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  1 / 59609 MEDLINE  
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[PMID]:29520180
[Au] Autor:Gwon DI; Ko GY; Kim JW; Ko HK; Yoon HK; Sung KB
[Ad] Dirección:Department of Radiology and Research Institute of Radiology, University of Ulsan College of Medicine, Asan Medical Center, Seoul 05505, Korea.
[Ti] Título:Double-Stent System with Long Duodenal Extension for Palliative Treatment of Malignant Extrahepatic Biliary Obstructions: A Prospective Study.
[So] Fuente:Korean J Radiol;19(2):230-236, 2018 Mar-Apr.
[Is] ISSN:2005-8330
[Cp] País de publicación:Korea (South)
[La] Idioma:eng
[Ab] Resumen:Objective: To investigate the technical safety and clinical efficacy of a double-stent system with long duodenal extension in patients with malignant extrahepatic biliary obstruction. Materials and Methods: This prospective study enrolled 48 consecutive patients (31 men, 17 women; mean age, 61 years; age range, 31-77 years) with malignant extrahepatic biliary obstructions from May 2013 to December 2015. All patients were treated with a double-stent system with long duodenal covered extension (16 cm or 21 cm). Results: The stents were successfully placed in all 48 patients. There were five (10.4%) procedure-related complications. Minor complications were self-limiting hemobilia (n = 2). Major complications included acute pancreatitis (n = 1) and acute cholecystitis (n = 2). Successful internal drainage was achieved in 42 (87.5%) patients. Median patient survival and stent patency times were 92 days (95% confidence interval [CI], 61-123 days) and 83 days (95% CI, 46-120 days), respectively. Ten (23.8%) of the 42 patients presented with stent occlusion due to food impaction with biliary sludge, and required repeat intervention. Stent occlusion was more frequent in metastatic gastric cancer patients with pervious gastrectomy, but did not reach statistical significance ( = 0.069). Conclusion: Percutaneous placement of a double-stent system with long duodenal extension is feasible and safe. However, this stent system does not completely prevent stent occlusion caused by food reflux.
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1803
[Cu] Fecha actualización por clase:180311
[Lr] Fecha última revisión:180311
[St] Status:In-Data-Review
[do] DOI:10.3348/kjr.2018.19.2.230


  2 / 59609 MEDLINE  
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[PMID]:29515732
[Au] Autor:Chouchaine A; Fodha M; Abdelkefi MT; Helali K; Fodha M
[Ad] Dirección:Service de Chirurgie Générale, Hôpital Taher Sfar, Mahdia, Tunisie.
[Ti] Título:[Gallbladder agenesis: about three cases].
[Ti] Título:Agénésie de la vésicule biliaire: à propos de trois cas..
[So] Fuente:Pan Afr Med J;28:114, 2017.
[Is] ISSN:1937-8688
[Cp] País de publicación:Uganda
[La] Idioma:fre
[Ab] Resumen:Gallbladder agenesis is a rare congenital anomaly. This study aimed to highlight the epidemiological aspects of this condition as well as the peculiarities of its diagnostic and therapeutic management through three case reports. Two adults were admitted to Hospital with hepatic colics and dyspepsia. Ultrasound showed multilithiasic scleroatrophic vesicle. In one of the two patients, CT scan results showed a stone at the level of scleroatrophic vesicle. These two patients were wrongly operated for vesicular lithiasis by using conventional method. The absence of gallbladder was detected during surgery. In order to confirm post-operative diagnosis, the first patient underwent biliary MRI. The other patient was lost to follow-up. The third patient was a 13-year old child hospitalized with acute pancreatitis. Vesicular agenesis was suspected based on its scannographic aspect and then confirmed using biliary MRI. This patient didn't underwent surgery.
[Pt] Tipo de publicación:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Mes de ingreso:1803
[Cu] Fecha actualización por clase:180311
[Lr] Fecha última revisión:180311
[St] Status:In-Process
[do] DOI:10.11604/pamj.2017.28.114.11919


