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New serum markers for the detection of severe acute pancreatitis in humans.

Acute pancreatitis is an inflammatory process which occurs in a normal organ and which is diagnosed mainly by acute abdominal pain associated with a concomitant rise of serum amylase and lipase concentrations (1, 2). Gallstone migration into the common bile duct and alcohol abuse account for most of the etiologies of the disease. Usually the injury is mild, but 20% of the patients have a severe injury and, among them, 15 to 25% will die. Because it is important to predict the severity of the illness as early as possible in order to optimize the therapy and to prevent organ dysfunction and local complications, several scores of severity have been proposed. Criteria of severity, such as Ranson (3‐5), Glasgow (6), and Acute Physiology and Chronic Health Evaluation (APACHE) (7) scores have been used for a long time. These scores assess the multiple organ dysfunction induced by the disease and consequently, the greater the number of organs injured, the greater the score. New serum markers have recently emerged and their potential for providing additional information on the severity of the disease is currently being evaluated. However, to become useful such markers must be assessed in a large consecutive series of patients, including a significant proportion of severe cases, and the timing of the assessment must be related to the onset of the disease. Moreover, the usefulness of the new marker must be compared with established ones; the results must be reproducible; and the detection of the new marker must be easy to detect in clinical chemistry laboratories. Interestingly, when seeking medical attention (usually 12 to 24 h after the onset of pain) most patients do not exhibit multiple organ dysfunction, which is likely to emerge by the second or third day and, at admission, numerous mediators can be detected in serum. If the concentration of these biologic factors is correlated to the severity of the disease, and if they are detected before the occurrence of multiple organ dysfunction, it is then conceivable that the therapeutic antagonism of these mediators might prevent or attenuate the severity of the multiple organ dysfunction, and consequently the outcome of the disease. These new factors might be important for the rapid scoring of the disease severity in the acute phase and some of them might be used as potential therapeutic targets.