Risk Of Gastrointestinal Cancer Research Articles

Assessing age-related risks of gastrointestinal pathologies: a comparative study of gastroscopy outcomes across decades.

Esophagogastroduodenoscopy (EGD) is the gold standard method for diagnosing upper gastrointestinal (GI) pathology. Swedish guidelines recommend patients over 50 years with new-onset dyspeptic symptoms undergo direct gastroscopy to rule out malignancy. However, the incidence of dysplasia or cancer in patients aged 61-70 years remains unclear. To investigate the referral factors and endoscopic findings in patients aged 61-70 years and compare the result with age groups 51-60 and 41-50 years from our previous studies to establish whether there is an age cutoff for upper GI cancer risk. A retrospective observational study was conducted to evaluate EGD referrals and outcomes in patients aged 61-70 years. We analyzed EGD referrals for patients aged 61-70 years within Region Örebro County from January 2019-April 2020 to January 2022-2023. Clinical data, including symptoms, medications, and laboratory results, were collected from medical records. Statistical analysis, including odds ratios (OR) and positive predictive values (PPV), was conducted to evaluate pathological outcomes based on referral factors. A total of 1003 referrals were analyzed. Statistically significant differences in pathological findings were observed between the 41-50 years reference group and the older groups (51-60 years: OR 2.08, p < 0.001; 61-70 years: OR 3.05, p < 0.001). However, no statistically significant difference in cancer incidence was found between the age groups. The most common pathological findings were benign, including hiatal hernia, gastroesophageal reflux disease/esophagitis, or gastritis. The incidence of cancer was low in all three groups. These results suggest that the "test-and-treat" strategy, currently recommended for patients under 50 years, may be appropriate for patients aged 51-70 years as well. NCT04585516.

Infectious pathogens and risk of esophageal, gastric and duodenal cancers and ulcers in China: A case-cohort study.

Infection by certain pathogens is associated with cancer development. We conducted a case-cohort study of ~2500 incident cases of esophageal, gastric and duodenal cancer, and gastric and duodenal ulcer and a randomly selected subcohort of ~2000 individuals within the China Kadoorie Biobank study of >0.5 million adults. We used a bead-based multiplex serology assay to measure antibodies against 19 pathogens (total 43 antigens) in baseline plasma samples. Associations between pathogens and antigen-specific antibodies with risks of site-specific cancers and ulcers were assessed using Cox regression fitted using the Prentice pseudo-partial likelihood. Seroprevalence varied for different pathogens, from 0.7% for Hepatitis C virus (HCV) to 99.8% for Epstein-Barr virus (EBV) in the subcohort. Compared to participants seronegative for the corresponding pathogen,Helicobacter pylori seropositivity was associated with a higher risk of non-cardia (adjusted hazard ratio [HR] 2.73 [95% CI: 2.09-3.58]) and cardia (1.67 [1.18-2.38]) gastric cancer and duodenal ulcer (2.71 [1.79-4.08]). HCV was associated with a higher risk of duodenal cancer (6.23 [1.52-25.62]) and Hepatitis B virus was associated with higher risk of duodenal ulcer (1.46 [1.04-2.05]). There were some associations of antibodies again some herpesviruses and human papillomaviruses with risks of gastrointestinal cancers and ulcers but these should be interpreted with caution. This first study of multiple pathogens with risk of gastrointestinal cancers and ulcers demonstrated that several pathogens are associated with risks of gastrointestinal cancers and ulcers. This will inform future investigations into the role of infection in the etiology of these diseases.