  3 / 59609 MEDLINE  
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[PMID]:29515728
[Au] Autor:Patel J; Madan A; Gammon A; Sossenheimer M; Samadder NJ
[Ad] Dirección:Division of Gastroenterology, University of Utah, Salt Lake City, Utah, USA.
[Ti] Título:Rare hereditary cause of chronic pancreatitis in a young male: SPINK1 mutation.
[So] Fuente:Pan Afr Med J;28:110, 2017.
[Is] ISSN:1937-8688
[Cp] País de publicación:Uganda
[La] Idioma:eng
[Ab] Resumen:Hereditary chronic pancreatitis associated with a mutation in the serine protease inhibitor, Kazal Type-1 (SPINK-1 gene) is extremely rare. The SPINK1 mutation results in trypsinogen activation which predisposes to chronic pancreatitis predominately when combined with CFTR gene mutations. It presents as either chronic or recurrent acute pancreatitis. Symptom control and management of complications is important. Active surveillance with cross-sectional imaging for pancreatic malignancy in individuals with hereditary pancreatitis is advocated due to individuals being high risk. We present an unusual case of a young male who initially presented with renal colic and was incidentally diagnosed with severe chronic pancreatitis on abdominal imaging, with genetic testing confirming a homozygous SPINK1 mutation.
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1803
[Cu] Fecha actualización por clase:180311
[Lr] Fecha última revisión:180311
[St] Status:In-Process
[do] DOI:10.11604/pamj.2017.28.110.13854


  4 / 59609 MEDLINE  
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[PMID]:29269704
[Au] Autor:Nakamura M; Yoshida T; Eguchi A; Inohana M; Nagahara R; Shiraki A; Ito N; Shibutani M
[Ad] Dirección:Laboratory of Veterinary Pathology, Veterinary Science, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu-shi, Tokyo 183-8509, Japan.
[Ti] Título:Intermediate-grade mammary gland adenocarcinoma in an 18-year-old female black leopard (Panthera pardus) with acute pancreatic necrosis and chronic interstitial nephropathy.
[So] Fuente:J Vet Med Sci;80(2):337-340, 2018 Mar 02.
[Is] ISSN:1347-7439
[Cp] País de publicación:Japan
[La] Idioma:eng
[Ab] Resumen:An 18-year-old female black leopard (Panthera pardus) showed renal failure, leukocytosis and presence of subcutaneous masses in the lower abdominal region and right shoulder; she eventually died. Histopathological observations included a mammary gland carcinoma with comedo, solid and tubulopapillary patterns in subcutaneous tissue, and highly proliferated tumor cells in systemic organs. The tumor cells were positive for cytokeratin AE1/AE3. The mammary gland tumor was diagnosed as intermediate-grade adenocarcinoma, based on a previously reported histological grading system of feline mammary carcinomas. Chronic interstitial nephritis was estimated to have been ongoing for 5 years, whilst acute necrotic pancreatitis in relation to tumor metastasis could have been the cause of death.
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1712
[Cu] Fecha actualización por clase:180311
[Lr] Fecha última revisión:180311
[St] Status:In-Process
[do] DOI:10.1292/jvms.17-0570


