1652 – A clinical description of acute pancreatitis was first presented in 1652 by the Dutch anatomist Nicholas Tulp.
1788 – Cawley first describes link between chronic alcohol use and pancreatitis -- but not until 1878 (Friedrich) identified this as drunkard’s pancreas (Chronic Pancreatitis).
1868 – Fles in 1868 administered pancreatic substances to their patients with pancreatic disease, thereby decreasing steatorrhea.
1878 – Friedrich identifies link between chronic alcohol use and pancreatitis (ie. see 1788) as drunkard#8217;s pancreas (now known as Chronic Pancreatitis).
1889 – Reginald Fitz firmly established pancreatitis as a disease entity.
1908 – In 1908, Julius Wohlgemuth, of Berlin, described a method for measuring the concentration of amylase ("diastase") in the serum, thereby introducing the potential for diagnosing acute pancreatitis prior to laparotomy or autopsy.
1925 – Lord Moynihan characterized the disease (acute pancreatitis). The introduction of his paper contains perhaps the most quoted description of acute pancreatitis.
1927 – The first case of hyperinsulinism due to a tumor of the islet cells was reported.
1946 – Comfort (et al) from the Mayo Clinic provide the first detailed description of Chronic Pancreatitis as a disesase entity. Their paper described 29 patients in detail including possible precipitating factors. (Alcohol was implicated in 68% of cases and they speculated that #8216;chronic relapsing pancreatitis may represent the summation of repeated attacks of acute interstitial pancreatitis#8217;.)
1952 – Hereditary Pancreatitis was first described by Comfort and Steinberg.
1963 – First attempt at classifying pancreatitis at the Marseilles symposium (organized by Henri Sarles).
1966 – The first human pancreatic transplant of the modern era was performed at the University of Minneapolis; the patient, a 28-year-old female with uncontrolled diabetes and renal failure. On December 17, 1966, a surgical team of Kelly, Lillehei, Merkel, Idezuki and Goetz, transplanted a cadaveric kidney and pancreas. The grafts function for almost two months.
1996 – Whitcomb (et al) isolated the first responsible mutation in the cationic trypsinogen gene (PRSS1) on the long arm of chromosome seven (7q35). (With 53% likelihood of developing pancreatic cancer – much higher than other forms of pancreatitis.).
1998 – Two groups report a strong association between idiopathic chronic pancreatitis and mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene. In the exocrine pancreas, the role of CFTR is to promote the secretion of fluid and bicarbonate by the ductal epithelum. Estimated that 20-40% of patients with idiopathic chronic pancreatitis will eventually prove to be compound heterozygotes for CTRF mutations.