review of literature on clinical pancreatology - The Pancreapedia

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single-centre experience <strong>of</strong> BD-IPMNs. Some 190 patients with radiological imaging orhistological findings consistent with BD-IPMN were enrolled between 1998 and 2005. Thosewith less than 6 months' follow-up and no histological confirmation were excluded. BD-IPMNwas diagnosed by computed tomography and pancreatography in 105 patients andpathologically in 85. Eighteen patients had adenoma, 53 borderline malignancy, fivecarcinoma in situ and nine invasive carcinoma. Findings associated with malignancy werethe presence <strong>of</strong> radiologically suspicious features and a cyst size <strong>of</strong> at least 30 mm. Hadconsensus guidelines been applied, 54 patients would have undergone pancreatic resection,whereas only 28 <strong>of</strong> these patients actually had a resection; 12 <strong>of</strong> the latter patients had amalignancy compared with none <strong>of</strong> the 26 patients who were treated conservatively. It wasconcluded that a simple increase in cyst size is not a reliable predictor <strong>of</strong> malignancy.Observation is recommended for patients with a BD-IPMN smaller than 30 mm showing nosuspicious features on imaging [582].Intraductal papillary mucinous neoplasm (IPMN) was first described by Ohashi et al as"mucin-producing cancer" that affected the main pancreatic duct and produced excessivequantities <strong>of</strong> mucus, which filled and distended the ductal system. Prediction <strong>of</strong> malignancy<strong>of</strong> IPMN is important not only for indication <strong>of</strong> operation but for selection <strong>of</strong> operativeprocedure. International Consensus Guidelines recommended to resect all main duct andmixed variant IPMNs, and also recommended to resect branch duct IPMNs with symptoms.However, the criteria for resection in the branch duct IPMNs are still unclear. One studyaimed to determine the predictive factors for malignancy in IPMN, particularly cancerinvasion in IPMNs. It was <strong>review</strong>ed 26 cases with IPMN operated from 2003 to 2007. Amongthem, 21 cases were branched type, and the others were main duct type. It was measureddiameter <strong>of</strong> main pancreatic duct, cystic lesion size and intramural nodule size by endoscopicultrasonography or computed tomography and serum levels <strong>of</strong> CEA and CA19-9. As forfactors to predict malignancy only in branched type, the intramural nodules size and wassignificantly larger in the cases with cancer than that in the cases without cancer. Theanalysis all types IPMNs showed significant difference in the main duct diameter between 15benign and 11 malignant cases (5.5 + 4.0 mm vs 10.9 + 4.5 mm). Moreover, among the 11cases whose diameter <strong>of</strong> main pancreatic duct was less than 7 mm, no malignancy wasdetected. These results suggest that the diameter <strong>of</strong> main pancreatic duct as well asintramural nodules size is useful for prediction <strong>of</strong> malignancy and that minimally-invasivesurgery such as spleen-preserving distal pancreatectomy can be safely indicated for thecases whose diameter <strong>of</strong> main pancreatic duct is less than 7 mm [583].It was investigated preoperative findings that are useful to distinguish intraductal papillarymucinousneoplasm (IPMN) subtypes. One hundred twenty-three patients who underwentpancreatectomy for IPMN were analyzed clinicopathologically and radiologically. InvasiveIPM carcinomas (IPMCs) were subdivided into early-stage nonaggressive (minimally invasiveIPMC [MI-IPMC]) and more advanced and aggressive (invasive carcinoma originating inIPMC [IC-IPMC]) subtypes according to recently proposed pathological criteria. The lesionsconsisted <strong>of</strong> 27 IPMNs with low-grade dysplasia, 14 IPMNs with moderate dysplasia, 21IPMNs with high-grade dysplasia, 30 MI-IPMCs, and 31 IC-IPMCs. Multidetector-rowcomputed tomography detected a component <strong>of</strong> invasive carcinoma in IC-IPMC with 86percent sensitivity and 100 percent specificity. In patients with IPMNs other than IC-IPMC,multivariate analysis demonstrated 3 significant predictive factors <strong>of</strong> malignancy: IPMN size(>40 mm), IPMN duct type (main pancreatic duct or mixed type), and the presence <strong>of</strong> a muralnodule or thick septum. The diagnostic score obtained using these 3 factors showed a strongcorrelation with the presence <strong>of</strong> malignancy. It was concluded that regarded preoperativeevaluation <strong>of</strong> patients with IPMN, it is recommended to rule out IC-IPMC using multidetectorrowcomputed tomography and then to categorize IPMN other than IC-IPMC according tomalignant potential based on the diagnostic score [584].
