ライフサイエンスコーパス: pancreatitis

1 onfirmed in serum samples from patients with pancreatitis).

2 ral pathological conditions, including acute pancreatitis.

3 T7K24R mice developed no spontaneous pancreatitis.

4 ients with pancreatic cancer from those with pancreatitis.

5 s associated with a higher rate of post-ERCP pancreatitis.

6 Piezo1-induced TRPV4 channel opening causes pancreatitis.

7 might be used to treat patients with severe pancreatitis.

8 les from patients with mild and severe acute pancreatitis.

9 llular calcium that is insufficient to cause pancreatitis.

10 ury during cholestasis, such as from biliary pancreatitis.

11 caused organ failure in the absence of acute pancreatitis.

12 pe 1 diabetes mellitus (T1D), and autoimmune pancreatitis.

13 n patients with predicted mild acute biliary pancreatitis.

14 d subjected to cerulein-induced experimental pancreatitis.

15 ce repeated injections of cerulein to induce pancreatitis.

16 d in vivo efficacy in a mouse model of acute pancreatitis.

17 WT littermates in two experimental models of pancreatitis.

18 cases of hepatotoxicity and 3 cases of acute pancreatitis.

19 ve treatment strategies in acute and chronic pancreatitis.

20 a preclinical mouse model of CTSB-dependent pancreatitis.

21 lso are more susceptible to cerulein-induced pancreatitis.

22 ivation, and necrosis, ultimately leading to pancreatitis.

23 visceral fat or systemic circulation during pancreatitis.

24 ms to be key pathogenic mechanism in chronic pancreatitis.

25 0.1%) events of adjudication-confirmed acute pancreatitis.

26 g the index admission for patients with mild pancreatitis.

27 by chylomicronemia and recurrent episodes of pancreatitis.

28 ality when compared with sterile necrotizing pancreatitis.

29 ed elevated diastase levels indicating acute pancreatitis.

30 We have studied its role in pancreatitis.

31 ted Hhip expression has been linked to human pancreatitis.

32 ntrol mice, with typical features of chronic pancreatitis.

33 increased severity of cerulein-induced acute pancreatitis.

34 astric pain and laboratory studies confirmed pancreatitis.

35 troperitoneal gas gangrene and emphysematous pancreatitis.

36 neutrophils, all cell types participating in pancreatitis.

37 R-216b KOs following caerulein-induced acute pancreatitis.

38 ion and cause hereditary or sporadic chronic pancreatitis.

39 nd extensive pancreatic injury seen in acute pancreatitis.

40 endpoint was overall frequency of post-ERCP pancreatitis.

41 c activation of trypsin is an early event in pancreatitis.

42 esponse and the cellular microenvironment in pancreatitis.

43 itor 1) have been found in familial forms of pancreatitis.

44 y responses of these cell types during acute pancreatitis.

45 st important determinant of outcome in acute pancreatitis.

46 iride group with adjudicated-confirmed acute pancreatitis.

47 tcome, and therapy of organ failure in acute pancreatitis.

48 aches for patients with infected necrotizing pancreatitis.

49 ier status who suffered from recurrent acute pancreatitis.

50 he pancreatic duct is commonly used to study pancreatitis.

51 use prolonged calcium changes and consequent pancreatitis.

52 ed from Piezo1 agonist- and pressure-induced pancreatitis.

53 m a cohort of patients presenting with acute pancreatitis.

54 occurs 3 to 5 weeks after the onset of acute pancreatitis.

55 ing and testing novel therapeutics for human pancreatitis.

56 Some mice were given cerulean to induce pancreatitis.

57 rritable bowel syndrome, Crohn's disease and pancreatitis.

58 hanisms between the development of POPFs and pancreatitis.

59 ncreas may contribute to the pathogenesis of pancreatitis.

60 evels and increased risk of life-threatening pancreatitis.

61 n of trypsinogen during secretagogue-induced pancreatitis.

62 te pancreatitis and has no effect on chronic pancreatitis.

63 ing in pancreatic acinar cells can result in pancreatitis.

64 tion to sensitize mice to the development of pancreatitis.

65 0), cholelithiasis (14.5%, 32/220) and acute pancreatitis (0.6%, 4/602), respectively.

