[Rare Incidental Finding during a Student Ultrasonography Course - A Case Report]. / Seltener Zufallsbefund in einem studentischen Sonografiekurs ­ ein Fallbericht.

Rare Incidental Finding during a Student Ultrasonography Course - A Case Report Abstract. During a sonography class in medical school, a large fluid-filled mass was discovered in the center of the lower abdomen in a healthy, asymptomatic female student; an overflow bladder was suspected. Despite various interdisciplinary investigations, the etiology of the cystic formation could not be clarified. Three months after discovery of the incidental finding, the increasingly symptomatic patient was diagnosed with a cystic tumor in the lower abdomen with secondary urinary retention, and surgical cyst excision was performed. A large, serous Paratubular cyst was found on the left side with torsion of the tube without signs of ischemia and without malignancy. Incidental findings in ultrasound teaching are not uncommon. Course participants, tutors, and course instructors must be aware of this and have a clear procedure at hand in order to deal with it.

Glucose-induced glucagon-like Peptide 1 secretion is deficient in patients with non-alcoholic fatty liver disease.

BACKGROUND & AIMS: The incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal peptide hormones regulating postprandial insulin release from pancreatic ß-cells. GLP-1 agonism is a treatment strategy in Type 2 diabetes and is evaluated in Non-alcoholic fatty liver disease (NAFLD). However, the role of incretins in its pathophysiology is insufficiently understood. Studies in mice suggest improvement of hepatic steatosis by GLP-1 agonism. We determined the secretion of incretins after oral glucose administration in non-diabetic NAFLD patients. METHODS: N=52 patients (n=16 NAFLD and n=36 Non-alcoholic steatohepatitis (NASH) patients) and n=50 matched healthy controls were included. Standardized oral glucose tolerance test was performed. Glucose, insulin, glucagon, GLP-1 and GIP plasma levels were measured sequentially for 120 minutes after glucose administration. RESULTS: Glucose induced GLP-1 secretion was significantly decreased in patients compared to controls (p<0.001). In contrast, GIP secretion was unchanged. There was no difference in GLP-1 and GIP secretion between NAFLD and NASH subgroups. All patients were insulin resistant, however HOMA2-IR was highest in the NASH subgroup. Fasting and glucose-induced insulin secretion was higher in NAFLD and NASH compared to controls, while the glucose lowering effect was diminished. Concomitantly, fasting glucagon secretion was significantly elevated in NAFLD and NASH. CONCLUSIONS: Glucose-induced GLP-1 secretion is deficient in patients with NAFLD and NASH. GIP secretion is contrarily preserved. Insulin resistance, with hyperinsulinemia and hyperglucagonemia, is present in all patients, and is more severe in NASH compared to NAFLD. These pathophysiologic findings endorse the current evaluation of GLP-1 agonism for the treatment of NAFLD.