The objective of this study was to compare the effects of various nutrients (fats, proteins, amino acids, and carbohydrates), given directly into the duodenum or the colon, on the release of peptide-YY (PYY) in conscious dogs. As reported previously, this study showed that plasma levels of PYY increased significantly (P less than 0.05) within 15 min in response to an oral mixed meal. Intraduodenal (ID) administration of a fatty acid (oleic acid; 100 mmol/L; 100 ml/h) stimulated a robust release of PYY, whereas ID administration of an amino acid mixture (phenylalanine plus tryptophan; 100 mmol/L each; 100 ml/h), glucose (1 g/kg), or a liver extract (10%; 100 ml/h) failed to elevate plasma levels of PYY. ID administration of glucose at 2 g/kg caused a mild but significant elevation in plasma PYY levels. Intracolonic administration of saline, a fatty acid, an amino acid mixture, glucose, or a liver extract significantly stimulated PYY release. This study suggests that as chyme moves from the stomach to the proximal bowel, fat is the primary constituent of food that stimulates the prompt release of PYY. However, unabsorbed nutrients can release PYY by a direct contact with the PYY-containing cells lining the intestinal lumen of the terminal ileum, colon, and rectum. Both mechanisms probably participate in the release of PYY.

INTRODUCTION: Dunbar Syndrome, also known as median arcuate ligament syndrome (MALS), is a rare condition with a reported incidence of 2 per 100,000. It is characterized by an extrinsic compression of the celiac trunk, and should be considered when evaluating patients with abdominal pain of unknown etiology. CASE DESCRIPTION/METHODS: A 78 year old female presented with a complaint of epigastric discomfort that was post-prandial in nature, with associated weakness and early satiety. Her symptoms had been persistent for one year. Workup prior to her presentation included a normal nuclear medicine (NM) gastric emptying scan and normal NM hepatobiliary scan with CCK. A detailed history revealed that her pain was particularly worse after eating and was associated with early satiety. Laboratory results on admission were unremarkable. Contrast-enhanced CT scan of the abdomen and pelvis showed external compression and indentation of the superior aspect of the proximal celiac axis with post-stenotic dilation. Further diagnostic evaluation utilized end-inspiratory phase CT angiography of the abdomen, which showed an approximately 1 cm length segment of proximal celiac arterial narrowing, measuring 70% maximally at its origin. She was diagnosed with MALS after review of the CTA reconstructive images which showed moderate external compression of the celiac artery. DISCUSSION: MALS predominantly affects women between the ages of 30 and 50 and is marked by the hallmark feature of postprandial abdominal pain. Other signs and symptoms may include nausea, vomiting, and consequent weight loss from an inability to tolerate oral intake. Symptoms are thought to have both a vascular (mesenteric ischemia) as well as neurogenic component (somatic pain thought to originate from the splanchnic plexus). CT angiography and conventional angiography are considered to be gold standard imaging modalities for Dunbar syndrome. They demonstrate focal stenosis that has a characteristic hooked appearance due to the indentation of the celiac trunk on its superior surface. Imaging for an accurate diagnosis should ideally be performed during the end-inspiratory phase, as indentation of the celiac trunk may be seen normally during expiration. Additional imaging features may include post-stenotic dilation, prominent collateral vessels, and thickening of the median arcuate ligament. Treatment includes endovascular transluminal angioplasty and stent placement, as well as laparoscopic division of the arcuate ligament and resection of the celiac plexus.

INTRODUCTION: Acute Myelogenous Leukemia (AML) is a heterogenous group of cancers of blood cells associated with many dysfunctions due to monoclonal expansion of blood marrow. AML typically presents with symptoms of pancytopenia, including general fatigue, weakness, infections, ecchymoses, epistaxis, or menorrhagia. Overt GI bleeding is not a common initial presentation for AML. CASE DESCRIPTION/METHODS: Our patient was an 85-year-old female with a past medical history of gastrointestinal bleed while taking DOAC for pulmonary embolism, gastroesophageal reflux disease, hypertension, and uterine adenoma with subsequent hysterectomy and bilateral oophorectomy. She presented with complaint of “jet black” stools for 12 hours and accompanying weakness. She had no other alarm symptoms including pallor, bruising, neurological complaints, weight loss, hematochezia, or night sweats. She was known to have a hiatal hernia on previous EGDs and a bleeding distal rectal mucosal lesion concerning for a Dieulafoy lesion, both of which were two years prior to admission. Her initial labs were significant for hemoglobin 8.4, platelets 24, INR 1.0, and white blood cell count 5.1 with normal differential. Upper GI bleed was suspected, despite her previous lower GI bleeding, and the first upper endoscopy was performed; this revealed a possible Dieulafoy lesion that was hemoclipped. Her anemia and melena continued to worsen and Hematology performed a bone marrow biopsy. In the intervening time, two more upper endoscopies were performed yielding no further evidence of bleeding. Given her continued symptoms, colonoscopy was performed showing blood in the terminal ileum and right colon with no obvious lesion; there was, however, discrete mucosal bleeding sites in the rectum with no lesions noted after extensive cleaning. Multiple hemoclips were placed in the rectum but,ultimately, none of the endoscopic interventions proved durative. Shortly after colonoscopy, bone marrow biopsy revealed AML. DISCUSSION: Our case highlights a unique presentation of AML, where gastrointestinal bleeding is the first major presenting symptom. Bruising, epistaxis, and vaginal bleeding are the most typical types of bleeding in AML, none were found in this patient. AML is due to dysfunctions due to monoclonal expansion blood marrow that can lead to preferentially nonfunctional blood lines. This patient had significant thrombocytopenia with cells that were dysfunctional, leading to diffuse gastrointestinal hemorrhage without the presence of bleeding lesions.

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