66 3), which included recurrence/progression of pancreatitis (2 early, 1 control) and a cystic duct stum

67 s correlated with a higher rate of post-ERCP pancreatitis (20%, p = 0.020) compared to the other type

68 Although most patients develop mild pancreatitis, 20% develop severe and/or necrotizing panc

69 l four toxicities, reaching significance for pancreatitis (6-month risk, 5.8% v 1.3%; P = .002).

70 Acute pancreatitis, a common cause of hospitalization in the U

71 er 2016, a total of 88 patients with chronic pancreatitis, a dilated main pancreatic duct, and who on

72 Asparaginase-associated pancreatitis (AAP) is common in patients with acute lymp

73 ecutive days, in patients with acute biliary pancreatitis (ABP).

74 cell is the initial step in pressure-induced pancreatitis, activation of Piezo1 produces only transie

75 e for human diseases, including myocarditis, pancreatitis, acute flaccid paralysis, and poliomyelitis

76 ncluded renal proximal tubular injury, focal pancreatitis, adrenocortical hyperplasia, and lymphocyte

77 In addition, the PAK patient developed acute pancreatitis after CAR-T therapy.

78 ve in reducing the frequency and severity of pancreatitis after endoscopic retrograde cholangiopancre

79 diameter balloon decreases the occurrence of pancreatitis after endoscopic retrograde cholangiopancre

80 indometacin on the frequency and severity of pancreatitis after ERCP in high-risk patients.

81 Pancreatitis after ERCP occurred in 141 (14%) of 1037 pa

82 n addition to the 141 patients who developed pancreatitis after ERCP, were considered serious as all

83 outcome of the study was the development of pancreatitis after ERCP.

84 al timing of their administration to prevent pancreatitis after ERCP.

85 re those at high risk for the development of pancreatitis after ERCP.

86 us approach to reporting features of chronic pancreatitis aimed to standardize diagnosis and assessme

87 ent presents and defines features of chronic pancreatitis along with recommended reporting metrics.

88 early in disease progression include chronic pancreatitis, alterations in epigenetic regulators, and

89 tern of visceral adipose injury during acute pancreatitis and acute diverticulitis to determine its r

90 ents reporting rash, and colitis, gastritis, pancreatitis and arthritis, and diabetic ketoacidosis ea

91 and PRSS1 mutation carriers with hereditary pancreatitis and at age 35 years in the setting of Peutz

92 group (0.87%); this patient developed acute pancreatitis and bacteremia after the procedure.

93 ms underlying pancreatic diseases, including pancreatitis and cancer, is essential to improve clinica

94 ion, which can lead to complications such as pancreatitis and cholangitis.

95 n in approximately 20% of all cases of acute pancreatitis and defines "severe acute pancreatitis." Or

96 e (PNLIP) increased in adipose tissue during pancreatitis and entered adipocytes by multiple mechanis

97 s the severity of secretagogue-induced acute pancreatitis and has no effect on chronic pancreatitis.

98 n ex vivo and in vivo rodent models of acute pancreatitis and human pancreatic acini.

99 tricture occurs frequently after necrotizing pancreatitis and is associated with splanchnic vein thro

100 tein-1) associates with a history of chronic pancreatitis and occurs in 25% of pancreatic ductal aden

101 findings implicate CA19-9 in the etiology of pancreatitis and pancreatic cancer and nominate CA19-9 a

102 pared levels of CDH11 messenger RNA in human pancreatitis and pancreatic cancer tissues and cells wit

103 found levels of IL22 to be increased during pancreatitis and pancreatic tumor development and to be

104 table similarities in matrix changes between pancreatitis and PDAC.

105 oncogenic Kras signaling, thereby promoting pancreatitis and progression to PDA.

106 ous cholecystitis associated with gangrenous pancreatitis and retroperitoneal gangrene.

107 ly between patients with initial-stage acute pancreatitis and those without imaging or laboratory fin

108 h other tissues in mice; IL22 increased with pancreatitis and tumorigenesis.

109 WON is a common consequence of severe pancreatitis and typically occurs 3 to 5 weeks after the

110 dilation reduced the frequency of post-ERCP pancreatitis and was determined to be the optimum dilati

111 y disease samples (of which 119 were chronic pancreatitis), and 199 PDAC samples (102 stage I-II and

112 o of colitis, and one each of transaminitis, pancreatitis, and cholecystitis.

