review of literature on clinical pancreatology - The Pancreapedia

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markedly irregular ductal contours, ruptured ducts, nuclear enlargement, pleomorphism andhyperchromatism, and mitotic figures. Immunohistologic markers that are helpful arecarcinoembryonic antigen, MUC1, p53, and Ki-67/ MIB1. There are a few features that arediagnostic and a number that are suggestive <strong>of</strong> PDAC. Therefore, a combination <strong>of</strong> severalfeatures may be required to clearly distinguish chronic pancreatitis from invasive PDAC[450].PseudotumorA variety <strong>of</strong> nonneoplastic conditions may form pancreatic masses that mimic carcinoma.Approximately 5-10 percent <strong>of</strong> pancreatectomies performed with the clinical diagnosis <strong>of</strong>pancreatic cancer prove on microscopic evaluation to be pseudotumors. To illustrate theclinical and pathologic characteristics <strong>of</strong> the 2 most frequent pseudotumoral inflammatoryconditions, autoimmune pancreatitis and paraduodenal pancreatitis, and describe the criteriathat may be useful in the differential diagnosis versus pancreatic carcinoma recent <strong>literature</strong>and the authors' experience with the clinical and pathologic characteristics <strong>of</strong> autoimmunepancreatitis and paraduodenal pancreatitis were <strong>review</strong>ed. The knowledge <strong>of</strong> the clinical,radiologic, and pathologic findings in both autoimmune pancreatitis and paraduodenalpancreatitis is crucial in making the correct preoperative diagnosis. Autoimmune pancreatitis,which occurs in isolated or syndromic forms, is characterized by a distinctivefibroinflammatory process that can either be limited to the pancreas or extend to the biliarytree. Its correct preoperative identification on biopsy material with ancillaryimmunohistochemical detection <strong>of</strong> dense immunoglobulin G4-positive plasma cell infiltrationis possible and crucial to prevent major surgery and to treat these patients with steroidtherapy. Paraduodenal pancreatitis is a special form <strong>of</strong> chronic pancreatitis that affects youngmales with a history <strong>of</strong> alcohol abuse and predominantly involves the duodenal wall in theregion <strong>of</strong> the minor papilla. Pathogenetically, the anatomical and/or functional obstruction <strong>of</strong>the papilla minor, resulting from an incomplete involution <strong>of</strong> the intraduodenal dorsalpancreas, associated with alcohol abuse represents the key factor [451].Special symptoms and signsHemosuccus pancreaticusThe major symptoms <strong>of</strong> cancer <strong>of</strong> the pancreas, even those <strong>of</strong> the head, are insidious weightloss, abdominal pains, back pain, anorexia, nausea, vomiting and generalized malaise.Jaundice is present in about 90 percent <strong>of</strong> the patients with cancer <strong>of</strong> the head and 10-40percent <strong>of</strong> those with cancer <strong>of</strong> body and tail. Massive haemorrhage is an uncommonpresentation. Most causes <strong>of</strong> gastrointestinal haemorrhage respond to conservativetreatment. Haemosuccus pancreaticus is a care cause <strong>of</strong> gastrointestinal hemorrhage andcan prove difficult to diagnose. It was presented two with upper gastrointestinal bleeding.Both patients were found to have pancreatic caranoma with bleding into the pancreatic ducts.I was concluded that haemosuccus pancreaticus may present as one <strong>of</strong> the early symptoms<strong>of</strong> carcinoma <strong>of</strong> the pancreas in young patients in our environment [452].Venous tromboembolismSeveral recent studies have shown that the incidence <strong>of</strong> venous thromboembolism is highestin patients who present with metastatic cancer, particularly cancers associated with a highone-year mortality rate, such as pancreatic cancer. The incidence rate <strong>of</strong> VTE is highest inthe first few months after the diagnosis <strong>of</strong> cancer, and it decreases over time thereafter. Formost cancers, it is not clear to what extent undergoing major surgery adds to the alreadyhigh risk <strong>of</strong> VTE associated with the presence <strong>of</strong> the cancer. However, patients with glioma
clearly have a very high incidence <strong>of</strong> VTE soon after they undergo any invasiveneurosurgical procedure. Active chemotherapy, the use <strong>of</strong> erythropoetin agents, and the use<strong>of</strong> certain anti-cancer therapies such as thalidomide, high-dose steroids, and anti-angiogenictherapy also increase the risk <strong>of</strong> thrombosis. Similar to patients without cancer, the risk <strong>of</strong>venous thromboembolism is higher in patients with coexisting chronic medical illnesses.Development <strong>of</strong> VTE is clearly associated with decreased survival and this effect is greateramong patients initially diagnosed with local or regional stage cancer compared to patientswith metastatic cancer [453].Venous thrombosis with and without pulmonary embolism is a frequent complication <strong>of</strong>malignancies and second among the causes <strong>of</strong> death in tumor patients. Its incidence isreported to be 10 to 15 percent. Since for methodological reasons, this rate can be assumedto be too low and to disregard asymptomatic venous thrombosis, a combined retrospectiveand prospective study was performed to examine the actual frequency <strong>of</strong> venous thrombosisin tumor patients. The histories <strong>of</strong> 409 patients with different tumors, consecutively enrolledin the order <strong>of</strong> their altogether 426 inpatient treatments, were checked in retrospect for thefrequency <strong>of</strong> venous thrombosis and pulmonary embolism. Subsequently, 97 tumorinpatients were systematically screened, by means <strong>of</strong> duplex sonography and/orvenography, for venous thromboses in the veins <strong>of</strong> the pelvis and both legs. In theretrospective analysis, where no systematic screening for thromboses was performed andonly symptomatic thrombosis was recorded, venous thrombosis was found in 6.6 percent <strong>of</strong>all tumor patients, whereas in the prospective examination with systematic duplexsonography and / or venography <strong>of</strong> all patients, the percentage was 33 percent. In theprospective