Experimental and clinical evidence of antioxidant therapy in acute pancreatitis

Abstract

Oxidative stress has been shown to play an important role in the pathogenesis of acute pancreatitis (AP). Antioxidants, alone or in combination with conventional therapy, should improve oxidative-stress-induced organ damage and therefore accelerate the rate of recovery. In recent years, substantial amounts of data about the efficiency of antioxidants against oxidative damage have been obtained from experiments with rodents. Some of these antioxidants have been found beneficial in the treatment of AP in humans; however, at present there is insufficient clinical data to support the benefits of antioxidants, alone or in combination with conventional therapy, in the management of AP in humans. Conflicting results obtained from experimental animals and humans may represent distinct pathophysiological mechanisms mediating tissue injury in different species. Further detailed studies should be done to clarify the exact mechanisms of tissue injury in human AP. Herein I tried to review the existing experimental and clinical studies on AP in order to determine the efficiency of antioxidants. The use of antioxidant enriched nutrition is a potential direction of clinical research in AP given the lack of clues about the efficiency and safety of antioxidant usage in patients with AP.

Acute kidney injury following acute pancreatitis: A review

“…Esrefoglu M. summarized experimental and clinical evidence of antioxidant therapy e.g ascorbic acid, alpha tocopherol, beta-carotene, melatonin, carnitine and N-acetyl-cysteine in cases of AP. Use of antioxidant regimens in the management of AP as a supplement and combined with conventional therapy are reasonable, but there are no sufficient data for using them alone 17 . Another study on rats showed an anti-inflammatory effect of pentoxifylline by inhibiting NF-κB activation in acute pancreatitis and pancreatic ischaemia-reperfusion (I-R) models.…”

“…In pancreatics acinar cells, induction of oxygen free radicals promote apoptosis whereas their inhibition leads to an increase in necrosis accompanied by reduced ATP (ref. 17 ). The apoptotic pathway is an active process requiring specific proteins, proteases (now called caspases).…”

“…Recent studies provide a more comprehensive view. A large amount of PLA 2 is released by polymorphonuclear leukocytes and mononuclear macrophages when SAP occurs and this causes degradation of phospholipids characterized by acute inflammation and necrosis of pancreatic parenchyma, necrosis of pancreatic fat, hemorrhage and inflammatory infiltration 16,17 . Pancreatic and kidney cells may die according to either necrosis or apoptosis mechanisms.…”

Changes of Prooxidant-Antioxidant Systems in Experimental Acute Pancreatitis

“…Thus, acute destructive pancreatitis provokes and deepens the formation of LPO and leads to significant violations of the balance of the prooxidative-antioxidative systems, as it was pointed out by the number of certain authors [10,12,13].…”

“…Damaged acinar cells release AFO, LPO products that are able to activate neutrophils with subsequent potentiation of SIR and microcirculatory disorders. Unsatisfactory results of treatment and a high mortality rate in severe forms of AP are largely determined by complications and inadequately studied pathogenesis, as well as prediction of the course of pancreatic inflammation [13].…”