Cancer risks in patients with ankylosing spondylitis and the effects of biologic agents: a population-based study

Abstract Objective The objective of this study was to conduct a population-based analysis of the malignancy risks of patients with AS. Methods A total of 1796 patients with AS and 7184 age- and sex-matched controls (1:4 ratio) were selected from the Korea National Health Insurance Service–National Sample Cohort database. Data of patients diagnosed with AS (code M45) according to the International Classification of Diseases (ICD) 10th edition, between 2002 and 2019, were reviewed. These data were extracted based on the ICD codes assigned to cancer patients. Results Cancer developed in 168/1796 patients (9.3%) after the AS diagnosis. After adjusting for confounders, the cancer risk of patients with AS was not significantly increased compared with that of controls [adjusted hazard ratio (HR): 1.1; 95% CI: 0.93–1.31]. However, the risks for upper gastrointestinal (GI) cancer (adjusted HR: 1.51; 95% CI: 1.07–2.12) and haematologic malignancy (adjusted HR: 2.36; 95% CI: 1.2–4.65) were significantly higher in patients with AS than in controls. There were no significant differences in the risks for other major cancers between patients with AS and controls. Regarding medication for AS, the HR of upper GI cancer was higher in patients with AS compared with controls (adjusted HR: 1.51; 95% CI: 1.00–2.29). Conclusion The overall cancer risk in patients with AS was not significantly different compared with that in the controls. However, while the effect of NSAIDs on upper GI cancer cannot be ruled out, patients with AS exhibited a significant increase in the risk of both upper GI cancer and haematologic malignancy.

The Role of Crohn Disease on Breast Cancer Incidence: A Clinical Analysis.

Crohn disease is a chronic inflammatory disease that can affect the entire gastrointestinal tract. The pathophysiology of this disease characteristically involves transmural inflammation, which predisposes patients to various gastrointestinal cancers such as colon cancer. Although the increased risk of gastrointestinal cancers in Crohn disease has been well established, the risk of extra-gastrointestinal cancers remains unknown. We sought to study the risk of breast cancer in patients with Crohn disease. The data for this retrospective study were compiled using the International Classification of Disease Ninth Revision (ICD-9) and ICD 10th Revision (ICD-10) codes from the national Health Insurance Portability and Accountability Act (HIPAA)-compliant PearlDiver database from 2010 to 2019. Patients were matched for age, sex, and Charlson Comorbidity Index (CCI). Statistical analyses were implemented to assess Chi-squared, logistic regression, and odds ratio. The database query resulted in 70,027 patients in both the control and Crohn disease groups. The incidence of breast cancer was 4,087 in the control group compared to 654 in the Crohn disease group. The P value was < 2.2 × 10-16 and the odds ratio was 0.15 (95% confidence interval (CI)). Patients without Crohn disease had an increased prevalence of breast cancer throughout all age ranges compared to patients with Crohn disease. Additionally, patients without Crohn disease had higher rates of breast cancer throughout the four major regions of the United States. In terms of healthcare costs, patients with breast cancer and a history of Crohn disease paid $23.87 more per hospital visit compared to patients with breast cancer and no history of Crohn disease. The results of this study indicate a statistically significant correlation between Crohn disease and a reduced incidence of breast cancer. This finding is true across all age groups and across the United States. Further study is required to investigate a possible mechanism between the pathophysiology of Crohn disease ultimately leading to reduced tumorigenesis in the breast.

Healthy dietary patterns, genetic risk, and gastrointestinal cancer incident risk: a large-scale prospective cohort study

