eosinophilic esophagitis

There is growing evidence that gastroesophageal disease is influenced by the esophageal microbiome, and that commensal bacteria of the oropharynx, stomach, and colon are thought to have a role in modulatiing pathogenesis. These emerging hypotheses are based on observed changes in the composition of the esophageal flora, notably, repeated observations: 1. There is an abundance of gram-positive bBacteria in the healthy esophagus. are more gram positive prevalent 2. The esophageal bacterial population becomes increasingly gram negative with disease progression. Associated with this shift to a more gram negative prevalence is an increase in the potential for the presence of antigenic lipopolysaccharide (LPS). The immunoreactivity of LPS endotoxin thought to promote susceptibility to inflammation and disease. The pathogenesis of the more common diseases of the esophagus e.g. gastroesophageal reflux disease (GERD), esophageal dysmotility (achalasia), eosinophilic esophagitis (EoE), Barrett’s esophagus (BE), and esophageal cancer, are well-established. Emerging data suggest however, that these are all characterized by an immune-mediated inflammatory cascade, propogated by a dysbiotic state. Thereby, the ability of the healthy “normative state” to protect against foreign bacteria is compromised. This dysbiosis thereby can create adverse inflammatory or immunoregulatory responses with progression of disease. In the normal healthy state, the esophageal microbiome is constituted in-part, by a multitude of gram positive bacteria, many of which produce antibacterial peptides called bacteriocins. Bacteriocins are selective and used to maintain population integrity by killing off foreign bacteria. When the “normative biome” is interrupted (e.g. antibiotics, medications, diet, environmental factors), the constitutional changes may allow a more hospitable imbalance favoring the proliferation of opportunistic pathogens. Therefore it seems rational that defining, perhaps that defining, perhaps cultivating, a protective bacterial community that could help prevent or mitigate inflammatory diseases of the esophagus. Furthermore, in conjunction with evidence demonstrating that some bacteriocins are cytotoxic or antiproliferative toward cancer cell lines, further exploration might provide a rich source of effective peptide-based drug targets. Therapeutic options targeting the microbiome, including prebiotics, probiotics, antibiotics and bacteriocins, have been studied, albeit the attributable effects on the esophagus for the most part, have been unrecognized by clinicians. This review focuses on the current knowledge of the involvement of the microbiome in esophageal diseases (most notably GERD/Barrett’s esophagus/esophageal cancer) and identifies emerging new concepts for treatment.

Acute pancreatitis is inflammation of the pancreas that may be accompanied by a systemic inflammatory response which results in impairment of the functioning of various organs, systems. Pancreatitis associated vascular complications very often cause morbidity and mortality. There are various cardiovascular complications like shock, hypovolemia, pericardial effusion, and sometimes ST–T changes in the electrocardiogram (ECG) presenting as acute myocardial infarction (AMI). Acute myocardial infarction complicating acute pancreatitis has rarely been studied and the exact process of myocardial injury still remains unclear. We here report a case of Acute Pancreatitis associated with acute myocardial Infarction.

Studies in children with eosinophilic esophagitis (EoE) have reported esophageal strictures but none have examined risk factors associated with strictures. Aim: To assess risk factors associated with strictures in children with EoE. Methods: In this retrospective study, children with EoE seen over 20 years were separated into two groups; with and without strictures. Physical features, CBC, endoscopic findings, and biopsy of the distal and mid-esophagus were captured. Statistical significance with p - value and multivariate logistic regression was done. Results: Total patients 222 and 20 (9.1%) had strictures. Mean age of stricture patients 12.7 years (range 7-18) and non-stricture 9.3 years (range 1-17) (p = 0.006). Among stricture patients following were prevalent and significant; dysphagia (stricture 100% vs. non-stricture 41.6%, p = 0.0005) and food impaction (70.04% vs. 4%, p = 0.0005); EGD: rings and exudates were strongly associated with stricture, 45.0% vs. 4.5%, p = 0.0005 and 60% vs. 30.7%, p = 0.008, respectively. Abdominal pain was lower in the stricture group (5% vs. 31.2%, p = 0.017). Eosinophil counts were numerically more in the stricture group but not significant. Multivariate logistic regression confirmed that strictures are likely to occur among patients with dysphagia (p = 0.02, OR = 11.7, 95% LCL 2.0) and food impaction (p = 0.0001, OR = 80.9, 95% LCL 15.4), respectively, adjusted for age and gender. Conclusion: EoE children with dysphagia or food impaction have a higher chance of having an esophageal stricture. These EoE children 12 years or over with exudates or rings on endoscopy, should be treated and carefully monitored, to reduce the risk of stricture formation.