study, 31 percent <strong>of</strong> venous thromboses were symptomatic and 69 percentasymptomatic. In 39 percent <strong>of</strong> the cases in the retrospective analysis and 25 percent in theprospective analysis, venous thrombosis occurred during chemotherapy, surgery or radiationtherapy. Venous thrombosis was most <strong>of</strong>ten seen in metastasizing tumors and in colorectalcarcinoma (40 %), haematological system diseases (29 %), gastric cancer (30 %), bronchial,pancreas and ovarian carcinoma (29 %), and carcinoma <strong>of</strong> the prostate (17 %). It wasconcluded that regular screening for thrombosis is indicated even in asymptomatic tumorpatients because asymptomatic venous thrombosis is frequent, can lead to pulmonaryembolism and has to be treated like symptomatic venous thrombosis. This is particularly truefor metastasization during chemotherapy, surgical interventions, or radiation [454].Cancer is the most important acquired but <strong>of</strong>ten overlooked risk factor for the development <strong>of</strong>venous thromboembolism (VTE). Tumors can express procoagulant proteins, for example,and tumor masses may compromise venous blood flow by extrinsic compression <strong>of</strong> adjacentvessels. Cancers can also induce the production <strong>of</strong> inflammatory cytokines that indirectlycontribute to the development <strong>of</strong> hypercoagulability and the risk <strong>of</strong> thromboembolism.Additional risk factors for VTE experienced by patients with cancer include immobilization,because <strong>of</strong> cancer or its treatment, and the potential presence <strong>of</strong> thrombophilic geneticfactors. Many common therapeutic modalities also increase VTE risk, including surgery,chemotherapy agents, adjuvant hormonal manipulation, the use <strong>of</strong> angiogenesis inhibitors,and the presence <strong>of</strong> central venous access devices. The risk <strong>of</strong> VTE seems to be greaterwith certain tumor types, such as cancers <strong>of</strong> the pancreas, kidney, or brain. The value <strong>of</strong>extensive screening <strong>of</strong> patients with the first episode <strong>of</strong> idiopathic thromboembolism for thepresence <strong>of</strong> an occult malignancy remains debatable at this time. VTE continues to pose asubstantial risk to patients with cancer because <strong>of</strong> a variety <strong>of</strong> tumor-, host-, and therapyrelatedfactors [455].Venous thromboembolism (VTE) is a well-recognized and relatively frequent complication <strong>of</strong>malignancy, whereas tumor thrombosis is a rare complication <strong>of</strong> solid cancers. The correctdiagnosis <strong>of</strong> tumor thrombosis and its differentiation from VTE can alter patient managementand prevent unnecessary long-term anticoagulation treatment. To evaluate the contribution<strong>of</strong> 18 F-fluorodeoxyglucose positron emission tomography (PET)/computed tomography to the
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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
Page 109 and 110: TNF-alpha promoter were performed.
Page 111 and 112: were validated in another series <s
Page 113 and 114: vascular invasion (14/15). Abnormal
Page 115 and 116: and other lymph nodes, salivary gla
Page 117 and 118: HEREDITARY PANCREATITISPatients wit
Page 119 and 120: Classification of
Page 121 and 122: historically, but recent life-style
Page 123 and 124: carcinogen exposure with cancer ris
Page 125 and 126: the risk of pancre
Page 127 and 128: conducted a cohort analysis <strong
Page 129 and 130: emain to be solved in screening for
Page 131 and 132: considered for women with Lynch syn
Page 133 and 134: Annexin A5Protein misfolding is a c
Page 135 and 136: CTNNB1To use fluorescence in situ h
Page 137 and 138: expression was not associated with
Page 139 and 140: (ECM) are not fully understood. In
Page 141 and 142: lines. However, the role of
Page 143 and 144: andomized to high-dose vitamin A, t
Page 145 and 146: Synuclein-gammaPerineural invasion
Page 147 and 148: 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: Quantum dotsIt was reported the suc
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 and 200: adenocarcinoma must be addressed at
Page 201 and 202: Molecular biologyCD44v6The purpose
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
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The tumor cells were negative for p
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Duodenal tumorsColorectal polyposis
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Colorectal carcinomaPancreatic meta
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It was described a case of<
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evaluation. The purpose of<
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perforation of a p
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the 28 had pancreatic duct injury <
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ENDOCRINE PANCREATIC TUMORSHistoryA
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25-111 pg/mL). Mean Hemoglobin A1C
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clinical features, misdiagnosis occ
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achieved in selected cases by tissu
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Overall survivalPancreatic neuroend
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REFERENCES001. Metter CC. History <
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044. Fitz RH. The symptomatology an
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089. McClusky DA, Skandalakis LJ, C
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126. Toouli J. Sphincter of
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162. Deshpande AV, Thomas G, Shun A
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196. Park JH, Lee TH, Cheon SL, Sun
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226. Botoi G, Andercou A. Early and
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260. Nakamura H, Morifuji M, Muraka
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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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517. Isayama H, Nakai Y, Togawa O,
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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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