Systemic Complications Of Acute Pancreatitis Research Articles

MODERN IDEAS ON THE ROLE OF HEMODYNAMIC DISORDERS IN THE PATHOGENESIS OF ACUTE PANCREATITIS

Acute pancreatitis remains one of the most common abdominal diseases, causing a large number of both local and systemic complications. Acute pancreatitis has a high death rate. The pathogenesis of acute pancreatitis is complex and needs careful examination. Many authors suppose, that hemodynamic disorders lead to the development of complications, often fatal. Thus, such disorders need be studied separately. 
 The review is based on the analysis of articles included in such databases as elibrary.ru, cyberleninka.ru, and e-versions of specialized open access journals. All the articles outline modern views on the role of hemodynamic disorders in the pathogenesis of acute pancreatitis.
 The causes and mechanisms of development of hemodynamic disorders are considered in terms of central and regional hemodynamics, and microcirculation. The authors describe their mutual influence and role in the development of both local and systemic complications of acute pancreatitis.
 Contractility disorders can be observed in the pathogenesis of central hemodynamics. They can be caused by a highly active myocardial depressant factor. These disorders are supported and aggravated by other organs and systems with the development of multiple organ failure.
 Violations of regional hemodynamics are associated mainly with an increase in intra-abdominal pressure. A direct dependence of intestinal wall perfusion on intra-abdominal pressure is established. Intestinal barrier dysfunction contributes to the infection of necrosis foci.
 Microcirculation disorders are the most important element in the pathogenesis of acute pancreatitis, often defining its outcome. Microcirculation disorders include angiospasm, venous stasis, microthrombi formation, and interstitial edema. A decrease in local perfusion due to impaired gland microcirculation can cause tissue ischemia and pancreonecrosis.

The role of biomarkers in the early diagnosis of acute kidney injury associated with acute pancreatitis: Evidence from 582 cases.

One of the systemic complications of acute pancreatitis (AP) is acute kidney injury (AKI). AKI development in patients with AP increases mortality, morbidity, and the cost of treatment. Therefore, early diagnosis and prevention of AKI is important. The purpose of our study was to present biomarkers and case management of AKI developing in patients with AP. The participants of this retrospective study consisted of 582 patients who were followed up with the diagnosis of AP. Atlanta classification was used for the diagnosis and the identification of severity of AP. The laboratory values of patients at the time of first application to the emergency room were recorded. Blood tests were checked 48 h/l. Their blood tests were monitored daily until the day of discharge. Of the 582 patients who were admitted with the AP diagnosis, 344 were female. AKI was detected in 147 patients (25.2%) of the patients admitted with AP diagnosis. The mean age of patients developing AKI was higher than those who did not develop AKI. The albumin and calcium levels in patients developing AKI were significantly lower than the group without AKI. The C-reactive protein (CRP)/albumin and neutrophil/lymphocyte ratios were statistically significantly higher in the group with AKI than the group without AKI. The increase values in AST and ALT levels between the group with AKI and the group without AKI were not statistically significant. The mean leukocyte, CRP, procalcitonin levels, and immature granulocyte percentage (IG%) ratio were higher in patients with AKI in comparison to the patient group without AKI. The decrease in the lymphocyte, hematocrit, and platelet levels was higher in the patient group with AKI compared to the patient group without AKI. Urea and creatinine levels of the group with AKI at the time of admission were higher than the group without AKI. The clinical picture in 13 of the patients we followed up with AP diagnosis was mortal. The values of hematocrit, platelet, leukocyte, lymphocyte, albumin, CRP, CRP/albumin ratio, neutrophil/lymphocyte ration, IG%, procalcitonin, urea, and creatinine that were examined at the time of hospital admission can be useful biomarkers in predicting the development of AKI in patients with AP. In addition, accompanying diseases and age are among the factors affecting AKI development.

