review of literature on clinical pancreatology - The Pancreapedia

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percent kidney, 2 percent omentum, 3 percent appendix, 3 pecent pancreas, and 1 percentfor gallbladder and lung. One hundred twelve <strong>of</strong> 113 grossly normal specimens had normalpathology. One grossly normal specimen exposed abnormal pathology revealing benignappendiceal mucocele. Therefore, 99 percent <strong>of</strong> grossly normal specimens sent forhistological examination after trauma laparotomy were normal. Based on this <strong>review</strong>, inselect patients routine histological examination <strong>of</strong> tissues removed for traumatic injury isunnecessary [661].
ENDOCRINE PANCREATIC TUMORSHistoryA search on PubMed using the keywords “neuroendocrine”, “pancreas” and “carcinoid” wasperformed to identify relevant <strong>literature</strong> over the last 30 years. The introduction <strong>of</strong> a revisedclassification <strong>of</strong> neuroendocrine tumours by the World Health Organisation (WHO) in 2000significantly changed our understanding <strong>of</strong> and approach to the management <strong>of</strong> thesetumours. Advances in laboratory and radiological techniques have also led to an increaseddetection <strong>of</strong> PNETs. Surgery remains the only treatment that <strong>of</strong>fers a chance <strong>of</strong> cure withincreasing number <strong>of</strong> non-surgical options serving as beneficial adjuncts. The betterunderstanding <strong>of</strong> the behaviours <strong>of</strong> PNETs together with improvements in tumour localisationhas resulted in a more aggressive management strategy with a concomitant improvement insymptom palliation and a prolongation <strong>of</strong> survival. Due to their complex nature and the widerange <strong>of</strong> therapeutic options, the involvement <strong>of</strong> specialists from all necessary disciplines in amultidisciplinary team setting is vital to provide optimal treatment <strong>of</strong> this disease [662].Reported cases <strong>of</strong> diffuse nesidioblastosis have had common clinical features: postprandialhyperinsulinemic hypoglycemia, no abnormal findings in radiological examinations, and thepresence <strong>of</strong> the ductulo-insular complex on histological examination. Surgical resection isrecommended, but the extent <strong>of</strong> surgery is controversial. Our case had some clinical features<strong>of</strong> insulinoma but was diagnosed as diffuse nesidioblastosis according to histopathologiccriteria. Because arterial stimulation and veneous sampling showed that the pancreatic bodyand tail had a lesion producing insulin abnormally, we performed a distal pancreatectomy tocure the hypoglycemia. Clinically, it is very difficult to distinguish diffuse nesidioblastosis frominsulinkoma [663].GeneticsPancreatic endocrine neoplasms (PENs) are diagnostically challenging tumors whose naturalhistory is largely unknown. Histopathology allows the distinction <strong>of</strong> two categories: poorlydifferentiated high-grade carcinomas and well-differentiated neoplasms. The latter includemore than 90percent <strong>of</strong> PENs whose clinical behavior varies from indolent to malignant andcannot be predicted by their morphology. The diagnosis <strong>of</strong> PEN is generally easy, butunusual features may induce misdiagnosis. Immunohistochemistry solves the issue, providedthat the possibility <strong>of</strong> a PEN has been considered. Morphology allows the distinction <strong>of</strong> poorlydifferentiated aggressive carcinomas from well-differentiated neoplasms. The World HealthOrganization classification criteria allow for the discernment <strong>of</strong> the latter into neoplasms andcarcinomas with either benign or uncertain behavior. The recently proposed staging andgrading systems hold great promise for permitting a stratification <strong>of</strong> carcinomas into clinicallysignificant risk categories. To date, inactivation <strong>of</strong> the MEN1 gene remains the onlyascertained genetic event involved in PEN genesis. It is inactivated in roughly one-third <strong>of</strong>PENs. The degree <strong>of</strong> genomic instability correlates with the aggressiveness <strong>of</strong> the neoplasm.Gene silencing by promoter methylation has been advocated, but a formal demonstration <strong>of</strong>the involvement <strong>of</strong> specific genes is still lacking. Expression pr<strong>of</strong>iling studies are furnishingvaluable lists <strong>of</strong> mRNAs and noncoding RNAs that may advance further the research todiscover novel markers and/or therapeutic targets [664].Gastrointestinal and pancreatic neuroendocrine tumors (GEP-NETs) originate from cells <strong>of</strong>the diffuse endocrine system. Most GEP-NETs are sporadic, however, some <strong>of</strong> them,especially pancreatic endocrine tumors, may occur as part <strong>of</strong> familial syndromes. Thegenetic and molecular pathology <strong>of</strong> neuroendocrine tumor development is incomplete andremains largely unknown. However, the WHO classification introduced in clinical practice will
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REVIEW OF LITERATURE ONCLINICAL PAN
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ABBREVIATIONAAPacute alcoholicABPac
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FMF AIPfocal mass-forming autoimmun
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ODPopen distal pancreatectomyOForga
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USUTDTVESDVTEZESWHOXIAPUnited State
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Ectopic pancreasCircumportal annula
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SymptomsEndocopic ultrasography (EU
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HSP27HuRIGF-1 receptorIntegrinesInt
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HemodialysisSerous cystadenomasSero
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CRPC-reactive proteinCRTchemoradiot
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ITNPintrathecal narcotics pumpJCGAI
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QSRquantitative systematic
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PANCREATIC HISTORYEarly conceptsPan
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derived from broadly Harveian anato
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acute appendicitis, intestinal obst
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dogma and its implied presence <str
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In the late 19th century, explorato
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performed. In 1880, Carl Thiersch <
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cancer was reported by Nestor Dimit
