I am also interesting in your question.Even though the patients may have similar reasons at the beginning but have so different clinical outcome between mild and severe acute pancreatitis. I collected clinical materials of more than 500 patients of acute pancreatitis several years later, but did find why they were different at the beginning.Now, I also want to study in this field. Now my hypothesis is that "the severe patients are more sensitive for inflammation". I want to know how to detect the sensitive patients.

I expect to your idea.

Patients with acute pancreatitis (AP) with normal hematocrit and serum creatinine seem to be unlikely to develop severe AP (PPV: 98%).

In contrast age, cancer, previous heart failure, chronic kidney or liver disease, alcoholic consumption and obesity are considered at risk of severe AP

In the ED the Bedside Index of severe AP based upon five criteria (BUN> 25mg/dl, SIRS, impaired mental status, age >60 years and pleural effusion could be of interest. A BISAP >2 within the first 24 hours increase the risk of organ failure of 7 fold.

You may use retrospectively these criteria to your 500 AP and validate or not. I will be interested with yours results; unfortunately our pro and anti-inflammatory cytokines study enrolled only severe AP admitted to an ICU. Thus, I cannot evaluate retrospectively these criteria.

You can found all the references in the Wu and Banks review (Clinical management of patients with AP), Gastroenterology 2013, 144: 1272

Thank you for your suggestion. It is well known that the severity criteria for AP , such as Ranson score, CT, Banks, or BISAP in 24 or 48 hs after admission. These criteria could predict for SAP, but It is not known why is different from the onset for the AP patient.

I am sorry but i do not understand what is the purpose of this discussion.

In clinical practice, the most important is to classify AP in mild or potentially severe. Whereas Ranson's and CT scan scales are of interest, they cannot be used at the ED, BISAP seems to be of interest for patients without organ dysfunction.

In a physiopathologic point of view, some comorbidities may increase the severity of illness.

Now, why 10-15%of AP may be severe? Does they are more sensitive to the inflammation? Nobody can answer these questions.

Indeed CRP and cytokines pro and inflammatory should be compared in ALL AP, and not only in SAP. It will of interest to evaluate the AP prevalence in patients treated with corticosteroids, chemotherapy and anti TNF alpha.

Dear colleques,

Although the scoring systems, clinical findings, some labarotory findings, and radiologic findings help for differentiation between severe and mild acute pancreatitis (although most of them needs to development) none of them guests the differentation from the beginning phase of the disease. I think the true response has already not given yet. I think a selection is present.

There are a set of interacting factors which all contribute.

First of these is the initial insult, commonly gall stones or alcohol. In the case of the latter dose is important. For gall stones it is my experience that after mild AP when a per operative chill angiogram is done the ducts are nearly alway clear, which is to say a small stone caused a transient insult and passed away. In severe AP early ERCP is beneficial to clear the duct, a larger stone has not passed and the insult goes on.

Lastly patients do vary in their response to any equivalent insult.

Later infection plays a determining role.

How to predict more accurately which AP would progress to SAP, Any one has better and more update, my colleagues, please share!?

In the past, I had read an article that spoke of the increased risk of more severe pancreatitis with those who are obese. I have noted more protracted and indolent cases, in this sub group.