Statin treatment linked to reduced severity of acute pancreatitis
Statins appear to reduce the severity of acute pancreatitis (AP), as demonstrated by a decrease in overall incidence of multisystem organ failure (MSOF), according to a study.
Researchers examined the medical records of adult patients with AP admitted in the Cleveland Clinic Health System between 2007 and 2014. They performed a propensity-matched analysis to assess the effect of statin exposure on the severity of pancreatitis and incidence of organ failure. The propensity model included factors that influence statin use to minimize selection bias.
A total of 110 AP patients on statin at admission were matched with 210 AP patients who were not exposed to the drug. The two patient groups were evenly matched in terms of known baseline factors that may influence statin use and severity of pancreatitis.
Outcomes of interest were pancreatitis severity (Revised Atlanta Classification), incidence of MSOF, new MSOF, acute necrosis, and death. Additional surrogate markers of severity, such as hospital length of stay, Bedside Index of Severity of Acute Pancreatitis (BISAP), and presence of systemic inflammatory response syndrome, were also assessed.
Results revealed that statin use was associated with a lower likelihood of developing MOSF, severe AP, and necrosis. While there were fewer cases of in-hospital death in the statin group than in the unexposed group, the difference was not statistically significant (2 vs 4 percent; p=0.38).
In a previous animal study, statin administration resulted in lower severity of AP, reduced serum levels of interleukin-10, and diminished myeloperoxidase activity. Statins also demonstrated antioxidant effects and helped prevent cell damage. Specifically, pravastatin significantly attenuated the progression of pancreatic inflammation, fibrosis, and exocrine dysfunction, possibly through the drug’s antioxidative properties and overproduction of interleukin-10. On the other hand, lovastatin was associated with the inhibition of pancreatic stellate cell activation through the interruption of RAS signalling. [Am J Gastroenterol 2017;112:1765–1767]