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Patients with Barrett's esophagus (BE) are at risk of progression esophageal adenocarcinoma (EAC). We developed a model to predict histologic progression in patients with non-dysplastic BE (NDBE).A longitudinal study in three referral centers, performed between January 2010 and-December 2019. As progression to LGD can be considered as indication for ablative therapy, the study endpoint was histopathologic progression to LGD, HGD or EAC at 3 years after diagnosis. We used logistic regression to create the model. Seventy percent of the cohort were used to stem the model and remaining 30% for internal validation.A total of 542 patients were included, 69.4% males, mean age 62.2 years. Long segment BE at index endoscopy was diagnosed in 20.8% of the patients. After mean follow up of 6.7 years, 133 patients (24.5%) had histologic progression. Our model identified neutrophil to lymphocyte ratio (NLR, OR 2.08, 95% confidence interval, CI, 1.77-2.32, p0.001), BE length (OR 1.22, 95% CI 1.09-1.36, p0.001), age (OR 1.03, 95% CI 1.02-1.05, p=0.02), smoking (OR 1.66, 95% CI 1.09-2.75, p=0.04) and renal failure (OR 1.51. 95% CI 0.93-2.43, p=0.07) as predictors of histologic progression at 3 years. The area under the receiver operating characteristic curves of this model were 0.88 and 0.76 in the training and validation cohort, respectively.This novel, internally validated model may predict histologic progression, even in patients with NDBE who generally have low rates of progression over time, and may contribute to enhance patient selection for more intense surveillance programs.

Type 2 diabetes mellitus is a multifactorial disease in which genetic susceptibility and environmental factors induce pancreatic β-cell dysfunction and insulin resistance. Additional factors such as hyperglycemia and hyperlipidemia have roles in β-cell dysfunction and disease progression. The phenomenon of lipid-induced pancreatic β-dysfunction, designated as lipotoxicity, has been observed in several in vitro and in vivo experiments; however, there is still no solid evidence for the occurrence of this event in humans. The toxic effect of high lipid levels on β-cell function consists of impaired insulin gene expression, apoptosis, and reduced glucose-stimulated insulin secretion.To demonstrate the importance of treating hypertriglyceridemia in reducing glucose intolerance and the need for insulin therapy in hospitalized diabetic patients.We evaluated five clinical case reports and conducted a detailed literature review via the PubMed search engine.Reduction in elevated blood triglyceride and glucose levels in hospitalized diabetic patients resulted in a rapid decline in glucose levels and in the need for insulin therapy.A decrease in high triglyceride levels in "lipotoxic" diabetic patients may improve insulin intolerance and glucose homeostasis and reduce the need for insulin therapy.