BackgroundDietary patterns have been associated with several cancers, especially gastrointestinal cancer (GIC). However, whether a healthy dietary pattern could modify the risk of GIC among people with different genetic backgrounds is not clear. ObjectiveThe objective of the study was to investigate how dietary patterns and genetic susceptibility contribute to the risk of GIC independently and jointly. MethodsThis large-scale prospective cohort study included 105,463 participants in UK Biobank who were aged 40–72 y and cancer-free at baseline. Dietary intake (Oxford WebQ) was used to calculate dietary pattern scores including dietary approach to stop hypertension (DASH) score and healthful plant-based diet index (hPDI). Genetic risk was quantified by a polygenic risk score (PRS) comprising 129 known GIC-associated loci. Cox proportional hazards regression was performed to estimate the associations of dietary patterns and PRS with GIC incidence after adjusting for potential confounders. ResultsOver a median follow-up of 11.70 y, 1,661 participants were diagnosed with GIC. DASH and hPDI were associated with 20% and 36% reductions, respectively, in GIC risk. Low PRS was associated with a 30 % decrease in GIC risk (HR: 0.70; 95% CI: 0.62, 0.79). Participants with healthy dietary scores at high-genetic risk had a lower GIC risk with HR of 0.77 (95% CI: 0.60, 0.98) for DASH and 0.66 (95% CI: 0.52, 0.84) for hPDI than those with unhealthy dietary score. Participants with both high-dietary score and low-genetic risk showed the lowest risk of GIC, with HR of 0.58 (95% CI: 0.45, 0.75) for DASH and 0.45 (95% CI: 0.34, 0.58) for hPDI. ConclusionsAdherence to DASH and hPDI were associated with a lower risk of some gastrointestinal cancers, and these 2 dietary patterns may partly compensate for genetic predispositions to cancer. Our results advance the development of precision medicine strategies that consider both dietary patterns and genetics to improve gastrointestinal health.

Proton pump inhibitors and risk of gastrointestinal cancer: A meta‑analysis of cohort studies

Proton pump inhibitors and risk of gastrointestinal cancer: A meta‑analysis of cohort studies

Alcohol Drinking Without Meals Is Associated With Risk of Gastrointestinal Cancers, Including Early-Onset Cases

Alcohol Drinking Without Meals Is Associated With Risk of Gastrointestinal Cancers, Including Early-Onset Cases

Bariatric Surgery and Risk of Hospitalization for Gastrointestinal Cancers in the USA: a Propensity Score Matched Analysis of National Inpatient Sample Study.

There are some concerns about the higher risk of certain gastrointestinal (GI) cancers in patients with a history of bariatric metabolic surgery (BMS). The current study aimed to investigate the association of BMS with GI cancer hospital admission including esophageal, gastric, colorectal, small intestinal, liver, gallbladder, bile duct, and pancreatic cancers. The analysis utilized the US national inpatient sample (NIS) data from 2016 to 2020, employing ICD-10 codes. A propensity score matching in a 3:1 ratio was done to match the BMS and non-BMS groups. A total of 328,369 patients with a history of BMS and 4,989,154 with obesity and without a history of BMS were included in this study. BMS was independently associated with a higher risk of gastric and pancreatic cancers hospital admission (OR: 1.69 (CI 95%: 1.42-2.01) and OR: 1.46 (CI 95%: 1.27-1.68)), respectively. In addition, BMS was independently associated with a lower risk of colorectal and liver cancer hospital admission (OR: 0.57 (CI 95%: 0.52-0.62) and OR: 0.72 (CI 95%: 0.52-0.98)), respectively. Besides, esophageal, gallbladder, bile duct, and small intestinal cancer were not significantly different between the two groups. In patients with GI cancer, although the BMS group had significantly lower total charges and length of hospital stay compared to the non-BMS group, the rate of in-hospital mortality was not significantly different. The current study showed that bariatric surgery may be associated with a higher risk of gastric and pancreatic cancer and a lower risk of colorectal and liver cancer hospital admission. Further research is needed to explore this association.

Gastrointestinal cancers in lean individuals with non-alcoholic fatty liver disease: A systematic review and meta-analysis.

