Peptic ulcer historical perspective
|
Peptic ulcer Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Surgery |
|
Case Studies |
|
2017 ACG Guidelines for Peptic Ulcer Disease |
|
Guidelines for the Indications to Test for, and to Treat, H. pylori Infection |
|
Guidlines for factors that predict the successful eradication when treating H. pylori infection |
|
Guidelines to document H. pylori antimicrobial resistance in the North America |
|
Guidelines for evaluation and testing of H. pylori antibiotic resistance |
|
Guidelines for when to test for treatment success after H. pylori eradication therapy |
|
Guidelines for penicillin allergy in patients with H. pylori infection |
|
Peptic ulcer historical perspective On the Web |
|
American Roentgen Ray Society Images of Peptic ulcer historical perspective |
|
Risk calculators and risk factors for Peptic ulcer historical perspective |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ;Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]
Overview
Historical Perspective
In 1997, the Centers for Disease Control and Prevention, with other government agencies, academic institutions, and industry, launched a national education campaign to inform health care providers and consumers about the link between H. pylori and ulcers. This campaign reinforced the news that ulcers are a curable infection, and the fact that health can be greatly improved and money saved by disseminating information about H. pylori.[1]
Helicobacter pylori was rediscovered in 1982 by two Australian scientists Robin Warren and Barry Marshall[2]. In their original paper, Warren and Marshall contended that most stomach ulcers and gastritis were caused by colonization with this bacterium, not by stress or spicy food as had been assumed before.[3]
The H. pylori hypothesis was poorly received, so 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, since halitosis is one of the symptoms of infection.[4] This experiment was published in 1984 in the Australian Medical Journal and is among the most cited articles from the journal.
In 2005, the Karolinska Institute in Stockholm awarded the Nobel Prize in Physiology or Medicine to Dr. Marshall and his long-time collaborator Dr. Warren "for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease". Professor Marshall continues research related to H. pylori and runs a molecular biology lab at UWA in Perth, Western Australia.
- Gastric ulcer was first discovered by Goldstein, a [nationality + occupation], in [year]/during/following [event].
- Spiral-shaped microorganism described by Polish clinical researcher Professor W.Jaworski at Cracow Jagiellonian University 100 years ago but it was confirmed in the animal by G.Bizzazero.In late 1970, J.R Warren, a pathologist in Perth, Australia found the appearance of spiral bacteria overlying gastric mucosa.
In 1982 Warren and B.J marshall cultured the organism and demonstrate a strong association between Helicobacter pylori and inflammation of gastric mucosa ,it is not due to spicy food and stress [5][6] 1994 A National Institutes of Health Consensus Development Conference concludes that there is a strong association between H. pylori and ulcer disease, and recommends that ulcer patients with H. pylori infection be treated with antibiotics.
Overview
Historical Perspective
Discovery
- In 16th, 17th century, 18th and 19th centuries,Smith , Rivers and Goldstein wrote chapters on the peptic ulcer disease[7]
- In pre 16th century
- Hippocrates first describes symptoms of peptic ulcer
- Avicenna described the relationship between gastric pain and mealtimes in peptic ulcer patient [8]
- In 1586, Marcellus Donatus of Mantua described gastric ulcers by performing autopsies
- In 1688, duodenal ulcers observed by Johannes von Murault
- In 1812, Broussais found that if acute gastritis is untreated, it can lead to chronic gastritis
- In 1821, Nepveu found a relationship between gastritis and gastric cancer
- In 1857, William Brintonin in his book on ulcer of the stomach described ulcer disease and gastric cancer
- In 1868, Kussmaul discovered that an antibacterial agent containing bismuth used to treat peptic ulcers
- In 1875, G. Bottcher and M. Letulle hypothesize 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 organisms in sediment washings of humans and described organisms may be involved with gastric disease
- In 1910 ,Moynihan wrote a book on duodenal ulcer[9]
- In 1913, Rosenow found that streptococci produce ulcers
- Spiral-shaped microorganism described by Polish clinical researcher Professor W.Jaworski at Cracow Jagiellonian University 100 years ago but it was confirmed in the animal by G.Bizzazero.In late 1970, J.R Warren, a pathologist in Perth, Australia found the appearance of spiral bacteria overlying gastric mucosa.[5][5][6]
A National Institutes of Health Consensus Development Conference 1994 concludes that there is a strong association between H. pylori and ulcer disease, and recommends that ulcer 951 J. Allende publishes a book describing the treatment of gastric ulcers with penicillin.[2] 1953 Dintzis and Hastings are able to stop urease production in mice with antibiotics, suggesting a relationship between urease and a bacterial infection.[19] 1954 Palmer publishes a study which finds no bacteria in the human stomach. He concludes earlier discoveries were a result of contamination. Unfortunately, he chooses not to use a silver staining method, which will be later used to reveal H. pylori by Warren and Marshall.[20] 1955 Tarnopolskaya observes that penicillin seems to cure some peptic ulcers.[13] Moutier and Cornet suggest treating gastritis with antibiotics.[13] Kornberg and Davies observe that antibiotics reduce urease in cats.[21]
