Terrible Triglycerides: A Fatal Side Effect

Poster #: 94
Session/Time: A
Author: Ryan Park
Mentor: Naveen Voore, MD
Co-Investigator(s): 1. Ryan Park, EVMS MD Program MS4 2. Lily Nguyen, MD, Department of Medicine Residency Program 3. Sam Stein, MD, Department of Medicine Residency Program 4. Ogochukwu Ilobi, MD, Department of Medicine Residency Program 5. Naveen Voore, MD, Department of Medicine
Research Type: A Case Report

Abstract

Introduction: Acute pancreatitis is an inflammatory disorder of the pancreas characterized by elevated pancreatic enzymes, abdominal pain and correlating imaging findings. Severe cases can lead to necrosis of the pancreas with eventual development of shock and organ failure. While gallstones and alcohol are the most common causes of acute pancreatitis, hypertriglyceridemia is another notable cause.

Case Information: A 37-year-old male with past medical history of PTSD, bipolar disorder (on valproic acid), HIV (on dolutegravir-rilpivirine), and polysubstance abuse presented to the emergency department with a 1-day history of severe abdominal pain, nausea, vomiting, fever and chills. Initial labs were most notable for a cholesterol of 434, lactic acid of 6.9, glucose of 398, and an anion gap metabolic acidosis. His blood was described as lipemic by the laboratory thus an initial lipase level could not be read. An abdominal CT scan revealed interstitial pancreatitis. He was admitted and initiated on IV fluids and analgesic medications. A lipid panel revealed a triglyceride level of >4000 and he was subsequently started on an insulin drip. A few hours after admission, he developed progressive lethargy with marked hypotension warranting central line placement for pressor support with norepinephrine, vasopressin, phenylephrine as well as broad spectrum antibiotics. He was transferred to a nearby hospital for emergent plasmapheresis. Upon arrival, he was intubated for respiratory acidosis and his repeat triglyceride level was 8,029. Other notable labs were a valproic acid level of 9.4 and lipase of 4,006. He received plasma exchange with continued pressor support and IV steroids were initiated. Renal replacement therapy was also initiated for shock-induced renal failure. Despite these measures, he continued to decompensate, developing profound transaminitis secondary to shock liver. Additionally, he developed abdominal compartment syndrome for which he was to undergo a decompressive laparotomy. However, on preparation for the procedure, he went into cardiac arrest with eventual ROSC. Given his continued clinical decline, his family decided to transition to comfort care, and the patient passed away.

Discussion/Clinical Findings: This patient notably had a benign triglyceride level of 120 two months prior to the described hospitalization; the profound increase is a unique aspect of this case. Triglycerides can be elevated from several causes, including HIV, hypertension, sedentary lifestyles, liver disease, and medications. On review of the patient's medications which included dolutegravir-rilpivirine and valproic acid, it was concluded that valproic acid was the most likely cause of the abrupt triglyceride elevation and development of acute pancreatitis. Valproic acid has a dose- independent relationship with pancreatitis. The association between metabolic derangements (such as increased weight and triglycerides) and valproic acid use has been well established in prior literature. Valproic acid-induced pancreatitis was first reported in 1979 and over 120 cases have been reported since. The mechanism behind valproic acid's effect on lipid profiles is multifactorial, including an increase in both insulin resistance and fatty acid oxidation.

Conclusion: We present this case to highlight a severe adverse effect of a commonly used medication and its potentially fatal consequences.