Obesity and non-alcoholic fatty liver disease (NAFLD) are known risk factors for gastrointestinal (GI) cancers. However, GI carcinogenesis in lean NAFLD patients remains unclear. This systematic review and meta-analysis aims to investigate the association between lean NAFLD and GI cancer risk. PubMed, Embase and Cochrane Library databases were systematically searched (from inception date to April 2023) for cohort studies assessing GI cancers in lean (body mass index [BMI] < 25 kg/m2 or < 23 kg/m2 in Asians) and non-lean (BMI ≥25 kg/m2 or ≥ 23 kg/m2 in Asians) NAFLD individuals. Data from eligible studies were extracted, and meta-analysis was carried out using a random effects model to obtain risk ratios (RRs) with 95% confidence intervals (CIs). Subgroup analyses, meta-regressions and sensitivity analyses were also performed. This study was registered in PROSPERO (CRD42023420902). Eight studies with 56,745 NAFLD individuals (11% were lean) and 704 cases of incident GI cancers were included. Lean NAFLD was associated with higher risk of hepatic (RR 1.77, 95% CI 1.15-2.73), pancreatic (RR 1.97, 95% CI 1.01-3.86) and colorectal cancers (RR 1.53, 95% CI 1.12-2.09), compared to non-lean NAFLD. No significant differences were observed for oesophagus, gastric, biliary and small intestine cancers. This study shows that lean NAFLD patients have an increased risk of liver, pancreatic and colorectal cancers compared to non-lean NAFLD patients, emphasizing the need to explore tailored cancer prevention strategies for this specific patient group. Further research is required to explore the mechanisms underlying the association between lean NAFLD and specific GI cancers.

Acute pancreatitis increases the risk of gastrointestinal cancer in type 2 diabetic patients: a Korean nationwide cohort study

Acute pancreatitis increases the risk of gastrointestinal cancer in type 2 diabetic patients: a Korean nationwide cohort study

Genome-Wide Association and Two-Sample Mendelian Randomization Analyses of Plasma Ghrelin and Gastrointestinal Cancer Risk.

Observational studies have suggested that the gut hormone ghrelin is an early marker of future risk of developing gastrointestinal cancer. However, whether ghrelin is a causal risk factor remains unclear. We conducted a genome-wide association study (GWAS) of plasma ghrelin and used Mendelian randomization (MR) to investigate the possible causal association between ghrelin and gastrointestinal cancer risk. Genetic variants associated with plasma ghrelin were identified in a GWAS comprising 10,742 Swedish adults in the discovery (N = 6,259) and replication (N = 4,483) cohorts. The association between ghrelin and gastrointestinal cancer was examined through a two-sample MR analysis using the identified genetic variants as instruments and GWAS data from the UK Biobank, FinnGen, and a colorectal cancer consortium. GWAS found associations between multiple genetic variants within ±200 kb of the GHRL gene and plasma ghrelin. A two-sample MR analysis revealed that genetically predicted higher plasma ghrelin levels were associated with a lower risk of gastrointestinal cancer in UK Biobank and in a meta-analysis of the UK Biobank and FinnGen studies. The combined OR per approximate doubling of genetically predicted plasma ghrelin was 0.91 (95% confidence interval, 0.85-0.99; P = 0.02). Colocalization analysis revealed limited evidence of shared causal variants for plasma ghrelin and gastrointestinal cancer at the GHRL locus (posterior probability H4 = 24.5%); however, this analysis was likely underpowered. Our study provides evidence in support of a possible causal association between higher plasma ghrelin levels and a reduced risk of gastrointestinal cancer. Elevated plasma ghrelin levels might reduce the risk of gastrointestinal cancer.

Vegetarian diets and the risk of gastrointestinal cancers: a meta-analysis of observational studies.

