A prospective evaluation of fatty pancreas by using EUS.

BACKGROUND: Fatty liver is associated with obesity, diabetes, hyperlipidemia, and the metabolic syndrome. The pathophysiology of fatty pancreas is poorly understood, but it may be closely related to fatty liver. OBJECTIVE: The aim of our study was to determine the prevalence of fatty pancreas and risk factors associated with its development. DESIGN: Prospective, single center study. SETTING: Tertiary-care academic medical center. PATIENTS: This study involved 250 consecutive patients referred for EUS examination. INTERVENTION: All patients undergoing EUS at our institution were prospectively identified. Information regarding demographics, tobacco use, alcohol use, blood test results, and comorbidities were collected before EUS. Pancreatic echogenicity was graded in comparison to the spleen at the time of EUS by using an a priori specified grading scheme. MAIN OUTCOME MEASUREMENTS: Prevalence of fatty pancreas and factors associated with its development. RESULTS: During the study period, 250 consecutive patients were prospectively enrolled. The prevalence of fatty pancreas was 27.8% (95% CI, 22.1-34.1). Fatty liver was seen in 22.6% of patients. Factors associated with fatty pancreas on univariate analysis were increasing body mass index (BMI) (P=.004), fatty liver (P<.0001), hyperlipidemia (P=.04), and the metabolic syndrome (odds ratio [OR] 3.13, P=.004). The presence of any metabolic syndrome components, that is, BMI≥30, hyperlipidemia, diabetes, or hypertension, increased the prevalence of fatty pancreas by 37% (OR 1.37, P=.01). Factors independently associated with fatty pancreas on multivariate analysis were increasing BMI (OR 1.05, P=.03) and fatty liver (OR 3.61, P<.001). We found no association between fatty pancreas and chronic pancreatitis or adenocarcinoma of the pancreas. LIMITATIONS: Single institution study. All patients were referred for EUS, which limits generalizability. Lack of histological confirmation of pancreatic fat. CONCLUSION: We found a strong association between fatty pancreas and the metabolic syndrome.

Drug-Induced Liver Injury After COVID-19 Vaccine.

The first case of coronavirus disease 2019 (COVID-19) was reported in December 2019 in China. World Health Organization declared it a pandemic on March 11, 2020. It has caused significant morbidity and mortality worldwide. Persistent symptoms and serious complications are being reported in patients who survived COVID-19 infection, but long-term sequelae are still unknown. Several vaccines against COVID-19 have been approved for emergency use around the globe. These vaccines have excellent safety profiles with few reported side effects. Drug-induced hepatotoxicity is mainly seen with different drugs or chemicals. There are only a few reported cases of hepatotoxicity with vaccines. We present a case of liver injury after administration of the vaccine against the COVID-19 infection.

Triage of General Gastrointestinal Endoscopic Procedures During the COVID-19 Pandemic: Results From a National Delphi Consensus Panel.

BACKGROUND AND AIMS: As the COVID-19 pandemic moves into the postpeak period, the focus has now shifted to resuming endoscopy services to meet the needs of patients who were deferred. By using a modified Delphi process, we sought to develop a structured framework to provide guidance regarding procedure indications and procedure time intervals. METHODS: A national panel of 14 expert gastroenterologists from throughout the US used a modified Delphi process, to achieve consensus regarding: (1) common indications for general endoscopy, (2) critical patient-important outcomes for endoscopy, (3) defining time-sensitive intervals, (4) assigning time-sensitive intervals to procedure indications. Two anonymous rounds of voting were allowed before attempts at consensus were abandoned. RESULTS: Expert panel reached consensus that procedures should be allocated to one of three timing categories: (1) time-sensitive emergent = scheduled within 1 week, (2) time-sensitive urgent = scheduled within 1-8 weeks, (3) nontime sensitive = defer to > 8 weeks and reassess timing then. The panel identified 62 common general endoscopy indications (33 for EGD, 21 for colonoscopy, 5 for sigmoidoscopy). Consensus was reached on patient-important outcomes for each procedure indication, and consensus regarding timing of the procedure indication was achieved for 74% of indications. Panelists also identified adequate personal-protective-equipment, rapid point-of-care testing, and staff training as critical preconditions before endoscopy services could be resumed. CONCLUSION: We used the validated Delphi methodology, while prioritized patient-important outcomes, to provide consensus recommendations regarding triaging a comprehensive list of general endoscopic procedures.

Gastrointestinal prophylaxis in critically ill patients.

Physiologic stress associated with illness and hospitalization is known to result in gastrointestinal ulceration, especially among the critically ill. The complication of this stress-related mucosal disease could be prevented with appropriate application of pharmacologic prophylaxis. Vigilance by the nursing staff is required to properly detect and manage the condition.

R-Etodolac decreases beta-catenin levels along with survival and proliferation of hepatoma cells.

BACKGROUND/AIMS: Inhibition of hepatoma cells by cyclooxygenase (COX)-2-dependent and -independent mechanisms has been shown previously. Here, we examine the effect of Celecoxib, a COX-2-inhibitor and R-Etodolac, an enantiomer of the nonsteroidal anti-inflammatory drug Etodolac, which lacks COX-inhibitory activity, on the Wnt/beta-catenin pathway and human hepatoma cells. METHODS: Hep3B and HepG2 cell lines were treated with Celecoxib or R-Etodolac, and examined for viability, DNA synthesis, Wnt/beta-catenin pathway components, and downstream target gene expression. RESULTS: Celecoxib at high doses affected beta-catenin protein by inducing its degradation via GSK3beta and APC along with diminished tumor cell proliferation and survival. R-Etodolac at physiological doses caused decrease in total and activated beta-catenin protein secondary to decrease in its gene expression and post-translationally through GSK3beta activation. In addition, increased beta-catenin-E-cadherin was also observed at the membrane. An associated inhibition of beta-catenin-dependent Tcf reporter activity, decreased levels of downstream target gene products glutamine synthetase and cyclin-D1, and decreased proliferation and survival of hepatoma cells was evident. CONCLUSIONS: The antitumor effects of Celecoxib (at high concentrations) and R-Etodolac (at physiological doses) on HCC cells were accompanied by the down-regulation of beta-catenin demonstrating a useful therapeutic strategy in hepatocellular cancer.

Fibroblast growth factor enriches the embryonic liver cultures for hepatic progenitors.

Fibroblast growth factors (FGFs) play an important role in hepatic induction during development. The aim of our study was to investigate the effect of exogenous FGFs on ex vivo liver development. We begin our analysis by examining FGF signaling during early mouse liver development. Phospho-FGF receptor (Tyr653/654) was detected in embryonic day 10 (E10) to E12 livers only. Next, E10 livers were cultured in the presence of FGF1, FGF4, or FGF8 for 72 hours and examined for histology, proliferation, apoptosis, and differentiation. FGFs especially FGF8 promoted sheet-like architecture, cell proliferation, and survival as compared to the control. All FGFs induced a striking increase in the number of c-kit and alpha-fetoprotein-positive progenitors, without altering albumin staining. However these progenitors were CK-19-positive (biliary and bipotential progenitor marker) only in the presence of FGF1 or FGF4 and not FGF8. FGFs also induced beta-catenin, a stem cell renewal factor in these cultures. In conclusion, the presence of activated FGFR indicates a physiological role of FGF during early liver development. FGF1 and FGF4 enrich the embryonic liver cultures for bipotential hepatic progenitors. FGF8 promotes such enrichment and induces a one-step differentiation toward a unipotential hepatocyte progenitor. Thus, FGFs might be useful for enrichment and propagation of developmental hepatic progenitors.