Нейтрофільні позаклітинні пастки як терапевтична мішень при системних ускладненнях гострого панкреатиту

The review focuses on the role of neutrophilic extracellular traps (NETs) in systemic complications of acute pancreatitis. NETs can activate trypsin, cause inflammation and pancreatic tissue damage, and clog the excretory ducts. The main fatal complications of acute pancreatitis, such as acute lung injury, kidney, myocardial and CNS damage, intestinal dysfunction, hemocoagulation disorders are associated with NETs. Focusing on the formation and degradation of NETs may be a way to develop strategies for treating organ damage in severe acute pancreatitis. Current data on the use of NET-targeted therapy in experimental severe acute pancreatitis, which is aimed at blocking the NETs formation and disassembly of the DNA scaffold, inhibition of proteins toxicity in NETs, are considered.

Serum Lactate Dehydrogenase Is a Sensitive Predictor of Systemic Complications of Acute Pancreatitis.

Acute pancreatitis (AP) is a common and potentially life-threatening inflammatory disease that can cause various complications, including systemic inflammatory response syndrome (SIRS), pleural effusion, ascitic fluid, myocardial infarction, and acute kidney injury (AKI). However, there is still a lack of rapid and effective indicators to assess the disease. The aim of this study was to investigate the associations of high serum lactate dehydrogenase (LDH) levels with AP severity and systemic complications. AP patients treated from July 2014 to December 2020 were retrospectively enrolled. They were divided into elevated (n = 93) and normal (n = 143) LDH groups. Their demographic data, clinical data, hospital duration, and hospital expenses were analyzed. Linear and binary logistic regression analyses were used to determine whether elevated LDH is a risk factor for AP severity and complications after adjusting for confounders. There were significant differences in AP severity scores (Ranson, MODS, BISAP, APACHE II, and CTSI), hospital duration, hospital expenses, and the incidences of complications (SIRS, pleural effusion, ascitic fluid, myocardial infarction, and AKI) between the elevated and normal LDH groups. After adjusting for confounders, elevated LDH was associated with AP severity scores and hospital duration and expenses (based on linear regression analyses) and was a risk factor for the occurrence of AP complications and interventions, that is, diuretic and vasoactive agent use (based on binary logistic regression analyses). Elevated LDH is associated with high AP severity scores and high incidences of complications (SIRS, pleural effusion, ascitic fluid, myocardial infarction, and AKI).

Predictors and classifications of the degree of severity of acute pancreatitis

Severe acute panreatitis is a life-threatening disease with mortality rates of about 15%. With the development of infected necrotizing pancreatitis, complicated by the development of organ failure, the mortality rate is 35.2%. Due to the fact that acute pancreatitis is a highly variable pathological process, leading to a wide range of clinical outcomes, predicting the severity of the disease and early identification of patients at risk of developing severe complications is critical to optimize treatment outcomes for this disease. Currently, there are no uniquely accurate and practically available laboratory tests to predict the severity of patients with acute pancreatitis. The review presents literature data on the terminology and classifications of the severity of acute pancreatitis, taking into account the possibilities of their practical application. Information on clinical scale systems for assessing the severity of acute pancreatitis with an assessment of their effectiveness in predicting various treatment outcomes is presented in detail. The characteristics and capabilities of various laboratory markers in the assessment of organ failure and diagnosis of systemic complications of acute pancreatitis are presented. Currently, for the best assessment of the severity of acute pancreatitis, it is necessary to use a multidisciplinary clinical examination of patients and a combination of various predictive tools.

