Purpose: To determine the characteristic magnetic resonance imaging (MRI) features of mass-forming autoimmune pancreatitis (AIP), which allow its differentiation from pancreatic adenocarcinoma (PAC).Materials and Methods: MR images of 37 patients with either pathologically proven, mass-forming AIPs (n ¼ 9) or PACs (n ¼ 28) were retrospectively reviewed. The pancreatic MR protocol included unenhanced images, contrastenhanced dynamic images, diffusion-weighted imaging (DWI), and MR-cholangiopancreatography (MRCP). Two reviewers analyzed the MR images regarding the number, location, morphologic features, and enhancement degree and pattern of the lesions as well as secondary changes of the pancreatic parenchyma, the biliary and pancreatic ducts. The size and apparent diffusion coefficient (ADC) values of the lesions were measured.Results: Although sensitivities were low (28.6%-44.4%), specificities of multiplicity, capsule-like rim enhancement, and skipped stricture of the biliary or pancreatic duct in mass-forming AIP were high (100%). Sensitivities and specificities of irregular or geographic shape, delayed enhancement, and a low ADC value <1.26 Â 10 À3 mm 2 /s in mass-forming AIP were favorable (71.4%-83.3% and 78.5%-89.3%).
Conclusion:Although to differentiate mass-forming AIP from pancreatic cancer is difficult, the combination of MRI findings including contrast-enhanced dynamic images, MRCP, and DWI can be a help.
Infection and systemic inflammatory response syndrome play an important role in the development of alcohol-related ACLF in Asian patients with active alcoholism. The CLIF-C ACLFs may be more useful for predicting mortality in ACLF cases than liver-specific scoring systems.
Corrosive esophagitis and gastritis are characterized by caustic damage due to ingestion of chemical agents. Caustic agents cause tissue destruction through liquefaction or coagulation reactions. Here, we report a case of corrosive esophagitis and gastritis caused by accidental ingestion of glutaraldehyde in Korea. A 62-year-old man presented to the emergency department 8 hours after ingesting glutaraldehyde, which is widely used for the prevention of foot-and-mouth disease in pigs. Urgent endoscopic examination revealed severely damaged mucosae of the esophagus and stomach. With conservative treatment, the patient’s condition was improved, and he was discharged on the 35th day of admission.
Genetic polymorphism can result in abnormal pharmacodynamics that subsequently leads to the individual variance in sedative effects and adverse reactions. The aim of this study was to elucidate the association between midazolam-related genetic polymorphism and sedative effects, including adverse reactions, under conscious sedation during upper gastrointestinal endoscopy. We prospectively enrolled 100 eligible patients undergoing upper gastrointestinal endoscopy. The efficacy of the sedation, adverse reactions, plasma concentration of midazolam and 1-hydroxymidazolam were investigated as well as the genetic polymorphism of MDR1 and CYP3A5. The correlation between genetic polymorphism and sedative effects was assessed. Regarding MDR1 gene, the plasma concentration of midazolam was greater in patients with CGC haplotype (P = 0.012), while it was lower in patients with CAC haplotype (P = 0.005) than in those with other haplotypes. However, genetic polymorphism of neither MDR1 nor CYP3A5 correlated with the plasma concentration of 1-hydroxymidazolam. CGT haplotype of MDR1 was significantly correlated with sedation grade after midazolam administration (P = 0.042). In contrast, genetic polymorphism of CYP3A5 was not correlated with sedation grade. There was no association between genetic polymorphism of MDR1 or CYP3A5 and selected adverse reactions related to midazolam. Genetic polymorphism of MDR1 influences the concentration of midazolam and the sedation grade. However, it is not associated with adverse reactions such as paradoxical response and retrograde amnesia.
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