The systematic review aimed to assess the association between vegetarian diet and the risk of gastrointestinal tumorigenesis. PubMed, Embase, Cochrane Library, and Web of Science were searched from inception to August 2022 for observational studies on vegetarian diets and the risk of gastrointestinal tumorigenesis. The primary outcome was morbidity due to gastrointestinal cancer. The Newcastle-Ottawa Scale was used to assess the quality of included studies. Pooled effects were analyzed using a random-effects model. The study protocol was registered in PROSPERO (no. CRD42022310187). Eight original studies (seven cohorts and one case-control), involving 686 691 participants, were included. Meta-analysis showed a negative correlation between vegetarian diets and gastrointestinal tumorigenesis risk [relative risk (RR) equals 0.77, 95% confidence interval (CI) is (0.65-0.90)], compared with non-vegetarian diets. Subgroup analysis indicated that vegetarian diets were negatively correlated with the risks of gastric cancer [RR = 0.41, 95% CI (0.28-0.61)] and colorectal cancer [RR = 0.85, 95% CI (0.76-0.95)], but not with that of upper gastrointestinal cancer (excluding stomach) [RR = 0.93, 95% CI (0.61-1.42)]. Vegetarian diets were negatively correlated with the risk of gastrointestinal tumorigenesis in men [RR = 0.57, 95% CI (0.36-0.91)], but were uncorrelated in women [RR = 0.89, 95% CI (0.71-1.11)]. Vegetarian diets were negatively correlated with the risk of gastrointestinal tumorigenesis in North American [RR = 0.76, 95% CI (0.61-0.95)] and Asian populations [RR = 0.43, 95% CI (0.26-0.72)] and were uncorrelated in the European population [RR = 0.83, 95% CI (0.68-1.01)]. Adhering to vegetarian diets reduces the risk of gastrointestinal tumorigenesis. More data from well-conducted cohort and other studies are needed.

Comprehensive Review of Red Meat Consumption and the Risk of Cancer.

Red and processed meat consumption rates are increasing in the United States. In this review, we present the current evidence that links red meat consumption and cancer development. A literature search was conducted in the PubMed and Google Scholar databases to review red meat consumption and its association with breast cancer and gastrointestinal cancer. Due to the presence of heme iron, which triggers oxidative reactions that eventually result in tumor formation, red meat consumption is strongly associated with the development of breast cancer. Ingestion of red meat increases Helicobacter pylori infections, resulting in enhanced expression of the CagA gene and the secretion of pro-inflammatory cytokines. This is the leading cause of gastric cancer. There is a strong correlation between heterocyclic amines and polycyclic aromatic hydrocarbons in red meat and the development of pancreatic cancer. However, additional research is necessary to confirm this finding. Adult colorectal cancer is caused by the formation of heterocyclic amines and DNA adducts due to the intake of red and processed meats cooked at higher temperatures. The consumption of poultry is associated with a reduced risk of breast and gastrointestinal cancers, but the results are inconsistent. The evidence is strong for the association between red meat and breast cancer and most gastric cancers. The presence of aromatic hydrocarbons, heterocyclic amines, and heme iron in red meat has been found to be behind tumorigenesis. Poultry has been shown to have a low association with cancer, but additional research is needed.

Consumption of Sugar-Sweetened Soft Drinks and Risk of Gastrointestinal Cancer: A Systematic Review and Meta-Analysis of Observational Studies

Introduction: Previous observational studies have reported inconsistent findings on the association between consumption of sugar-sweetened soft drinks (SSSDs) and the risk of gastrointestinal (GI) cancer. This study investigated the associations between SSSD consumption and the risk of GI cancer using a systematic review and meta-analysis. Methods: Observational epidemiological studies were searched from the PubMed and EMBASE databases until June 2021. We conducted a meta-analysis of all included studies and subgroup meta-analyses based on various factors. Results: In a meta-analysis of 27 studies with nine case-control studies and 18 cohort studies, the consumption of SSSDs was modestly associated with an increased risk of GI cancer (odds ratio [OR]/relative risk [RR]: 1.08; 95% confidence interval [CI]: 1.01–1.16), with a significant positive dose-response relationship. In the subgroup meta-analysis by study design, there was a significant positive association between the consumption of SSSDs and GI cancer in cohort studies (RR: 1.11; 95% CI: 1.03–1.20; n = 18), but not in case-control studies. In the subgroup meta-analysis by type of cancer, consumption of SSSDs was significantly associated with an increased risk of colorectal cancer (OR/RR: 1.13; 95% CI: 1.07–1.19). Conclusions: This meta-analysis suggests that SSSD consumption significantly increases the risk of GI cancer, specifically colorectal cancer.

