Hepatic Steatosis May Predispose to More Severe Acute Pancreatitis

Abstract

Purpose: Obesity is implicated in the severity and outcome of acute pancreatitis. The impact of abdominal fat and the influence of hepatic steatosis on the severity and outcome of the acute pancreatitis (AP) have not been studied. Hepatic dysfunction associated with obesity might enhance the systemic inflammatory response by altering the detoxification of inflammatory mediators. We aim to study the relationship of abdominal adiposity and hepatic steatosis with the severity and outcome of acute pancreatitis. Methods: A retrospective chart review on 108 (mean age 53 yrs, male 52%) of 257 patients with AP seen between January 2002 and December 2009 meeting the inclusion criteria were included. Ranson's and CT severity index score calculations were performed. Hepatic attenuation index (HSA) was obtained by calculating the ratio of hepatic to splenic attenuation (Hounsfield units); HSA < 1.0 was used to diagnose moderate to severe macrovesicular steatosis. Total abdominal fat was calculated using sagital and coronal reformation images on CT of the abdomen and pelvis using data from the superior end plate of T10 to the inferior symphysis pubis. Hounsfield units < - 200 HU and > -20 HU were excluded yielding total abdominal fat content; a histogram profile of this remaining volume using a post processing Workstation, GE AW 4.2 (GE Milwaukee, WI) was used to calculate the fat volume. Results: Etiology of AP was alcohol in 19 (17.6%), ERCP-induced 8 (7.4%), gallstone 42 (38.9%) and other etiologies 39 (36.1%). Based on Ranson's score at 48 hrs, 22 (20.4%) had severe AP (score ≥3), and of the 87(80.6%) subjects whose CT severity index was available 20 (23%) had severe AP (score ≥3). HSA < 1.0 was noted in 44 (40.7%) patients. The severity of pancreatitis on Ranson's criteria at 48 hrs (1.57±1.43 vs. 1.20±1.3, p=0.14) and by CT severity index (3.13±2.51 vs. 2.15±1.75, p=0.08) trended to be higher in patients with low-HSA (with fatty liver) compared to high-HSA (without fatty liver). When patients with ERCP induced pancreatitis were excluded, subjects with low-HSA had significantly more severe AP on CT severity index (3.21±2.5 vs. 2.12±1.8, p=0.04). Mean total abdominal fat content was not significantly different in patients with severe (score > 3) vs. milder (score < 3) pancreatitis by Ranson's criteria (15.6±6.7 vs. 13±4.7 liters, p=0.14). No significant difference was noted in the need for ICU admission (31.8% vs. 28.1%), fraction of patients with necrosis (13.6% vs. 12.5%) or pseudocyst formation (9.1 vs. 7.8%), or length of hospital stay (11.6±9.4 vs. 12.2±19.2, p=0.07) in patients with low-HSA and high-HSA. Conclusion: Patients with hepatic steatosis may be predisposed to more severe acute pancreatitis.