Hypertriglyceridemia Acute Pancreatitis Research Articles

Predictive value of hyperglycemia on infection in critically ill patients with acute pancreatitis

To analyze the predictive value of hyperglycemia on the extrapancreatic infection (EPI) and infected pancreatic necrosis (IPN) of severe patients with acute pancreatitis (AP). We enrolled 234 patients with acute pancreatitis admitted to the intensive care unit (ICU) of the Second Affiliated Hospital of Nanchang University from July 2017 to July 2022 for a retrospective cohort study. We collected maximum blood glucose values three times after admission to the ICU within 120 h (Glu1: 0–24 h, Glu2: 24–48 h, Glu3: 48–120 h), the levels of leucocyte, blood urea nitrogen (BUN), C-reactive protein (CRP), procalcitonin (PCT), and albumin within 24 h after admission to the ICU, and the BISAP and SIRS scores of all patients within 24 h. EPI was taken as the primary outcome indicator and IPN as the secondary outcome indicator. The accuracy of blood glucose values in predicting acute pancreatitis infection was measured by the area under the curve (AUC). A total of 56 patients appeared EPI. Univariate analysis showed that Glu3 was associated with IPN in critically ill patients with AP. Multivariate logistic regression analysis showed that Glu2, Glu3, and SIRS > 48 h were associated with EPI in critically ill patients with AP. The AUCs of Glu2 and Glu3 to predict EPI were 0.805(95%CI: 0.717–0.892) and 0.782(95%CI: 0.685–0.878), respectively, and the cutoff values were 12.60 mmol/L and 14.75 mmol/L, respectively. The AUC of Glu2 combined with Glu3 to predict EPI was 0.812(0.725–0.899). The maximum blood glucose on Day2-5 after admission to the ICU can predict infection in critically ill patients with AP. There are differences in etiology while glucose predicting infection. Patients with hypertriglyceridemia AP need to intervene blood glucose levels more actively and earlier, and control it more strictly.

Dysregulated B7H4/JAK2/STAT3 Pathway Involves in Hypertriglyceridemia Acute Pancreatitis and Is Attenuated by Baicalin.

Patients with hypertriglyceridemia (HTG) are prone to develop more severe acute pancreatitis (AP). However, the specific molecular mechanism still has not been elaborated clearly, and effective drugs for treating HTG-AP are not yet readily available. Baicalin is an ingredient isolated from a natural product that with potential to attenuate inflammation and pain in AP. The aim of the present study was to explore the effect of baicalin on HTG-AP and the possible mechanism involved. A mouse model of HTG-AP was successfully established by administering Poloxamer 407 and L-arginine intraperitoneally. We analyzed pathological changes, and performed TUNEL staining, DHE staining, and western blot to detect apoptosis, inflammation, oxidative stress, and B7H4/JAK2/STAT3 signaling in the pancreas. Treatment with baicalin decreased serum triglyceride, cholesterol, lipase, amylase levels, and attenuated pancreatic edema. After intervention with baicalin, apoptosis and inflammation in HTG-AP mice were alleviated, as indicated by the decrease of Bax, cleaved-caspase-3, IL-6, TNF-α, and IL-1β. Baicalin also alleviated oxidative stress by decreasing NOX2, increasing SOD2 protein expression, and regulating Nrf2/Keap1 signaling in HTG-AP mice. Furthermore, baicalin decreased the upregulated B7H4/JAK2/STAT3 pathway in HTG-AP. In conclusion, our data suggested that baicalin could attenuate HTG-AP, possibly through regulating B7H4/JAK2/STAT3 signaling.

S106 Acute Pancreatitis from Hypertriglyceridemia Is More Severe and Associated with Longer Length of Stay

