Prevalence of gastrointestinal malignancy in non-anemic iron deficiency and significance for endoscopic screening: A Western Australian multicenter cohort study.

BACKGROUND AND AIM: There is a paucity of evidence regarding non-anemic iron deficiency as a predictor for colorectal cancer and therefore the indication for endoscopic evaluation. This study explores the rates of malignancy in adults with iron deficiency with and without anemia. METHODS: A retrospective multicenter diagnostic cohort study was conducted across two Australian health services. All cases that underwent both esophagogastroduodenoscopy and colonoscopy between September 1, 2018, and December 31, 2019, for the investigation of iron deficiency were included, and the cohort was divided into anemic and non-anemic arms. Multivariate binomial logistic regression was performed to establish clinical characteristics associated with neoplasia. RESULTS: Five hundred eighty-four patients underwent endoscopic evaluation over a 16-month period. There was a significantly higher rate of malignancy in the iron deficiency anemia arm as compared with those without anemia (8.76% vs 1.20%, P < 0.01). Gastrointestinal pathology to account for iron deficiency was identified in > 60% of the total cohort. The presence of anemia (odds ratio [OR] 6.87, P < 0.01) and male gender (OR 3.01, P = 0.01) were significant predictors of malignancy. CONCLUSION: This study demonstrates that anemic iron deficiency confers a significantly greater risk of gastrointestinal cancer compared with non-anemic iron deficiency. Additionally, over 60% of patients had gastrointestinal pathology to account for iron deficiency overall, supporting the need to perform baseline endoscopy in patients with iron deficiency.

A population-based study of IGF axis polymorphisms and the esophageal inflammation, metaplasia, adenocarcinoma sequence.

BACKGROUND & AIMS: Insulin-like growth factor (IGF) axis plays a key role in cell development, proliferation, and survival and is implicated in the etiology of several cancers. Few studies have examined the relationship between genetic variation of this axis and esophageal adenocarcinoma (EAC) or its precursors. METHODS: In a population-based case-control study, we investigated the association of common polymorphisms of IGF-1, IGF-2, IGF-1 receptor, IGF binding protein-3, growth hormones (GH) 1 and GH2, and GH receptor with reflux esophagitis (RE), Barrett esophagus (BE), and EAC. Two hundred and thirty RE, 224 BE, 227 EAC cases, and 260 controls were studied. Gene polymorphisms were identified using publicly available online resources; 102 IGF axis tag and putatively functional single-nucleotide polymorphisms (SNPs) were analyzed using MassARRAY iPLEX and Taqman assays. Results were analyzed using Haploview. RESULTS: Three polymorphisms were disease-associated. IGF1 SNP rs6214 was associated with BE (adjusted P = .039). Using GG genotype as reference, odds ratio for BE in AA (wild-type) was 0.43 (95% confidence interval [CI], 0.24-0.75). GH receptor SNP rs6898743 was associated with EAC (adjusted P = .0112). With GG as reference, odds ratio for EAC in CC (wild-type) genotype was 0.42 (95% CI, 0.23-0.76). IGF1 (CA)(17) 185-bp allele was associated with RE (adjusted P = .0116). Using IGF1(non17) as reference, odds ratio for RE in IGF1(17) carriers was 7.29 (95% CI, 1.57-46.7). CONCLUSIONS: In this study, 3 polymorphisms of IGF genes were associated with EAC or its precursors. These polymorphisms may be markers of disease risk; independent validation of our findings is required. These results suggest the IGF pathway is involved in EAC development.