Impact of Body Overweight and Class I, II and III Obesity on the Outcome of Acute Biliary Pancreatitis

Waele, Boudewijn De; Vanmierlo, Bert; Nieuwenhove, Yves Van; Delvaux, Georges

doi:10.1097/01.mpa.0000220857.55378.7b

Cited by 62 publications

(65 citation statements)

References 19 publications

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“…In a meta-analysis, obesity (defined as BMI >30) was associated with significantly higher incidence of systemic and local complication and higher rate of mortality [1][2][3]. Several independent studies have also confirmed this observation [4][5][6].…”

Section: Discussionsupporting

confidence: 55%

“…Results from meta-analysis show that obesity (defined as BMI>30) was associated with significantly higher incidence of systemic and local complication and higher rate of mortality from AP [1][2][3]. Several independent studies have also confirmed this observation [4][5][6]. Visceral obesity, which is a component of metabolic syndrome, has been recognized to have a stronger correlation with poor outcomes in patients with AP [1][2][3][4][5][6][7].…”

Section: Introductionsupporting

confidence: 48%

“…Several independent studies have also confirmed this observation [4][5][6]. Visceral obesity, which is a component of metabolic syndrome, has been recognized to have a stronger correlation with poor outcomes in patients with AP [1][2][3][4][5][6][7]. NAFLD is an objective marker of visceral obesity.…”

Section: Introductionmentioning

confidence: 53%

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NAFLD Diagnosed with Abdominal Ultrasound is a Marker of Severity in Acute Pancreatitis

Jasdanwala¹

2015

J Gastrointest Dig Syst

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Objective: Obesity, particularly metabolic obesity, is associated with an increased incidence and enhanced severity of acute pancreatitis (AP). Non Alcoholic Fatty Liver Disease (NAFLD) is a marker of metabolic obesity, which can be easily diagnosed, with the help of initial abdominal ultrasound (AUS) routinely performed in all patients with AP upon admission to assess a biliary etiology. The aim of this study is to identify the clinical utility of detecting NAFLD by AUS in determining the severity of patients with AP Methods: Five hundred and seventy four patients with non-alcoholic AP were divided into two groups on the basis of presence or absence of NAFLD detected by AUS at the time of admission. The diagnosis of NAFLD was based solely on imaging findings. Well-established single markers of prognosis as well as scoring systems were studied in both groups. The data was analyzed using the student's t-test, chi-square test and multivariate regression analysis. Results:Patients with NAFLD had a more severe disease as compared to patients without NAFLD as measured by single markers of prognosis like serum albumin, mean length of stay, ICU admission and mortality as well as scoring systems like BISAP score and Modified Atlanta Classification system ( P value < 0.05) BMI, by itself, was not associated with any difference in outcomes in patients with and without NAFLD as assessed by multivariate regression analysis. Age, sex and individual components of metabolic syndrome also had no influence on the prognostic markers Conclusion: Presence of NAFLD as diagnosed by early AUS can be used as an additional single marker of prognosis in AP. The diagnosis of NAFLD is objective and almost always available at the time of initial presentation of AP.

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Section: Discussionsupporting

confidence: 55%

Section: Introductionsupporting

confidence: 48%

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NAFLD Diagnosed with Abdominal Ultrasound is a Marker of Severity in Acute Pancreatitis

Jasdanwala¹

2015

J Gastrointest Dig Syst

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“…In 35 reports the exact Atlanta definitions for organ failure were specifically stated and used 23,61,62 . Seven articles restricted organ failure to two of the four Atlanta determinants for organ failure: respiratory and renal insufficiency 63 -65 .…”

Section: Organ Failurementioning

confidence: 99%

The Atlanta Classification on Acute Pancreatitis Revisited

Bollen

Santvoort²,

Besselink³

et al. 2006

Pancreas

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Results: A total of 447 articles was assessed, including 12 guidelines and 82 reviews. Alternative definitions of predicted severity of acute pancreatitis, actual severity and organ failure were used in more than half of the studies. There was a large variation in the interpretation of the Atlanta definitions of local complications, especially relating to the content of peripancreatic collections. Conclusion:The Atlanta definitions for acute pancreatitis are often used inappropriately, and alternative definitions are frequently applied. Such lack of consensus illustrates the need for a revision of the Atlanta Classification.

