Ensayos clínicos

Overview

Información sobre este estudio

Acute pancreatitis (AP) is the most common gastrointestinal cause of hospital admission resulting in an estimated $2.6 billion per year in costs. Each year, there are more than 300,000 admissions to the hospital for treatment of AP. The incidence of AP is rising and hospital admissions due to pancreatitis have increased by at least 15% over the past 10 years. Unfortunately, despite over 100 years of experimental and clinical studies, there are still no targeted drugs available to treat this painful condition. Current treatment is limited to supportive care such as fluids, nutrition, and pain control and complication management. Although the mechanisms of AP remain unclear, pathologic intra-acinar trypsinogen activation plays important roles in the disease initiation and progression. Clinically, however, medications targeting trypsin alone have not been effective in treating AP patients. Recently, we have found pre-treatment with Dabigatran, an FDA approved drug for anticoagulation which not only inhibits thrombin but also trypsin, dramatically alleviated pancreatic edema, serum amylase levels and pancreas histology. In contrast, Camostat, a trypsin inhibitor which is used in other countries for AP, has limited effects. In addition, 5-20 hours after AP induction, Dabigatran, but not Camostat, effectively prevented parenchymal cell death and the development of chronic pancreatitis. Our study suggested that coagulation may be a novel mechanism for AP initiation and progression. We retrospectively studied the role of anti-coagulation in AP using the Nationwide Inpatient Sample (NIS) 2014. After matched by gender and age, comorbidity index, patients who were on anti-coagulation for their pre-existing condition had lower mortality, fewer ICU admissions, fewer complications, shorter hospital stay and lower hospital costs than those who were not on anti-coagulations. Therefore, anti-coagulation is a promising treatment for AP.

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