Ammonia 1957 Charles Lieber and Andre Lefèvre discover that antibiotics reduce gastric urea to ammonia conversion.[22] 1958 Gordon observes that penicillin cures some peptic ulcers.[13] John Lykoudis successfully treats his own gastroenteritis with antibiotics.[23] Lieber and Lefèvre present their results at the World Congress of Gastroenterology in Washington. It is not well received because of the widespread belief that bacteria cannot survive in the human stomach, due to Palmer.[24] 1959 Lieber and Lefèvre publish a follow-up study demonstrating that antibiotics prevent the conversion of urea to ammonia in the human stomach.[25] Conway et al. call into question the extent of urease produced by bacteria in mice, as an argument against the bacterial theory of PUD.[26]
Campylobacter fetus 1960 Vital and Orrego observe Campylobacter-like organisms in the stomachs of cats and dogs.[27] Lykoudis is awarded a Greek patent (#22,453) for his antibiotic treatment of PUD.[23] 1962 Susser and Stein publish a paper identifying a cohort phenomenon of PUD in England. This is taken as evidence for stress causing PUD.[28] 1964 Lykoudis presents his antibiotic treatment for PUD at a meeting of the Medico-Surgical Society in Greece. He is largely shunned by the medical establishment.[23] 1966 Lykoudis' manuscript is rejected by the Journal of the American Medical Association.[23] 1967 Susumu Ito describes Campylobacter-like organisms attached to a gastric epithelial cell.[29] 1968 Lykoudis is fined 4,000 drachmas for treating PUD patients with his treatment, which includes antibiotics.[23] 1970–21st century[edit] 1971 Howard Steer observes H. pylori from biopsies of a patient with ulcers.[30] 1972 The first report of successfully using furazolidone (an antibacterial agent) to treat PUD in China.[31] 1974 Morozov observes H. pylori; he does not connect this discovery to PUD.[13] A well regarded study of PUD is published which does not mention bacteria.[30][32]
Pseudomonas aeruginosa 1975 Steer and Colin-Jones publish their results regarding H. pylori and its relation to PUD. They decide that it was Pseudomonas, a contaminant, and not related to PUD.[33] 1978 At a meeting of the American Gastroenterology Association in Las Vegas, several papers are presented which suggest that acid control via H2 blockers is ineffective at curing PUD.[34] 1979 Ramsey publishes a study demonstrating that bismuth can help eradicate PUD. Bismuth is an antibacterial agent, although this is not recognized by Ramsey.[35] J. Robin Warren first observes H. pylori in a gastric biopsy.[36] Fung, Papadimitriou, and Matz observe H. pylori.[37] 1981 Yao Shi observes bacteria in the stomach, but he believes they are passing through the stomach and not colonizing it.[31] July: Barry Marshall joins gastroenterology division of Royal Perth Hospital and meets Robin Warren[38] October: Marshall and Warren successfully treat their first PUD patient with antibiotics.[38] 1982 Satoha et al. find evidence for an infectious cause of ulcers in rats.[39] Marshall and Warren begin their first study to determine the relationship between H. pylori and PUD.[38] First successful culturing of H. pylori performed; it occurs almost by accident.[38] October: Marshall discovers the bacteria he is investigating are not campylobacteria, by looking at electron micrographs.[38] October 2: Marshall presents his and Warren's results at a local College of Physicians meeting. He meets with criticism, which Marshall later admits was well-founded (at least in part).[38]
Cimetidine 1983 January: Two letters authored by Warren and Marshall, respectively, are sent to The Lancet describing their results.[38] February: Gastroenterological Society of Australia rejects Marshall's abstract to present his research at their yearly conference. They deem it in the bottom 10% of papers submitted. The same abstract is accepted for presentation at a Campylobacter workshop in Brussels.[38] April: Marshall and Ian Hislop begin a study to compare bismuth treatment with cimetidine. The study is abandoned because it is inconclusive.[38] June: Warren and Marshall's letter appears in The Lancet.[40] September: H. pylori is observed in patients outside of Australia.[38] After the appearance of the letters in The Lancet, groups around the world begin isolating H. pylori.[38] 1984 A paper describing Marshall and Warren's results is accepted by the Gastroenterological Society of Australia for presentation.[38] Marshall and Goodwin attempt to infect pigs with H. pylori in an attempt to demonstrate that it causes PUD. The experiment fails.[38] Marshall and Warren's paper is accepted by The Lancet in May and published in June. Many reviewers dislike the paper.[38] McNulty and Watson are able to reproduce Marshall and Warren's results.[41] June 12: Marshall intentionally consumes H. pylori and becomes ill. He takes antibiotics and is relieved of his symptoms.