Molecular biologyCD44v6The purpose <strong>of</strong> thone is study was to examine CD44v6 expression in intraductal papillarymucinous neoplasms (IPMNs) and clarify the role <strong>of</strong> CD44v6 in progression, invasion,metastasis, and morphogenesis <strong>of</strong> IPMNs. One hundred fifty-one samples <strong>of</strong> IPMNs and 30normal controls were subjected to immunohistochemical analysis for CD44v6. The IPMNswere divided into 4 groups according to the grade <strong>of</strong> atypia (adenoma, borderline IPMN,noninvasive carcinoma, and invasive carcinoma) and 5 subtypes according to histologicalphenotype (gastric, intestinal, pancreatobiliary, oncocytic, and unclassified). Whereas normalductal epithelium did not express CD44v6, CD44v6 expression was observed from the earlystage <strong>of</strong> IPMNs and up-regulated in the progression <strong>of</strong> IPMNs to invasive carcinoma.CD44v6 expression in intestinal-type IPMNs was significantly lower compared with that inother subtypes. Whereas no correlation was observed between lymph node metastasis andCD44v6 expression in invasive IPM carcinomas, the invasion pattern was significantlycorrelated to CD44v6 expression. These data indicate that CD44v6 expression determinesthe morphology and aggressiveness <strong>of</strong> IPMNs and is involved in development and invasion<strong>of</strong> IPMNs [585].CD133The rate <strong>of</strong> intraductal papillary mucinous neoplasm (IPMN) progression is much slower thanthat <strong>of</strong> invasive ductal adenocarcinomas. The identification <strong>of</strong> a clinicopathological marker todistinguish IPMNs from ductal adenocarcinomas is important for understanding the molecularmechanisms <strong>of</strong> pancreatic cancer. It was examined the expression pattern <strong>of</strong> the cell surfacemarker CD133, which has been used to identify putative cancer stem cells from solid tumors,in adult pancreatic ductal adenocarcinomas (n=10) and IPMNs (n=34). CD133 expressionwas detected in the centroacinar region and intralobular ductal cells <strong>of</strong> normal pancreas.CD133 expression was also observed in ductal adenocarcinomas. In contrast, CD133expression was not observed in the mucin-producing epithelial cells and carcinoma cells onIPMNs. These results demonstrate that the expression <strong>of</strong> CD133 is down-regulated inIPMNs, suggesting that loss <strong>of</strong> CD133 expression might be a useful clinicopathologicalmarker distinguishing IPMNs from ductal adenocarcinomas [586].KOCTo evaluate if immunocytochemical expression <strong>of</strong> K homology domain containing proteinoverexpresssed in cancer (KOC) in biliary brushings and fine needle aspiration improves thediagnostic capability <strong>of</strong> cytology for intraductal papillary mucinous neoplasm (IPMN) andpancreatic ductal adenocarcinoma 14 pancreatic cancers, 15 IPMNs and 7 chronicpancreatitis cases were investigated. The cytology smears and surgical specimens werestained with antibody to KOC (1:500). The intensity (scale 0-3+) and percentage <strong>of</strong> cellsstaining were evaluated in pathologic lesions, and diffuse (>75 % <strong>of</strong> cells) staining <strong>of</strong> 3+intensity was considered positive. There was 100 percent specificity for diagnosingpancreatic cancer. The sensitivity was greater in histology (79 %) than cytology (71 %). Allchronic pancreatitis and IPMN cases, including IPMN with high grade dysplasia, werenegative. Benign epithelium adjacent to pancreatic cancer or IPMN was also negative. Thisstudy demonstrated that pancreatic adenocarcinoma can be differentiated from IPMN andbenign ductal epithelium using KOC expression. This could be useful in cytologic caseswhere atypical features preclude a definitive diagnosis <strong>of</strong> malignancy [587].WWOXIt has previously been shown that WW domain-containing oxidoreductase (WWOX) hastumour-suppressing effects and that its expression is frequently reduced in pancreaticcarcinoma. In one study, it was examined WWOX expression in intraductal papillarymucinous neoplasm <strong>of</strong> the pancreas (IPMN) to assess the function <strong>of</strong> WWOX in pancreatic
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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
Page 149 and 150: the optimal combination of<
Page 151 and 152: which is essential in tumor and nod
Page 153 and 154: provide conclusive evidence for the
Page 155 and 156: MD-CT is suitable for evaluating tu
Page 157 and 158: approved study and imaged during sh
Page 159 and 160: Quantum dotsIt was reported the suc
Page 161 and 162: clearly have a very high incidence
Page 163 and 164: patients for operation and when cou
Page 165 and 166: demonstrated using the confocal mic
Page 167 and 168: cancer [468].To evaluate pancreatic
Page 169 and 170: pancreaticoduodenectomy (PD). The s
Page 171 and 172: safe option as an interposition gra
Page 173 and 174: a curative surgery, while double-by
Page 175 and 176: %), pseudocyst (3 %), and trauma (3
Page 177 and 178: procedure is failing to progress la
Page 179 and 180: Glucos metabolism after pancreatect
Page 181 and 182: Quality of lifeOne
Page 183 and 184: was observed in the NACRT group. Th
Page 185 and 186: interval 0.80 to 0.96]. On subgroup
Page 187 and 188: ate in patients with pancreatic can
Page 189 and 190: median survival time was 7 versus 7
Page 191 and 192: and the endoscopic ultrasound-guide
Page 193 and 194: local recurrence of1.5 cm (odds ratio 2.4), and
Page 199: adenocarcinoma must be addressed at
Page 203 and 204: IPMN were studied. Two-dimensional
Page 205 and 206: the NT-IPMN-Br group. Eleven patien
Page 207 and 208: metastatic neoplasms showing cystic
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
Page 217 and 218: It was described a case of<
Page 219 and 220: evaluation. The purpose of<
Page 221 and 222: perforation of a p
Page 223 and 224: the 28 had pancreatic duct injury <
Page 225 and 226: ENDOCRINE PANCREATIC TUMORSHistoryA
Page 227 and 228: 25-111 pg/mL). Mean Hemoglobin A1C
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Page 231 and 232: achieved in selected cases by tissu
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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292. Borak GD, Romagnuolo J, Alsola
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324. Oh HC, Kim MH, Choi KS, Moon S
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358. Koornstra JJ, Mourits MJ, Sijm
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391. Chen JY, Amos CI, Merriman KW,
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421. Horwhat JD, Gerke H, Acosta RD
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451. Zamboni G, Capelli P, Scarpa A
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483. Rosa F, Pacelli F, Papa V, Tor
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545. Pino MS, Milella M, Gelibter A
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637. Nagar AM, Raut AA, Morani AC,
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670. Lejonklou M, Edfeldt K, Johans
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