Lipid apheresis in the management of severe hypertriglyceridaemia in an adolescent girl with global developmental delay.

Hypertriglyceridaemia-induced acute pancreatitis (HTG-AP) remains one of the common metabolic causes of acute pancreatitis in the paediatric population and the third most common cause after alcohol and gallstones in the adult population. We report a case of an early adolescent girl with global developmental delay and moderate cognitive impairment of unknown aetiology who presented with recurrent acute pancreatitis and uncompensated hypovolaemic shock. She was found to have serum triglyceride level of 7877 mg/dL (reference range<150 mg/dL) and hyperglycaemia with ketosis (no prior history of diabetes mellitus) that was successfully treated with lipid apheresis. This sometimes is an early modality for treatment in adults; however, it remains a last resort in children, used only for severe cases. A brief literature review on severe HTG-AP and its management is also provided.

Primary Sjogren's syndrome presenting as hypokalaemic periodic paralysis and acute pancreatitis.

Renal tubular acidosis is a well-known consequence of primary Sjogren's syndrome (pSS), but a rare manifestation similar to acute pancreatitis in pSS. Here, we discuss the case of a woman in her 50s, who presented to a tertiary care hospital with recurrent episodes of sudden-onset weakness in all four limbs, recurrent vomiting and epigastric pain. She had non-anion gap metabolic acidosis with hypokalaemia and was diagnosed with pSS with hypokalaemic periodic paralysis. She was also diagnosed with acute pancreatitis based on elevated amylase and lipase levels and CT findings. The article highlights the diverse spectrum of clinical manifestations of pSS, including renal and pancreatic involvements, which can be rare consequences of the disease.

Less Aggressive Hydration May Be More in Acute Pancreatitis?

Consider a more conservative approach to fluid resuscitation in mild acute pancreatitis to avoid fluid overload without sacrificing patient-oriented clinical outcomes.

Association Between Hemoglobin-to-Red Blood Cell Distribution Width Ratio and 30-Day Mortality in Patients with Acute Pancreatitis: Data from MIMIC-III and MIMIC-IV.

To investigate the relationship between hemoglobin-to-red blood cell distribution width (RDW) ratio (HRR) and the 30-day mortality risk in acute pancreatitis (AP), and assess the predictive ability of HRR. Data from 2001 to 2019 in the Medical Information Mart for Intensive Care-III/IV (MIMIC-III/IV) were analyzed. The outcome of this retrospective cohort study was 30-day mortality. Hemoglobin-to-RDW ratio (0-24 hours) and HRR (24-48 hours) were divided into 4 groups based on quartiles (Q1, Q2, Q3, and Q4). The predictive effect was evaluated by the C-index. A total of 1736 patients were included, and 30-day mortality occurred in 204 (11.75%) patients. Compared with Q1 of HRR (0-24 hours), Q2 (HR = 0.60, 95% CI : 0.42-0.86), Q3 (HR =0.47, 95% CI : 0.31-0.71), and Q4 (HR = 0.45, 95% CI : 0.29-0.68) of HRR levels reduced the 30-day mortality risk. Hemoglobin-to-RDW ratio (24-48 hours) was consistent with the results of HRR (0-24 hours). For changes in HRR, Q4 for changes in HRR levels (HR = 1.64, 95% CI : 1.09-2.45) increased the 30-day mortality risk. Hemoglobin-toRDW ratio significantly improved the predictive effect of Sequential Organ Failure Assessment (C-index = 0.736) and Bedside Index of Severity in Acute Pancreatitis (C-index = 0.704) on 30-day mortality. Higher HRR levels reduced the 30-day mortality risk in AP and may improve the prediction of other tools.

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This study presents a multi-center clinical data management platform that facilitates unified and structured management of real-world data and serves as an ideal tool to enhance the quality and progress of clinical research related to severe acute pancreatitis (SAP). The use of the platform enables clinical teams to obtain safe, accurate, structurally unified, traceable, scene-clear, and fully functional real-world medical data in the diagnosis, treatment, and research of acute pancreatitis (AP).

