Dyspepsia historical perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

The current understanding of the pathogenesis of dyspepsia began with the first description of gastric ulcer disease in 1799. The term was first used in its current form in 1916 by Walter Alvarez.

• Indigestion is an old english word meaning ‘lack of digestion’, and the symptoms of dyspepsia have known since the birth of medicine. However, the underlying pathogenesis of dyspepsia only began to be understood when Baillie in 1799 first described the pathology and symptoms of gastric ulcer disease.
• Development of barium X-ray radiology by Cannon in 1897 led to the clinical recognition of peptic ulcer disease and its relationship with symptoms.
• Walter Alvarez at the Mayo Clinic in Rochester, MN was the first to apply the term ‘functional dyspepsia’ in 1916 to describe patients with ulcer-like symptoms and a normal X-ray.
• In pre-16th century:
  • Hippocrates gave a detailed describtion of the symptoms of peptic ulcer disease
  • Avicenna described the relationship between abdominal pain and mealtimes in peptic ulcer patients^[1]
• In 1586, Marcellus Donatus of Mantua described gastric ulcers by performing autopsies
• In 1688, Johannes von Murault gave detailed description of duodenal ulcers
• In 1812, Broussais found that if acute gastritis is left untreated, it may lead to chronic gastritis
• In 1821, Nepveu found a relationship between gastritis and gastric cancer
• In 1857, William Brintonin described ulcer of the stomach and gastric cancer in his book
• In 1875, G.Bottcher and M. Letulle hypothesized that ulcers are caused by bacteria
• In 1880, J.Cohnheim found that ulcers may be caused by chemical factors
• In 1889, Walery Jaworski found spiral-shaped organisms in sediment washings of humans and proposed that these organisms may be involved with gastric disease
• In 1910, Moynihan wrote a book on duodenal ulcer^[2]
• In 1971, Howard Steer found H. pylori from biopsies of a patient with ulcers^[3][4]
• In late 1970, J.R Warren, a pathologist in Perth, Australia found the appearance of spiral bacteria overlying gastric mucosa^[4][5]
• In 1982 , Warren and B.J marshall cultured the organism and found a strong association between Helicobacter pylori and inflammation of gastric mucosa^[4][5]
• In an act of self-experimentation Marshall drank a petri-dish containing a culture of organisms extracted from a patient and soon developed gastritis.
• His symptoms disappeared after two weeks, but he took antibiotics to kill the remaining bacteria at the urging of his wife.This experiment was published in 1984 in the Australian Medical Journal^[6]
• In 1994, Parsonnet et al found an association between H. pylori and lymphomas of the gastrointestinal tract^[7]
• In 1997 Tomb et al. completed sequencing of the entire 1,667,867 base pairs of the H. pylori genome. This helped in identifying new virulence factors for the infectivity of H. pylori at the molecular level^[8]
• In 2001, Chan et al. showed that eradication of H. pylori prevents bleeding from ulcers that is caused by aspirin and non-steroidal anti-inflammatory drugs^[9]
• In 2002, European Helicobacter pylori Study Group published the Maastricht 2-2000 Consensus Report, and found a “test-and-treat” strategy for H. pylori in young patients without typical symptoms. It suggested the use of noninvasive testing to evaluate for H. pylori ^[10]
• In 2005 Warren and Marshall awarded the Nobel Prize in medicine by Karolinska Institute in Stockholm for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease^[11]

• In 1992,Covacci discovered CagA gene, which encodes for a cytotoxin-associated surface protein, related with strains of H. pylori that caused duodenal ulcers and was discovered by molecular techniques were first involved in the pathogenesis of peptic ulcer disease ^[12]

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