English

BACKGROUND Acute pancreatitis (AP) is described as acute inflammation of the pancreas with or without peripancreatic abnormalities. The present study describes the role of computed tomography in the evaluation and grading of acute pancreatitis. Acute pancreatitis is a dynamic disease having biphasic mortality peaks due to two overlapping phases, which include early and late due to increased obesity, ageing of population, alcohol abuse, increased gall stone incidence, the worldwide AP incidence is increasing. Most important causes of AP in developing countries such as India include increased alcohol consumption. Contrast enhanced computed tomography plays an important role in diagnosis of the disease and helps in determining the prognosis of the disease. Modified CT severity index scoring system is the most commonly used scoring system for assessment of the severity of the disease. METHODS The present study is a prospective study of patients presenting with signs and symptoms of acute pancreatitis referred to the Department of Radio Diagnosis at Katuri medical college. This study comprised of 50 patients with clinical suspicion / diagnosis of acute pancreatitis, raised pancreatic biochemical parameters like serum amylase and serum lipase. Contrast enhanced computed tomography was performed in these patients, findings reported, and the disease was classified using modified CT scoring index system (MCTSI). RESULTS The mean age of the patients in the present study was 42.3 ± 12.28 years. Most of the patients presented with abdominal epigastric pain, abdominal distension. Acute pancreatitis was divided into acute oedematous pancreatitis and necrotising pancreatitis, the former being common. Complications included, ascites, pleural effusions, splenic vein thrombosis, portal venous thrombosis, and haemorrhages. CONCLUSIONS Contrast enhanced CT is useful to differentiate between oedematous and necrotising types of pancreatitis. The MCTSI helps in better evaluation of pancreatic necrosis grading. The modified computed tomography score index correlation with the development of local and systemic complications in acute pancreatitis is well established. Ideally, conducting contrast enhanced computed tomography (CECT) after 48 - 72 hours of acute attack, increases the probability of identifying necrotising pancreatitis. CT in particular has an overall accuracy of about 87 % and sensitivity and specificity of 100 % in the recognition of pancreatic necrosis. KEYWORDS Computed Tomography, Acute Pancreatitis, Pseudocyst, Modified CT Score Index

Elevated Serum Triglyceride Level as a Predictor of Local and Systemic Complications in Acute Pancreatitis

Elevated Serum Triglyceride Level as a Predictor of Local and Systemic Complications in Acute Pancreatitis

On admission severe and sharp pain is associated with local and systemic complications of acute pancreatitis: a prospective cohort-analysis of 1435 cases

On admission severe and sharp pain is associated with local and systemic complications of acute pancreatitis: a prospective cohort-analysis of 1435 cases

Outcomes of Acute Pancreatitis in Patients with Heart Failure: Insights from the Nationwide Inpatient Sample

Introduction Acute pancreatitis (AP) is an inflammatory process involving the pancreas that presents as severe epigastric pain, associated with nausea and vomiting. Aggressive fluid resuscitation is extremely important to prevent local and systemic complications of AP and has been shown to reduce mortality from AP. However, limited data exists to assess the safety of fluid resuscitation among patients predisposed to volume overload, specifically congestive heart failure (CHF). The aim of our study was to assess mortality outcomes and complications of AP in patients with a concurrent CHF. Methods Using the Nationwide Inpatient Sample (NIS), retrospective analysis of hospitalized patients ≥18 years, with a primary diagnosis of acute pancreatitis during a five-year period (2010-2014) was performed. Patients were divided into two groups - with and without CHF. Primary outcomes were inpatient mortality and length of stay. Secondary outcomes were respiratory failure, mechanical ventilation, and need for vasopressors. Descriptive analyses were compared using the t-test for continuous data and chi-square test for categorical data. Statistical significance was assigned at P Results A total of 1,356,659 patients were hospitalized with a primary diagnosis of AP, out of which 69,657 patients had CHF. Patients in the CHF group were older (68.29 vs 51.13 years, p Conclusion Our study showed that patients with AP associated with CHF have significantly higher mortality in comparison with those without CHF. While acute respiratory distress syndrome is a known complication of AP, concomitant CHF was shown to have a higher rate of respiratory failure, requiring intubation and mechanical ventilation. Volume resuscitation in patients with CHF and AP can be challenging, as there is a very fine balance to tip them from euvolemic to volume overload state. Future studies are needed to determine methods to improve volume resuscitation in these patients.

Serum triglyceride level dose dependently elevates the risk of local or systemic complications in acute pancreatitis. A multicenter international cohort analysis of 716 patients

Serum triglyceride level dose dependently elevates the risk of local or systemic complications in acute pancreatitis. A multicenter international cohort analysis of 716 patients

Aging and Comorbidities in Acute Pancreatitis II.: A Cohort-Analysis of 1203 Prospectively Collected Cases.