Serum uric acid concentration in acute pancreatitis is significantly higher than healthy population.

Acute pancreatitis (AP) is a common disease caused by a variety of causes. Is uric acid associated with the onset of AP? The objective of this study was to assess whether uric acid concentration in AP patients was higher than that in healthy population, and whether there were associations between uric acid concentration and serological indicators related to AP. A total of 205 AP patients were included in this study. Two hundred and five people who underwent physical examination in our hospital were randomly selected as controls. We analyzed whether there was difference in uric acid concentrations between the two groups. If the difference was statistically significant, the correlations between uric acid concentration and serological indicators in AP patients was further analyzed. There was significant difference in uric acid concentration (P < 0.001) between AP patients and healthy population. Serum uric acid concentration in AP group was significantly higher than that in control group. Two hundred and five AP patients were divided into mild AP group and non-mild AP group. There was no statistically significant difference in uric acid concentration between the two groups (P = 0.176). There was a low linear correlation between serum uric acid concentration and triglyceride level (r = 0.316, P < 0.001). But there was no linear correlation between serum uric acid concentration and hypersensitive C-reactive protein (r = 0.126, P = 0.072), white blood cell (r = 0.192, P = 0.006), albumin (r = 0.183, P = 0.009), total cholesterol concentration (r = 0.133, P = 0.058), fasting blood-glucose (r = 0.133, P = 0.058) and blood calcium (r = 0.155, P = 0.026). Uric acid concentration in patients with AP was significantly higher than healthy population. There was correlation between uric acid concentration and triglyceride in AP patients.

Early Endoscopic Retrograde Cholangiopancreatography in Gallstone Pancreatitis Is Safe: Results From a Large Single-Center Retrospective Study.

OBJECTIVES: There is concern that performing early endoscopic retrograde cholangiopancreatography (ERCP) in the setting of gallstone pancreatitis (GSP) with choledocholithiasis can worsen underlying pancreatitis. This study was designed to assess outcomes of early versus delayed ERCP in patients with GSP with choledocholithiasis in the absence of cholangitis. MATERIALS AND METHODS: In this single-center retrospective study, we identified 124 patients who underwent ERCP for choledocholithiasis in the setting of GSP without cholangitis between 2012 and 2022. Timing of ERCP was categorized as early (<48 hours after time of diagnosis) versus delayed (>48 hours). Data on patient demographics, complications, length of stay (LOS), and mortality were collected. RESULTS: Cannulation success rates were similar for early and delayed ERCP (97% vs 100%). The adverse event rate for early ERCP was 15% compared to 29% for delayed ERCP. LOS for patients with predicted mild pancreatitis was shorter for early versus delayed ERCP (4.2 vs 7.1 days, P = 0.007). There were no deaths in either group. CONCLUSIONS: There was a trend toward fewer adverse events and there was a shorter LOS among patients with GSP with choledocholithiasis undergoing early versus delayed ERCP. Early ERCP should be considered, particularly in patients with predicted mild pancreatitis.

Pancreas and pancreatitis: Exocrine pancreatic insufficiency.

Exocrine pancreatic insufficiency (EPI) is highly prevalent among individuals with cystic fibrosis (CF). Individuals diagnosed with EPI are often labeled as having "pancreas insufficient cystic fibrosis (PI-CF)" while those with normal exocrine function are labeled as "pancreas sufficient CF (PS-CF)." This diagnosis of EPI relies on clinical and laboratory features and management involves consumption of pancreas enzyme replacement therapy. In this review, we discuss the nuances of diagnosis and management of EPI in CF. We also present emerging evidence on the effects of CFTR modulating agents on the management of EPI, and speculate that these medications may lead to greater heterogeneity in management of EPI in CF moving forward.

Retinal microvascular changes in patients with pancreatitis and their clinical significance.