  5 / 59609 MEDLINE  
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[PMID]:29248457
[Au] Autor:Zolghadri Y; Pal Choudhuri S; Ocal O; Layeghi-Ghalehsoukhteh S; Berhe F; Hale MA; Wilkie TM
[Ad] Dirección:Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas; Department of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran.
[Ti] Título:Malnutrition in Pancreatic Ductal Adenocarcinoma (PDA): Dietary Pancreatic Enzymes Improve Short-Term Health but Stimulate Tumor Growth.
[So] Fuente:Am J Pathol;188(3):616-626, 2018 Mar.
[Is] ISSN:1525-2191
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:Pancreatic ductal adenocarcinoma (PDA) is a deadly cancer that resists efforts to identify better chemotherapeutics. PDA is associated with chronic pancreatitis and acinar cell dedifferentiation. This reduces enzyme production by the exocrine pancreas, resulting in digestive insufficiencies. Malabsorption of partially digested food causes bloating, overfilled intestines, abdominal pain, excessive feces, steatorrhea, and malnutrition. These maladies affect quality of life and restrict treatment options for pancreatitis and PDA. Here, we characterize health benefits and risks of dietary pancreatic enzymes in three mouse models of PDA-KC, KCR8-16, and KIC. KC expresses oncogenic Kras in pancreatic tissue whereas KCR8-16 also has deletions of the Rgs8 and Rgs16 genes. Rgs proteins inhibit the release of digestive enzymes evoked by G-protein-coupled-receptor agonists. KC and KCR8-16 mice developed dedifferentiated exocrine pancreata within 2 months of age and became malnourished, underweight, hypoglycemic, and hypothermic. KC mice adapted but KCR8-16 mice rapidly transitioned to starvation after mild metabolic challenges. Dietary pancreatic enzyme supplements reversed these symptoms in KC and KCR8-16 animals, and extended survival. Therefore, we tested the benefits of pancreatic enzymes in an aggressive mouse model of PDA (KIC). Median survival improved with dietary pancreatic enzyme supplements and was extended further when combined with warfarin and gemcitabine chemotherapy. However, dietary pancreatic enzymes stimulated tumor growth in the terminal stages of disease progression in KIC mice.
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1712
[Cu] Fecha actualización por clase:180311
[Lr] Fecha última revisión:180311
[St] Status:In-Data-Review


  6 / 59609 MEDLINE  
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[PMID]:29248441
[Au] Autor:He P; Yang JW; Yang VW; Bialkowska AB
[Ad] Dirección:Department of Medicine, Stony Brook University School of Medicine, Stony Brook, New York.
[Ti] Título:Krüppel-like Factor 5, Increased in Pancreatic Ductal Adenocarcinoma, Promotes Proliferation, Acinar-to-Ductal Metaplasia, Pancreatic Intraepithelial Neoplasia, and Tumor Growth in Mice.
[So] Fuente:Gastroenterology;, 2017 Dec 15.
[Is] ISSN:1528-0012
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:BACKGROUND & AIMS: Activating mutations in KRAS (Kirsten rat sarcoma viral oncogene homolog) are detected in most pancreatic ductal adenocarcinomas (PDACs). Expression of an activated form of KRAS (KrasG12D) in pancreata of mice is sufficient to induce formation of pancreatic intraepithelial neoplasia (PanINs)-a precursor of PDAC. Pancreatitis increases formation of PanINs in mice that express KrasG12D by promoting acinar-to-ductal metaplasia (ADM). We investigated the role of the transcription factor Krüppel-like factor 5 (KLF5) in ADM and KRAS-mediated formation of PanINs. METHODS: We performed studies in adult mice with conditional disruption of Klf5 (Klf5 ) and/or expression of Kras (LSL-Kras ) via Cre recombinase regulated by an acinar cell-specific promoter (Ptf1a). Activation of KrasG12D and loss of KLF5 was achieved by administration of tamoxifen. Pancreatitis was induced in mice by administration of cerulein; pancreatic tissues were collected, analyzed by histology and immunohistochemistry, and transcriptomes were compared between mice that did or did not express KLF5. We performed immunohistochemical analyses of human tissue microarrays, comparing levels of KLF5 among 96 human samples of PDAC. UN-KC-6141 cells (pancreatic cancer cells derived from Pdx1-Cre;LSL-Kras mice) were incubated with inhibitors of different kinases and analyzed in proliferation assays and by immunoblots. Expression of KLF5 was knocked down with small hairpin RNAs or CRISPR/Cas9 strategies; cells were analyzed in proliferation and gene expression assays, and compared with cells expressing control vectors. Cells were subcutaneously injected into flanks of syngeneic mice and tumor growth was assessed. RESULTS: Of the 96 PDAC samples analyzed, 73% were positive for KLF5 (defined as nuclear staining in more than 5% of tumor cells). Pancreata from Ptf1a-Cre ;LSL-Kras mice contained ADM and PanIN lesions, which contained high levels of nuclear KLF5 within these structures. In contrast, Ptf1a-Cre ;LSL-Kras ;Klf5 mice formed fewer PanINs. After cerulein administration, Ptf1a-Cre ;LSL-Kras mice formed more extensive ADM than Ptf1a-Cre ;LSL-Kras ;Klf5 mice. Pancreata from Ptf1a-Cre ;LSL-Kras ;Klf5 mice had increased expression of the tumor suppressor NDRG2 and reduced phosphorylation (activation) of STAT3, compared with Ptf1a-Cre ;LSL-Kras mice. In UN-KC-6141 cells, PI3K and MEK signaling increased expression of KLF5; a high level of KLF5 increased proliferation. Cells with knockdown of Klf5 had reduced proliferation, compared with control cells, had reduced expression of ductal markers, and formed smaller tumors (71.61 ± 30.79 mm vs 121.44 ± 34.90 mm from control cells) in flanks of mice. CONCLUSION: Levels of KLF5 are increased in human PDAC samples and in PanINs of Ptf1a-Cre ;LSL-Kras mice, compared with controls. KLF5 disruption increases expression of NDRG2 and reduces activation of STAT3 and reduces ADM and PanINs formation in mice. Strategies to reduce KLF5 activity might reduce progression of acinar cells from ADM to PanIN and pancreatic tumorigenesis.
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1712
[Cu] Fecha actualización por clase:180310
[Lr] Fecha última revisión:180310
[St] Status:Publisher