Introduction: Our meta-analysis indicated that aging influences the outcomes of acute pancreatitis (AP), however, a potential role for comorbidities was implicated, as well. Here, we aimed to determine how age and comorbidities modify the outcomes in AP in a cohort-analysis of Hungarian AP cases.Materials and Methods: Data of patients diagnosed with AP by the revised Atlanta criteria were extracted from the Hungarian Registry for Pancreatic Patients. Outcomes of interest were mortality, severity, length of hospitalization, local, and systemic complications of AP. Comorbidities were measured by means of Charlson Comorbidity Index (CCI) covering pre-existing chronic conditions. Non-parametric univariate and multivariate statistics were used in statistical analysis. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated.Results: A total of 1203 patients from 18 centers were included. Median age at admission was 58 years (range: 18–95 years), median CCI was 2 (range: 0–10). Only severe comorbidities (CCI ≥ 3) predicted mortality (OR = 4.48; CI: 1.57–12.80). Although severe comorbidities predicted AP severity (OR = 2.10, CI: 1.08–4.09), middle (35–64 years) and old age (≥65 years) were strong predictors with borderline significance, as well (OR = 7.40, CI: 0.99–55.31 and OR = 6.92, CI: 0.91–52.70, respectively). Similarly, middle and old age predicted a length of hospitalization ≥9 days. Interestingly, the middle-aged patients (35–64 years) were three times more likely to develop pancreatic necrosis than young adults (OR = 3.21, CI: 1.26–8.19), whereas the old-aged (≥65 years) were almost nine times more likely to develop systemic complications than young adults (OR = 8.93, CI: 1.20–66.80), though having severe comorbidities (CCI ≥ 3) was a predisposing factor, as well.Conclusion: Our results proved that both aging and comorbidities modify the outcomes of AP. Comorbidities determine mortality whereas both comorbidities and aging predict severity of AP. Regarding complications, middle-aged patients are the most likely to develop local complications; in contrast, those having severe comorbidities are prone to develop systemic complications. Studies validating the implementation of CCI-based predictive scores are awaited.

Obesity causes PGC-1α deficiency in the pancreas leading to marked IL-6 upregulation via NF-κB in acute pancreatitis.

Obesity is associated with local and systemic complications in acute pancreatitis. PPARγ coactivator 1α (PGC-1α) is a transcriptional coactivator and master regulator of mitochondrial biogenesis that exhibits dysregulation in obese subjects. Our aims were: (1) to study PGC-1α levels in pancreas from lean or obese rats and mice with acute pancreatitis; and (2) to determine the role of PGC-1α in the inflammatory response during acute pancreatitis elucidating the signaling pathways regulated by PGC-1α. Lean and obese Zucker rats and lean and obese C57BL6 mice were used first; subsequently, wild-type and PGC-1α knockout (KO) mice with cerulein-induced pancreatitis were used to assess the inflammatory response and expression of target genes. Ppargc1a mRNA and protein levels were markedly downregulated in pancreas of obese rats and mice versus lean animals. PGC-1α protein levels increased in pancreas of lean mice with acute pancreatitis, but not in obese mice with pancreatitis. Interleukin-6 (Il6) mRNA levels were dramatically upregulated in pancreas of PGC-1α KO mice after cerulein-induced pancreatitis in comparison with wild-type mice with pancreatitis. Edema and the inflammatory infiltrate were more intense in pancreas from PGC-1α KO mice than in wild-type mice. The lack of PGC-1α markedly enhanced nuclear translocation of phospho-p65 and recruitment of p65 to Il6 promoter. PGC-1α bound phospho-p65 in pancreas during pancreatitis in wild-type mice. Glutathione depletion in cerulein-induced pancreatitis was more severe in KO mice than in wild-type mice. PGC-1α KO mice with pancreatitis, but not wild-type mice, exhibited increased myeloperoxidase activity in the lungs, together with alveolar wall thickening and collapse, which were abrogated by blockade of the IL-6 receptor glycoprotein 130 with LMT-28. In conclusion, obese rodents exhibit PGC-1α deficiency in the pancreas. PGC-1α acts as selective repressor of nuclear factor-κB (NF-κB) towards IL-6 in pancreas. PGC-1α deficiency markedly enhanced NF-κB-mediated upregulation of Il6 in pancreas in pancreatitis, leading to a severe inflammatory response. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