Acute pancreatitis, a common exocrine inflammatory disease affecting the pancreas, is characterized by intense abdominal pain and multiple organ dysfunction. However, the alterations in retinal blood vessels among individuals with acute pancreatitis remain poorly understood. This study employed optical coherence tomography angiography (OCTA) to examine the superficial and deep retinal blood vessels in patients with pancreatitis. Sixteen patients diagnosed with pancreatitis (32 eyes) and 16 healthy controls (32 eyes) were recruited from the First Affiliated Hospital of Nanchang University for participation in the study. Various ophthalmic parameters, such as visual acuity, intraocular pressure, and OCTA image for retina consisting of the superficial retinal layer (SRL) and the deep retinal layer (DRL), were recorded for each eye. The study observed the superficial and deep retinal microvascular ring (MIR), macrovascular ring (MAR), and total microvessels (TMI) were observed. Changes in retinal vascular density in the macula through annular partitioning (C1-C6), hemispheric quadrant partitioning (SR, SL, IL, and IR), and early diabetic retinopathy treatment studies (ETDRS) partitioning methods (R, S, L, and I). Correlation analysis was employed to investigate the relationship between retinal capillary density and clinical indicators. Our study revealed that in the superficial retinal layer, the vascular density of TMI, MIR, MAR, SR, IR, S, C2, C3 regions were significantly decreased in patients group compared with the normal group. For the deep retinal layer, the vascular density of MIR, SR, S, C1, C2 regions also reduced in patient group. The ROC analysis demonstrated that OCTA possesses significant diagnostic performance for pancreatitis. In conclusion, patients with pancreatitis may have retinal microvascular dysfunction, and OCTA can be a valuable tool for detecting alterations in ocular microcirculation in pancreatitis patients in clinical practice.

Regulatory axis of circular RNA DTNB, microRNA-485-5p, and myeloid cell leukemia 1 attenuates inflammation and apoptosis in caerulein-treated AR42J cells.

Acute pancreatitis (AP) is an inflammatory disease of the pancreas and the main cause of hospital admissions for gastrointestinal diseases. Here, the work studied the circular RNA DTNB/microRNA-485-5p/MCL1 axis in AP and hoped to unravel the related mechanism. Caerulein exposure replicated an AP model in AR42J cells, and caerulein-mediated expression of circDTNB, miR-485-5p, and MCL1 was recorded. After exposure, cells were intervened with transfection plasmids and tested for LDH release, apoptosis, and inflammation. To determine the interwork of circDTNB, miR-485-5p, and MCL1, prediction results and verification experiments were conducted. Caerulein exposure reduced circDTNB and MCL1, while elevated miR-485-5p levels in AR42J cells. Upregulating circDTNB protected AR42J cells from caerulein-induced LDH cytotoxicity, apoptosis, and inflammation, but circDTNB upregulation-induced protections could be muffled by inhibiting MCL1. On the contrary, downregulating circDTNB further damaged AR42J cells under caerulein exposure, however, this phenomenon could be partially rescued after silencing miR-485-5p. miR-485-5p was mechanistically verified to be a target of circDTNB to mediate MCL1. Overall, the circDTNB/miR-485-5p/MCL1 axis protects inflammatory response and apoptosis in caerulein-exposed AR42J cells, promisingly identifying circDTNB as a novel molecule for AP treatment.

mTORC2 knockdown mediates lipid metabolism to alleviate hyperlipidemic pancreatitis through PPARα.