[38] The National Health and Medical Research Council of Australia fully funds Marshall's research into H. pylori.[38] A study is published in China about the effectiveness of treating PUD with an antibacterial agent.[31] July 31: The New York Times publishes an article by its medical correspondent Dr. Lawrence K. Altman on the possible link between H. pylori and PUD.[42] He states in 2002, "I’ve never seen the medical community more defensive or more critical of a story" since he joined the newspaper in 1969.[43] Thomas Borody developed the bismuth-based "Triple Therapy" consisting of bismuth and two antibiotics. This became the first truly successful treatment for H. pylori with an eradication rate greater than 90%.[44][45][46] 1985 Marshall publishes the results of self-induced infection.[38] Borody patents the bismuth-based triple therapy.[47] 1987 Drumm and colleagues following a study of children reported in the New England Journal of Medicine that Helicobacter pylori was specifically associated with primary or unexplained gastric inflammation and primary duodenal ulceration whereas the bacteria were not found in association with secondary gastric inflammation and ulcers due to causes such as Crohn's disease or critical illness. Because gastritis and duodenal ulceration are rare in children this study had the capacity to demonstrate that Warren and Marshall were correct in claiming that H. pylori was a specific pathogen rather than as had been suggested by some, merely an opportunistic colonizer of an inflamed or ulcerated mucosal surface. This was the first time that New England Journal of Medicine, the worlds leading medical journal published a study [48] on Helicobacter pylori.
Morris intentionally consumes H. pylori. Like Marshall, he becomes ill, but unlike Marshall, he is not completely cured by antibiotics. The infection will remain with him for three years.[49] An extensive study in Dublin demonstrates that eradicating H. pylori substantially reduces recurrence of ulcers.[50] 1990 Borody's triple therapy became commercialized in the United States under the product name Helidac.[51] Rauws and Tytgat describe cure of duodenal ulcer by eradication of H. pylori using Borody's triple therapy combination.[52] Triple-therapy, modernized to a proton pump inhibitor and two antibiotics, soon becomes first line therapy for eradication. World Congress of Gastroenterology recommends eradicating H. pylori to cure duodenal ulcers.[53] First report of resistance of H. pylori to the antibiotic metronidazole.[54] Resistance of H. pylori to treatment will lead to the development of many different antibiotic and proton pump inhibitor regimens for eradication.[55] 1992 Fukuda et al. prove ingestion of H. pylori causes gastritis in rhesus monkeys.[4] Covacci et al. sequence the CagA gene, which encodes for a cytotoxin-associated surface protein, which correlated strongly with strains of H. pylori that caused duodenal ulcers. This was the first description of a virulence factor for H. pylori infection determined by molecular techniques.[56]
Gastric cancer
Fujioka et al. prove similar results as those from Fukuda et al.[4] Patents for acid reducing drugs expire, removing financial incentive to resist antibiotics as treatment of PUD.[38] A conference held by National Institute of Health (USA) demonstrates the general acceptance of H. pylori as cause of PUD in the US.[38] The World Health Organization's International Agency for Research on Cancer declares H. pylori a Group 1 carcinogen.[57]
- In 1994, Parsonnet et al found an association between H. pylori and lymphomas of the gastrointestinal tract.Malignant ulcers can be treated by eradicating Helicobacter[10]
- 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 on the molecular level[11]
- In 2001 , Chan et al. showed that eradication of H. pylori even prevents bleeding from ulcers that is caused by aspirin and non-steroidal anti-inflammatory drugs[12]
- In 2002, European Helicobacter Pylori Study Group published the Maastricht 2-2000 Consensus Report, found a "test-and-treat" strategy for H. pylori in young patients without atypical symptoms. It suggests the use of noninvasive testing to evaluate for H. pylori and simply treating if found, even in the absence of ulcer disease documented on endoscopy[13]
- In 2005 Warren and Marshall awarded the Nobel Prize in Physiology or Medicine by Karolinska Institute in Stockholm for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease"[14]
- In 1994 CagA gene, which encodes for a cytotoxin-associated surface protein, related strongly 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 discovered by Covacci et al.[15]
Outbreaks
- There have been several outbreaks of [disease name], which are summarized below:
Landmark Events in the Development of Treatment Strategies
- In 1996 first antibiotic was developed by the Food and Drug Administration to treat peptic ulcer disease.[16]
Impact on Cultural History
Famous Cases
- The following are a few famous cases of disease name:
References
- ↑ Ulcer, Diagnosis and Treatment - CDC Bacterial, Mycotic Diseases
- ↑ Marshall BJ (1983). "Unidentified curved bacillus on gastric epithelium in active chronic gastritis". Lancet. 1 (8336): 1273–1275. PMID 6134060.
