Abstract
Background/Objective: Evidence from basic and clinical studies suggests that unsaturated fatty acids (UFAs) might be relevant mediators of the development of complications in acute pancreatitis (AP). Objective: The aim of this study was to analyze outcomes in patients with AP from regions in Spain with different patterns of dietary fat intake.Materials and Methods: A retrospective analysis was performed with data from 1,655 patients with AP from a Spanish prospective cohort study and regional nutritional data from a Spanish cross-sectional study. Nutritional data considered in the study concern the total lipid consumption, detailing total saturated fatty acids, UFAs and monounsaturated fatty acids (MUFAs) consumption derived from regional data and not from the patient prospective cohort. Two multivariable analysis models were used: (1) a model with the Charlson comorbidity index, sex, alcoholic etiology, and recurrent AP; (2) a model that included these variables plus obesity.Results: In multivariable analysis, patients from regions with high UFA intake had a significantly increased frequency of local complications, persistent organ failure (POF), mortality, and moderate-to-severe disease in the model without obesity and a higher frequency of POF in the model with obesity. Patients from regions with high MUFA intake had significantly more local complications and moderate-to-severe disease; this significance remained for moderate-to-severe disease when obesity was added to the model.Conclusions: Differences in dietary fat patterns could be associated with different outcomes in AP, and dietary fat patterns may be a pre-morbid factor that determines the severity of AP. UFAs, and particulary MUFAs, may influence the pathogenesis of the severity of AP.
Highlights
Acute pancreatitis (AP) is a common health issue [1]
Patients with AP from regions with high unsaturated fatty acid (UFA) intake had significantly higher rates of local complications [odds ratio (OR) = 1.53; 95% CI: 1.15– 2.05; p = 0.004], persistent (>48 h) organ failure (POF) [OR = 2.1; 95% CI: 1.18–3.74; p = 0.01], mortality [OR = 2.37; 95% CI: 1.12–5.03; p = 0.02], and moderate-to-severe disease [OR = 1.42; 95% CI: 1.1–1.85; p = 0.007] in the model without obesity compared to patients from areas with low UFA intake; after entering the variable obesity into the model, high UFA intake remained a risk factor
The Atlantis prospective cohort study confirmed that obesity is associated with a higher mortality and with a higher incidence of POF [4], and fatty acids could be relevant mediators in the physiopathogenesis of moderate-tosevere AP in obese patients
Summary
While most patients have a mild disease course, one-third experience local and/or systemic complications that produce an increase of morbidity [2]. In vitro experiments using acinar cells of the pancreas have shown that unsaturated fatty acids (UFAs) are associated with inflammation and necrosis, while saturated fatty acids (SFAs) are not harmful. These experiments suggest that UFAs produce necrosis of acinar pancreatic cells and uncontrolled UFA release results in high UFA levels in the bloodstream and is associated with kidney failure and with cell damage in lung alveoli [6, 7]. This study aimed to compare clinical course of disease of AP in regions of Spain that have different dietary fat intake patterns
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