The effect of serum triglyceride concentration on the outcome of acute pancreatitis: systematic review and meta-analysis

Elevated serum triglyceride concentration (seTG, >1.7 mM or >150 mg/dL) or in other words hypertriglyceridemia (HTG) is common in the populations of developed countries. This condition is accompanied by an increased risk for various diseases, such as acute pancreatitis (AP). It has been proposed that HTG could also worsen the course of AP. Therefore, in this meta-analysis, we aimed to compare the effects of various seTGs on the severity, mortality, local and systemic complications of AP, and on intensive care unit admission. 16 eligible studies, including 11,965 patients were retrieved from PubMed and Embase. The results showed that HTG significantly elevated the odds ratio (OR = 1.72) for severe AP when compared to patients with normal seTG (<1.7 mM). Furthermore, a significantly higher occurrence of pancreatic necrosis, persistent organ failure and renal failure was observed in groups with HTG. The rates of complications and mortality for AP were significantly increased in patients with seTG >5.6 mM or >11.3 mM versus <5.6 mM or <11.3 mM, respectively. We conclude that the presence of HTG worsens the course and outcome of AP, but we found no significant difference in AP severity based on the extent of HTG.

Preexisting Diabetes Elevates Risk of Local and Systemic Complications in Acute Pancreatitis: Systematic Review and Meta-analysis.

The prevalence of diabetes mellitus (DM) and acute pancreatitis (AP) increases continuously, therefore, to understand the effects of preexisting diabetes on AP is crucially needed. Here, we performed a systematic review and meta-analysis in which AP patients including DM and non-DM groups were sorted. Several outcome parameters were analyzed, and the odds ratio (OR) and standardized mean difference with 95% confidence intervals (CIs) were calculated.We found 1417 articles, of which 9 articles involving 354,880 patients were analyzed. More complications were seen in diabetic patients than in non-DM patients (OR, 1.553 [95% CI, 1.266-1.904]; P < 0.001). Intensive care unit admission (OR, 1.799 [95% CI, 1.442-2.243]; P < 0.001) and renal failure (OR, 1.585 [95% CI, 1.278-1.966]; P < 0.001) were more frequent in DM patients. There was a tendency of higher mortality and local complications (OR, 1.276 [95% CI, 0.991-1.643]; P = 0.059; and OR, 1.267 [95% CI, 0.964-1.659]; P = 0.090, respectively) in preexisting DM. Length of hospitalization was longer in DM patients (standardized mean difference, 0.217 [95% CI, 0.075-0.360]; P = 0.003). Preexisting DM negatively influences the outcome of AP and increases the risk of renal failure, local complications, and mortality.

Pre-existing diabetes elevates risk of local and systemic complications in acute pancreatitis

Pre-existing diabetes elevates risk of local and systemic complications in acute pancreatitis

Resistin aggravates the expression of proinflammatory cytokines in cerulein‑stimulated AR42J pancreatic acinar cells.

Resistin, an adipocytokine secreted by fat tissues, has been shown to be associated with increased local and systemic complications in acute pancreatitis (AP). However, the mechanism underlying the effect of resistin in the aggravation of AP remains to be elucidated. The aim of the present study was to investigate the functional consequences of exposing rat pancreatic acinar cells to resistin and to determine whether it amplifies proinflammatory signaling in an invitro AP model. AR42J cells pretreated with recombinant resistin were activated by cerulein as an invitro model of AP. The secretion of amylase was measured to evaluate the cytotoxic effect. The mRNA expression levels of tumor necrosis factor (TNF)‑α and interleukin (IL)‑6 were determined using reverse transcription‑quantitative polymerase chain reaction analysis. The nuclear protein expression levels of the nuclear factor (NF)‑κB p65 subunit were determined using western blot analysis. Resistin treatment significantly increased the secretion of amylase, and the mRNA expression levels of TNF‑α and IL‑6 in the cerulein‑induced invitro AP model. High protein levels of the NF‑κB p65 subunit were observed in the nuclei of cells in the resistin‑treated AP model, compared with the untreated AP model. Pretreatment of the invitro resistin‑treated AP model with the NF‑κB inhibitor, pyrrolidine dithiocarbamate decreased the protein expression of the NF‑κB p65 subunit in nuclei, and significantly attenuated the increased mRNA expression levels of TNF‑α and IL‑6 induced by resistin. The results of the present study showed that resistin increased the production of the TNF‑α and IL‑6 proinflammatory cytokines via the NF‑κB‑dependent pathway during AP. Thus, the overproduction of obesity‑associated resistin and the associated amplification of the inflammatory response may result in the aggravation of AP severity.