Hyperlipidemic pancreatitis (HP) is an inflammatory injury of the pancreas triggered by elevated serum triglyceride (TG) levels. The mechanistic target of rapamycin (mTOR) signaling pathway plays a crucial role in regulating lipid homeostasis and inflammation. This study aimed to investigate whether the activity of mTOR complex 2 (mTORC2) affects the progression of HP and its underlying mechanisms. In vivo, a high-fat diet and retrograde administration of sodium taurocholate were employed to establish the HP models in rats, with pancreatic tissue pathology evaluated. The expression of Rictor and peroxisome proliferator-activator receptor (PPAR) was examined. The serum levels of TG, fatty acid metabolites, inflammatory and lipid metabolism-related factors were determined. In vitro, pancreatic acinar cells (PACs) were exposed to palmitic acid and cholecystokinin-8. PAC apoptosis, pyroptosis, and ferroptosis were assessed. In the HP models, rats and PACs exhibited upregulated Rictor and downregulated PPARα, and Rictor knockdown promoted PPARα expression. In vivo, Rictor knockdown decreased the serum levels of TG, α-amylase, total cholesterol, low-density lipoprotein cholesterol, lactate dehydrogenase, and inflammatory factors, while increasing high-density lipoprotein cholesterol levels. Rictor knockdown increased ACOX1 and CPT1α and decreased SREBP-1, CD36, SCD1, ACLY, and ACACA. Rictor knockdown reduced damage to pancreatic tissue structure. In vitro, Rictor knockdown inhibited PAC apoptosis, pyroptosis, and ferroptosis. Treatment with the PPARα antagonist GW6471 abolished the beneficial effects of Rictor knockdown. Rictor/mTORC2 deficiency reduces serum TG levels, maintains lipid homeostasis, and suppresses inflammation by inhibiting PPARα expression. Weakening mTORC2 activity holds promise as a novel therapeutic strategy for HP.

Accuracy of ChatGPT3.5 in answering clinical questions on guidelines for severe acute pancreatitis.

BACKGROUND: Guidelines must be interpreted comprehensively and correctly to standardize the clinical process. However, this process is challenging and requires interpreters to have a medical background and qualifications. In this study, the accuracy of ChatGPT3.5 in answering clinical questions related to the 2019 guidelines for severe acute pancreatitis was evaluated. METHODS AND RESULTS: An observational study was conducted using the 2019 guidelines for severe acute pancreatitis. The study compared the accuracy of ChatGPT3.5 in English versus Chinese and found that it was more accurate in English (71%) than in Chinese (59%) (P value: 0.203). Additionally, the study assessed the accuracy of ChatGPT3.5 in answering short-answer questions versus true/false questions and found that it was more accurate in answering short-answer questions (76%) than in answering true/false questions (60%) (P value: 0.405). CONCLUSIONS: For clinicians managing severe acute pancreatitis, ChatGPT3.5 may have potential value. However, it should not be relied upon excessively for clinical decision making.

Role of Interleukin 6 in Acute Pancreatitis: A Possible Marker for Disease Prognosis.

Acute pancreatitis (AP) is a significant cause of morbidity, even in children, and is frequently associated with systemic manifestations. There are many cytokines involved in the inflammatory response characteristic of this disease. Interleukin 6 (IL-6) is one of the most important cytokines involved in AP, beginning from cellular injury and continuing to the systemic inflammatory response and distant organ involvement. IL-6 is a multifunctional cytokine that regulates acute-phase response and inflammation. It is produced by various cells and exerts its biological role on many cells through its high-affinity complex receptor. IL-6 has been investigated as a predicting maker for severe forms of AP. Many studies have validated the use of IL-6 serum levels in the first 48 h as a reliable marker for severe evolution and multisystemic involvement. Still, it has not been used in daily practice until now. This review discusses the main binding mechanisms by which IL-6 triggers cellular response and the AP pathogenetic mechanisms in which IL-6 is involved. We then emphasize the promising role of IL-6 as a prognostic marker, which could be added as a routine marker at admission in children with AP.

Presentation of Acute Pancreatitis in Sickle Cell Disease Patients: A Single Hospital Experience.

