At this point in time, pancreatitis caused by excessive alcohol consumption is treated symptomatically. It can be managed, but little emphasis is placed on preventing the progression of the disease. Physicians must start paying attention to the root cause, which is alcoholism. They can no longer just react to the effects of the problem.
Recently, the very first controlled clinical trial investigating the effect of intervention type strategies for alcohol abuse and their influence on the progression of alcoholic pancreatitis concluded. Severe and prolonged abuse of alcohol has been identified as a primary cause of acute and chronic pancreatitis in not only developed countries but also in developing countries.
Usually, the disease first presents as an attack of acute pancreatitis. Further attacks allow it to progress to chronic pancreatitis, which progresses through a series of fibrotic and necrotic occurrences. The first cellular events leading to an instance of necroinflammation are the subject of terrific scrutiny. It is believed they include the premature intracellular activation of digestive enzymes, which can lead to auto-digestion.
Continued abuse of alcohol for anywhere from five to 10 years will usually instigate the first occurrence of acute alcoholic pancreatitis. At this time, research indicates that isolated binge drinking causes pancreatitis rarely if at all.
Two recent observations have prompted research into the cause, development and effects of the disease. First of all, the chance of contracting alcoholic pancreatitis is amplified by the amount of alcohol a person consumes. This suggests an absolute causal effect of alcohol on the pancreas.
Further research on alcohol’s effects on the gland through experiments on animal subjects and in vitro models suggests that as the pancreas metabolizes alcohol, it is subjected to oxidative stress. This encourages the synthesis of pancreatic digestive enzymes. It also destabilizes intracellular membranes and initiates the pancreas to begin autodigestion.
The key effector cells in the regulation of pancreatic fibrosis are known to be the pancreatic stellate cells. Excess collagen is produced when these cells are activated by cytokines that are released during necroinflammation or through alcohol consumption directly.
The other recent observation driving research regarding the pathogenesis of alcoholic pancreatitis is that a mere 5 percent of chronic alcoholics present with pancreatitis. This would imply that some people have specific susceptibility or another trigger factor, but there has been no concrete evidence that any single factor is responsible up to now despite several studies researching the roles that genetic factors and lifestyle may play.
Smoking can be a major factor for mortality in patients with pancreatitis by developing cancers in their autodigestive tract and cardiovascular disease. There is also some evidence that smoking may hasten the progression of pancreatitis that is already established.
Recent studies in human subjects indicate that variations of the genes responsible for encoding anionic trypsinogen and cholesteryl ester lipase, an enzyme that metabolizes ethanol to fatty-acid ethyl esters, may have some effect on a person’s likelihood to develop pancreatitis. Another study has implied that bacterial endotoxin plays a role in developing the condition for some people. Despite such promising findings, identifying the reasons that some individuals are susceptible to alcoholic pancreatitis is open to far more research.
Physicians can only offer medical, endoscopic and surgical therapies for pancreatic attacks. Enzyme-replacement therapy, insulin and analgesics can be prescribed for chronic pancreatitis presenting with maldigestion, diabetes and pain. There are some surgical and endoscopic options meant to treat the pain of pancreatitis, but none has been compared to medical therapy during a random trial. It has been suggested through a recent study that a cocktail of common antioxidants may be of benefit to ameliorate pain associated with chronic pancreatitis.
However, evidence suggests that little attention is given to the predominant factor that causes pancreatitis, which is the excessive intake of alcohol. Many published guidelines do not even mention that patients should reduce alcohol consumption to manage their pancreatitis. That is why the majority of treatment is symptomatic and not preventive.
Some studies suggest that abstinence from alcohol does not prevent the destruction of the pancreatic parenchyma. However, it may lessen the frequency and reduce the intensity of the attacks. Even in light of those studies, there remains a bias among doctors regarding encouraging abstinence to their patients with pancreatitis. This same bias may be the reason that so few studies have researched the effects of interventions for chronic alcoholics with alcoholic pancreatitis.