Obesity In Acute Pancreatitis Research Articles

Obesity in acute pancreatitis: a meta-analysis based on 9,997 patients

Obesity in acute pancreatitis: a meta-analysis based on 9,997 patients

Mo1419 Health Burden of Obesity in Acute Pancreatitis

Mo1419 Health Burden of Obesity in Acute Pancreatitis

Human pancreatic fibroblasts promote epithelial to mesenchymal transition (EMT) in pancreatic cancer cells through ZEB dependent and independent signaling

E.J.M. van Geenen , T.L. Bollen , M.M. Smits , H.C. van Santvoort , M.G. Besselink , H.G. Gooszen , M.J. Bruno . Department of Gastroenterology, VUMC, Amsterdam, Netherlands Department of Radiology, St Antonius Hospital, Nieuwegein, Netherlands Department of Surgery, UMCU, Utrecht, Netherlands Department of Surgery, UMC St Radboud, Nijmegen, Netherlands Department of Gastroenterology, Erasmus UMC, Rotterdam, Netherlands Introduction: Recent meta-analyses on obesity in acute pancreatitis show an increased risk for complications and death, but did not take into account the predicted severity of disease. In several conditions, other than pancreatitis, a so called “obesity paradox” has been described meaning that certain obese patients have an improved outcome. In the current study we examined whether the obesity paradox exists in acute pancreatitis and (central) obesity is associated with an increased risk of complications in patients with predicted severe acute pancreatitis (SAP). Methods: In the current post-hoc analysis, we included patients with a primary episode of predicted (SAP) from a larger cohort of patients enrolled in a previous multicenter randomized clinical trial. The primary endpoint was mortality. Secondary endpoints were morbidity. Anthropometric assessment included body mass index (BMI), CT measurements including waist circumferences (WC), and the WC/BMI. Results: 144 patients with SAP were evaluated. Multivariable analysis showed an association between mortality and highWC/BMI (OR 10.0; 1.8952.7), and a lower BMI (OR 0.84; 0.71-0.99). For morbidity, multivariable analysis showed an association with a higher WC/BMI (OR 11.5; 2.07-63.8) and CTSI (OR 9.81; 3.22-29.2) and a lower BMI (OR 0.79; 0.66-0.94). Conclusion: This is the first study to show that the “obesity paradox” also exists in patients with predicted SAP; obese patients suffering from a predicted SAP have a better outcome than non-obese patients, unless a patient has central obesity.

Adiponectin Polymorphisms and Serum Adiponectin Levels in Severe Acute Pancreatitis

Purpose: Acute pancreatitis (AP) is an acute inflammatory event that originates within the pancreas. Most patients develop mild AP (MAP); however, in some patients, there is an exaggerated systemic inflammatory response that results in severe AP (SAP). Obesity is a known risk factor for developing SAP. Adipokines released from adipose tissue play a role in the inflammatory response to injury. We hypothesize that adipokines such as adiponectin mediate the effect of obesity in AP. Methods: AP patients and controls were enrolled. SAP was defined as the presence of remote organ failure. The single nucleotide polymorphisms (SNPs) of interest in adiponectin (+45 T/G and +276 G/T) were evaluated by polymerase chain reaction (PCR) amplification and DNA sequencing. Serum samples were quantitatively assayed for adiponectin levels. Results: There were 133 patients with AP (108 with MAP and 25 with SAP) and 133 healthy controls. No associations between the two adiponectin SNPs and AP susceptibility or severity were found. There were 60 patients (27 with MAP and 33 with SAP) for whom serum adiponectin levels were available. Serum adiponectin levels from days 1–3 were significantly lower in SAP patients (N = 10; median: 3.74; range: 0.83–8.92 mg/ml) than in MAP patients (N = 26; median: 6.58; range: 1.31–15.37 mg/ml) (P= 0.02). There were no statistically significant differences in serum adiponectin levels among patients with different genotypes at the +45 and +276 loci. However, when the analysis was restricted to lean patients only, serum adiponectin levels were lower in patients with the +45 T/G genotype (N = 2; median: 3.18; range: 1.18–5.18 mg/ml) than the +45 T/T genotype (N = 20; median: 8.07; range: 3.02–18.20) (P= 0.05); there were no patients with the G/G genotype in this subgroup. Multivariate logistic regression controlling for BMI, +45 locus genotype, and sex showed that serum adiponectin level from days 1–3 was a significant predictor of SAP (P= 0.03; OR:0.36, 95% CI: 0.14–0.90). A receiver operating characteristics (ROC) curve using serum adiponectin levels from days 1–3 as the predictor for severity had an area under the curve (AUC) of 0.75. Conclusion: Adiponectin polymorphisms did not alter the risk of developing AP or SAP. Serum adiponectin levels were lower in patients with SAP and can be helpful in predicting the severity of AP.Figure

Obesity Is a Definitive Risk Factor of Severity and Mortality in Acute Pancreatitis: An Updated Meta-Analysis

