Location
Moultrie, GA
Start Date
17-4-2026 12:00 PM
End Date
17-4-2026 1:00 PM
Description
Background: Familial hyperlipidemia encompasses a group of inherited lipid metabolism disorders characterized by elevated serum cholesterol and/or triglyceride levels. Severe hypertriglyceridemia, particularly levels exceeding 1,000 mg/dL, is a well-established but less common cause of acute pancreatitis (1). Acute pancreatitis is an inflammatory condition of the pancreas most frequently attributed to gallstones or alcohol use; however, hypertriglyceridemia accounts for approximately 1–10% of cases and is associated with increased morbidity when not promptly recognized and treated.
Introduction: Hypertriglyceridemia-induced acute pancreatitis results from excessive circulating triglyceride-rich lipoproteins, leading to free fatty acid release and pancreatic inflammation (2). Young patients without traditional risk factors may present with pancreatitis as the first manifestation of an underlying genetic lipid disorder. We report the case of an 18-year-old male with no significant past medical history who presented with acute abdominal pain and was subsequently diagnosed with acute pancreatitis secondary to previously undiagnosed familial hypertriglyceridemia. This case highlights the importance of maintaining a broad differential diagnosis and considering metabolic etiologies in young patients presenting with acute abdomen.
Methods: An 18-year-old male presented to the emergency department with one day of diffuse abdominal pain radiating to the back, accompanied by nausea and vomiting. Initial evaluation included a comprehensive history, physical, laboratory studies, and imaging. The patient reported mild social alcohol use, denied trauma, and had no established primary care provider. Physical examination revealed epigastric and upper abdominal tenderness with radiation to the back. Laboratory testing included complete blood count (CBC), comprehensive metabolic panel (CMP), lipid panel, serum lipase, thyroid-stimulating hormone (TSH), and urinalysis. Imaging studies included right upper quadrant ultrasound and abdominal computed tomography (CT).
Results: Laboratory evaluation revealed markedly elevated triglycerides (1,943 mg/dL), total cholesterol (370 mg/dL), and very-low-density lipoprotein (VLDL) (389 mg/dL). Serum lipase was elevated at 1,217 U/L. Leukocytosis was present with a white blood cell count of 17.7 ×10³/µL, and total bilirubin was mildly elevated at 2.2 mg/dL. CT imaging demonstrated peripancreatic fluid and inflammatory changes consistent with acute pancreatitis, as well as mild hepatic steatosis. No gallstones or biliary obstruction were identified. Based on clinical presentation, laboratory findings, and imaging results, the patient was diagnosed with hypertriglyceridemia-induced acute pancreatitis secondary to suspected familial hyperlipidemia. He was treated with intravenous fluids, bowel rest, and analgesia, resulting in symptomatic improvement. Given clinical stability and response to therapy, insulin infusion was not required. The patient was discharged on atorvastatin and fenofibrate with close outpatient follow-up arranged for long-term lipid management.
Discussion: This case underscores the importance of considering severe hypertriglyceridemia in the differential diagnosis of acute pancreatitis, particularly in young patients without gallstones or significant alcohol use. Undiagnosed familial hypertriglyceridemia may first present with acute pancreatitis, emphasizing the need for lipid evaluation in unexplained cases. Early recognition allows for targeted therapy to reduce triglyceride levels and prevent recurrence. Long-term management with lipid-lowering pharmacotherapy and primary care follow-up is essential to reduce the patient’s future risk of recurrent pancreatitis and cardiovascular disease.
Embargo Period
5-26-2026
Included in
A Case Study: Undiagnosed Familial Hypertriglyceridemia Inciting Acute Pancreatitis
Moultrie, GA
Background: Familial hyperlipidemia encompasses a group of inherited lipid metabolism disorders characterized by elevated serum cholesterol and/or triglyceride levels. Severe hypertriglyceridemia, particularly levels exceeding 1,000 mg/dL, is a well-established but less common cause of acute pancreatitis (1). Acute pancreatitis is an inflammatory condition of the pancreas most frequently attributed to gallstones or alcohol use; however, hypertriglyceridemia accounts for approximately 1–10% of cases and is associated with increased morbidity when not promptly recognized and treated.
Introduction: Hypertriglyceridemia-induced acute pancreatitis results from excessive circulating triglyceride-rich lipoproteins, leading to free fatty acid release and pancreatic inflammation (2). Young patients without traditional risk factors may present with pancreatitis as the first manifestation of an underlying genetic lipid disorder. We report the case of an 18-year-old male with no significant past medical history who presented with acute abdominal pain and was subsequently diagnosed with acute pancreatitis secondary to previously undiagnosed familial hypertriglyceridemia. This case highlights the importance of maintaining a broad differential diagnosis and considering metabolic etiologies in young patients presenting with acute abdomen.
Methods: An 18-year-old male presented to the emergency department with one day of diffuse abdominal pain radiating to the back, accompanied by nausea and vomiting. Initial evaluation included a comprehensive history, physical, laboratory studies, and imaging. The patient reported mild social alcohol use, denied trauma, and had no established primary care provider. Physical examination revealed epigastric and upper abdominal tenderness with radiation to the back. Laboratory testing included complete blood count (CBC), comprehensive metabolic panel (CMP), lipid panel, serum lipase, thyroid-stimulating hormone (TSH), and urinalysis. Imaging studies included right upper quadrant ultrasound and abdominal computed tomography (CT).
Results: Laboratory evaluation revealed markedly elevated triglycerides (1,943 mg/dL), total cholesterol (370 mg/dL), and very-low-density lipoprotein (VLDL) (389 mg/dL). Serum lipase was elevated at 1,217 U/L. Leukocytosis was present with a white blood cell count of 17.7 ×10³/µL, and total bilirubin was mildly elevated at 2.2 mg/dL. CT imaging demonstrated peripancreatic fluid and inflammatory changes consistent with acute pancreatitis, as well as mild hepatic steatosis. No gallstones or biliary obstruction were identified. Based on clinical presentation, laboratory findings, and imaging results, the patient was diagnosed with hypertriglyceridemia-induced acute pancreatitis secondary to suspected familial hyperlipidemia. He was treated with intravenous fluids, bowel rest, and analgesia, resulting in symptomatic improvement. Given clinical stability and response to therapy, insulin infusion was not required. The patient was discharged on atorvastatin and fenofibrate with close outpatient follow-up arranged for long-term lipid management.
Discussion: This case underscores the importance of considering severe hypertriglyceridemia in the differential diagnosis of acute pancreatitis, particularly in young patients without gallstones or significant alcohol use. Undiagnosed familial hypertriglyceridemia may first present with acute pancreatitis, emphasizing the need for lipid evaluation in unexplained cases. Early recognition allows for targeted therapy to reduce triglyceride levels and prevent recurrence. Long-term management with lipid-lowering pharmacotherapy and primary care follow-up is essential to reduce the patient’s future risk of recurrent pancreatitis and cardiovascular disease.