review of literature on clinical pancreatology - The Pancreapedia

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Fatty pancreasTo investigate the clinical implications <strong>of</strong> lipid deposition in the pancreas (fatty pancreas) 293patients who had undergone abdominal computed tomography (CT) and sonography werestudied. Fatty pancreas was diagnosed by sonographic findings and subdivided into mild,moderate, and severe fatty pancreas groups comparing to the retroperitoneal fatechogenicity. Fatty pancreas was associated with higher levels for visceral fat, waistcircumference, aspartate aminotransferase (AST), alanine aminotransferase (ALT), totalcholesterol, triglyceride, high density lipoprotein, free fatty acid, gamma-GTP, insulin, and thehomeostasis model assessment <strong>of</strong> insulin resistance (HOMA-IR) than the control group (P
PANCREATIC PHYSIOLOGYSphincter <strong>of</strong> OddiThe most common functional disorder <strong>of</strong> the biliary tract and pancreas relates to the activity<strong>of</strong> the Sphincter <strong>of</strong> Oddi. The Sphincter <strong>of</strong> Oddi is a small smooth muscle sphincterstrategically placed at the junction <strong>of</strong> the bile duct, pancreatic duct, and duodenum. Thesphincter controls flow <strong>of</strong> bile and pancreatic juices into the duodenum and prevents reflux <strong>of</strong>duodenal content into the ducts. Disorder in its motility is called Sphincter <strong>of</strong> Oddidysfunction. Clinically this presents either with recurrent abdominal biliary type pain orepisodes <strong>of</strong> recurrent pancreatitis. Manometry may identify the motility abnormalities, themost clinically significant being an abnormally elevated basal pressure. The most effectivetreatment once an abnormal basal pressure is identified is division <strong>of</strong> the sphincter. This isassociated with good long-term results [126].Modulatory drugs <strong>of</strong> gastrointestinal (GI) motility are a possibility for use to relieve the mainclinical presentation <strong>of</strong> sphincter <strong>of</strong> Oddi (SO) dysfunctions which are not easily distinguishedfrom those occurring in high prevalence functional GI disorders. The aim <strong>of</strong> one study was toinvestigate the effects <strong>of</strong> GI motility modulators including pinaverium, domperidone,trimebutine, and tegaserod on the contractile activity <strong>of</strong> SO stimulated by carbachol in therabbit. The contraction responses precontracted by carbachol (0.1 µM) <strong>of</strong> in vitro rabbit SOrings were evaluated before and after the addition <strong>of</strong> a series concentration (10 -13 to 10 -3 M) <strong>of</strong>pinaverium, domperidone, trimebutine, and tegaserod. Pinaverium induced a concentrationdependentrelaxation <strong>of</strong> isolated SO rings precontracted with carbachol (0.1 µM). Tegaseroddid not significantly effect SO motility, but domperidone seemed to stimulate SOcontractions. At low doses (10 -13 to 10 -7 M), trimebutine stimulated SO contraction; however,high doses (10 -6 to 10 -3 M) <strong>of</strong> trimebutine inhibited SO motility. It was concluded thatpinaverium totally inhibits contractions induced by carbachol and tegaserod has no effect oncarbachol-induced contractions. Domperidone stimulates contractions induced by carbachol.Trimebutine could either stimulate or inhibit SO contractions depending on its dosage [127].FeedingThe complex control <strong>of</strong> food intake and energy metabolism in mammals relies on the ability<strong>of</strong> the brain to integrate multiple signals indicating the nutritional state and the energy level <strong>of</strong>the organism and to produce appropriate responses in terms <strong>of</strong> food intake, energyexpenditure, and metabolic activity. Central regulation <strong>of</strong> feeding is organized as a long-loopmechanism involving humoral signals and afferent neuronal pathways to the brain,processing in hypothalamic neuronal circuits, and descending commands using vagal andspinal neurons. Sensor mechanisms or receptors sensitive to glucose and fatty acidmetabolism, neuropeptide and cannabinoid receptors, as well as neurotransmitters andneuromodulators synthesized and secreted within the brain itself are all signals integrated inthe hypothalamus, which therefore functions as an integrator <strong>of</strong> signals from central andperipheral structures. Homeostatic feedback mechanisms involving afferent neuroendocrineinputs from peripheral organs, like adipose tissue, gut, stomach, endocrine pancreas,adrenal, muscle, and liver, to hypothalamic sites thus contribute to the maintenance <strong>of</strong>normal feeding behavior and energy balance. In addition to transcriptional events, peripheralhormones may also alter firing and/or connection (synaptology) <strong>of</strong> hypothalamic neuronalnetworks in order to modulate food intake. Moreover, intracellular energy sensing andsubsequent biochemical adaptations, including an increase in AMP-activated protein kinaseactivity, occur in hypothalamic neurons. Understanding the regulation <strong>of</strong> appetite is clearly amajor research effort but also seems promising for the development <strong>of</strong> novel therapeuticstrategies for obesity [128].