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Modern pancreatic historyHoward Reb
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PANCREATIC DEVELOPMENT, EMBRYOLOGY
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preparations. They were also employ
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pancreas can be diagnosed without t
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PANCREATIC PHYSIOLOGYSphincter <str
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acid profile and d
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hormones. The roles of</str
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ACUTE PANCREATITISAcute pancreatiti
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necrosis or a severe course, and lo
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of 245 cases <stro
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plasty of the mino
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no significant difference. The stro
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Urinary trypsinogen-2There is not a
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groups. None of th
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evaluated the presence or absence <
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adical, etc, further studies are st
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Precut at sphincterotomyPrecut is p
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indications [204].Hypercalcemia-ind
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endoscopic retrograde cholangiopanc
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(before ERCP), serum TAP was detect
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concentration and clinical symptoms
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However, the recipients of<
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less safe for predominantly cephali
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increased mortality. Mortality in p
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Epidemiology and demographyChinaCHR
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for the first time the significance
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endoscopic ultrasound accurately de
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possible to at least reduce relapse
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etiologies have been proposed and a
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patients, can be performed with mod
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negative binomial model. One hundre
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Halofuginone did n
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years, the risk of
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patients with a proven exocrine pan
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high-risk patients [296].Cystic fib
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TNF-alpha promoter were performed.
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were validated in another series <s
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vascular invasion (14/15). Abnormal
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and other lymph nodes, salivary gla
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HEREDITARY PANCREATITISPatients wit
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Classification of
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historically, but recent life-style
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carcinogen exposure with cancer ris
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the risk of pancre
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conducted a cohort analysis <strong
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emain to be solved in screening for
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considered for women with Lynch syn
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Annexin A5Protein misfolding is a c
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CTNNB1To use fluorescence in situ h
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expression was not associated with
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(ECM) are not fully understood. In
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lines. However, the role of
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andomized to high-dose vitamin A, t
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Synuclein-gammaPerineural invasion
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interventions. Cancer nests were ma
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the optimal combination of<
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which is essential in tumor and nod
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provide conclusive evidence for the
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MD-CT is suitable for evaluating tu
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approved study and imaged during sh
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Quantum dotsIt was reported the suc
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clearly have a very high incidence
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patients for operation and when cou
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demonstrated using the confocal mic
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cancer [468].To evaluate pancreatic
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pancreaticoduodenectomy (PD). The s
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safe option as an interposition gra
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Page 181 and 182: Quality of lifeOne
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Page 185 and 186: interval 0.80 to 0.96]. On subgroup
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Page 201 and 202: Molecular biologyCD44v6The purpose
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Page 209 and 210: Solid pseudopapillary neoplasms <st
Page 211 and 212: The tumor cells were negative for p
Page 213 and 214: Duodenal tumorsColorectal polyposis
Page 215 and 216: Colorectal carcinomaPancreatic meta
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Page 233 and 234: Overall survivalPancreatic neuroend
Page 235 and 236: REFERENCES001. Metter CC. History <
Page 237 and 238: 044. Fitz RH. The symptomatology an
Page 239 and 240: 089. McClusky DA, Skandalakis LJ, C
Page 241 and 242: 126. Toouli J. Sphincter of
Page 243 and 244: 162. Deshpande AV, Thomas G, Shun A
Page 245 and 246: 196. Park JH, Lee TH, Cheon SL, Sun
Page 247 and 248: 226. Botoi G, Andercou A. Early and
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670. Lejonklou M, Edfeldt K, Johans
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