ライフサイエンスコーパス: pancreatic necrosis

1 ic fibrosis can be initiated by little or no pancreatic necrosis.

2 or the need of intervention in patients with pancreatic necrosis.

3 tibiotic administration to all patients with pancreatic necrosis.

4 ry, renal) and on the presence and extent of pancreatic necrosis.

5 ic morphology and the presence and extent of pancreatic necrosis.

6 ted clinical course, multiorgan failure, and pancreatic necrosis.

7 t pancreatitis and high FA concentrations in pancreatic necrosis.

8 rainage in patients with extensive organized pancreatic necrosis.

9 mortality without affecting AP induction or pancreatic necrosis.

10 with the exception of transmural drainage of pancreatic necrosis.

11 Eleven patients with organized pancreatic necrosis (8 sterile and 3 infected) after sev

12 remain symptomatic after an episode of acute pancreatic necrosis after the necrosis has become organi

13 iple organ failure, increasing percentage of pancreatic necrosis and heterogeneity of the collection

14 Pretreatment with IRS954 reduced pancreatic necrosis and lung inflammation in taurolithoc

15 Pancreatic necrosis and organ failure are principal dete

16 uch that the presence of both infected (peri)pancreatic necrosis and persistent organ failure have a

17 ming and indications for surgery in cases of pancreatic necrosis and pseudocyst assessed.

18 ipases convert mild AP to SAP independent of pancreatic necrosis and the inflammatory response.

19 bridement or drainage to those with infected pancreatic necrosis and/or abscess confirmed by radiolog

20 on (serum amylase and lipase), fat necrosis, pancreatic necrosis, and multisystem organ failure, and

21 um OA, a severe inflammatory response, worse pancreatic necrosis, and multisystem organ failure.

22 asive approaches to the drainage of infected pancreatic necrosis are beginning to gain acceptance.

23 ategies for asymptomatic or oligosymptomatic pancreatic necrosis are still poorly defined.

24 The treatment of pancreatic necrosis at a tertiary referral center was re

25 was a composite of major infection (infected pancreatic necrosis, bacteremia, or pneumonia) or death

26 moval of viable tissue.Accurate diagnosis of pancreatic necrosis by dynamic CT led to new approaches

27 (18 male, median age 58 yrs.) diagnosed with pancreatic necrosis by endoscopic ultrasound, in whom a

28 ough to be good, management of patients with pancreatic necrosis can be labor intensive and require e

29 The management of pancreatic necrosis demands the allocation of extensive

30 bpopulation of patients with extensive acute pancreatic necrosis develop complex, organized collectio

31 and January 1, 2000, focusing on those with pancreatic necrosis documented by contrast-enhanced comp

32 Debridement of pancreatic necrosis followed by closed packing and drain

33 ued aggressive approach to the management of pancreatic necrosis, given that long-term outcome about

34 ed computerized tomography showed > or = 50% pancreatic necrosis in 10 of 11 patients in whom endosco

35 reviously, pancreata of dying alcoholics and pancreatic necrosis in severe AP, respectively, showed h

36 Infectious pancreatic necrosis (IPN) is a viral disease currently p

37 Infectious pancreatic necrosis (IPN) is a viral disease with a sign

38 n to be effective for patients with infected pancreatic necrosis (IPN), but the data from individual

39 Pancreatic necrosis is a devastating disease that leads

40 ical intervention for secondary infection of pancreatic necrosis is associated with a death rate of 2

41 The optimal management of severe pancreatic necrosis is evolving with a few large center

42 95% CI: 0.04-0.62; P < 0.01), percentage of pancreatic necrosis (<30%/30%-50%/>50%: OR = 0.54; 95% C

43 luid collections (PFCs) including walled-off pancreatic necrosis, management of refractory gastrointe

44 Forty-eight patients had evidence of pancreatic necrosis on computed tomography scan.

45 eterminant relates to whether there is (peri)pancreatic necrosis or not, and if present, whether it i

46 major pancreatic complications that included pancreatic necrosis, pancreatic abscess, pseudocyst, hem

47 bclassified as multiorgan dysfunction (MOF), pancreatic necrosis (PN >30% on contrast CT), and death.

48 n, alcohol was shown to increase the risk of pancreatic necrosis regardless of the cause of acute pan

49 The role of surgery in patients with sterile pancreatic necrosis remains controversial.

50 The treatment of patients with extensive pancreatic necrosis remains controversial; a subpopulati

51 The presence of high liquid content in the pancreatic necrosis resulted in a 64% predicted endpoint

52 eate-induced increase in serum lipase, UFAs, pancreatic necrosis, serum inflammatory markers, systemi

53 d acute UFA generation via lipolysis worsens pancreatic necrosis, systemic inflammation, and injury a

54 Infectious pancreatic necrosis virus (IPNV), a member of the family

55 ped a reverse genetics system for infectious pancreatic necrosis virus (IPNV), a prototype virus of t

56 of three different fish viruses: infectious pancreatic necrosis virus (IPNV), infectious hematopoiet

57 The major capsid protein, VP2, of infectious pancreatic necrosis virus, a nonenveloped icosahedral vi

58 Infectious pancreatic necrosis viruses (IPNVs) exhibit a wide range

59 Pancreatic necrosis was identified by characteristic fin

60 perative management of patients with sterile pancreatic necrosis was superior to surgical interventio

61 ndoscopic drainage/debridement of walled-off pancreatic necrosis (WOPN) after necrotizing pancreatiti