Introduction: Hypertriglyceridemia (HTG) is a relatively uncommon cause of Acute Pancreatitis (AP) representing <10% of cases. Studies comparing outcomes of HTG-AP with other causes of AP have yielded inconsistent results, likely due in part to non-standardized AP management, which lead to varied outcomes and prognosis in HTG-AP patients. This study aimed to investigate the clinical characteristics and outcomes of patients admitted with HTG-AP versus AP from other etiologies. Methods: This single-center study compared the clinical course and outcomes of AP patients from January 2015 to August 2020. All of the patients presenting with AP were diagnosed and managed according to a standardized protocol (Methodist Acute Pancreatitis Protocol) which is comprised of computer physician orders (e.g. fluid resuscitation, enteral feeding), physician and nursing education, and a patient navigator to optimize adherence to AP published guidelines (APPG). Measured outcomes included length of stay (LOS), in-patient mortality, 30-day readmission, and final pancreatitis severity characterized as mild, moderately severe, or severe as defined by the APPG. Fisher's exact test and Wilcoxon rank-sum (Mann-Whitney) tests were used for statistical analyses. Results: Data from 42 patients admitted with HTG-AP and 243 patients with non-HTG-AP were analyzed (Table 1). The mean age (SD) was 39.95 (± 10.95) years for the HTG-AP group and 50.55 (± 17.78) years for the non-HTG-AP group (P=0.0003). The mean LOS was 7.74 (± 11.54) days for the HTG-AP group and 4.20 (± 4.16) days for the non-HTG-AP group (P=0.0014). Also, 9.52% of the HTG-AP group and 2.88% of the non-HTG-AP group had severe pancreatitis. The odds of having moderately severe and severe pancreatitis were higher than mild AP in the HTG group compared to that in the non-HTG group. The difference in mortality between the HTG-AP group (0%) and non-HTG-AP group (1.65%) was not statistically significant (P=1.000). Thirty-day readmission rates were 7.14% for the HTG-AP group and 2.93% for the non-HTG-AP group (P=0.175). Conclusion: The HTG-AP group had a longer LOS and higher pancreatitis severity compared to the non-HTG-AP group, despite the fact that all patients were managed with a standardized early medical management protocol. These findings suggest a need to improve risk stratification based on AP etiology and identify opportunities to improve management of HTG-AP.Table 1.: Differences in demographics and outcomes between patients with hypertriglyceridemia acute pancreatitis and acute pancreatitis from other etiologies.

Digenic Inheritance and Gene-Environment Interaction in a Patient With Hypertriglyceridemia and Acute Pancreatitis.

The etiology of hypertriglyceridemia (HTG) and acute pancreatitis (AP) is complex. Herein, we dissected the underlying etiology in a patient with HTG and AP. The patient had a 20-year history of heavy alcohol consumption and an 8-year history of mild HTG. He was hospitalized for alcohol-triggered AP, with a plasma triglyceride (TG) level up to 21.4 mmol/L. A temporary rise in post-heparin LPL concentration (1.5–2.5 times of controls) was noted during the early days of AP whilst LPL activity was consistently low (50∼70% of controls). His TG level rapidly decreased to normal in response to treatment, and remained normal to borderline high during a ∼3-year follow-up period during which he had abstained completely from alcohol. Sequencing of the five primary HTG genes (i.e., LPL, APOC2, APOA5, GPIHBP1 and LMF1) identified two heterozygous variants. One was the common APOA5 c.553G > T (p.Gly185Cys) variant, which has been previously associated with altered TG levels as well as HTG-induced acute pancreatitis (HTG-AP). The other was a rare variant in the LPL gene, c.756T > G (p.Ile252Met), which was predicted to be likely pathogenic and found experimentally to cause a 40% loss of LPL activity without affecting either protein synthesis or secretion. We provide evidence that both a gene-gene interaction (between the common APOA5 variant and the rare LPL variant) and a gene-environment interaction (between alcohol and digenic inheritance) might have contributed to the development of mild HTG and alcohol-triggered AP in the patient, thereby improving our understanding of the complex etiology of HTG and HTG-AP.

Clinical characteristics of acute pancreatitis in children: a single-center experience in Western China

BackgroundThe diagnosis of pediatric pancreatitis has been increasing over the last 20 years. We aimed to compare the clinical characteristics for pediatric acute pancreatitis (AP) with adult AP, and investigate the risk factor for acute recurrent pancreatitis (ARP) in children.MethodFrom June 2013 to June 2019, a total of 130 pediatric patients with AP at the inpatient database were enrolled. Univariate analysis and multivariate Cox regression analysis were performed to identify the risk factors for ARP in children.ResultMajor etiologic factors in 130 patients were biliary (31.5%), idiopathic (28.5%). The etiology of pancreatitis in children was markedly different from that in adults (p < 0.001). Compared with the adult patients, the pediatric patients had significantly lower severity (p = 0.018) and occurrence rate of pancreatic necrosis (p = 0.041), SIRS (p = 0.021), acute peripancreatic fluid collection (p = 0.014). Univariate and Multivariate Cox regression analysis showed that female (p = 0.020; OR 3.821; 95% CI 1.231–11.861), hypertriglyceridemia (p = 0.045; OR 3.111; 95% CI 1.024–9.447), pancreatic necrosis (p = 0.023; OR 5.768; 95% CI 1.278–26.034) were the independent risk factors of ARP. Hypertriglyceridemia AP had the highest risk of recurrence compared to other etiology (p = 0.035).ConclusionBiliary and idiopathic disease were the major etiologies of AP in children. Children have simpler conditions than adults. Female, hypertriglyceridemia, and pancreatic necrosis were associated with the onset of ARP.

