8/12/2019 Community Acquired Acute Helicobacter Pylori Gastritis

http://slidepdf.com/reader/full/community-acquired-acute-helicobacter-pylori-gastritis 1/3

 Journal of Gastroenterology and Hepatology (2000) 15, 1353–1355

authors suggested that the diagnosis of acute H. pylori infection should prompt antibiotic therapy to ensure H.

 pylori  eradication and prevention of chronic H. pylori 

gastritis.Proton pump inhibitors have potent anti-H. pylori 

activity and their use is associated with a marked fall inbacterial load; more than 20% become negative by his-tology or urea breath test (UBT). The anti-H. pylori activity of the proton pump inhibitor casts some doubton the interpretation of the 80% (e.g. four of five)‘spontaneous remission’ rate reported by Nomura et 

al.1–4 When acute H. pylori gastritis involves the gastriccorpus, marked hypochlorhydria or achlorhydria isexpected.5–10 Proton pump inhibitors would not beexpected to be beneficial, based on antisecretory activ-ity. It is therefore unclear whether the symptomaticresponse reported was related to the therapy given, the

natural history of the disease, or both.The presumptionof the authors was that those patients with one daysymptoms would continue to have symptoms and belike the group that had them for 4–6 days.The differentpattern and duration of symptoms in the prospectivelyinfected individuals suggests that that presumptionmight not have been valid.

Although there are a number of publications, verylittle is known about the acute phase of H. pylori gas-tritis.5–26 This study shows that the prepared mind canprospectively identify some cases. Nevertheless, thespectrum of the initial presentation remains unknown.The presentation may depend on the inoculum size, thevirulence of the infecting strain of H. pylori , and/orundetermined host factors.The endoscopic findings inthis study included multiple erosions and or ulcers withfriable mucosa.These findings are suggestive of, but notspecific for acute H. pylori gastritis. The authors actu-ally evaluated 18 patients with a similar presentationand excluded eight patients (44%) because of evidenceof chronic H. pylori  infection (anti-H. pylori IgG posi-tive in seven) or negative culture and histology for H.

 pylori (in one patient).

See article on page 1377

Nomura et al. reported results of a prospective study of 

community acquired acute Helicobacter pylori gastritis.1

Patients underwent endoscopy because of a recentonset of upper gastrointestinal symptoms. The diagno-sis of acute H. pylori gastritis was suspected based uponendoscopic findings of acute mucosal damage (e.g. mul-tiple erosions, ulcers and friability). Histologic findingsshowed acute inflammation without a significantchronic inflammatory reaction. In each case H. pylori 

infection was confirmed by the use of a positive rapidurease test, as well as by culture and histology. AcuteH. pylori  infection was also suspected because of thepresence of infection in the absence of a postive im-munoglobulin (Ig)G serology for H. pylori antibodies.

The authors prospectively divided the patients into

two groups; those who presented within 24 h of symptom onset and those who presented 4–6 days aftersymptoms appeared. Those with an acute presentationwere randomized to receive either antimicrobial therapywith lansoprazole or lansoprazole alone. All patientswho presented after prolonged symptoms receivedantimicrobial and antisecretory therapy. There was arapid resolution of symptoms following the institutionof therapy. The authors attributed the response to thetherapy but as all patients received lansoprazole it isimpossible to exclude spontaneous remission. Treat-ment with lansoprazole plus antibiotics resulted in aresolution of the endoscopic finding within 1 week.However, lansoprazole alone did not accelerate thehealing of the endoscopic damage,because those receiv-ing lansoprazole alone had a similar course to those whopresented with symptoms several days before receivingantibiotic therapy. All patients had normal endoscopyby the third week.1

Four of the five patients who received only lansopra-zole had a ‘spontaneous’ clearing of the infection.Because one of the five patients (20%, 95% CI=1–72%) did not have a clearing of the infection, the

EDITORIAL 

Community acquired acute Helicobacter pylori gastritis

DAVID Y GRAHAM

Department of Medicine,Veterans Affairs Medical Center and the Departments of Medicine and Molecular 

Virology and Microbiology, Baylor College of Medicine, Houston Texas, USA

Correspondence: Dr DY Graham, Rm 3A-320 (111D), Veterans Affairs Medical Center, 2002 Holcombe Blvd., Houston,

Texas 77030, USA. Email: dgraham@bcm.tmc.edu

Accepted for publication 23 August 2000.

© 2000 Blackwell Science Asia Pty Ltd

8/12/2019 Community Acquired Acute Helicobacter Pylori Gastritis

http://slidepdf.com/reader/full/community-acquired-acute-helicobacter-pylori-gastritis 2/3

In our experience with feeding H. pylori  to normalvolunteers, approximately 70% developed dyspepsia,whereas no patient had abnormal gastric mucosa after2 weeks, despite them not receiving any therapy.27 Weused a cagA negative strain and yet all our patients hadan intense polymorphonuclear infiltrate in the gastric

mucosa. Whether cagA status is a critical determinantwith respect to the endoscopic finding is unknown.Eventually, prospective challenge studies using cagApositive and negative strains will provide a better insightwith regards to the spectrum of the initial manifesta-tions than are possible from studies in the community.

