Sitagliptin-induced Pancreatitis: Chronic Use Would Not Spare You the Complication.

Medication-induced pancreatitis is an overlooked cause of acute pancreatitis. We present an 81-year-old male patient with acute sharp epigastric pain radiating to his back, who was found to have lipase of more than 30,000 U/L. The patient denied current alcohol use. Abdominal ultrasound and abdominal computed tomography scan revealed no gallstones or biliary duct abnormalities. The patient had been taking sitagliptin for eight years. Supportive treatment with intravenous fluids, pain medications, and early feeding adequately treated his disease. With our case, we aim to increase awareness of sitagliptin-induced pancreatitis, regardless of the duration of use.

Endoscopic Ultrasound-Guided Drainage of Intramural Duodenal Abscess Caused by Foreign Body Ingestion.

A 63-year-old man presented with fever and generalized weakness for 2 days. Computed tomography scan showed an intramural duodenal abscess and a linear radiolucent foreign body penetrating the duodenal wall. Endoscopic drainage was performed. Endoscopic ultrasound showed fluid collection in the second portion of the duodenum. The duodenal lumen was punctured with the creation of stoma using a lumen-apposing metal stent and electrocautery system. The stent was deployed, and the drainage of purulent fluid followed. The foreign body was suspected to be a wire brush bristle. The patient received intravenous antibiotics for 14 days. Follow-up images showed the resolution of the abscess.

An in vitro model for studying the effects of continuous ethanol exposure on N-methyl-D-aspartate receptor function.

Long-term ethanol exposure has deleterious effects on both glial and neuronal function. We assessed alterations in both astrocytic and neuronal viability, and alterations in N-methyl-d-aspartate receptor (NMDAR) function, in cocultures of rat cerebellar granule cells (CGCs) and astrocytes after continuous ethanol exposure (CEE). Treatment of cells with 100 mM EtOH once every 24 h for 4 days resulted in a mean ethanol concentration of 57.3 ± 2.1 mM. Comparisons between control and post-ethanol-treated cells were made 4 days after the last ethanol treatment. CEE did not alter glial cell viability, as indicated by the absence of either changes in astrocytic morphology, actin depolymerization, or disruption of astrocytic intracellular mitochondrial distribution at any day postethanol treatment. The CGCs were healthy and viable after CEE, as indicated by phase-contrast microscopy and the trypan-blue exclusion method. Whole-cell patch-clamp experiments indicated that NMDA-induced currents (I(NMDA)) were altered by CEE treatment. Similar to previous results obtained during the withdrawal phase from chronic ethanol exposure, I(NMDA) from CEE-treated cells were significantly larger than I(NMDA) from NMDARs in control CGCs, but returned to control values by the fourth day post-CEE. However, after the last ethanol dosing and during a time when ethanol concentrations remained high, I(NMDA) were significantly smaller than control values. Identical results were observed in CGCs expressing the NR2A or NR2B subunit. In summary, both neurons and astrocytes remained healthy following exposure to CEE with no signs of neurotoxicity at the cellular level, and modulation of NMDAR function is consistent with findings from prior experiments. Thus, we conclude that the CEE paradigm in glial-neuronal cocultures readily lends itself to long-term in vitro studies of ethanol effects that include glial-neuronal interactions and the ability to study ethanol withdrawal-induced neurotoxicity.