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“…In severe cases, progress to circulatory shock, acute lung injury, renal failure, and eventual death may occur (1). Despite some controversy, numerous studies have demonstrated that obesity is associated with increased risk of the severe form of AP and with development of life-threatening complications (2)(3)(4)(5)(6)(7)(8). However, the mechanism by which increased adiposity worsens AP remains unknown.…”

mentioning

confidence: 99%

Interleukin-18, together with interleukin-12, induces severe acute pancreatitis in obese but not in nonobese leptin-deficient mice

Sennello¹,

Fayad²,

Pini³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Obesity is associated with increased severity of acute pancreatitis (AP). The cytokines IL-18 and IL-12 are elevated in patients with AP, and IL-18 levels are high in obesity. We aimed to develop a pathologically relevant model to study obesity-associated severe AP. Lean WT and obese leptin-deficient ob/ob mice received two injections of IL-12 plus IL-18. Survival, pancreatic inflammation, and biochemical markers of AP were measured. Dosing with IL-12 plus IL-18 induced 100% lethality in ob/ob mice; no lethality was observed in WT mice. Disruption of pancreatic exocrine tissue and acinar cell death as well as serum amylase and lipase levels were significantly higher in ob/ob than in WT mice. Edematous AP developed in WT mice, whereas obese ob/ob mice developed necrotizing AP. Adipose tissue necrosis and saponification were present in cytokine-injected ob/ob but not in WT mice. Severe hypocalcemia and elevated acute-phase response developed in ob/ob mice. The cytokine combination induced high levels of regenerating protein 1 and pancreatitis-associated protein expression in the pancreas of WT but not of ob/ob mice. To differentiate the contribution of obesity to that of leptin deficiency, mice received short-and long-term leptin replacement therapy. Shortterm leptin reconstitution in the absence of major weight loss did not protect ob/ob mice, whereas leptin deficiency in the absence of obesity resulted in a significant reduction in the severity of the pancreatitis. In conclusion, we developed a pathologically relevant model of AP in which obesity per se is associated with increased severity.cytokines ͉ inflammation ͉ obesity ͉ pancreas A cute pancreatitis (AP) is an inflammatory disorder that ranges from interstitial edema to confluent necrosis and hemorrhage. In severe cases, progress to circulatory shock, acute lung injury, renal failure, and eventual death may occur (1). Despite some controversy, numerous studies have demonstrated that obesity is associated with increased risk of the severe form of AP and with development of life-threatening complications (2-8). However, the mechanism by which increased adiposity worsens AP remains unknown.Leptin, a protein mainly produced by adipocytes, is a critical regulator of appetite (9). Leptin exerts important regulatory effects on inflammation (10). In the context of AP, the role of leptin remains controversial. In patients with AP, a correlation between serum leptin and disease severity has been reported by some investigators but not by others (11,12). Although in animal models administration of leptin decreases AP severity (13-16), more severe disease is present in leptin-deficient ob/ob and leptin receptordeficient db/db mice as well as leptin-receptor mutant fa/fa rats (17, 18). However, the differential effect of obesity versus leptin deficiency has not been fully investigated.IL-12 and IL-18 are two proinflammatory cytokines that drive the Th1 cell response, characterized by high levels of IFN-␥ (19). Both cytokines are mainly produced by monocytes/macrophages....

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Impact of Body Overweight and Class I, II and III Obesity on the Outcome of Acute Biliary Pancreatitis

Abstract: In acute biliary pancreatitis, body overweight and obesity represent a risk of more "severe" disease and the number and type of complications increase in categories of increasing BMI.

Cited by 62 publications

References 19 publications

NAFLD Diagnosed with Abdominal Ultrasound is a Marker of Severity in Acute Pancreatitis

NAFLD Diagnosed with Abdominal Ultrasound is a Marker of Severity in Acute Pancreatitis

The Atlanta Classification on Acute Pancreatitis Revisited

Interleukin-18, together with interleukin-12, induces severe acute pancreatitis in obese but not in nonobese leptin-deficient mice

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