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lüll Ritonavir and disulfiram may be synergistic in lowering active interleukin-18 levels in acute pancreatitis, and thereby hasten recovery Kast REJOP 2008[May]; 9 (3): 350-3Interleukin-18 (IL-18) is one of the mediators of both pancreas damage and systemic complications like hypotension and multi-organ dysfunction during acute pancreatitis. IL-18 is generated intracellularly from pro-IL-18 by caspase-1 mediated proteolysis. Active caspase-1 itself is generated intracellularly by the action of the inflammasome, autocatalysis and other stimuli. The anti-retroviral drug ritonavir inhibits conversion of inactive pro-caspase-1 to active caspase-1. Since ritonavir is well tolerated in short-term use it may therefore prove useful in treating acute pancreatitis by lowering caspase-1 mediated IL-18 formation and the many inflammatory mediators downstream from that. The alcoholism treatment drug disulfiram has been in continuous use since the 1950s. It likewise has a low risk profile. Disulfiram inhibits several human proteases, among them caspase-1. Given the current morbidity and mortality of pancreatitis, research should be directed to ritonavir and disulfiram as treatment options for illnesses like pancreatitis where excessive IL-18 contributes to pathology. The first clinically used angiotensin converting enzyme inhibitor, captopril, has shown potent caspase-1 inhibiting activity as well and should be investigated in rodent models of human pancreatitis.|Acute Disease[MESH]|Animals[MESH]|Antihypertensive Agents/pharmacology[MESH]|Captopril/pharmacology[MESH]|Caspase Inhibitors[MESH]|Disulfiram/administration & dosage/*pharmacology[MESH]|Drug Synergism[MESH]|Enzyme Inhibitors/administration & dosage/pharmacology[MESH]|Humans[MESH]|Interleukin-18/*blood/metabolism/physiology[MESH]|Models, Biological[MESH]|Pancreatitis/blood/*drug therapy/etiology[MESH]|Remission Induction[MESH]|Ritonavir/administration & dosage/*pharmacology[MESH]|Time Factors[MESH] |