Hyperglycemia During Acute Pancreatitis and Progression to Early-Onset Diabetes After Recovery: Preliminary Findings From the Diabetes Related to Acute Pancreatitis and Its Mechanisms (DREAM) Study.

Long-Term Prognosis of Acute Pancreatitis in Japan

High risk of complications and mortality in cirrhotic patients with acute pancreatitis

32-Year-Old-Woman With Abdominal Pain

Surgical Management of Acute Pancreatitis

Pre-Existing Pancreatitis and Elevated Risks of COVID-19 Severity and Mortality

Acute pancreatitis (AP) is increasingly recognized as a major cause of diabetes, however, the frequency and risk factors associated with new-onset diabetes are not well established. We aimed to assess the frequency and risk factors associated with new-onset diabetes, the time of diabetes occurrence, and the difference between early and late-onset diabetes following an AP episode. This prospective study included adult patients with AP admitted to a tertiary referral center, followed-up for one year to assess the occurrence of postpancreatitis diabetes. Diabetes was defined in accordance with World Health Organization criteria and the severity of AP was assessed based on the 2012 revised Atlanta classification. Of 329 patients with AP, 29 (8.8%) were diagnosed with diabetes secondary to AP. Of these, 21 (6.37%) had early-onset diabetes (within one month after the acute episode) whereas 8 (2.42%) had late-onset diabetes (more than one month after the AP episode). Obesity and acute necrosis were more frequent in patients with new-onset diabetes compared to those without (55.2% vs. 33.4%, p=0.040 and 31% vs. 7.7%, p<0.01), and remained statistically significant in multivariate analysis. No statistically significant differences were found between these groups regarding sex, age, etiology and severity of AP. The patients with early-onset diabetes were older than those with late-onset (61 vs. 45 years old), in univariate and multivariate analysis (p=0.018 and p=0.038, OR=0.87). Less than 10% of patients with AP developed diabetes within 1 year, particularly obese patients and those with acute pancreatic necrosis of more than 50%. Patients aged over 61 years old developed diabetes in the first month after the acute episode of AP.

Can Too Much Acid Sour Your Pancreas?

Recent Developments in Acute Pancreatitis

Background: Acute pancreatitis is a relatively common disease with variable prevalence in different countries. Different modalities are available for predicting aetiology, severity and outcome of acute pancreatitis with different sensitivity and specificity. Moreover, some are not widely available, some are very expensive. A single, cheap, widely available marker with high sensitivity and specificity is yet to be identified. The present study intends to find out the utility of serum lipase amylase ratio in predicting the aetiology, severity and outcome of acute pancreatitis.Methods: This prospective, observational study was done at the Department of Gastrointestinal Hepatobiliary &amp; Pancreatic Disorders (GHPD), BIRDEM General Hospital, Dhaka, during the period of July 2014 to March 2016. A total of 71 patients with acute pancreatitis were included. Complete blood count, serum amylase, serum lipase, serum calcium, liver function test, renal function test, fasting lipid profile, ultrasonography of whole abdomen, CT scan of upper abdomen and arterial blood gas (ABG) were done in all patients. Statistical analysis was done with SPSS version 16.Results: Among 71 patients, 23(32.4%) were due to biliary cause, 15(21.1%) were due to hypertriglyceridaemia, 4(5.6%) were due to alcohol and 22(31%) were due to unknown causes. 45 (63.4%) patients had mild attack, 10(14.1%) patients had moderate attack and 16(22.5%) patients had severe attack of acute pancreatitis. Out of 71 patients, 17(23.9%) developed complication whereas 54(76.1%) developed no complication. Serum lipase amylase ratio in patients with biliary pancreatitis was 1.40±0.39 and in patients with non-biliary pancreatitis was 2.39±0.84(p &lt;0.001). Again, serum lipase amylase ratio in patients with acute alcoholic pancreatitis was 2.89±0.79 and in patients with non-alcoholic acute pancreatitis was 1.95±0.81 (p=0.002). Serum lipase amylase ratio in patients with acute pancreatitis due to hypertriglyceridaemia was 2.75±0.68 and in patients with acute pancreatitis due to other than hypertriglyceridaemia was 1.62±.65(p&lt; 0.001). This study showed that serum lipase amylase ratio was &lt;2.0 in acute biliary pancreatitis and this ratio was &gt;2.5 in acute alcoholic pancreatitis and in acute pancreatitis due to hypertriglyceridaemia. Serum lipase amylase ratio in patients with mild acute pancreatitis was 1.95±0.89; in patients with moderately severe acute pancreatitis the ratio was 2.37±0.92 and in patients with severe acute pancreatitis, the ratio was 2.22±0.70. The difference of lipase amylase ratio among these groups of patients was not statistically significant (p=0.273). Mean lipase amylase ratio among the patients without complication of acute pancreatitis was 2.03±0.92 whereas this ratio among the patients with complication was 2.17±0.68. This difference of lipase amylase ratio was not statistically significant (p=0.557).Conclusion: Role of serum lipase amylase ratio in predicting the aetiology and severity of acute pancreatitis has been addressed in several recent studies. This study was another attempt to achieve this goal. Predicting the aetiology of acute pancreatitis by such a cheap tool will guide further diagnostic work up and management strategy will avoid unnecessary investigations.Bangladesh Crit Care J September 2017; 5(2): 88-92

