ライフサイエンスコーパス: pancreatic necrosis

1 t pancreatitis and high FA concentrations in pancreatic necrosis.

2 mortality without affecting AP induction or pancreatic necrosis.

3 with the exception of transmural drainage of pancreatic necrosis.

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

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

6 nd teaching others to care for patients with pancreatic necrosis.

7 tibiotic administration to all patients with pancreatic necrosis.

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

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

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

11 rainage in patients with extensive organized pancreatic necrosis.

12 with a microbiologically confirmed infected pancreatic necrosis.

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

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

15 rentiation between infected and non-infected pancreatic necrosis and assist medical therapy in acute

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

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

18 ificant health risk due to the potential for pancreatic necrosis and multi-organ failure.

19 Pancreatic necrosis and organ failure are principal dete

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

21 ent may be required in patients with sterile pancreatic necrosis and persistent unwellness marked by

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

23 ted efferocytosis is critical for preventing pancreatic necrosis and suggest that targeting the TRIM2

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

25 regarding the clinical care of patients with pancreatic necrosis and to offer concise best practice a

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

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

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

29 stric local pancreatic hypothermia decreases pancreatic necrosis, apoptosis, inflammation, and marker

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

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

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

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

34 In rats with AP, cooling decreased pancreatic necrosis by 48%, decreased serum levels of cy

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

36 (18 male, median age 58 yrs.) diagnosed with pancreatic necrosis by endoscopic ultrasound, in whom a

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

38 Infected pancreatic necrosis correlated with high morbidity, but

39 The management of pancreatic necrosis demands the allocation of extensive

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

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

42 BEST PRACTICE ADVICE 4: In patients with pancreatic necrosis, enteral feeding should be initiated

43 Debridement of pancreatic necrosis followed by closed packing and drain

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

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

46 regulation of efferocytosis and reduction of pancreatic necrosis in AP, we used miR-133a-agomir and p

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

48 , but also may develop later due to infected pancreatic necrosis-induced sepsis.

49 evolution comprising multiple organ failure, pancreatic necrosis, infected collections and high morta

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

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

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

53 n acute pancreatitis, secondary infection of pancreatic necrosis is a complication that mostly necess

54 Pancreatic necrosis is a devastating disease that leads

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

56 BEST PRACTICE ADVICE 1: Pancreatic necrosis is associated with substantial morbi

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

58 ICE ADVICE 5: Drainage and/or debridement of pancreatic necrosis is indicated in patients with infect

59 95% CI: 0.04-0.62; P < 0.01), percentage of pancreatic necrosis (<30%/30%-50%/>50%: OR = 0.54; 95% C

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

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

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

63 st indicated for culture-proven infection in pancreatic necrosis or when infection is strongly suspec

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

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

66 Pancreatic necrosis (PN) is the most common complication

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

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

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

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

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

72 PRACTICE ADVICE 8: Percutaneous drainage of pancreatic necrosis should be considered in patients wit

73 venous antibiotics with ability to penetrate pancreatic necrosis should be favored (eg, carbapenems,

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

75 l Step-Up Approach in Patients With Infected Pancreatic Necrosis (TENSION) trial, demonstrated that t

76 en to transferring patients with significant pancreatic necrosis to an appropriate tertiary-care cent

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

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

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

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

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

82 Pancreatic necrosis was identified by characteristic fin

83 For decades, infected or symptomatic pancreatic necrosis was managed by open surgical necrose

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

85 ansgastric necrosectomy (TGN) for walled-off pancreatic necrosis (WON) in selected patients.

86 roaches in managing patients with walled-off pancreatic necrosis (WON).

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