113 of mice with cerulean- or L-arginine-induced pancreatitis, and in an oncogenic Kras murine model of s

114 statin usage is protective against post ERCP pancreatitis, and our findings suggest a potential role

115 d key safety outcomes (severe hypoglycaemia, pancreatitis, and pancreatic cancer).

116 atory bowel disease, celiac disease, chronic pancreatitis, and primary sclerosing cholangitis.

117 trols (100 healthy subjects; 50 with chronic pancreatitis; and 125 with noncancerous pancreatic cysts

118 fferent classifications of severity in acute pancreatitis (AP) and to investigate which characteristi

119 Acute Pancreatitis (AP) is sudden onset pancreas inflammation

120 Acute pancreatitis (AP) of different etiologies is associated

121 somal-dominant disorder with recurrent acute pancreatitis (AP) progressing to chronic pancreatitis (C

122 r circulating triglycerides may worsen acute pancreatitis (AP)-associated local and systemic injury.

123 duces inflammatory diseases, including acute pancreatitis (AP).

124 i for inflammatory bowel disease and chronic pancreatitis are associated with PDAC and may provide in

125 ase, inflammatory bowel disease, and chronic pancreatitis are associated with PDAC.

126 atic ductal adenocarcinoma (PDA) and chronic pancreatitis are characterized by a dense collagen-rich

127 stromal tumours, Crohn's disease, and groove pancreatitis are discussed.

128 ches to the debridement of acute necrotizing pancreatitis are preferred to open surgical necrosectomy

129 Criteria for the diagnosis of early chronic pancreatitis are still under discussion and need prospec

130 we address research needs such as staging of pancreatitis, aspects of malnutrition and pain, and canc

131 people diagnosed with CP may have hereditary pancreatitis, associated with cationic trypsinogen (PRSS

132 Acute pancreatitis-associated adipose tissue had ongoing lipol

133 Differentiation from pancreatitis based on static imaging 1 h after injection

134 Given his history of chronic pancreatitis, baseline abdominal MRI was performed to de

135 Given his history of chronic pancreatitis, baseline abdominal MRI was performed to de

136 Furthermore, similar analyses in chronic pancreatitis biopsy samples showed the presence of acina

137 ically develops early in the course of acute pancreatitis, but also may develop later due to infected

138 on of adaptive immune responses in mice with pancreatitis by flow cytometry analysis of T cells (CD25

139 We induced severe acute pancreatitis by partial duct ligation with caerulein sti

140 e chymotrypsin protects the pancreas against pancreatitis by reducing harmful trypsin activity.

141 There were no differences in the risk of pancreatitis (CACPR: 2.9%, non-CACPR: 2.4%; weighted OR

142 el diagnostic algorithms, definitive chronic pancreatitis can be diagnosed by imaging criteria alone,

143 en and lysosomal fraction occurs early after pancreatitis-causing stimulus.

144 The cumulative incidence of grade 3-4 pancreatitis, central neurotoxicity, and thromboses was

145 he incidence rate of complications including pancreatitis, cholangitis, bleeding, and perforation bet

146 In patients with predicted mild gallstone pancreatitis, cholecystectomy within 24 hours of admissi

147 (11% vs 5%; P = .43), or in recurrent acute pancreatitis, chronic pancreatitis, Izbicki pain scores,

148 cantly increased the occurrence of post-ERCP pancreatitis compared with shorter balloon dilation (p=0

149 The incidence of acute pancreatitis continues to rise, inducing substantial med

150 ute pancreatitis (AP) progressing to chronic pancreatitis (CP) and a markedly increased risk of pancr

151 ts containing healthy controls (HC), chronic pancreatitis (CP) and PDAC cases, identified 13 miRNAs i

152 Chronic pancreatitis (CP) is a chronic inflammatory and fibrotic

153 Chronic pancreatitis (CP) is a fibro-inflammatory syndrome in in

154 Chronic pancreatitis (CP) is a fibrotic disorder of the pancreas

155 Chronic pancreatitis (CP) is considered an irreversible fibroinf

156 also required for acinar regeneration after pancreatitis, demonstrating a general role in control of

157 ning conditions, including acute and chronic pancreatitis, diabetes, and pancreatic cancer, which aff

158 T-cell activation and severity of acute pancreatitis did not differ significantly between IL12B-

159 Among patients with chronic pancreatitis, early surgery compared with an endoscopy-f

160 Early oral refeeding in mild acute pancreatitis (EORVsUOR).

161 h clinical features as abdominal pain, acute pancreatitis, eruptive xanthomas, and lipemia retinalis.