Association of meat consumption with the risk of gastrointestinal cancers: a systematic review and meta-analysis

BackgroundThe association between gastrointestinal cancer and types of meat consumption, including red meat, processed meat, or a combination of both, remains disputable. Therefore, we performed a systematic review and meta-analysis of prospective cohort studies to estimate the association between meat consumption and gastrointestinal cancer risk.MethodsPubMed, EmBase, and the Cochrane library databases were searched systematically for eligible studies that investigated the relation between meat consumption and the risk of developing gastrointestinal cancers, including esophageal cancer (EC), gastric cancer (GC), colorectal cancer (CRC), colon cancer (CC), rectal cancer (RC), pancreatic cancer (PC), and hepatocellular carcinoma (HCC) throughout February, 2023. The pooled relative risk (RR) with 95% confidence interval (CI) was assigned as an effect estimate and calculated using a random-effects model with inverse variance weighting.ResultsForty cohorts comprising 3,780,590 individuals were selected for the final quantitative analysis. The summary results indicated that a higher red meat consumption was associated with an increased risk of CRC (RR: 1.09; 95% CI: 1.02–1.16; P = 0.007) and CC (RR: 1.13; 95% CI: 1.03–1.25; P = 0.011). Moreover, a higher processed meat consumption was associated with an increased risk of CRC (RR: 1.19; 95% CI: 1.13–1.26; P < 0.001), CC (RR: 1.24; 95% CI: 1.13–1.26; P < 0.001), and RC (RR: 1.24; 95% CI: 1.08–1.42; P = 0.002). Furthermore, a higher total consumption of red and processed meat was associated with an increased risk of CRC (RR: 1.13; 95% CI: 1.06–1.20; P < 0.001), CC (RR: 1.17; 95% CI: 1.04–1.33; P = 0.012), and RC (RR: 1.20; 95% CI: 1.04–1.39; P = 0.016). Finally, the strength of higher consumption of total red and processed meat with the risk of GC, and higher consumption of red meat with the risk of RC in subgroup of high adjusted level was lower than subgroup of moderate adjusted level, while the strength of higher consumption of processed meat with the risk of RC and HCC in subgroup of follow-up ≥ 10.0 years was higher than subgroup of follow-up < 10.0 years.ConclusionsThis study found that meat consumption was associated with an increased risk of CRC, CC, and RC, and dietary intervention could be considered an effective strategy in preventing CRC.

Psychiatric disorder and its association with gastrointestinal cancer: a retrospective cohort study with 45,842 patients in Germany.

Psychiatric disorders and cancer are both common, and comorbidity has detrimental impacts on cancer outcomes. Previous studies focus on affective disorders which arise after cancer diagnosis, not on the impact of psychiatric disorders on cancer risk. We investigate the association between psychiatric disorders and subsequent gastrointestinal cancer in a large cohort in Germany. This case-control study used secondary data (electronic medical records) from the national IQVIA Disease Analyzer database.We evaluated the association between previous psychiatric diagnosis in 44,582 matched patients with and without gastrointestinal (GI) cancer. Regression analyses were stratified by psychiatric diagnosis and adjusted by chronic comorbidities and previous psychiatric treatments. No association between any previous psychiatric disease and GI cancers was found (OR = 0.98 (0.95-1.02 95%CL, p = 0.39). Previous psychosomatic disorder and GI cancer showed a significant negative association (OR: 0.86, 0.81-0.90 95%CL, p < 0.0001). No association was found between previous diagnosis with depression or PTSD and GI cancer. These results remained consistent when including previous psychiatric treatments in the regression analyses. Psychiatric disease was not associated with GI cancer risk. Further investigation into the pathways linking psychiatric disease and cancer needs to be conducted, taking into consideration psychiatric treatments administered, to enhance our understanding of the relationship between these two common and devastating diseases.

Association between Metabolically Healthy Status and Risk of Gastrointestinal Cancer.