In the USA, it would be unlikely that any of thepatients presenting with the symptoms of acute H.pylori gastritis would have received an endoscopic evaluation.The criteria for the presumptive diagnosis of acute H.

 pylori  infection do not require endoscopy, but dorequire objective evidence of H. pylori  infection (e.g.[13C]-UBT positivity) and an absence of serum IgGantibodies to H. pylori . Most of the patients in the USA

and Japan who presented symptoms would most likelyhave received symptomatic therapy with an antisecre-tory drug. The data from the Nomura et al. studysuggest that a spontaneous cure may be common. If aspontaneous cure or cure related to the use of a protonpump inhibitor occurs commonly, it is unlikely that thecorrect diagnosis would be considered or confirmed. Inour local experience with children, over a 5-monthperiod, 52 children (aged less than 13 years) who pre-sented with acute upper gastrointestinal symptoms hada [13C]-UBT and H. pylori IgG serology.Twelve (21%)had a positive [13C]-UBT, but only three had positiveserology, suggesting that the results from Japan are notunique and deserve wider appreciation (MA Gilger and

AR Opekun, unpubl. obs., 2000).As with most studies, new information brings up asmany questions as it answers. Even when one is lookingfor acute H. pylori , it is uncommon even in a countrywith a high background prevalence of the infection. Onepresumes that only the tip of the iceberg was sampled.For example, why did these particular individualsdecide to come to the doctor after having symptoms foronly one day? How many patients who had symptomsfor one day would have had symptoms at 4–6 days?Do symptoms correlate with the extent, severity ortypographic distribution of endoscopic or histologicdamage? Where did they acquire the infection? Werethere any common characteristics in the week or twoprior to presentation? Was the infecting strain the sameas that of their spouse? One can list many more ques-tions illustrating how little we know and how muchthere is yet to learn.

In conclusion, one should suspect acute H. pylori when acute gastric mucosal damage (erosions andulcers) is not otherwise expected (e.g. chronic non-steroidal anti-inflammatory drug (NSAID) use). Apositive rapid urease test would clinch the diagnosis of H. pylori , but would not differentiate between acute H. pylori , chronic H. pylori  and other processes suchas syphilis, NSAID damage or an unknown disease.28

Nevertheless, most agree that the diagnosis of H. pylori infection should prompt therapy.The choice of therapyshould be based on which combination (drugs, doses,

1354   DY Graham

duration) provide the optimum results. The quest forthe shortest duration of therapy has resulted in an unac-ceptable rate of failures.29 In my opinion, the choiceshould be an antibiotic combination that is proven toprovide the best results in the population, taking intoaccount the local prevalence of antibiotic resistance.29

REFERENCES

1 Nomura H, Miyake K, Kashiwsagi S, Sugiyama T,

Asaka M. A short-term eradication therapy for Helicobac-

ter pylori acute gastritis. J.Gastroenterol.Hepatol. 2000; 15:

1377–81.

2 Graham DY, Genta R, Evans DG, Reddy R, Clarridge JE,

Olson CA, Edmonds AL, Siepman N. Helicobacter pylori 

does not migrate from the antrum to the corpus in

response to omeprazole. Am. J. Gastroenterol. 1996; 91:

2120–4.

3 Bravo LE,Realpe JL,Campo C, Mera R, Correa P. Effects

of acid suppression and bismuth medications on the per-formance of diagnostic tests for Helicobacter pylori  infec-

tion. Am. J. Gastroenterol. 1999; 94: 2380–3.

4 Connor SJ, Seow F, Ngu MC, Katelaris PH.The effect of 

dosing with omeprazole on the accuracy of the 13C-urea

breath test in Helicobacter pylori -infected subjects. Aliment 

Pharmacol.Ther. 1999; 13: 1287–93.

5 Hirschowitz BI, Streeten DHP, Londong WA   et al. A

steroid-induced gastric ulcer. Lancet 1956; 2: 1081–3.

6 Hirschowitz BI, Streeten DHP, Pollard HM. Role of 

gastric secretion in activation of peptic ulcers by corti-

cotropin (ACTH). JAMA 1955; 158: 27–32.

7 Epidemic hypochlorhydria [letter]. BMJ (Clin. Res. Ed).

1985; 291: 52–3.

8 Gledhill T, Leicester RJ, Addis B et al. Epidemic hypo-

chlorhydria. BMJ (Clin. Res. Ed). 1985; 290: 1383–6.

