Complex interplay between hypertriglyceridemia and acute pancreatitis: a narrative review

Recent Developments in Acute Pancreatitis

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32-Year-Old-Woman With Abdominal Pain

Dear Editor, Acute pancreatitis induced by hypercalcemia due to primary hyperparathyroidism (PHPT) is a very rare condition, and its prevalence is estimated to be between 1.5% and 7%.1 Studies from India report an incidence between 6.8% and 12%.2 However, in patients with PHPT and resulting hypercalcemia, pancreatitis occurs 10 to 20 times more often than in the general population. Normally, hypocalcemia is expected during an attack of acute pancreatitis and hypercalcemia is a strong clue for suspecting PHPT. Hence, elevated serum calcium associated with pancreatitis should alert the physician to either hyperparathyroidism or malignancy.3 The metabolic causes of acute pancreatitis include diabetic ketoacidosis, hypertriglyceridemia, and hypercalcemia with or without hyperparathyroidism.4 Gallstones and alcoholism are the commonest etiological agents of pancreatitis in India. Serum calcium is not routinely measured in all patients diagnosed with the first attack of acute pancreatitis as it is not the common cause. Some patients suffer from 2 or more attacks of pancreatitis before the diagnosis of PHPT. We describe a 40-year-old female patient who presented to a gastroenterology unit with severe upper abdominal pain, vomiting, and fever of 3 days’ duration. She had a similar episode of symptoms 2 months previously, for which she was admitted to a civil hospital, where she was diagnosed as a case of acute pancreatitis and was managed conservatively and discharged after 7 days. No additional risk factors causing acute pancreatitis such as alcohol consumption, hyperlipidemia, and gallstones were present. She had a history of cholecystectomy 1.5 years earlier for stone. After proper evaluation, a diagnosis of post-cholecystectomy acute pancreatitis was made, and the patient was managed conservatively. Within the next 5 months, she was again admitted with dyspeptic symptoms and pain in the abdomen of 20 days’ duration. On examination, the abdomen was soft with diffuse tenderness, especially in the right hypochondrium. The clinical picture was suggestive of acute pancreatitis. Investigations revealed serum amylase of 1772 IU/L, serum lipase of 86 IU/L, serum alkaline phosphatase of 104 IU/L, serum albumin of 3.84 g/dL, and total serum cholesterol of 128 mg/dL. During the first 2 episodes of pancreatitis, serum calcium was not estimated; and during the third episode, serum calcium was 12.4 mg/dL and serum phosphorus was 2.3 mg/dL. Computed tomography (CT) scan of the abdomen was suggestive of acute edematous pancreatitis (figure 1). After the acute episode of pancreatitis subsided, serum biochemical parameters were repeated. Repeat serum calcium was 11.2 mg/dL (reference range=8.7-10.2), and serum phosphorus was 2.7 mg/dL. Repeated serum estimations confirmed persistent hypercalcemia. The initial suspicion of PHPT was confirmed when her intact parathyroid hormone (iPTH) level was found to be 486 pg/mL (reference range=15-68). Ultrasonography of the neck revealed a 3.4×1.2 cm, well-defined, low echogenic mass below the lower pole of the right lobe of the thyroid, which was later confirmed with a radionuclide parathyroid scan (technetium [99 mTc] sestamibi), showing a right inferior parathyroid adenoma (figure 1). PHPT was diagnosed after the third episode of hypercalcemia-induced pancreatitis. After conservative management, she was advised parathyroid surgery but she refused surgical intervention. Later on, she was again admitted with a fourth episode of recurrent pancreatitis and this time she underwent right inferior parathyroidectomy. The histopathological report confirmed the diagnosis, which was consistent with parathyroid adenoma. PTH postoperatively was within the normal range. The postoperative period was uneventful. She was doing very well at 3 months’ postoperative follow-up, with her pancreatitis resolved clinically and serum calcium returning to normal biochemically. Presently, the patient is asymptomatic, and there was no recurrence of pancreatitis at the latest follow-up. Figure 1 Technetium (99 mTc) sestamibi scan shows increased activity in the right inferior parathyroid, suggestive of adenoma, and the CT scan of the abdomen shows a diffusely enlarged pancreas with an irregular outline. Conflict of Interest: None declared.

Can Too Much Acid Sour Your Pancreas?

Past, Present, and Future of Endoscopic Retrograde Cholangiopancreatography: Perspectives on the National Institutes of Health Consensus Conference

Does bile of patients with acute gallstone pancreatitis cause pancreatic inflammatory lesions? A study of the pancreatic toxicity of choledochal secretions collected at ERCP