Evolocumab in treatment of acute pancreatitis induced by hypertriglyceridemia

Acute pancreatitis (AP) is a common emergency resulting from inflammation of the pancreas. The mechanism involves premature activation of enzyme precursors in the acinar cells triggering a self-digestive inflammatory cascade. Hypertriglyceridemia is the most common etiology of pancreatitis after gall stones and alcohol. It usually follows a sudden surge such as diabetic ketoacidosis on top of hereditary hyperlipidemia. In the present case report; we describe a patient with type-I diabetes mellitus who had developed recurrent attacks of hypertriglyceridemia AP (HTG-AP) despite Fenfibrate-therapy and report on our experience with Evolocumab in his treatment and prophylaxis. &#x0D; Keywords: diabetes mellitus, hypertriglyceridemia, pancreatitis, prophylaxis, treatment.

Significantly different clinical features between hypertriglyceridemia and biliary acute pancreatitis: a retrospective study of 730 patients from a tertiary center

BackgroundUnlike western world, gallstones and hypertriglyceridemia (HTG) are among the first two etiologies of acute pancreatitis (AP) in China. But yet, detailed differences in clinical features and outcomes between hypertriglyceridemia and biliary acute pancreatitis have not been well described.MethodsThis retrospective study enrolled 730 acute pancreatitis patients from July 1, 2013 to October 1, 2016 in Jinling Hospital. The causes of the study patients were defined according to specific diagnostic criteria. The clinical features and outcomes of patients with hypertriglyceridemia acute pancreatitis (HTG-AP) and biliary acute pancreatitis (BAP) were compared in terms of general information, disease severity, laboratory data, system complications, local complications, and clinical outcome.ResultsIn the enrolled 730 AP patients, 305 (41.8%) were HTG-AP, and 425 (58.2%) were BAP. Compared to BAP, the HTG-AP patients were found to be younger, with higher body mass Index (BMI), and much higher proportion of diabetes, fatty liver and high fat diet. Besides that, HTG-AP patients had significantly higher C-reactive protein (CRP) (p<0.01) and creatinine (p = 0.031), together with more acute respiratory distress syndrome (ARDS) (p = 0.039), acute kidney injury (AKI) (p<0.001), deep venous thrombosis (p = 0.008) and multiple organ dysfunction syndrome (MODS) (p = 0.032) in systematic complications. As for local complications, HTG-AP patients had significantly less infected pancreatitis necrosis (p = 0.005). However, there was no difference in mortality, hospital duration and costs between the groups.ConclusionHTG-AP patients were younger, more male, having high fat diet and with higher BMI compared to BAP patients. The prevalence of AKI/ARDS/DVT/MODS in HTG-AP patients was higher than BAP patients, while BAP patients had a greater possibility in development of infected pancreatitis necrosis (IPN). According to the multivariate analysis, only the complication of AKI was independently related with the etiology of HTG, however, BMI contributes to AKI, ARDS and DVT.

A Rare Case of Acute Pancreatitis Due to Very Severe Hypertriglyceridemia (>10 000 mg/dL) Successfully Resolved With Insulin Therapy Alone: A Case Report and Literature Review.

A 48-year-old male presented to the psychiatric emergency room for dysmorphic mood. He was admitted to medical service for the management of hyponatremia, which was discovered in his initial laboratory workup. After the first day of admission, he developed abdominal pain and fever, and subsequent laboratory work revealed a triglyceride level of 10 612 mg/dL (reference range = 0-194 mg/dL). Computed tomography scan of the abdomen and pelvis revealed a hypodense lesion in the pancreas surrounded by a moderate amount of peripancreatic fluid suggestive of hemorrhagic pancreatitis. Based on the laboratory findings and imaging, we diagnosed acute pancreatitis (AP) secondary to hypertriglyceridemia. The patient was initiated on intravenous fluids and insulin to help decrease the triglyceride level with the plan to initiate apheresis. However, the patient improved on insulin therapy alone, which negated the need for apheresis, and the patient was discharged with fenofibrate with no further complications. While elevated triglycerides are a well-known cause of AP, we sought to assess various treatment options in management, especially considering a severely elevated triglyceride level of >10 000 mg/dL. Along with supportive care in AP, there are additional options in hypertriglyceridemia AP, including heparin, insulin, apheresis, antioxidants, and fibrates. Currently, there are no clear guidelines favoring one therapeutic option over the other.