Background/Aims: Obesity is considered a risk factor in patients with acute pancreatitis. However, the relationship between obesity and mortality in this disease has not been confirmed definitively even in a previous meta-analysis. Since the publication of our previous meta-analysis, one study has been reported about the prognostic value of obesity in acute pancreatitis. We have performed a new meta-analysis to confirm the relationship between obesity and the outcome of acute pancreatitis. Data Sources: A MEDLINE search using ‘pancreatitis’, ‘obesity’ and ‘body mass index’ as search terms. Review Methods: Clinical studies which investigated the prognostic value of obesity in acute pancreatitis with the following criteria: (a) inclusion of mild and severe acute pancreatitis; (b) use of body mass index (BMI) as the measure of obesity; (c) definition of obesity as BMI ≧30 kg/m²; (d) definition of severity of acute pancreatitis according to the criteria established in the Atlanta Symposium. Five studies including patients with mild and severe acute pancreatitis and obesity measured by BMI were analyzed. The end points of the meta-analysis were the severity of acute pancreatitis, local complications, systemic complications and mortality. Pooled odds ratio (OR) and confidence intervals (CI) were calculated according to the Mantel-Haenszel method, and heterogeneity was assessed by the multiplicative inverse variance method. Results: Seven hundred and thirty-nine patients were included. There was no heterogeneity for the variables severity, systemic complications, local complications and mortality among the included studies. Severe acute pancreatitis was significantly more frequent in obese patients (OR 2.9, 95% CI 1.8–4.6). Furthermore, those patients developed significantly more systemic (OR 2.3, 95% CI 1.4–3.8) and especially local complications (OR 3.8, 95% CI 2.4–6.6). In this new analysis, mortality was also higher in obese patients (OR 2.1, 95% CI 1.0–4.8). Conclusion: Obesity is not only a risk factor for the development of local and systemic complications in acute pancreatitis: it also increases the mortality of this disease.

Obesity

This study was conducted to assess the prognostic value of obesity in acute pancreatitis and to determine the role played by obesity-associated diseases in the course of the disease. We prospectively studied 49 patients with acute pancreatitis who were divided into three groups according to their body mass index (BMI). There were 22 patients in group I (BMI < or = 25 kg/m2, normal or low weight); 15 in group II (BMI >25 and < or = 29 kg/m2, overweight); and 12 in group III (BMI >29 kg/m2, obese). Other anthropometric parameters also were measured. The severity of pancreatitis was assessed according to the Atlanta classification system. Systemic complications were significantly more common among obese than nonobese patients (p < 0.05). Patients with severe pancreatitis had a higher body-fat percentage, measured by the subscapular skin-fold thickness, and a larger abdominal circumference than patients with mild pancreatitis. Although hypertensive or diabetic patients developed more systemic complications, the multivariate analysis demonstrated that the presence of these underlying diseases did not modify the prognostic role of obesity in acute pancreatitis. We conclude that obesity is a prognostic factor of outcome in acute pancreatitis. Obesity-associated diseases do not vary the prognostic value of obesity. It seems that truncal adiposity is the kind of obesity related to worse outcome of acute pancreatitis.

Obesity: a risk factor for severe acute biliary and alcoholic pancreatitis

Objective: In this study we evaluate the association between obesity and complication development in patients with a first-attack acute pancreatitis (AP), and investigate the influence of comorbid factors on this association. Methods: Medical records of 150 patients with AP were reviewed. General data, AP etiology, admission AP prognostic criteria, and occurrence of complications were recorded. Patients were classified according to body mass index (BMI) as obese (BMI > 25 kg/m 2) and nonobese (BMI ≤ 25 kg/m 2). Results: Prevalence of obesity was 57%. Thirty-eight percent of the obese patients developed complications as compared with 21% of the nonobese (RR = 1.74; 95% CI, 1–2.9). The risk for severe AP increased according to the degree of obesity. Pancreatic and peripancreatic necrosis was more common in obese patients (17.6% vs 6%), as was the incidence of infectious complications. The risk for severe AP was highest in obese patients with either alcoholic (RR = 5.3; 95% CI, 1.2–23) or biliary etiology (RR = 5.2, 95% CI, 1–26). Conclusion: Obesity may predispose to a complicated course of AP, especially if it is secondary to alcohol or gallstones. Further studies are needed to establish the precise prognostic value of obesity in AP, as well as the pathogenic mechanisms involved in the process.

Is obesity a significant prognostic factor in acute pancreatitis?

The role of obesity in acute pancreatitis has not been fully investigated. Based on the new internationally recognized classification system for acute pancreatitis since 1993, the aim of the present study is to evaluate the implications of obesity as an early prognostic indicator for the development of complications in the course of acute pancreatitis. Three hundred twenty patients with acute pancreatitis were consecutively evaluated in a prospective cohort study. Severe acute pancreatitis was defined by the development of organ failure and/or local complications. Obesity was evaluated by measurement of body mass index. The body mass index did not differ significantly between the patients who lived or died (P = 0.51). The obese (body mass index > or =30 kg/m2) had a higher incidence of developing local complications than the nonobese (P < 0.0001). There was no statistical difference in the incidence of developing systemic complications (P = 0.21) or in the mortality (P = 1.0) between the obese and nonobese. These data demonstrated that obese patients had a higher risk of developing local complications in the course of acute pancreatitis. Obesity did not carry an increased risk of developing organ failure or fatal outcome.