Page 1 and 2: REVIEW OF LITERATURE ONCLINICAL PAN
Page 3 and 4: ABBREVIATIONAAPacute alcoholicABPac
Page 5 and 6: FMF AIPfocal mass-forming autoimmun
Page 7 and 8: ODPopen distal pancreatectomyOForga
Page 9 and 10: USUTDTVESDVTEZESWHOXIAPUnited State
Page 11 and 12: Ectopic pancreasCircumportal annula
Page 13 and 14: SymptomsEndocopic ultrasography (EU
Page 15 and 16: HSP27HuRIGF-1 receptorIntegrinesInt
Page 17 and 18: HemodialysisSerous cystadenomasSero
Page 19 and 20: CRPC-reactive proteinCRTchemoradiot
Page 21 and 22: ITNPintrathecal narcotics pumpJCGAI
Page 23 and 24: QSRquantitative systematic
Page 25 and 26: PANCREATIC HISTORYEarly conceptsPan
Page 27 and 28: derived from broadly Harveian anato
Page 29 and 30: acute appendicitis, intestinal obst
Page 31 and 32: dogma and its implied presence <str
Page 33 and 34: In the late 19th century, explorato
Page 35 and 36: performed. In 1880, Carl Thiersch <
Page 37 and 38: cancer was reported by Nestor Dimit
Page 39 and 40: Modern pancreatic historyHoward Reb
Page 41 and 42: PANCREATIC DEVELOPMENT, EMBRYOLOGY
Page 43 and 44: preparations. They were also employ
Page 45: pancreas can be diagnosed without t
Page 49 and 50: acid profile and d
Page 51 and 52: hormones. The roles of</str
Page 53 and 54: ACUTE PANCREATITISAcute pancreatiti
Page 55 and 56: necrosis or a severe course, and lo
Page 57 and 58: of 245 cases <stro
Page 59 and 60: plasty of the mino
Page 61 and 62: no significant difference. The stro
Page 63 and 64: Urinary trypsinogen-2There is not a
Page 65 and 66: groups. None of th
Page 67 and 68: evaluated the presence or absence <
Page 69 and 70: adical, etc, further studies are st
Page 71 and 72: Precut at sphincterotomyPrecut is p
Page 73 and 74: indications [204].Hypercalcemia-ind
Page 75 and 76: endoscopic retrograde cholangiopanc
Page 77 and 78: (before ERCP), serum TAP was detect
Page 79 and 80: concentration and clinical symptoms
Page 81 and 82: However, the recipients of<
Page 83 and 84: less safe for predominantly cephali
Page 85 and 86: increased mortality. Mortality in p
Page 87 and 88: Epidemiology and demographyChinaCHR
Page 89 and 90: for the first time the significance
Page 91 and 92: endoscopic ultrasound accurately de
Page 93 and 94: possible to at least reduce relapse
Page 95 and 96: etiologies have been proposed and a
Page 97 and 98:
patients, can be performed with mod
Page 99 and 100:
negative binomial model. One hundre
Page 101 and 102:
Halofuginone did n
Page 103 and 104:
years, the risk of
Page 105 and 106:
patients with a proven exocrine pan
Page 107 and 108:
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 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 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
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
Page 229 and 230:
clinical features, misdiagnosis occ
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
Page 249 and 250:
260. Nakamura H, Morifuji M, Muraka
Page 251 and 252:
292. Borak GD, Romagnuolo J, Alsola
Page 253 and 254:
324. Oh HC, Kim MH, Choi KS, Moon S
Page 255 and 256:
358. Koornstra JJ, Mourits MJ, Sijm
Page 257 and 258:
391. Chen JY, Amos CI, Merriman KW,
Page 259 and 260:
421. Horwhat JD, Gerke H, Acosta RD
Page 261 and 262:
451. Zamboni G, Capelli P, Scarpa A
Page 263 and 264:
483. Rosa F, Pacelli F, Papa V, Tor
Page 265 and 266:
517. Isayama H, Nakai Y, Togawa O,
Page 267 and 268:
545. Pino MS, Milella M, Gelibter A
Page 269 and 270:
576. Tanno S, Sasajima J, Koizumi K
Page 271 and 272:
605. Ayadi L, Ellouze S, Khabir A,
Page 273 and 274:
637. Nagar AM, Raut AA, Morani AC,
Page 275 and 276:
670. Lejonklou M, Edfeldt K, Johans
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