1.Clinical Features of Pseudoaneurysms Complicating Pancreatitis: Single Center Experience and Review of Korean Literature.
Ji Hyun KIM ; Jae Seon KIM ; Chang Duck KIM ; Hong Sik LEE ; Young Jig CHO ; Jong Sup LEE ; Do Won CHOI ; Woo Sik HAN ; Youn Ho KIM ; Jong Eun YEON ; Jong Jae PARK ; Kwan Soo BYUN ; Young Tae BAK
The Korean Journal of Gastroenterology 2007;50(2):108-115
BACKGROUND/AIMS: Pseudoaneurysm is a life-threatening complication of chronic or acute pancreatitis. This study was undertaken to evaluate the clinical features of pseudoaneurysm complicating pancreatitis. METHODS: We reviewed the medical records of 7 patients diagnosed as pseudoaneurysms with chronic pancreatitis in Korea University Guro and Anam Hospital from January 1995 to March 2006 and analyzed their demographics, clinical courses and outcomes. RESULTS: All patients were men and mean age was 54.6 years (range, 43-67 years). All the cases occurred in the setting of chronic alcoholic pancreatitis complicated by pseudocyst. Abdominal pain was the unique initial clinical symptom in 5 cases, hematemesis in 1 case, and simultaneous abdominal pain with hematemesis in 1 case. Bleeding into pseudocyst developed in 5 cases, flowing into duodenum through pancreatic duct in 1 case and rupture into the descending colon in 1 case. Mean duration between onset of symptom and diagnosis of pseudoaneurysm was 7.8 days (range, 1-23 days). Six cases were diagnosed by abdominal computed tomography disclosing characteristic finding of focal high density area in the pseudocyst. Pulsed doppler abdominal sonography was performed before computed tomography in 3 cases and results were negative in 2 cases. Transcatheter arterial embolizations were initially performed in 6 cases, and there was no recurrent bleeding except one case of splenic infarction. Distal pancreatectomy was initially performed in 1 case. CONCLUSIONS: Pseudoaneurysms complicating chronic pancreatitis shows various clinical features. Transcatheter arterial embolization can be recommended as a primary therapeutic modality.
Adult
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Aged
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Aneurysm, False/*diagnosis/etiology/ultrasonography
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Arteries/injuries
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Demography
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Embolization, Therapeutic
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Hemorrhage/etiology/surgery
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Humans
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Korea
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Male
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Middle Aged
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Pancreatic Pseudocyst/etiology/surgery
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Pancreatitis, Alcoholic/*complications/pathology
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Retrospective Studies
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Tomography, X-Ray Computed
2.Emodin prevents intima thickness via Wnt4/Dvl-1/beta-catenin signaling pathway mediated by miR-126 in balloon-injured carotid artery rats.
Jun Yi HUA ; Yu Zhou HE ; Yun XU ; Xu Hong JIANG ; Wu YE ; Zhi Min PAN
Experimental & Molecular Medicine 2015;47(6):e170-
Neointimal proliferation after vascular injury is a key mechanism of restenosis, a major cause of percutaneous transluminal angioplasty failure and artery bypass occlusion. Emodin, an anthraquinone with multiple physiological activities, has been reported to inhibit proliferation of vascular smooth muscle cells (VSMCs) that might cause intimal arterial thickening. Thus, in this study, we established a rat model of balloon-injured carotid artery and investigated the therapeutic effect of emodin and its underlying mechanism. Intimal thickness was analyzed by hematoxylin and eosin staining. Expression of Wnt4, dvl-1, beta-catenin and collagen was determined by immunohistochemistry and/or western blotting. The proliferation of VSMC was evaluated by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and electron microscopy. MicroRNA levels were quantified by real-time quantitative PCR. Emodin relieved injury-induced artery intimal thickness. Results of western blots and immunohistochemistry showed that emodin suppressed expression of signaling molecules Wnt4/Dvl-1/beta-catenin as well as collagen protein in the injured artery. In addition, emodin enhanced expression of an artery injury-related microRNA, miR-126. In vitro, MTT assay showed that emodin suppressed angiotensin II (AngII)-induced proliferation of VSMCs. Emodin reversed AngII-induced activation of Wnt4/Dvl-1/beta-catenin signaling by increasing expression of miR-126 that was strongly supported by transfection of mimic or inhibitor for miR-126. Emodin prevents intimal thickening via Wnt4/Dvl-1/beta-catenin signaling pathway mediated by miR-126 in balloon-injured carotid artery of rats.
Adaptor Proteins, Signal Transducing/*metabolism
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Animals
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Carotid Arteries/drug effects/metabolism/pathology
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Carotid Artery Injuries/*drug therapy/metabolism/pathology
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Cell Proliferation/drug effects
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Emodin/*therapeutic use
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Male
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MicroRNAs/*metabolism
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Phosphoproteins/*metabolism
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Rats
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Rats, Sprague-Dawley
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Signal Transduction/drug effects
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Tunica Intima/*drug effects/metabolism/pathology
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Wnt4 Protein/*metabolism
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beta Catenin/*metabolism