The hunt for microlithiasis in idiopathic acute recurrent pancreatitis: Should we abandon the search or intensify our efforts?

Background and Aims: Patients who have an episode of acute pancreatitis (AP) frequently develop diabetes mellitus (DM) over time. The reported incidence of DM after AP varies depending on the severity, etiology and the extent of pancreatic necrosis during AP. We performed a systematic review to determine the incidence of new-onset DM after AP episode (s), and compared the rate of DM in AP patients based upon different disease characteristics.Methods: A total of 31 relevant studies with 13894 subjects were collected from Medline, Embase, and Web of Science. Stata 15 software was used for data analyses in the meta-analysis.Results: The random-effects pooled incidence was 23.0% for DM (95% CI 16.0–31.0%) and 15.0% (95% CI 9.0–23.0%) for DM treated with insulin. We noted substantial heterogeneity in incidence estimates for DM and DM treated with insulin (I2 = 95.61 and 71.78%; both p < 0·001). The DM incidence was higher in the populations that had a severe AP (SAP) episode than in those with mild acute pancreatitis (MAP) (39 vs. 14%). Patients that displayed pancreatic necrosis during the AP attack(s) had a higher frequency of DM than those without necrosis (37 vs. 11%). In addition, the pooled incidence of DM was higher after alcoholic compared to biliary AP (28 vs. 12%). The incidence of insulin use after SAP and alcoholic AP was 21 and 18%, respectively, with very low heterogeneities. According to duration of follow-up, the pooled rate of DM and insulin use within 5 years after AP was 20 and 14%, while the rate associated with follow-up duration of more than 5 years was elevated to 37 and 25%, respectively. On meta-regression, year of publication, male proportion, age at DM test, and duration of follow-up were neither positively nor negatively associated with the incidence of DM and DM treated with insulin in patients who had a prior AP attack.Conclusion: Patients with AP developed DM after discharge from hospital with a frequency of about 23%. SAP, alcoholic AP and acute necrotizing pancreatitis (ANP) were associated with increased incidence of DM. Assessments of severity, etiology, and pancreatic necrosis are critical for predicting DM development after AP.

Alcoholic pancreatitis: is it a priori chronic disease?

Introduction: Pancreatitis is closely associated with an intense inflammatory response. Monocyte chemotactic protein-1 (MCP-1) is a chemokine that plays a central role establishing and maintaining the inflammatory process. Polymorphism -2518 G of the regulatory region of monocyte MCP1 affects the level of expression of this chemokine increasing the inflammatory response. Aims: To determine whether: MCP1 2518 G allele is associated with the severity of acute pancreatitis (AP). MCP1 2518 G polymorphism is associated to acute recurrent pancreatitis (ARP). Patients and Methods: Determination of MCP1 2518 G polymorphism was achieved by PCR/Restriction Fragment Length Polymorphism (RFLP) in 101 patients affected from a single episode of biliary AP (59.4% Male); 67 patients affected from non-biliary acute recurrent pancreatitis (61.2% Male) and 73 healthy normal controls of the same ethnical group (56.3% Male). The severity of pancreatitis (AP + ARP) was based upon the Atlanta criteria: 129 patients had mild pancreatitis (76.8%), 39 had severe pancreatitis (23.2%). Results: MCP1 2518 G polymorphism is associated with ARP (Fisher's exact test, p = 0.003, OR = 2.74, CI = [1.42-5.30]). The heterozygous polymorphism 2518 G of MCP1 was found in 35 ARP patients (52.2%); the homozygous polymorphism 2518 G of MCP1 was found in 6 ARP patients (9.0%) and 26 ARP patients did not present the G allele (38.8%). The heterozygous polymorphism 2518 G of MCP1 was found in 46 AP patients (45.5%); the homozygous polymorphism 2518 G of MCP1 was found in 2 AP patients (2%) and 53 AP patients did not present the G allele (52.5%). The heterozygous polymorphism 2518 G of MCP1 was found in 21 normal controls subjects (28.8%); the homozygous polymorphism 2518 G of MCP1 was found in 5 controls (6.8%) and 47 controls did not present the G allele (64.4%). No statistically significance association has been observed between MCP1 2518 G polymorphism and single episode biliary AP. No statistically significance relationship between MCP1 2518 G polymorphism and severity of acute pancreatitis was detected. Conclusions: MCP-1 polymorphism is associated with ARP. This polymorphism could increase the inflammatory response leading to a recurrence of the disease and possibly to chronic pancreatitis. In our series the MCP-1 2518 G allele is not associated with the severity of AP.TABLE 1: MCP genotype in Acute Pancreatitis (AP) and Acute Recurrent Pancreatitis (ARP)TABLE 2: MCP Genotype in Mild Acute Pancreatitis (AP) and Severe Acute Pancreatitis (ARP)

