Alcohol abuse and gallstones were the two most common causes of acute pancreatitis (AP). Hypertriglyceridemia is an uncommon etiology of acute pancreatitis, with a reported incidence of 2-4 % (1). Typically, triglyceride(TGL) levels >1000 mg/dL have been associated with AP; however, the level above which AP may occur is unknown and varies with individuals. Here we discuss management of a patient with acute pancreatitis presented to our ICU with a rare cause with our multi-disciplinary approach.
Ηуреrtriglуϲeriԁеmia-induced pancreatitis (HTGP) causes 2 to 4 percent of all cases of acute pancreatitis(2). The risk of acute раոсreаtitiѕ increases progressively with serum triglyceride levels over 500 mg/dL, with the risk increasing markedly with levels over 1000 mg/dL(3). In this article we present a case of hypertriglyceridemia induced acute pancreatitis, managed in our ICU.
This is about a 40 years old female who is known case of diabetes mellitus presented to our hospital with history of abdominal pain and vomiting for 2 days. She was tachycardic and hyperglycemia was present at time of admission, hence she was admitted in ICU and started on IV hydration. Her CT abdomen was suggestive of acute pancreatitis Her initial Sr. Lipase levels were 4512 and Sr. triglycerides were 1447mg/dl at time of admission. She was started on insulin infusion. Medical gastroenterologist opinion was obtained and he suggested to start oral fibrates. Serum triglyceride levels were monitored periodically. IV insulin was stopped once Sr.triglyceride levels fall less than 500mg/dl. She improved clinically and she was shifted to ward and gradually discharged in stable condition. Her blood sample after collection was given in figure no.1.
The etiology of HTG can be broadly divided into primary and secondary. Primary one causes more severe HTG. Severe HTG is commonly seen with familial chylomicronemia syndrome (FCS), primary hypertriglyceridemia, and mixed hypertriglyceridemia also known as Fredrickson Type I, IV, and V. Common genetic defects leading to severe HTG include lipoprotein lipase deficiency, LPL gene mutation, and Apolipoprotein C II defciency(4). The exact mechanism of HTG induced AP is not clearly understood. Most accepted theories are from animal models which describe metabolism of excessive TGs by pancreatic lipase to free fatty acids (FFA) leading to pancreatic cell injury and ischemia(5). The initial presentation of HTGP is similar to that of acute раոϲrеаtitiѕ due to other causes. Most cases of HTGP that occur during pregnancy are attributable to underlying genetic causes of HTG. Αlϲоhοl may elevate triglyceride levels in patients with an underlying genetic hуреrliрiԁеmia. In most other patients, triglyceride elevations with аlсοhοl intake are transient and likely to be an epiphenomenon rather than a cause of раոϲrеatitiѕ . Αlcοhоl, in doses of >60 grams daily, increases serum triglyceride concentrations in a dose-dependent manner. In a study of approximately 8000 males and females, the prevalence of serum triglyceride concentrations above 227 mg/dL (2.5 mmol/L) increased from 8 to 20 percent with an increase in аlсοhоl intake from three to nine or more drinks per day. The excess triglyceride in a serum sample can displace water containing sodium and cause pseudo-hyponatremia(6). Insulin therapy has been used for more than a decade to lower TG level along with heparin. Insulin activates lipoprotein lipase (LPL) activity which in turn accelerates chylomicron degradation thus lowering TGs levels. Insulin will also rest pancreatic tissue and cause by immunoparalysis via upregulating the expression of human leukocyte antigen on monocytes and decreasing cell apoptosis(7). Heparin releases stored lipoprotein lipase from the endothelial cell thus lowering TGs levels. There is a concern of rebound hypertriglyceridemia as long term or continuous heparin infusion has been shown to deplete LPL, leading to reduction of chylomicrons catabolism and increase in TGs levels. Plasmapheresis (PEX) rapidly removes TGs and chylomicron from the circulation removing the inciting factor and halting the further inflammation and damage to the pancreas(8).
HTG is likely to be associated with severe pancreatitis as compared to other causes but no difference in mortality has been reported. Currently, there are no standardized treatment guidelines. Patients with severe HTG-AP and those with APACHE II score ≥8, organ dysfunction, or Balthazar grade D/E should be offered intensive care unit and non-pharmacologic treatments. TGs lowering treatment should be continued until TGs < 500 mg/dL. Oral lipid lowering therapy should be started when patient is able to t olerate oral intake. . Further research efforts are needed to guide future therapies and uniform guidelines of this important clinical entity.
Dr. Dhineshraj DrNB Critical Care Medicine Kauvery Hospital, Chennai
Dr. Vetriselvan P Associate Consultant Critical Care Medicine Kauvery Hospital, Chennai
Courtesy – https://pmc.ncbi.nlm.nih.gov/articles/PMC6083537