Although obesity is associated with numerous diseases, the risks of disease may depend on metabolically healthy status. Nevertheless, it is unclear to whether metabolically healthy status affects risk of gastrointestinal (GI) cancer in general Chinese population. A total of 114,995 participants who met the criteria were included from the Kailuan Study. The study participants were divided into four groups according to body mass index (BMI)/waist circumference (WC) and metabolic status. Incident of GI cancer (esophageal cancer, gastric cancer, liver cancer, biliary cancer, pancreatic cancer, and colorectal cancer) during 2006-2020 were confirmed by review of medical records. The Cox proportional hazard regression models were used to assess the association metabolically healthy status with the risk of GI cancer by calculating the hazard ratios (HR) and 95% confidence interval (CI). During a mean 13.76 years of follow-up, we documented 2,311 GI cancers. Multivariate Cox regression analysis showed that compared with the metabolically healthy normal-weight group, metabolically healthy obese (MHO) participants demonstrated an increased risk of developing GI cancer (HR, 1.54; 95% CI, 1.11 to 2.13) by BMI categories. However, such associations were not found for WC category. These associations were moderated by age, sex, and anatomical site of the tumor. Individuals with metabolic unhealthy normal-weight or metabolic unhealthy obesity phenotype also have an increased risk of GI cancer. MHO phenotype was associated with increased risk of GI cancer. Moreover, individuals who complicated by metabolic unhealthy status have an increased risk of developing GI cancer. Hence, clinicians should consider the risk of incident GI cancer in people with abnormal metabolically healthy status and counsel them about metabolic fitness and weight control.

Limitation of PET/CT for screening of synchronous upper gastrointestinal cancer in oral cancer patients

ObjectivePatients with squamous cell carcinoma (SCC) of the head and neck including the oral cavity have a high risk of upper gastrointestinal cancer, especially esophageal cancer. Synchronous upper gastrointestinal cancers affect the field of radiation or surgery, and undetected double cancer can cause poor prognosis. The purpose of this retrospective study was to evaluate the diagnostic performance of 18 F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT) for detecting synchronous upper gastrointestinal cancer at the initial staging of oral cancer patients. MethodsBetween September 2006 and August 2021, 804 newly diagnosed oral squamous cell carcinoma patients who undergo esophagogastroduodenoscopy (EGD) and FDG-PET/CT at the initial staging were enrolled in this study. The incidence of synchronous upper gastrointestinal cancer in EGD screening at the initial staging of oral cancer was retrospectively calculated. Furthermore, we evaluated the diagnostic performance of FDG-PET/CT for screening of synchronous upper gastrointestinal cancer in oral cancer patients. ResultsThe incidence of synchronous upper gastrointestinal cancer in EGD screening at the initial staging of oral cancer was 4.2% (34/804 patients). Of 34 oral cancer patients with synchronous upper gastrointestinal cancer, 26 (76.5%) had both smoking and drinking habits. The sensitivity, specificity, accuracy, false-negative rate, false-positive rate, positive predictive value, and negative predictive value of FDG-PET/CT for synchronous upper gastrointestinal cancer were 44.1%, 99.6%, 97.3%, 55.9%, 0.4%, 83.3%, and 97.6%, respectively. ConclusionsBecause PET/CT cannot sufficiently detect synchronous upper gastrointestinal cancer in oral SCC patients, EGD screening before the treatment may be suitable for the high-risk oral SCC patients.

Effects of ranitidine and nizatidine on the risk of gastrointestinal cancer.

