Acute Pancreatitis in Patients With Severe Hypertriglyceridemia in a Multi-Ethnic Minority Population

Ambika Amblee, MD; Divyanshu Mohananey, MD; Micheal Morkos, MD; Sanjib Basu, PhD; Ayokunle T. Abegunde, MD; Malini Ganesh, MD; Neil Bhalerao, MD; Amrutha Mary George, MD; Milli Jain, MD; Leon Fogelfeld MD


Endocr Pract. 2018;24(5):429-436. 

In This Article

Abstract and Introduction


Objective: To investigate the prevalence and predictors of hypertriglyceridemic acute pancreatitis (HTG-AP) in a multi-ethnic minority population.

Methods: A retrospective, cross-sectional study from 2003 to 2013 of 1,157 adults with a serum triglyceride (TG) level ≥1,000 mg/dL comparing baseline characteristics and risk factors between those with and without HTG-AP.

Results: Mean study population age was 49.2 ± 11.5 years; 75.6% were male, 31.6% African American, 38.4% Hispanic, 22.7% Caucasian, 5.7% Asian, and 1.6% Pacific Islander. Prevalence of HTG-AP was 9.2%. Patients with HTG-AP were significantly younger (41.3 years vs. 50.0 years; P<.001) than those without HTG-AP. Excessive alcohol intake (odds ratio [OR], 3.9; 95% confidence interval [CI], 2.5 to 6.0; P<.001), gallstone disease (OR, 3.9; 95% CI, 1.4 to 10.8; P = .008), and TG >2,000 mg/dL (OR, 4.8; 95% CI, 3.1 to 7.4; P<.001) remained significant independent risk factors. TG levels for patients with HTG-AP were higher (median TG, 2,394 mg/dL; interquartile range [IQR], 1,152 to 4,339 mg/dL vs. median TG, 1,406 mg/dL; IQR, 1,180.7 to 1,876.5 mg/dL). TG levels >2,000 mg/dL were associated with higher incidence of AP (22% vs. 5%). Patients with TG levels <2,000 mg/dL and no risk factors had prevalence of 2% compared to 33.6% with one risk factor and TG >2,000 mg/dL. Patients with HTG-AP had higher incidence of diabetic ketoacidosis at admission (7.5% vs. 2.5%; P = .004).

Conclusion: TG level ≥2,000 mg/dL is associated with higher HTG-AP prevalence in ethnic minorities. Presence of excessive alcohol intake and/or gallstones further accentuates risk.


Acute pancreatitis (AP) is an inflammatory condition of the pancreas, accounting for more than 220,000 annual hospital admissions[1] and associated with a mortality ranging from 3 to 30%.[1–3] Hypertriglyceridemia (HTG) as an underlying etiology is present in 1.3 to 3.8% of patients with AP, making it one of the most common etiologies for AP after gallstone disease and excessive alcohol intake.[4] Several pathophysiologic mechanisms have been suggested for AP in the presence of HTG (HTG-AP), with the most commonly accepted theory being that excess TGs are hydrolyzed by pancreatic lipase, resulting in free fatty acids (FFAs). These excess FFAs consequently overwhelm the binding capacity of albumin and cause acinar and pancreatic capillary injury. In addition, hyperviscosity resulting from chylomicronemia causes impaired pancreatic blood flow, leading to ischemia and acidosis, ultimately resulting in further pancreatic injury.[5–7]

The Endocrine Society clinical practice guidelines (2012) define severe HTG as TG levels between 1,000 and 1,999 mg/dL and very severe HTG as TG levels ≥2,000 mg/dL.[8] While a threshold TG value of ≥1,000 mg/dL is often cited as the cut-off for developing pancreatitis, not all patients with severe HTG develop AP.[8] At present, there is little information about the risk of AP in relation to TG levels. Some studies have reported cut-off TG values as high as 1,772 mg/dL, while other studies stratified patients based on TG levels >500 mg/dL.[9–12] Not only is there ambiguity in the level of HTG causative of pancreatitis, literature is also lacking on the correlation of increased TG levels and the risk of developing AP. Furthermore, the existing literature on HTG-AP has limited data on the prevalence in ethnic minority populations.[10,12–14] Given the above-mentioned gaps in the literature, we conducted a retrospective study in a large medical center with high rates of ethnic minorities with the aim of determining the prevalence of HTG-AP in patients with severe HTG (TG ≥1,000 mg/dL) and to study other risk factors of HTG-AP.