Acute pancreatitis (AP) is one of the most frequent inflammatory gastrointestinal disorders worldwide. The global pooled incidence is reported to be 34 cases per 100,000 people per year, with North America and the Western Pacific having the highest rates.1, 2 Most of the patients admitted have a mild disease and a short hospital stay.3 Nevertheless, in severe cases, the mortality rate rises to 30–50%, mainly due to its association with systemic inflammatory response syndrome (SIRS) and multiple organ failure.4, 5 As a result, an accurate and timely assessment of the AP severity is critical for identifying high-risk patients, which improves outcomes and lowers the mortality rate.

Obesity (defined as a body mass index [BMI] > 30 kg/m2) is a probed independent risk factor for AP, which is associated with a complicated course, especially abdominal obesity (characterized by a large waist circumference [WC]). This can be explained by the fact that visceral adipose tissue leads to a hypersecretion of proinflammatory mediators such as interleukin 6 and tumor necrosis factor, increasing the inflammatory response when pancreatitis is present.6, 7 In addition, hypertriglyceridemia (HTG), which is one of the most frequent lipometabolic disorders, is an independently significant risk factor for the development of organ failure in AP.8, 9, 10, 11

The concept of hypertriglyceridemic waist (HTGW) phenotype was formulated by Lemieux et al. in 2000, which includes HTG and a large WC.12 This phenotype has been used to identify the characteristics of excessive visceral adipose tissue. Furthermore, these comorbidities have been associated with metabolic syndrome, cardiovascular disease, diabetes, and hypertension. In recent years, interest in the relationship between HTGW and AP has increased.4, 5 This study was aimed to assess the influence of HTG and an enlarged WC on the severity of AP.