The effect of lornoxicam on TLR2 and TLR4 messenger RNA expression and tumor necrosis factor-α, interleukin-6, and interleukin-8 secretion in patients with systemic complications of acute pancreatitis.

To assess the effects of the cyclooxygenase-1/cyclooxygenase-2 inhibitor lornoxicam on systemic complications in patients with acute pancreatitis, Toll-like receptor (TLR)2 and TLR4 messenger RNA expression, and cytokine secretion (IL-6, IL-8, tumor necrosis factor-α). Adult patients with acute pancreatitis were randomized to standard therapy or standard therapy plus lornoxicam. Standard therapy included analgesics, spasmolytics, octreotide, pantoprazole, and intravenous fluids. The TLR2 and TLR4 expression levels and TLR2- and TLR4-mediated cytokine production in peripheral blood mononuclear cells were assessed in patients with severe complications and in healthy volunteers (n = 15). A total of 334 patients received standard therapy (n = 246) or standard therapy plus lornoxicam (n = 88), 172 (51.5%) of whom developed systemic complications. Occurrence of complications was higher with standard therapy compared with lornoxicam (57.3% versus 35.2%; P = 0.00034), as was mortality (19.1% versus 6.8%; P = 0.006). The TLR2 and TLR4 expression and TLR2 and TLR4-mediated cytokine production were significantly higher in patients with systemic complications of acute pancreatitis compared with healthy volunteers. Relative TLR2 expression and cytokine production were significantly reduced in patients receiving lornoxicam versus standard therapy. The use of lornoxicam at the onset of acute pancreatitis decreased TLR2 and TLR4 expression and the production of proinflammatory cytokines, thereby reducing the risk of systemic complications and mortality.

Dual pancreas- and lung-targeting therapy for local and systemic complications of acute pancreatitis mediated by a phenolic propanediamine moiety

To inhibit both the local and systemic complications with acute pancreatitis, an effective therapy requires a drug delivery system that can efficiently overcome the blood–pancreas barrier while achieving lung-specific accumulation. Here, we report the first dual pancreas- and lung-targeting therapeutic strategy mediated by a phenolic propanediamine moiety for the treatment of acute pancreatitis. Using the proposed dual-targeting ligand, an anti-inflammatory compound Rhein has been tailored to preferentially accumulate in the pancreas and lungs with rapid distribution kinetics, excellent tissue-penetrating properties and minimum toxicity. Accordingly, the drug–ligand conjugate remarkably downregulated the proinflammatory cytokines in the target organs thus effectively inhibiting local pancreatic and systemic inflammation in rats. The dual-specific targeting therapeutic strategy may help pave the way for targeted drug delivery to treat complicated inflammatory diseases.