Background Assessment of the biliary origin of acute pancreatitis (AP) is crucial because it affects patient treatment to avoid recurrence. Although CT is systematically performed to determine severity in AP, its usefulness in assessing AP biliary origin has not been evaluated. Purpose To assess abdominal CT features associated with acute biliary pancreatitis (ABP) and to evaluate the predictive value of a combination of CT and clinical data for determining a biliary origin in a first episode of AP. Materials and Methods From December 2014 to May 2019, all consecutive patients who presented with a first episode of AP and with at least 6 months of follow-up were retrospectively reviewed. Evidence of gallstones was mandatory for a clinical diagnosis of ABP. Abdominal CT images were reviewed by two abdominal radiologists. Univariable and multivariable statistical analyses were performed, and a nomogram was constructed on the basis of the combination of clinical and CT features. This nomogram was validated in a further independent internal cohort of patients. Results A total of 271 patients (mean age ± standard deviation, 56 years ± 20; 160 men) were evaluated. Of these, 170 (63%) had ABP. At multivariable analysis, age (odds ratio [OR], 1.06; 95% CI: 1.03, 1.09; P < .001), alanine aminotransferase level (OR, 1.00; 95% CI: 1.00, 1.01; P = .009), gallbladder gallstone (OR, 15.59; 95% CI: 4.61, 68.62; P < .001), choledochal ring sign (OR, 5.73; 95% CI: 2.11, 17.05; P < .001), liver spontaneous attenuation (OR, 1.07; 95% CI: 1.04, 1.11; P < .001), and duodenal thickening (OR, 0.17; 95% CI: 0.03, 0.61; P = .01) were independently associated with ABP. The matching nomogram combining both clinical and CT features displayed an area under the curve of 0.94 (95% CI: 0.91, 0.97) in the study sample (n = 271) and 0.91 (95% CI: 0.84, 0.99) in the validation cohort (n = 51). Conclusion Abdominal CT provided useful features for diagnosis of acute biliary pancreatitis (ABP). Combining CT and clinical features in a nomogram showed good diagnostic performance for early diagnosis of ABP. © RSNA, 2021 Online supplemental material is available for this article. See also the editorial by Chang in this issue.

