) were dispensed CGRPi. Individuals with high or middle SES had an increased probability of being dispensed CGRPi, compared to individuals with low SES (adjusted odds ratio = 1.68; 95% confidence interval = 1.46–1.92 and adjusted odds ratio = 1.41; 95% confidence interval = 1.24–1.61, respectively). Conclusions: Higher SES was associated with dispensation of CGRPi, which suggests unequal access to CGRPi.

Background: It remains open whether gastric precancerous lesions are associated with an elevated risk of pancreatic cancer. Our aim was to investigate the association between gastric mucosal status and pancreatic cancer risk. Methods: Patients with gastric biopsies [normal, minor changes, superficial gastritis, and atrophic gastritis/intestinal metaplasia/dysplasia (AG/IM/Dys)] from the Swedish histopathology registers during 1979 to 2011 were included. Cross-linkages with several nationwide registries allowed complete follow-up and identification of pancreatic cancer cases until 2014. Standardized incidence ratios (SIR) and HRs were estimated. Results: During 3,438,248 person-years of follow-up with 318,653 participants, 3,540 cases of pancreatic cancer were identified. The same pattern of excess risk of pancreatic cancer compared with the general population was observed across all groups: a peak of 12- to 21-fold excess risk in the first year after biopsy [e.g., normal: SIR = 17.4; 95% confidence interval (CI), 15.7–19.3; AG/IM/Dys: SIR = 11.5; 95% CI, 9.9–13.4], which dropped dramatically during the second and third years, followed by 20% to 30% increased risk after the third year (e.g., normal: SIR = 1.2; 95% CI, 1.1–1.4; AG/IM/Dys: SIR = 1.3; 95% CI, 1.1–1.5). However, no significant excess risk was observed with the normal gastric mucosa as reference. Conclusions: This unique, large pathologic cohort study did not find evidence that abnormal gastric mucosal status is causally associated with a long-term pancreatic cancer risk. However, a highly increased short-term risk was observed for people undergoing gastroscopy with biopsy sampling compared with the general population. Impact: Further studies for a long-term risk of pancreatic cancer in patients with gastric biopsies are needed, with further adjustments.