  7 / 59609 MEDLINE  
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[PMID]:29524184
[Au] Autor:Nor Hanipah Z; Punchai S; Brethauer SA; Schauer PR; Aminian A
[Ad] Dirección:Bariatric and Metabolic Institute, Department of General Surgery, Cleveland Clinic, 9500 Euclid Avenue/M61, Cleveland, OH, 44195, USA.
[Ti] Título:Development of De Novo Diabetes in Long-Term Follow-up After Bariatric Surgery.
[So] Fuente:Obes Surg;, 2018 Mar 09.
[Is] ISSN:1708-0428
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:INTRODUCTION: While bariatric surgery leads to significant prevention and improvement of type 2 diabetes, patients may rarely develop diabetes after bariatric surgery. The aim of this study was to determine the incidence and the characteristic of new-onset diabetes after bariatric surgery over a 17-year period at our institution. METHODS: Non-diabetic patients who underwent bariatric surgery at a single academic center (1997-2013) and had a postoperative glycated hemoglobin (HbA1c) ≥ 6.5%, fasting blood glucose (FBG) ≥ 126 mg/dl, or positive glucose tolerance test were identified and studied. RESULTS: Out of 2263 non-diabetic patients at the time of bariatric surgery, 11 patients had new-onset diabetes in the median follow-up time of 9 years (interquartile range [IQR], 4-12). Bariatric procedures performed were Roux-en-Y gastric bypass (n = 7), adjustable gastric banding (n = 3), and sleeve gastrectomy (n = 1). The median interval between surgery and diagnosis of diabetes was 6 years (IQR, 2-9). At the last follow-up, the median HbA1c and FBG values were 6.3% (IQR, 6.1-6.5) and 95 mg/dl (IQR, 85-122), respectively. Possible etiologic factors leading to diabetes were weight regain to baseline (n = 6, 55%), steroid-induced after renal transplantation (n = 1), pancreatic insufficiency after pancreatitis (n = 1), and unknown (n = 3). CONCLUSION: De novo diabetes after bariatric surgery is rare with an incidence of 0.4% based on our cohort. Weight regain was common (> 50%) in patients who developed new-onset diabetes suggesting recurrent severe obesity as a potential etiologic factor. All patients had good glycemic control (HbA1c ≤ 7%) in the long-term postoperative follow-up.
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1803
[Cu] Fecha actualización por clase:180310
[Lr] Fecha última revisión:180310
[St] Status:Publisher
[do] DOI:10.1007/s11695-018-3194-z


