Duodenal adenomas coincide with colorectal neoplasia.

BACKGROUND AND AIM: Small case series have alluded to an association between sporadic duodenal adenomas and colorectal neoplasia. The strength of the association remains uncertain. This case-control study was designed to test this association in a large national pathology database. METHODS: This study, performed at Miraca Life Sciences, a specialized pathology laboratory that receives gastrointestinal biopsy specimens from outpatient centers throughout the US, included all subjects who underwent a bidirectional endoscopy with biopsy results from both procedures between January 2008 and December 2011. The association between duodenal and colonic neoplasms was investigated using odds ratios (OR) and their 95 % confidence intervals (CIs) derived from univariate and multivariate analyses. RESULTS: There were 203,277 patients who underwent bidirectional procedures within the study period (mean age 58 years, 58 % females). Duodenal adenomas were present in 537 patients (median age 65 years, 51 % females; OR for male sex 1.34, 95 % CI 1.13-1.59). Hyperplastic colon polyps were present in 30,205 and colon adenomas in 85,801 patients. Hyperplastic polyps were more common in patients with duodenal adenomas (1.45, 1.07-1.95). Patients with duodenal adenomas also had a significantly greater prevalence of all types of colonic adenomas (2.65, 2.16-3.25), particularly of advanced adenomas (4.30, 3.24-5.70) and colorectal cancer (3.13, 1.38-7.12). Duodenal adenomas were associated with an equally increased risk for left and right colon adenomas. CONCLUSIONS: Patients with duodenal adenomas harbor an increased risk for any type of colonic neoplasm. This association may provide new insights into the general mechanisms underlying mucosal proliferation in the gastrointestinal tract.

Prevalence of esophageal eosinophilia varies by climate zone in the United States.

OBJECTIVES: The epidemiology of eosinophilic esophagitis (EoE) is rapidly evolving, and differences in climate could impact the prevalence of EoE. We aimed to examine the association between esophageal eosinophilia and climate zones in the United States. METHODS: This was a cross-sectional study of esophageal biopsies from 2008 to 2010 in a large US pathology database. Cases were patients with esophageal eosinophilia; controls had normal esophageal biopsies. A Köppen-Geiger (K-G) climate class was assigned to each patient, and the association between case-control status and the main K-G climate type (tropical, arid, temperate, or cold) was assessed. RESULTS: A total of 233,649 patients were included, 71,948 (30.8%) with normal esophageal biopsies and 9,995 (4.3%) with esophageal eosinophilia. Using the temperate zone as the referent and after multivariable analysis, the odds of esophageal eosinophilia were highest in the cold climate zone (odds ratio (OR)=1.39, 95% confidence interval (CI): 1.34-1.47), compared with the tropical zone (OR=0.87; 95% CI: 0.71-10.8) and the arid zone (OR=1.27; 95% CI: 1.19-1.36). Increased likelihood of EoE was also associated with increasing odds of being in the cold climate zone. Compared with patients with normal esophageal biopsies, patients with dysphagia, a clinical suspicion of EoE, no reflux or Barrett's esophagus, esophageal eosinophilia, and eosinophilic microabscesses had the highest adjusted odds of being in a cold climate zone (OR 2.02; 1.78-2.28). CONCLUSIONS: Esophageal eosinophilia differs significantly between K-G climate zones, with the highest prevalence in the cold and arid zones. Geographical and climate patterns may help identify candidate antigens characteristic to high-prevalence areas to be targeted for future investigation.

Histopathologic diagnosis of eosinophilic conditions in the gastrointestinal tract.

Eosinophils, a constitutive component of the columnar-lined gastrointestinal tract, play an essential role in allergic responses and parasitic infections. The tissue density of these cells also increases in a variety of conditions of uncertain etiology. With the exception of the esophageal squamous epithelium, in which no eosinophils are normally present, the population of normal eosinophils in the remainder of the luminal gut is poorly defined. Therefore, histopathologists must rely on their subjective judgment to determine when a diagnosis of eosinophilic gastritis, enteritis, or colitis should be rendered. Eosinophilic esophagitis is currently the best defined and most studied eosinophilic condition of the digestive tract; therefore, the confidence in accurate diagnosis is increasing. In contrast, the characteristic clinicopathologic features of eosinophilic conditions affecting other parts of the digestive tract remain somewhat elusive. This review was designed to present pathologists with simple and practical information for the biopsy-based histopathologic diagnosis of eosinophilic esophagitis, gastritis, enteritis, and colitis. It was prepared by critically reviewing more than 200 articles on the topic, along with incorporating evidence accumulated through our own collective experience. We anticipate that by increasing pathologists' confidence in reporting these abnormal but often nameless eosinophilic infiltrates, we can help better define and characterize their significance.

Inverse association of esophageal eosinophilia with Helicobacter pylori based on analysis of a US pathology database.

BACKGROUND & AIMS: Eosinophilic esophagitis (EoE) is of increasing prevalence and believed to result from allergic processes. Helicobacter pylori has been inversely associated with allergic diseases, but there is no known relationship between H pylori, EoE, and esophageal eosinophilia. We investigated the association between esophageal eosinophilia and H pylori infection. METHODS: We performed a cross-sectional study of data, collected from a US pathology database, on 165,017 patients in the United States who underwent esophageal and gastric biopsies from 2008 through 2010. Patients with and without H pylori on gastric biopsy were compared, and odds of esophageal eosinophilia were determined. RESULTS: From the data analyzed, 56,301 (34.1%) had normal esophageal biopsy specimens, 5767 (3.5%) had esophageal eosinophilia, and 11,170 (6.8%) had H pylori infection. Esophageal eosinophilia was inversely associated with H pylori (odds ratio [OR], 0.77; 95% confidence interval [CI], 0.69-0.87). Compared with patients with normal esophageal biopsy specimens, odds of H pylori were reduced among patients with ≥ 15 eosinophils per high-power field (eos/hpf) (OR, 0.79; 95% CI, 0.70-0.88), ≥ 45 eos/hpf (OR, 0.75; 95% CI, 0.61-0.93), ≥ 75 eos/hpf (OR, 0.72; 95% CI, 0.50-1.03), and ≥ 90 eos/hpf (OR, 0.52; 95% CI, 0.31-0.87) (P for trend <.001). A similar dose-response trend was observed for increasing clinical suspicion for EoE and decreasing prevalence of H pylori. Additionally, severity of histologic effects of H pylori was inversely associated with esophageal eosinophilia. All trends held in multivariate analysis. CONCLUSIONS: In a large cross-sectional analysis, H pylori infection was inversely associated with esophageal eosinophilia. This relationship could have implications for the pathogenesis and epidemiology of EoE.