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Pancreas Divisum

Pancreas divisum just showing a ventral pancreas, always to be distinguished from a tumor obstructing the main pancreatic ducts pancreas divisum, divided pancreas, split pancreas. Because of the anatomic abnormality in pancreas divisum, people have said, "Well, you should be protected against pancreatitis because only your ventral pancreas now, a relatively small portion of the pancreas, is attached to the papilla so you shouldnít be able to get pancreatitis." Pancreas divisum patients do indeed get chronic pancreatitis and in various series itís been variably reported. I donít want you to look so much at the variety of the numbers reported, just at the fact that it is reported. So that pancreas divisum does not protect you from microlithiasis and acute pancreatitis.

Now what is the incidence of pancreas divisum? Because itís based on the incidence that people first started looking at pancreas divisum as a cause for acute pancreatitis. In the general population itís generally about 5-13%. In idiopathic acute pancreatitis it has been reported to be as high as 50%. If you look at these many many studies, some will be within the normal limits. I think the Del Hayes study has turned out eventually to be the largest study - this is from Belgium - and they report, and they are big proponents of pancreatic therapies, endoscopic therapies, but they have finally reported that the incidence of pancreas divisum in patients with idiopathic pancreatitis is the same as in the general population. There is a tendency to over-report pancreas divisum in idiopathic pancreatitis because those are the patients who have more difficult ERCPís, who are then referred to major centers so there is a sort of in-built bias which is obvious when these things are reported. If you look at the balance of the studies, I think the balance favors the fact that the incidence of pancreas divisum in idiopathic pancreatitis is about the same as in population.

Here are the results of uncontrolled studies following evaluation of accessory papillotomy in patients with idiopathic acute pancreatitis and pancreas divisum. The surgeons of course are always as good or better than endoscopists and they have - the follow-up periods are given here - the number of patients and the number improved.

There is only one controlled trial of treatments in pancreas divisum and itís always very widely quoted, but I think itís actually a rather fragile study. You would think a study of that moment would be published in something more august than Gastrointestinal Endoscopy. And Iím not pointing this out as a very big criticism, but I think there are problems with the study.

So why should we challenge the acceptance of pancreas divisum as a cause of idiopathic acute pancreatitis? I think we should challenge it because not all studies systematically get rid of all the other etiologies that weíve been talking about. That the pathophysiology is not clear - not that thatís necessarily a reason we should not believe, but itís a reason we should doubt - and epidemiological association has not been well proven. There is objective evidence for obstruction confined to the dorsal duct, has not been identified. I might say that the argument goes that some patients with pancreas divisum have problems.

So, if we continue, definite improvement is variable and often includes partial responses. Follow-up after therapeutic interventions is short. You might say, "But you showed interventions of years" but weíve all see patients with idiopathic pancreatitis who may have an attack and an attack and an attack and then go five or six years without an attack. So itís very variable. Five or six years without having an attack doesnít mean to say you are not going to have another attack.

Patients, and many patients that we see, who have had these things done in our clinic often have symptoms consistent with irritable bowel syndrome or motility disorder. Somebody said yesterday, if all youíve got is a hammer (i.e. a ERCP scope) and all you can recognize is a nail, a lot of things start looking like nails. I think that this subject suffers quite a bit from that concept.

Finally for pancreas divisum, there have been no corroborating randomized trials evaluating stent therapy. Thereís just the one trial of Landís and others. We should be very suspicious of these studies because there are complications of stent therapy. I think putting a stent in a pancreatic duct for a matter of months almost invariably results in permanent duct changes. Quite frightening when you see this. They certainly get pancreatitis, stent occlusion, outward and inward stent migration, dorsal duct damage.

There is always a flip side and you can see some of the believers in the audience are beaming radio messages in my ear saying, "Donít you ever do it?" Well, the answer is, I do it very rarely. Here is a patient where we did do it. Here is a man - just for light relief - who I saw in the pancreas clinic who came to me at about the age of 65, having had about 40 years mind you, 40 years, of idiopathic attacks of pancreatitis, ostensibly no evidence of chronic pancreatitis clinically, who wanted to be cured. So after taking a deep breath, thinking, "But man, youíve had it for 40 years, why donít you just live with it? I can probably do you more harm than I can do you good"- I did, after discussion, we did proceed to ERCP. 

Sphincter of Oddi dysfunction: Even less data than Iíve presented to you on pancreas divisum. What is the incidence of sphincter of Oddi dysfunction in acute pancreatitis? You know, you can look and itís all over the board. You can get it from 15% to 60% and this just seems untenable. Sixty percent of people should have disease of their pancreas due to tight sphincters in a group of patients should make red lights flash in your head all the time. On the other hand, if you look at the results of uncontrolled studies - everything is uncontrolled in this particular area - evaluating sphincterotomy in patients with idiopathic acute pancreatitis.