Poster Presentation Australian & New Zealand Obesity Society 2016 Annual Scientific Meeting

Hypertriglyceridemia and Acute Pancreatitis in a Cohort of Overweight and Obese Patients (#282)

Hong Lin Evelyn Tan 1 , Tom Goodsall 1 2 3 , Georgina McDonald 1 2 , Tripti Joshi 1 2 , Shamasunder Acharya 1 2 , Katie-Jane Wynne 1 2
  1. Department of Diabetes & Endocrinology, John Hunter Hospital, Newcastle, NSW, Australia
  2. School of Medicine and Public Health, University of Newcastle, Newcastle, NSW, Australia
  3. Australian Gastrointestinal Research Alliance Group, John Hunter Hospital, Newcastle, NSW, Australia

Background: Hypertriglyceridemia (HTG>1.7mmol/l) commonly occurs with visceral obesity, metabolic syndrome and diabetes. The risk of hypertriglyceridemia-associated acute pancreatitis (HTGAP) increases with very high triglyceride levels (>5.6mmol/l) and is 12-fold in severe HTG (>11.2mmol/l). HTGAP accounts for 6% of all episodes of acute pancreatitis (AP).

Method: Data was collected on a retrospective cohort coded for HTG in two hospitals during 2010-15. The records for patients with HTG≥5.6mmol/l and a subset with HTGAP were reviewed and collated.

Results: 22 admissions with HTG occurred in 16 patients. All patients had BMI ≥25kg/m2; 12/16 (75%) were male; 6/16 (38%) had family history of dyslipidemia. Patients with type 2 (n=8, BMI=36.9kg/m2) were more overweight than type 1 (n=1, BMI=25kg/m2) and those without diabetes (n=7, BMI=30.0kg/m2).

HTGAP was diagnosed in 14/22 of admissions in 11/16 of patients; 5/14 required ICU care. Overweight/obesity (100%), diabetes (45%) and alcohol use (63%) were common, with 78% having multiple risk factors. The HTGAP group had a similar risk profile to those with HTG alone: BMI (33.2 vs. 34.8kg/m2; p=0.6) peak triglyceride level (37.9 vs. 39.6mmol/l; p=0.9), diabetes (45% vs. 80%; p=0.31) and alcohol use (63% vs. 80%; p=1.0).

HTG was diagnosed between 5 and 86 hours following AP admission. Insulin infusion resulted in rapid improvement (peak triglyceride 37.9mmol/l to 9.8mmol/l; p<0.001).  Medications (fibrates and omega-3) were added to very low fat diet. HTGAP accounted for 14 (0.8%) of our total 1685 AP admissions.

Discussion: Overweight/obesity is a common risk factor for HTG and HTGAP. Insulin resistance reduces lipoprotein lipase (LPL) action and increases VLDL production. Hydrolysis of triglyceride by pancreatic lipase produces excess unbound fatty acids that may damage acinar cells, precipitating HTGAP. All patients with AP should have HTG excluded at presentation. Insulin therapy activates LPL and reduces fatty acid production; early treatment reduces HTG and may improve outcome.