162 efit most from surgical treatment in chronic pancreatitis, especially in regard to pain relief.

163 Ivacaftor may be useful for recurrent pancreatitis, even in the absence of respiratory morbidi

164 ctivity of trypsin increases the severity of pancreatitis, even though loss of trypsin activity does

165 llowing initiation of azathioprine, 40 acute pancreatitis events occurred (incidence rate 49.1 events

166 estations ranging from abdominal pain, acute pancreatitis, exocrine and/or endocrine dysfunction, and

167 ts of CM4620 in preventing or reducing acute pancreatitis features and severity.

168 ion of pancreatitis significantly diminished pancreatitis features including pancreatic oedema, acina

169 uction; biliary obstruction; recurrent acute pancreatitis; fistulas; or persistent systemic inflammat

170 the pancreatic gland is the central cause of pancreatitis following abdominal trauma, surgery, endosc

171 e pancreas has been linked to development of pancreatitis for more than a century.

172 Spleen cells from mice with pancreatitis had increases in Th2 cells but not in Th1 c

173 y shortly after admission for mild gallstone pancreatitis has been proposed based on observational da

174 Acute, acute recurrent, and chronic forms of pancreatitis have been increasingly diagnosed in childre

175 Hereditary pancreatitis (HP) is a heritable, autosomal-dominant dis

176 tors, diagnosis, and management of pediatric pancreatitis, identifies features that are unique to the

177 of azathioprine and increased risk of acute pancreatitis in adult inflammatory bowel disease.

178 n the modern management of acute necrotizing pancreatitis in cases not amenable to less invasive endo

179 ioprine is associated with the risk of acute pancreatitis in children with inflammatory bowel disease

180 s associated with an increased risk of acute pancreatitis in children with inflammatory bowel disease

181 ransplantation is performed to treat chronic pancreatitis in children.

182 lays no significant role in cerulein-induced pancreatitis in mice.

183 tigated the role of CTRL in cerulein-induced pancreatitis in mice.

184 gh loss of trypsin activity does not prevent pancreatitis in mice.

185 , attenuates acinar cell pathology and acute pancreatitis in mouse experimental models.

186 in calcium signaling and the pathogenesis of pancreatitis in pancreatic acinar cells.

187 n of cerulein for 2 days induced progressive pancreatitis in T7K24R mice, but not in control mice, wi

188 ptoms requiring over 20 hospitalizations for pancreatitis in the last 10 years.

189 tion of CM4620 reduces the severity of acute pancreatitis in the rat, a hitherto untested species.

190 on of patients with predicted mild gallstone pancreatitis in whom early cholecystectomy is safe warra

191 pared with the standard 100 mg regimen, with pancreatitis incidence remaining high in high-risk patie

192 k patients, the optimal dose is unknown, and pancreatitis incidence remains high.

193 s associated with an increased risk of acute pancreatitis (incidence rate ratio 5.82 [95% CI 2.47-13.

194 Key features of acute pancreatitis include excess cellular Ca(2+) entry driven

195 ry without affecting NEFA signaling or acute pancreatitis induction.

196 (MORC4) is associated with acute and chronic pancreatitis, inflammatory disorders and cancer but it r

197 (environmental and genetic) that cause acute pancreatitis initially cause injury to organelles of the

198 s lent additional support to the notion that pancreatitis is a disease of autodigestion.

199 Infected necrotizing pancreatitis is a highly morbid disease with poor outcom

200 Chronic pancreatitis is a multifactorial, fibroinflammatory synd

201 Chronic pancreatitis is an inflammatory condition of the pancrea

202 Acute pancreatitis is an inflammatory disorder of the exocrine

203 Colon involvement in necrotizing pancreatitis is associated with substantial morbidity an

204 SUMMARY/BACKGROUND DATA: Necrotizing pancreatitis is characterized by a profound inflammatory

205 Acute pancreatitis is characterized by premature intracellular

206 The predominant symptom of chronic pancreatitis is chronic pain resulting in reduced qualit

207 Colon involvement in necrotizing pancreatitis is common; clinical deterioration should pr

208 ta cell area, even without overt diabetes or pancreatitis is consistently observed.