- ↑ Marshall BJ, Warren JR (1984). "Unidentified curved bacilli in the stomach patients with gastritis and peptic ulceration". Lancet. 1 (8390): 1311–1315. PMID 6145023.
- ↑ "Research Enterprise, The 2005 Nobel Prize in Physiology or Medicine". Retrieved 2007-08-26.
- ↑ 5.0 5.1 5.2 Konturek JW (2003). "Discovery by Jaworski of Helicobacter pylori and its pathogenetic role in peptic ulcer, gastritis and gastric cancer". J. Physiol. Pharmacol. 54 Suppl 3: 23–41. PMID 15075463.
- ↑ 6.0 6.1 "Home | CDC Ulcer".
- ↑ Graham DY (2014). "History of Helicobacter pylori, duodenal ulcer, gastric ulcer and gastric cancer". World J. Gastroenterol. 20 (18): 5191–204. doi:10.3748/wjg.v20.i18.5191. PMC 4017034. PMID 24833849.
- ↑ Kidd M, Modlin IM (1998). "A century of Helicobacter pylori: paradigms lost-paradigms regained". Digestion. 59 (1): 1–15. PMID 9468093.
- ↑ Barry, J (2002). Helicobacter pioneers : firsthand accounts from the scientists who discovered helicobacters, 1892-1982. Victoria, Australia Malden, MA, USA: Blackwell. ISBN 0867930357.
- ↑ Parsonnet J, Hansen S, Rodriguez L, Gelb AB, Warnke RA, Jellum E, Orentreich N, Vogelman JH, Friedman GD (1994). "Helicobacter pylori infection and gastric lymphoma". N. Engl. J. Med. 330 (18): 1267–71. doi:10.1056/NEJM199405053301803. PMID 8145781.
- ↑ Tomb JF, White O, Kerlavage AR, Clayton RA, Sutton GG, Fleischmann RD, Ketchum KA, Klenk HP, Gill S, Dougherty BA, Nelson K, Quackenbush J, Zhou L, Kirkness EF, Peterson S, Loftus B, Richardson D, Dodson R, Khalak HG, Glodek A, McKenney K, Fitzegerald LM, Lee N, Adams MD, Hickey EK, Berg DE, Gocayne JD, Utterback TR, Peterson JD, Kelley JM, Cotton MD, Weidman JM, Fujii C, Bowman C, Watthey L, Wallin E, Hayes WS, Borodovsky M, Karp PD, Smith HO, Fraser CM, Venter JC (1997). "The complete genome sequence of the gastric pathogen Helicobacter pylori". Nature. 388 (6642): 539–47. doi:10.1038/41483. PMID 9252185.
- ↑ Chan FK, Chung SC, Suen BY, Lee YT, Leung WK, Leung VK, Wu JC, Lau JY, Hui Y, Lai MS, Chan HL, Sung JJ (2001). "Preventing recurrent upper gastrointestinal bleeding in patients with Helicobacter pylori infection who are taking low-dose aspirin or naproxen". N. Engl. J. Med. 344 (13): 967–73. doi:10.1056/NEJM200103293441304. PMID 11274623.
- ↑ Malfertheiner P, Mégraud F, O'Morain C, Hungin AP, Jones R, Axon A, Graham DY, Tytgat G (2002). "Current concepts in the management of Helicobacter pylori infection-the Maastricht 2-2000 Consensus Report". Aliment. Pharmacol. Ther. 16 (2): 167–80. PMID 11860399.
- ↑ "The Nobel Prize in Physiology or Medicine 2005".
- ↑ Covacci A, Censini S, Bugnoli M, Petracca R, Burroni D, Macchia G, Massone A, Papini E, Xiang Z, Figura N (1993). "Molecular characterization of the 128-kDa immunodominant antigen of Helicobacter pylori associated with cytotoxicity and duodenal ulcer". Proc. Natl. Acad. Sci. U.S.A. 90 (12): 5791–5. PMC 46808. PMID 8516329.
- ↑ Ulcer, Diagnosis and Treatment - CDC Bacterial, Mycotic Diseases