Gastrointestinal (GI) cancer occurs in digestive organs such as the stomach, colon, liver, esophagus, and pancreas. About 83,034 cases occurred in Korea alone in 2020. Dietary factors, alcohol consumption, Helicobacter pylori (H. pylori), and lifestyle factors increase the incidence of diseases such as gastritis, peptic ulcer, pancreatitis, and gastroesophageal reflux disease (GERD), which can develop into GI cancer. However, in 2019, the US Food and Drug Administration announced that the drugs ranitidine and nizatidine, which are used for digestive disorders, contain carcinogens. In this study, we investigated the effects of ranitidine and nizatidine on the development of GI cancer. In this study, using National Health Insurance Service-National Sample Cohort (NHIS-NSC) version 2.5 (updated from 2002 to 2019), subjects who developed GI cancer were enrolled in the case group, and those who were at risk of, but did not develop, cancer were enrolled in the control group. Thereafter, risk-set matching was performed (1:3 ratio) by sex and age at the time of diagnosis of cancer in the case group. Through this procedure, 22,931 cases and 68,793 controls were identified. The associations of ranitidine and/or nizatidine with GI cancer were confirmed by adjusted odds ratios (aORs) and 95% confidence intervals (CIs) calculated through conditional logistic regression analysis. The aORs of ranitidine and/or nizatidine users were lower than those of nonusers in all average prescription days groups (< 30 days/year: aOR [95% CI] = 0.79 [0.75-0.82]; 30-59 days/year: aOR [95% CI] = 0.66 [0.59-0.73]; 60-89 days/year: aOR [95% CI] = 0.69 [0.59-0.81]; ≥ 90 days/year: aOR [95% CI] = 0.69 [0.59-0.79]). Sensitivity analyses were conducted with different lag periods for the onset of GI cancer after drug administration, and these analyses yielded consistent results. Additional analyses were also performed by dividing subjects into groups based on cancer types and CCI scores, and these analyses produced the same results. Our study, using nationwide retrospective cohort data, did not find evidence suggesting that ranitidine and nizatidine increase the risk of GI cancer. In fact, we observed that the incidence of GI cancer was lower in individuals who used the drugs compared to nonusers. These findings suggest a potential beneficial effect of these drugs on cancer risk, likely attributed to their ability to improve digestive function.

Ambient Air Pollution and Risk of Enterotomy, Gastrointestinal Cancer, and All-Cause Mortality among 4,708 Individuals with Inflammatory Bowel Disease: A Prospective Cohort Study.

Previous studies indicated that air pollution plausibly increases the risk of adverse outcomes in inflammatory bowel disease (IBD) via proinflammatory mechanisms. However, there is scant epidemiological data and insufficient prospective evidence assessing associations between ambient air pollution and clinical outcomes of IBD. We aimed to investigate the associations between ambient air pollution and clinical outcomes among individuals with IBD. Leveraging data from the UK Biobank, we included 4,708 individuals with IBD recruited in the period 2006-2010 in this study. A land use regression model was used to assess annual mean concentrations of ambient air pollutants nitrogen including oxides (), nitrogen dioxide (), and particulate matter (PM) with aerodynamic diameter () and PM with aerodynamic diameter (). Individuals with IBD were followed up for incident clinical outcomes of enterotomy, gastrointestinal cancer, and all-cause mortality, ascertained via death registry, inpatient, primary care, and cancer registry data. Cox proportional hazard model was used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) for the magnitude of the associations. During a mean follow-up of 12.0 y, 265 enterotomy events, 124 incident gastrointestinal cancer, and 420 death events were documented among individuals with IBD. We found that each interquartile range (IQR) increase in exposure to was associated with increased risk of enterotomy (; 95% CI: 1.00, 1.34, ), whereas an IQR increase in exposure to (; 95% CI: 1.01, 1.20, ), (; 95% CI: 1.03, 1.29, ), (; 95% CI: 1.03, 1.30, ), and (; 95% CI: 1.02, 1.28, ) was associated with increased risk of all-cause mortality among individuals with IBD. We did not observe any significant associations between air pollutants and gastrointestinal cancer in the primary analyses. Consistent results were observed in subgroup and sensitivity analyses. Ambient pollution exposure was associated with an increased risk of enterotomy and all-cause mortality among individuals with IBD, highlighting the important role of environmental health in improving the prognosis of IBD. https://doi.org/10.1289/EHP12215.