Hypertriglyceridemia (HTG) is the third most common cause of acute pancreatitis (AP) after gallstones and alcohol abuse. Early determination of the triglyceride (TG) level in patients with acute abdominal pain, particularly in cases of AP, is crucial, as an acute increase can be followed by a rapid decrease within 2days. HTG as a cause of acute abdominal pain and AP is often overlooked in clinical practice. In addition, manifest HTG is often underdiagnosed and inadequately treated. We investigated 1279 cases of acute abdominal pain, including 226 cases of AP, to assess the frequency and timing of TG level measurement. Additionally, we studied 237 patients with HTG levels above 500mg/dL to determine the frequency of HTG-related symptoms and the rate of initiation of adequate therapy, considering the specialty in which the elevated TG levels were identified. Triglycerides were determined in 22% of patients with acute abdominal pain and 55% with AP; fewer than 15% of all patients received a determination at the first contact with the physician. TG levels were measured at a median of 24h (1-54) in patients with acute abdominal pain and 48h (24-95) in those with AP after admission. Less than half of patients with HTG received TG-lowering therapy. Only 5 of 226 cases with AP was identified as HTG-induced, while 13.5% of all cases with HTG above 500mg/dL had a history of AP. Our findings support the assumption that HTG and its complications are often underestimated in clinical practice and require more attention. Furthermore, early initiation of appropriate therapy is crucial.

Acute biliary pancreatitis: when should the endoscopist intervene?

The most common causes of acute pancreatitis are microlithiasis and alcohol. In pediatrics, anomalies in pancreaticobiliary system should be considered as possible causes. Among many anomalies, pancreas divisum associated with anomalous pancreaticobiliary ductal union (APBDU) is very rare. APBDU is associated with acute pancreatitis, choledochal cyst, and gallbladder cancer. Pancreas divisum is also a well known cause of acute recurrent pancreatitis. In adult cases with such conditions, the role of endoscopic management including sphincterotomy or stenting through the Santorini duct is well documented. However, it is still controversial to perform endoscopic retrograde cholangiopancreatography in pediatrics. Herein, we experienced a case of 4 year 7 month old female patient suffered from recurrent attacks of acute pancreatitis, which were caused by APBDU and incomplete pancreas divisum. She was treated by endoscopic sphincterectomy of both openings to the Santorinis and Wirsungs ducts. Thus, we report this interesting case with literature review.

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.

Alcoholic pancreatitis: is it a priori chronic disease?

#1385190: Empagliflozin Induced Acute Pancreatitis

Although there are numerous causes of acute panc-reatitis, an etiology cannot always be found. Two potential etiologies, microlithiasis and sphincter of Oddi dysfunction, are discussed in this review. Gallbladder microlithiasis, missed on transcutaneous ultrasound, is reported as the cause of idiopathic acute pancreatitis in a wide frequency range of 6%-80%. The best diagnostic technique for gallbladder microlithiasis is endoscopic ultrasound although biliary crystal analysis and empiric cholecystectomy remain as reasonable options. In contrast, in patients who are post-cholecystectomy, bile duct microlithiasis does not appear to have a role in the pathogenesis of acute pancreatitis. Sphincter of Oddi dysfunction is present in 30%-65% of patients with idiopathic acute recurrent pancreatitis in whom other diagnoses have been excluded. It is unclear if this sphincter dysfunction was the original etiology of the first episode of pancreatitis although it appears to have a causative role in recurring episodes since sphincter ablation decreases the frequency of recurrent attacks. Unfortunately, this conclusion is primarily based on small retrospective case series; larger prospective studies of the outcome of pancreatic sphincterotomy for SOD-associated acute pancreatitis are sorely needed. Another problem with this diagnosis and its treatment is the concern over potential procedure related complications from endoscopic retrograde cholangiopancreatography (ERCP), manometry and pancreatic sphincterotomy. For these reasons, patients should have recurrent acute pancreatitis, not a single episode, and have a careful informed consent before assessment of the sphincter of Oddi is undertaken.

Objective To explore the causes and clinical features change of acute pancreatitis,to get early diagnosis of severe acute pancreatitis.Methods The clinical data of 1195 cases of patients with acute pancreatitis were retrospectively analyzed.Results Main causes of acute pancreatitis were still biliary disease 31.72％ (379/1195),engorgement 25.44％ (304/1195) and hyperlipidemia 16.82％ (201/1195).But the causes of severe acute pancreatitis had changed.Hyperlipidemia was 44.59％ (140/314),biliary disease accounted for 28.34％ (89/314),engorgement accounted for 17.52％ (55/314).The incidence of hyperlipidemia severe acute pancreatitis was 69.65％ (140/201),the incidence of biliary severe acute pancreatitis was 69.88％ (58/83).The incidence of severe acute pancreatitis on patients with body mass index (BMI) ≤25 kg/m2,BMI26-30 kg/m2,BMI≥31 kg/m2 were 5.41％ (17/314),24.84％ (78/314),69.75％ (219/314).There was significant difference (P ＜ 0.05).The incidence of severe acute pancreatitis on patients at age ≤54 years-old,55-69 years-old,≥70 years-old were 12.42％ (39/314),21.66％(68/314),65.92％ (207/314).There was significant difference (P ＜ 0.05).Conclusions In shanghai,the main causes of acute pancreatitis still is biliary disease and engorgement in the lastest ten years.The causes of severe acute pancreatitis have changed.Hyperlipidemia is main casuse; the second one is biliary disease.The incidence rate of severe acute pancreatitis as well as high BMI and elder age were very high and serious.Thus control of blood-lipid and weight should be strengthened. Key words: Pancreatitis; Hyperlipidemias; Cause of disease