209 n relief after surgical treatment in chronic pancreatitis is high and the commonly used procedures ca

210 Currently, an effective targeted therapy for pancreatitis is lacking.

211 The incidence and prevalence of chronic pancreatitis is rising and no curative treatment is avai

212 longed calcium elevation necessary to induce pancreatitis is unknown.

213 d our understanding of the mechanisms behind pancreatitis, it continues to afflict many families for

214 or in recurrent acute pancreatitis, chronic pancreatitis, Izbicki pain scores, or medical costs.

215 generation following acute caerulein-induced pancreatitis, leading to more severe damage, loss of the

216 ions previously linked to CF carriers (e.g., pancreatitis, male infertility, bronchiectasis), as well

217 Acute pancreatitis may be associated with both local and syste

218 rocess in the endocrine pancreas, suggesting pancreatitis might be a potential precursor to DM.

219 atrophy was a hallmark of both neoplasia and pancreatitis models in the absence of Ddr1.

220 CTSC deletion reduced the severity of pancreatitis (more prominently in the milder model) with

221 eads to pancreatic injury in early stages of pancreatitis, multiple parallel mechanisms, including ac

222 enzyme in human serum indicates the onset of pancreatitis, mumps, cancer, stress, and depression.

223 ensitivity [n = 13]; osteonecrosis [n = 29]; pancreatitis [n = 24]; thromboembolism [n = 17]) was 9.3

224 The risk of acute pancreatitis needs to be considered when deciding on opt

225 Its loss mitigates the severity of pancreatitis not by reducing intra-acinar cell zymogen a

226 Biliary stricture in necrotizing pancreatitis (NP) has not been systematically categorize

227 elopment of colon involvement in necrotizing pancreatitis (NP) negatively affects morbidity and morta

228 During pancreatitis, obese PNLIP-knockout mice, unlike obese ad

229 Overall, post-ERCP pancreatitis occurred in 199 (10%) of 1920 patients (44

230 Chronic pancreatitis often results in chronic abdominal pain and

231 increased lipase or amylase (two [4%]), and pancreatitis (one [2%]).

232 vation of digestive proteases is critical in pancreatitis onset.

233 grading of pathological conditions, such as pancreatitis or cancer.

234 ease, cancer, chronic liver disease, chronic pancreatitis, or alcohol-related conditions), and medica

235 e undergoing cholecystectomy for malignancy, pancreatitis, or choledocholithiasis.

236 acute pancreatitis and defines "severe acute pancreatitis." Organ failure typically develops early in

237 of asparaginase-associated hypersensitivity, pancreatitis, osteonecrosis, and thromboembolism were pr

238 uantification of disease severity in chronic pancreatitis, other than by using ductal features alone

239 Additionally, we describe the novel Chronic Pancreatitis Pain Relief Score (CPPR-Score) as a tool fo

240 The Chronic Pancreatitis Pain Relief Score allows identifying patien

241 ry signalling as central mechanisms in acute pancreatitis pathobiology.

242 and mouse genetic models, as well as chronic pancreatitis patient samples.

243 ding is safe in predicted mild acute biliary pancreatitis patients, does not cause adverse gastrointe

244 ents with Peutz-Jeghers syndrome, hereditary pancreatitis, patients with CDKN2A gene mutation, and pa

245 risk due to germline mutations, a history of pancreatitis, patients with mucinous pancreatic cysts, a

246 rate of adverse events, including post-ERCP pancreatitis (PEP) (16.1% vs. 6.4%, p = 0.17), and hemor

247 ith an incidence of 3.5 to 15%, is post ERCP pancreatitis (PEP).

