review of literature on clinical pancreatology - The Pancreapedia

observations on acute pancreatitis which were similar to those <strong>of</strong> Portal [030]. Interestingly,these early authors noted an association between swelling <strong>of</strong> the salivary glands andinflammation <strong>of</strong> the pancreas. Théodoric Lerminier (1770-1836) observed that there was ananalogy between the state <strong>of</strong> the pancreas and the parotid in severe fevers [031] and S.Neumann (1819-1908) and JT Mondière both proposed that inflammation could rapidlyspread from the salivary glands to the pancreas resulting in the death <strong>of</strong> the patient [010,032]. It was only in 1899 that HF Harris <strong>of</strong> Boston was convincingly able to link mumps andpancreatitis [033].The etiology <strong>of</strong> pancreatic inflammation was a matter <strong>of</strong> intense speculation. Some <strong>of</strong> theproposed causative factors included mercury, which was used to treat syphilis at that time[003, 034], gastritis and continuous vomiting (Claessen, 1842) [020], chronic hepatic disease(Portal, 1803) [029], excessive masturbation (A von Störck, 1799) [035], migration <strong>of</strong> a wormfrom the duodenum to the pancreatic duct (Shea [036] and Lieutaud [037]), perforated gastriculcer causing penetration <strong>of</strong> the pancreas (Andral) [031] and compression <strong>of</strong> the bile ductleading to pancreatitis with jaundice (Crampton, 1818) [038].Karl von Rokitansky (1804-1878), chair <strong>of</strong> pathology at the Wiener AllgemeinesKrankenhaus, was the first in 1842 to recognize acute hemorrhagic pancreatitis [039]followed by Theodor Albrecht Edwin Klebs (1834-1913) <strong>of</strong> Berne, who, in 1870, noted thathemorrhagic inflammation <strong>of</strong> the gland resulted in "purulent peripancreatitis with partialsequestration <strong>of</strong> the gland" [040]. TS Cullen (1867-1948) <strong>of</strong> Edinburgh describedperiumbilical discoloration in a patient with ectopic pregnancy, and this later came to berecognized as a sign <strong>of</strong> severe acute pancreatitis [041], whereas G Gray-Turner (1877-1951)<strong>of</strong> London, in 1920, reported flank discoloration associated with hemorrhagic pancreatitis[042].In 1856, the great French physiologist Claude Bernard (1813-1878) demonstrated thecapacity <strong>of</strong> pancreatic secretions to digest proteins, carbohydrate and fat. Bernard initiallydemonstrated fat necrosis in dogs in 1856 but failed to elucidate on his finding. He wasfollowed by Julius Klob, an assistant <strong>of</strong> Rokitansky, who identified fat necrosis in humans in1860. In 1882, F Balser described the process <strong>of</strong> fat necrosis in more detail but felt that thiswas a separate event from pancreatic inflammation. W Dettner, who, in 1894, proposed apancreatic ferment as the cause, and H Chiari (1851-1916), who considered it to be due topancreatic degeneration (1896), contested this. Further controversy was excited by ReginaldFitz (1843-1913), who thought the origin was bacterial infection and HD Rolleston whoproposed it to be a solar plexus-related event. Robert Langerhans postulated that it waspancreatic ferment that resulted in necrosis <strong>of</strong> fat tissue, and Simon Flexner, in 1897,suggested that this ferment was lipase [010].Reginald FitzIn a seminal article published in 1889, Reginald Huber Fitz (1843-1913) <strong>of</strong> Boston presentedthe first systematic analyses <strong>of</strong> acute pancreatitis [032]. Fitz was born in Chelsea,Massachusets, and entered Harvard College in 1858 but left in his junior year to work in acopper mine [043]. He returned in 1862 to complete BA and MD degrees and thenproceeded to Europe, where he acquired a unique blend <strong>of</strong> training in both clinical medicineand pathology under the guidance <strong>of</strong> such illustrious scientists as Rokitansky, Skoda, andBillroth. Fitz also worked in the laboratory <strong>of</strong> Rudolf Virchow (1821-1902), where he becamean expert in microscopy and also brought to the United States Virchow's teaching thatdisease is an expression <strong>of</strong> aberration in normal cellular function. Having returned toMassachusetts, as an instructor in Pathology and later as Shattuck Pr<strong>of</strong>essor <strong>of</strong> PathologicAnatomy, he pioneered integration <strong>of</strong> clinical information with pathologic findings, and hisperspicacity led to significant advances in surgical pathology including characterization <strong>of</strong>