The Significance of Etiology in Chronic Pancreat...
French authors（Durbec and Sarles 1978）have undoubtedly demonstrated that alcohol is a risk factor for chronic pancreatitis showing that the relative risk is multiplied by approximately a factor of 1.4 passing from 1 to 20-g of alcohol intake.In addition，the increase of risk to develop a chronic pancreatitis appears to be more rapid when passing from the class of non-drinkers to that of a 20-g alcohol intake per day.The mechanism which determines fibrosis of the pancreatic gland has been pointed out in a well-written paper by Talukdar et al.（2006）.The oxidation of ethanol to acetaldehyde determines the activation of the quiescent pancreatic stellate cells without any pre-activation；determining the development of pancreatic fibrosis even in the absence of necroinflammation process.We have also reported using breath analysis that oxidative stress is an important process in chronic pancreatitis patients（Morselli-Labate et al.2007）.In fact，using a mass spectrometer to analyze breath samples obtained from patients with chronic pancreatitis，having mainly alcoholic pancreatitis without pancreatic pain，we found that the volatile compounds H2S，NO and malononitrile were significantly higher in these chronic pancreatitis patients as compared to healthy subjects（Kuroda et al.1998）.We should underline that the above mentioned substances are the final products of ethanol and oxidative stress able to initiate fibrogenesis of the pancreas.
Thus，alcohol induces pancreatic fibrosis as has frequently been found in autoptic series of alcoholics without a clinical history of chronic pancreatitis（Kuroda et al.1998；Martin and Bedossa 1989；Suda et al.1996）.(https://www.daowen.com)
Unfortunately，in experimental animals the administration of alcohol is not able to induce pancreatic damage similar to that observed in human chronic pancreatitis because alcohol to damage the pancreas requires prior sensitization with other agents.
The etiology of tropical pancreatitis is different and several hypotheses have been proposed such as the malnutrition theory，the suggested role of Cassava metabolites in inducing chronic alterations of the pancreas and，finally，the oxidant stress hypothesis（Martin and Bedossa 1989）.Thus，it is possible that unknown substances cause an activation of the pancreatic stellate cells.In addition，the occurrence of the SPINK-1 mutation in patients with tropical pancreatitis suggests a combined etiology of this disease（Bhatia et al.2002；Schneider et al.2002）.