Mo1355 Factors Affecting Cholecystectomy in Acute Gallstone Pancreatitis in a Nationwide Inpatient Sample

Background: Age Adjusted Charlson Comorbidity Index (AACCI) has been studied in the past to predict morbidity and mortality in various clinical conditions. At the same time there has been various markers and scores developed to predict morbidity and mortality in acute pancreatitis. Most of the tools used in acute pancreatitis, were unable to reach adequate sensitivity and specificity. However AACCI was never studied in the setting of acute pancreatitis. We hypothesized that AACCI which reflects the influence of burden of comorbid conditions, may predict outcomes in acute pancreatitis. We studied correlation between AACCI and length of hospital stay in individuals admitted with acute pancreatitis.Methods: We conducted retrospective observational study between January 1, 2009 and June 30, 2011 including all individuals admitted to our institutionwith acute pancreatitis.We collected demographic, laboratory, and radiological data. We used Length of Stay (LOS) as a measure of inpatient morbidity and extracted LOS days from medical records. We calculated AACCI based on comorbid conditions noted in electronic medical records. We divided study population into 3 groups based on AACCI score, Group A (scores 0 to 2), Group B (scores 3 to 5) and Group C (score 6 and above). We analyzed data using standard statistical methods and JMP11 software. Results: There were 209 individuals who met the inclusion criteria as per current definition of acute pancreatitis. Men and women were represented equally. There were 51% Hispanics and 49% non-Hispanics of which 80% were African Americans. There were no significant differences in LOS between women and men (10.25 vs. 10.42 days, p 0.91), between Hispanics and non-Hispanics (9.23 vs. 10.82, p 0.28). Also we did not notice any difference in length of stay based on etiology of acute pancreatitis. However we found significant increase in length of stay parallel to increase in AACCI (Table 1). (Group A 8.31, Group B 11.09 and Group C 15.44 days, p 0.002) Conclusion: Increase in Age Adjusted Charlson Comorbidity Index predicted prolonged Length of Stay, in patients hospitalized with acute pancreatitis. Our study is unique in studying relation between AACCI and LOS in acute pancreatitis especially in minority populations. Further studies are needed to relate AACCI with various local and systemic complications in acute pancreatitis, which may give single tool to predict outcomes without elaborative laboratory or radiological work up. Table 1

Mo1354 Age Adjusted Charlson Comorbidity Index: A Prognostic Tool to Measure Disease Burden: Can We Use It in Acute Pancreatitis? A Retrospective Observational Study in Minority Populations

Background: Age Adjusted Charlson Comorbidity Index (AACCI) has been studied in the past to predict morbidity and mortality in various clinical conditions. At the same time there has been various markers and scores developed to predict morbidity and mortality in acute pancreatitis. Most of the tools used in acute pancreatitis, were unable to reach adequate sensitivity and specificity. However AACCI was never studied in the setting of acute pancreatitis. We hypothesized that AACCI which reflects the influence of burden of comorbid conditions, may predict outcomes in acute pancreatitis. We studied correlation between AACCI and length of hospital stay in individuals admitted with acute pancreatitis.Methods: We conducted retrospective observational study between January 1, 2009 and June 30, 2011 including all individuals admitted to our institutionwith acute pancreatitis.We collected demographic, laboratory, and radiological data. We used Length of Stay (LOS) as a measure of inpatient morbidity and extracted LOS days from medical records. We calculated AACCI based on comorbid conditions noted in electronic medical records. We divided study population into 3 groups based on AACCI score, Group A (scores 0 to 2), Group B (scores 3 to 5) and Group C (score 6 and above). We analyzed data using standard statistical methods and JMP11 software. Results: There were 209 individuals who met the inclusion criteria as per current definition of acute pancreatitis. Men and women were represented equally. There were 51% Hispanics and 49% non-Hispanics of which 80% were African Americans. There were no significant differences in LOS between women and men (10.25 vs. 10.42 days, p 0.91), between Hispanics and non-Hispanics (9.23 vs. 10.82, p 0.28). Also we did not notice any difference in length of stay based on etiology of acute pancreatitis. However we found significant increase in length of stay parallel to increase in AACCI (Table 1). (Group A 8.31, Group B 11.09 and Group C 15.44 days, p 0.002) Conclusion: Increase in Age Adjusted Charlson Comorbidity Index predicted prolonged Length of Stay, in patients hospitalized with acute pancreatitis. Our study is unique in studying relation between AACCI and LOS in acute pancreatitis especially in minority populations. Further studies are needed to relate AACCI with various local and systemic complications in acute pancreatitis, which may give single tool to predict outcomes without elaborative laboratory or radiological work up. Table 1