248 rates in CBD stones clearance, incidence of pancreatitis, perforation, bleeding, as well as, decreas

249 y breast ovarian cancer syndrome, hereditary pancreatitis, Peutz-Jeghers syndrome, familial atypical

250 Incident acute pancreatitis (physician-assigned diagnosis with ICD-10 c

251 with past medical history of recurrent acute pancreatitis presented for evaluation following a referr

252 Chronic pancreatitis represents a risk factor for the developmen

253 Management of chronic pancreatitis requires an interdisciplinary approach incl

254 ing criteria alone, whereas probable chronic pancreatitis requires clinical features and imaging crit

255 titis, 20% develop severe and/or necrotizing pancreatitis, requiring advanced medical and interventio

256 Genetic deficiency in chymotrypsin increases pancreatitis risk in humans and pancreatitis severity in

257 Prior U/S and CT imaging for pancreatitis ruled out gallstones or anatomical etiologi

258 yA 55-year-old man with a history of chronic pancreatitis secondary to chronic alcohol abuse presente

259 in increases pancreatitis risk in humans and pancreatitis severity in mice.

260 Acute pancreatitis severity scores have limited proficiency, a

261 nd APACHE II scores were used as measures of pancreatitis severity.

262 Patients with chronic pancreatitis should be seen at least once a year and re-

263 imaging after multiple time points, PDAC and pancreatitis showed a trend for differential uptake kine

264 infusion starting 30 min after induction of pancreatitis significantly diminished pancreatitis featu

265 dogs with spontaneous DM (sDM), spontaneous pancreatitis (sPanc), both (sDMPanc), toxin-induced DM (

266 Pancreatitis starts with primarily sterile local inflamm

267 0 Dutch hospitals participating in the Dutch Pancreatitis Study Group.

268 e prevention of surgical diabetes in chronic pancreatitis subjects undergoing total pancreatectomy (a

269 For patients with painful chronic pancreatitis, surgical treatment is postponed until medi

270 median duration of time between the onset of pancreatitis symptoms and operative intervention was 60

271 es have been previously linked to hereditary pancreatitis, this is the first known instance of a muta

272 e of CTRC as a key defense mechanism against pancreatitis through regulation of intrapancreatic tryps

273 e found the step-up approach for necrotizing pancreatitis to be superior to open necrosectomy, withou

274 r correction of organelle functions in acute pancreatitis to create a discussion for clinical trial t

275 (four [12%]), neutropenia (three [9%]), and pancreatitis (two [6%]).

276 Therefore, during pancreatitis, unlike diverticulitis, PNLIP leaking into

277 l 19 months, patient reported no episodes of pancreatitis until he discontinued ivacaftor.

278 sity of iodine was 2.5mg/ml in patients with pancreatitis vs. 3.65mg/ml in controls (p = 0.02).

279 s immunoglobulin group (atrial fibrillation, pancreatitis, vulvar pain, chest tube malfunction and co

280 al step-up approach for infected necrotizing pancreatitis was found to reduce the composite endpoint

281 CA19-9-mediated pancreatitis was reversible and could be suppressed with

282 The frequency of post-ERCP pancreatitis was significantly higher in the 0 s group t

283 The frequency of post-ERCP pancreatitis was significantly lower in the 30, 60, and

284 tivation, severity of cerulein-induced acute pancreatitis was similar in Ctrl-KO and C57BL/6N mice.

285 In mice with severe pancreatitis, we found systemic inflammatory response sy

286 ase, inflammatory bowel disease, and chronic pancreatitis were associated with PDAC at P values < 0.0

287 a diagnosis of predicted mild acute biliary pancreatitis were divided into Group A (early oral refee

288 e patients who underwent surgery for chronic pancreatitis were included.

289 Adults with predicted mild gallstone pancreatitis were randomized to cholecystectomy with cho

290 uspicion such as recurrent episodes of acute pancreatitis when imaging is normal or equivocal.

291 he context of a patient with recurrent acute pancreatitis who chooses to delay surgery until after ho

292 confirmed or suspected infected necrotizing pancreatitis who required intervention from May 12, 2014

293 contrast material in 27 patients with acute pancreatitis who underwent the examination 48 to 72hours

294 7H/7 T/F508del) who presented with recurrent pancreatitis who was effectively treated with ivacaftor

295 he genetics, cell biology, and immunology of pancreatitis with a focus on protease activation pathway

296 uses genomic instability, tissue damage, and pancreatitis with full penetrance.

297 ression in mice resulted in rapid and severe pancreatitis with hyperactivation of epidermal growth fa

298 e practical considerations in managing acute pancreatitis within the first 72 hours after the patient

299 CPDPC investigators from the Adult Chronic Pancreatitis Working Group were tasked with development

300 reatic cancer cases to subjects with chronic pancreatitis yielded 46% sensitivity at 99% specificity