9 Ramsey EJ, Carey KV, Peterson WL et al. Epidemic

gastritis with hypochlorhydria. Gastroenterology 1979; 76:

1449–57.

10 Graham DY, Alpert LC, Smith JL,Yoshimura HH. Iatro-

genic Campylobacter pylori infection is a cause of epidemic

achlorhydria. Am. J. Gastroenterol. 1988; 83: 974–80.

11 Sobala GM, Crabtree JE, Dixon MF et al. Acute Heli-

cobacter pylori  infection: clinical features, local and sys-

temic immune response, gastric mucosal histology, and

gastric juice ascorbic acid concentrations. Gut 1991; 32:

1415–18.

12 Frommer DJ, Carrick J, Lee A, Hazell SL. Acute presen-

tation of Campylobacter pylori gastritis. Am.J.Gastroenterol.

1988; 83: 1168–71.

13 Rocha GA, Queiroz DM, Mendes EN, Barbosa AJ,

Lima J, Oliveira CA. Helicobacter pylori acute gastritis: his-

tological, endoscopical, clinical, and therapeutic features.

 Am. J. Gastroenterol. 1991; 86: 1592–5.

14 Mitchell JD, Mitchell HM, Tobias V. Acute Helicobacter 

 pylori infection in an infant, associated with gastric ulcera-

tion and serological evidence of intra-familial transmis-

sion. Am. J. Gastroenterol. 1992; 87: 382–6.

15 Takata T, Shirotani T, Okada M, Kanda M, Fujimoto S,

Ono J. Acute hemorrhagic gastropathy with multiple

shallow ulcers and duodenitis caused by a laboratory

infection of Helicobacter pylori . Gastrointest. Endosc. 1998;

47: 291–4.

8/12/2019 Community Acquired Acute Helicobacter Pylori Gastritis

http://slidepdf.com/reader/full/community-acquired-acute-helicobacter-pylori-gastritis 3/3

16 Moriai T, Hirahara N. Clinical course of acute gastric

mucosal lesions caused by acute infection with Helicobac-

ter pylori [letter]. N. Engl. J. Med. 1999; 341: 456–7.

17 Langenberg W, Rauws EA, Oudbier JH, Tytgat GN.

Patient-to-patient transmission of Campylobacter pylori 

infection by fiberoptic gastroduodenoscopy and biopsy. J.

Infect. Dis. 1990; 161: 507–11.18 Miyaji H, Kohli Y, Azuma T et al. Endoscopic cross-

infection with Helicobacter pylori [letter]. Lancet 1995; 345:

464.

19 Morris A, Nicholson G. Ingestion of Campylobacter 

 pyloridis causes gastritis and raised fasting gastric pH. Am.

 J. Gastroenterol. 1987; 82: 192–9.

20 Barbosa AJ, Queiroz DM, Mendes EN, Rocha GA,

Carvalho AS, Roquete ML. Campylobacter pylori associ-

ated acute gastritis in a child [letter]. J.Clin. Pathol. 1989;

42: 779.

21 Marshall BJ, Armstrong JA, McGechie DB, Glancy RJ.

Attempt to fulfil Koch’s postulates for pyloric Campy-

lobacter . Med. J. Aust. 1985; 142: 436–9.

22 Waterfall W. Spontaneous decrease in gastric secretoryresponse to humoral stimuli. BMJ 1969; 4: 459–61.

Community acquired acute H. pylori gastritis 1355

23 Wiersinga WM, Tytgat GN. Clinical recovery owing to

target parietal cell failure in a patient with Zollinger– 

Ellison syndrome. Gastroenterology 1977; 73: 1413–17.

24 Desai HG, Zaveri MP, Antia FP. Spontaneous and per-

sisting decrease in maximal acid output. BMJ  1971; 2:

313–15.

25 Desai HG, Antia FP. Spontaneous achlorhydria withatrophic gastritis in the Zollinger–Ellison syndrome.  Gut 

1969; 10: 935–9.

26 McIntyre RL, Irani MS, Piris J. Histological study of the

effects of three anti-inflammatory preparations on the

gastric mucosa. J. Clin. Pathol. 1981; 34: 836–42.

27 Graham DY, Opekun AR, Osato MS et al. Challenge

model for H. pylori  infection in human volunteers. Gas-

troenterology 1999; 116: A176 (Abstract).

28 Rank EL, Goldenberg SA, Hasson J, Cartun RW, Grey N.

Treponema pallidum and Helicobacter pylori recovered in a

case of chronic active gastritis [published erratum appears

in Am. J. Clin. Pathol. 1992; 97: 897]. Am. J. Clin. Pathol.

1992; 97: 116–20.

29 Graham DY. Therapy of Helicobacter pylori : current statusand issues. Gastroenterology 2000 (Suppl.); 118: S2–8.