  8 / 59609 MEDLINE  
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[PMID]:29523472
[Au] Autor:Sharma M; Somani P
[Ad] Dirección:Department of Gastroenterology, Jaswant Rai Speciality Hospital, Saket, Meerut 250 001, Uttar Pradesh, India. Electronic address: sharmamalay@hotmail.com.
[Ti] Título:EUS of pancreatic ascariasis.
[So] Fuente:Arab J Gastroenterol;, 2018 Mar 06.
[Is] ISSN:2090-2387
[Cp] País de publicación:Egypt
[La] Idioma:eng
[Ab] Resumen:Ascaris is a common cause of acute pancreatitis in developing countries. The mechanism of ascariasis induced acute pancreatitis include obstruction of papilla of Vater, invasion of common bile duct, or pancreatic duct (PD). PD ascariasis is a rare diagnosis. Endoscopic ultrasound is a highly accurate method to diagnose the aetiology of idiopathic acute pancreatitis with reference to biliary and pancreatic ascariasis. Treatment usually consist of endoscopic removal of worms with dormia basket or forceps on side viewing endoscopy. Ascaris induced pancreatitis is generally mild and worm extraction is associated with rapid relief of symptoms. We present a case of PD ascariasis diagnosed on endoscopic ultrasound.
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1803
[Cu] Fecha actualización por clase:180310
[Lr] Fecha última revisión:180310
[St] Status:Publisher


  9 / 59609 MEDLINE  
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[PMID]:29523291
[Au] Autor:Zitinic I; Plavsic I; Poropat G; Hauser G
[Ad] Dirección:Centre for Emergency Medicine, Clinical Hospital Centre, Rijeka, Croatia.
[Ti] Título:ERCP induced and non-ERCP-induced acute pancreatitis: Two distinct clinical entities?
[So] Fuente:Med Hypotheses;113:42-44, 2018 Apr.
[Is] ISSN:1532-2777
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:Acute pancreatitis (AP) is a common gastrointestinal disease of varied etiology; however, the most common causes of AP are gallstones and alcohol abuse. AP has emerged as the most frequent complication after endoscopic retrograde cholangiopancreatography (ERCP). Post-ERCP pancreatitis is generally a clinically irrelevant condition; however, it can be severe or even fatal in up to 0.8% of cases. Different clinical courses and outcomes have been observed between mild and severe AP of different etiologies (i.e., non-ERCP AP and post-ERCP AP), which opens the discussion as to whether they are the same or distinct clinical entities.
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1803
[Cu] Fecha actualización por clase:180310
[Lr] Fecha última revisión:180310
[St] Status:In-Process


  10 / 59609 MEDLINE  
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[PMID]:29523189
[Au] Autor:Ralapanawa U; Jayalath T; Senadhira D
[Ad] Dirección:Faculty of Medicine, University of Peradeniya, Peradeniya, Sri Lanka. udayapralapanawa@yahoo.com.
[Ti] Título:A case of acute necrotizing pancreatitis complicated with non ST elevation myocardial infarction.
[So] Fuente:BMC Res Notes;11(1):167, 2018 Mar 09.
[Is] ISSN:1756-0500
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen:BACKGROUND: Acute pancreatitis is an inflammatory condition with varying severity and a range of local and systemic complications. Here we report a patient with acute necrotizing pancreatitis complicated with a true non ST elevation myocardial infarction. CASE PRESENTATION: A 58 year old lady was admitted to our unit with acute onset epigastric pain and vomiting for 4 h duration. Following admission she complained of retrosternal tightening type of a chest pain. She had elevated serum amylase and cardiac troponin. Electrocardiogram (ECG) revealed lateral ischaemia. Contrast computerized tomography abdomen revealed acute severe necrotizing pancreatitis. CONCLUSIONS: Nonspecific ECG changes can occur in patients with acute pancreatitis. But the diagnosis of true myocardial infarction in a context of acute pancreatitis using ECGs, 2D echocardiography, cardiac biomarkers and coronary angiograms can be challenging with the choice of revascularization therapy and safety of antiplatelet agents and anticoagulant therapy. Decision making regarding the management of such a patient is also critical.
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1803
[Cu] Fecha actualización por clase:180310
[Lr] Fecha última revisión:180310
[St] Status:In-Process
[do] DOI:10.1186/s13104-018-3274-0



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