INTRODUCTION: Sickle cell disease (SCD) is a haemoglobinopathy that leads to the formation of distorted sickle-shaped red blood cells that are prone to vaso-occlusion. This may lead to vaso-occlusive crises that may affect any organ. Acute pancreatitis (AP) in SCD patients may be mimicked by a vaso-occlusive crisis in the abdomen. The objective of this article is to analyse the clinical profiles of SCD patients with AP and understand the differences in the presentation of AP compared to an abdominal vaso-occlusive crisis and the difference between its presentation in SCD patients in comparison to other patients. MATERIALS AND METHODS: Twenty-eight SCD patients who were diagnosed with AP during their admission to the paediatric department at a tertiary hospital between January 2012 and December 2020 were retrospectively studied. Patients aged older than 14 years were excluded. The data collected concerned: demographics, the clinical course and the hospital course. The diagnosis and severity protocols followed the revised Atlanta Criteria. RESULTS: The patients were aged with a mean of 9.61 years. There were 15 males and 13 females. Demographics were not significantly correlated to complication rates (P > 0.05). The mean duration of hospitalisation was 6.43 days. The most common clinical presentations were abdominal pain, fever, then vomiting and nausea. Three patients experienced complications and they were all cases of cholangitis (10.71%). There were no cases of pseudocysts, acute necrotic collections, pancreatic or peripancreatic necrosis or walled-off necroses. All of the cases of AP in SCD children were mild according to the revised Atlanta classification. Leucocytosis was present in 29.29% of patients and 17.8% of patients had high C-reactive proteins (CRPs). There was no significant correlation between leucocyte counts, CRP levels, serum or urinary amylase levels and complications (P > 0.05). All patients had haemoglobin (Hb) levels above 7 g/dL. The levels of sickle Hb ranged from 40 to 70 g/dL and reticulocyte counts averaged at 3.57%. Haematologic parameters were not significantly correlated with complication rates (P > 0.05). There were no recurrences. CONCLUSION: AP in SCD patients presented with classic signs and symptoms. There were no associations between demographics and complications. The levels of leucocytes, CRP counts and serum and urinary amylase were not correlated with complications. The level of Hb and sickle cell Hb was not associated with complication rates. Reticulocytes were slightly elevated in SCD patients with AP. More studies are needed to demarcate factors distinguishing AP in SCD from abdominal vaso-occlusive crises.

Autophagy-mediated ferroptosis is involved in development of severe acute pancreatitis.

BACKGROUND: Ferroptosis is a newly recognized form of regulatory cell death characterized by severe lipid peroxidation triggered by iron overload and the production of reactive oxygen species (ROS). However, the role of ferroptosis in severe acute pancreatitis(SAP) has not been fully elucidated. METHODS: We established four severe acute pancreatitis models of rats including the sham control group, the SAP group, the Fer -1-treated SAP (SAP + Fer-1) group, the 3-MA-treated SAP (SAP + 3-MA) group. The SAP group was induced by retrograde injection of sodium taurocholate into the pancreatic duct. The other two groups were intraperitoneally injected with ferroptosis inhibitor (Fer-1) and autophagy inhibitor (3-MA), respectively. The model of severe acute pancreatitis with amylase crest-related inflammatory factors was successfully established. Then we detected ferroptosis (GPX4, SLC7A1 etc.) and autophagy-related factors (LC3II, p62 ect.) to further clarify the relationship between ferroptosis and autophagy. RESULTS: Our study found that ferroptosis occurs during the development of SAP, such as iron and lipid peroxidation in pancreatic tissues, decreased levels of reduced glutathione peroxidase 4 (GPX 4) and glutathione (GSH), and increased malondialdehyde(MDA) and significant mitochondrial damage. In addition, ferroptosis related proteins such as GPX4, solute carrier family 7 member 11(SLC7A11) and ferritin heavy chain 1(FTH1) were significantly decreased. Next, the pathogenesis of ferroptosis in SAP was studied. First, treatment with the ferroptosis inhibitor ferrostatin-1(Fer-1) significantly alleviated ferroptosis in SAP. Interestingly, autophagy occurs during the pathogenesis of SAP, and autophagy promotes the occurrence of ferroptosis in SAP. Moreover, 3-methyladenine (3-MA) inhibition of autophagy can significantly reduce iron overload and ferroptosis in SAP. CONCLUSIONS: Our results suggest that ferroptosis is a novel pathogenesis of SAP and is dependent on autophagy. This study provides a new theoretical basis for the study of SAP.