Does Incompetence of the Sphincter of Oddi Exist? Can It Account for Certain Cases of Acute Pancreatitis?.- Pancreatic Duct Reflux and Acute Pancreatitis.- Can Pancreaticoduodenal Reflux Explain Acute Pancreatitis? Yes, in Some Cases.- The Role of Biliary Millilithiasis in the Pathogenesis of Acute Pancreatitis.- Hemodynamic and Metabolic Impairment in Acute Pancreatitis.- Acute Pancreatitis Following Transduodenal Sphincterotomy.- Discussion.- Controversies in the Biological Diagnosis of Acute Pancreatitis.- The Cause of Hypophosphatemia in Acute Pancreatitis.- Fibronectin as a Prognostic Parameter in Patients Suffering from Pancreatogenic Shock.- The P3 Index in Acute Pancreatitis.- The Amylase to Creatinine Clearance Ratio.- Interest of Measuring Plasmatic and Urinary Lipase Activity in Pancreatic Disorders.- Ultrasonic Diagnosis of Acute Pancreatitis.- Contribution of Computed Tomography in the Diagnosis of Severe Acute Pancreatitis.- Possibilities and Limits of Sonography in Acute Pancreatitis.- Computed Tomography and Clinical Severity of Acute Pancreatitis.- Computed Tomography and Acute Pancreatitis.- Computer Tomography and Prognostics of Acute Pancreatitis.- Retrospective Value of Diagnostic Procedures in Acute Pancreatitis.- Computed Tomography and Anatomical Comparisons in Acute Pancreatitis.- Possibilities and Limits of Computed Tomography.- Contribution of Computed Tomography in the Management of Acute Necrotizing Pancreatitis.- Peritoneal Lavage for the Diagnosis and Prognosis of Acute Pancreatitis.- What can be Expected of Laparoscopy in the Diagnosis of Acute Pancreatitis?.- Objective Prognostic Evaluation of Patients with Acute Pancreatitis.- Prognostic Signs in Acute Pancreatitis.- Prognostic Value of Nystagmus in the Evolution of Acute Pancreatitis.- Pancreatic Necrosis and Acute Pancreatitis.- Functional Cardiorespiratory Patterns in Acute Pancreatitis.- Histopathology of Experimental Pancreatitis of Ductal Origin.- Current Status of Diagnosis and Conservative Treatment of Acute Pancreatitis.- Anatomopathological Findings in Acute Pancreatitis.- Acute Necrotic Pancreatitis: Anatomosurgical Correlations and Therapeutic Deductions.- Proteinase Inhibitors of Microbial Origin in the Treatment of Experimental Acute Haemorrhagic Pancreatitis.- Relationship of Glucagon to Exocrine Pancreatic Secretion and Its Use in Acute Pancreatitis.- Treatment of Acute Pancreatitis with Somatostatin. A Randomized Study.- Trypsinogen and Trypsin in Acute Pancreatitis. Physiopathology.- A Prospective Study to Determine the Efficacy of Dextran 40 in Acute Pancreatitis.- Our Experience in the Treatment of Acute Necrotizing Hemorrhagic Pancreatitis.- Acute Pancreatitis: Results of 42 Observations.- Acute Pancreatitis. Retrospective Study of 225 Cases.- Points of View on Necrosis in Acute Pancreatitis.- Peritoneal Lavage in Acute Pancreatitis.- Our Experience with Drainage-Lavage of the Peritoneal Cavity.- A Controlled Randomized Study on the Value of Peritoneal Lavage in Acute Pancreatitis (an Interim Report).- Therapeutic Peritoneal Lavage.- Peritoneal Dialysis in Acute Necrotic-Hemorrhagic Pancreatitis.- Acute Hemorrhagic-Necrotic Pancreatitis: Laparotomy or Peritoneal Lavage? Results of a Randomized Controlled Clinical Study.- Controversies in Acute Pancreatitis.- Endoscopic Papillotomy as a Therapeutic Alternative in Acute Biliary Pancreatitis.- Endoscopic Sphincterotomy in Acute Biliary Pancreatitis.- Endoscopic Sphincterotomy in Acute Pancreatitis.- Possibilities and Limits of Intensive Care in Acute Necrotic Pancreatitis.- Controversies in Possibilities and Limits of Intensive Care. Conclusions.- Acute Pancreatitis: Controversial Operative Indications.- Our Criteria for Surgical Intervention in Acute Necrotizing Pancreatitis.- Controversies in Surgical Indications.- Results of Exeresis in Acute Necrotico-hemorrhagic Pancreatitis.- Choice of Treatment in Acute Pancreatitis.- Surgical Treatment of Acute Necrotizing Pancreatitis: A Series of 30 Cases.- Surgical Treatment of Acute Necrotizing Hemorrhagic Pancreatitis: A Series of 46 Cases.- Acute Pancreatitis: Conservative Attitude, Expectant Vigilance.- Acute Pancreatitis: Results and Strategy of Operative Treatment.- Role of Total Pancreatectomy in the Treatment of Acute Necrotizing Pancreatitis. Indications and Results of 22 Cases.- Early and Iterative Interventions in Cases of Acute Necrotizing Pancreatitis: An Answer to the Absence of Correlation Between Their Anatomical and Clinical Expressions.- Enteral Nutrition by Alimentation Jejunostomy in 11 Cases of Severe Acute Pancreatitis.- The Role of Artificial Nutrition in the Treatment of Acute Pancreatitis.- Role of Complete Parenteral Treatment Nutrition in Acute Pancreatitis.- Amino Acid Metabolism in Acute Necrotizing Pancreatitis. Aspects of Parenteral Nutrition.- Secondary Colonic Lesions in Acute Pancreatitis.- Necrotizing Colitis and Acute Necrotizing Pancreatitis. Report of Eight Cases. Role of Shock.- Problems in the Management of Pancreatic Abscesses.- Treatment of Pancreatic Abscess.- Treatment of Fistulas Following Laparotomy for Acute Pancreatitis.- General Conclusions and Adoption of a Diagnostic and Therapeutic Programme for the Future.