helicobacter pylori and duodenal ulcer: guilty as...

ADULT INFECTIOUS DISEASE NOTES

Helicobacter pylori and duodenal ulcer: Guilty as

charged

A L TIIOUGII BOTTCHER FIRST OBSERVED SPIRAL BACTERIA IN the human stomach in 1874 (1). the s ignificance

of bacterial infection of the s tomach was largely ignored until the classic work of Warren and Marshall in 1982

(2). The organism they isola ted , named Campylobacier py loridis . is now known a s Helicobacter pylori (3). In the intervening 12 years, there has been a virtual explos ion of knowledge regarding the role of this bacterium in human disease and il is now accepted as a definite human pa thogen for a number of upper gastrointestinal disorders.

EPIDEMIOLOGY H pylori has been described worldwide. but higher

infection rates are seen in developing than in developed countries {4). Furthermore, persons in developing countries acquire infection a t earlier ages than do those in developed countries.

Although an environmen tal reservoir of infection has not been identified , there is considerable evidence implicating person to person transmission, including ou tbreaks from endoscopy equipmen t (5). As well. a lleasl in some third-world countries , there is evidence of waterbome transmission (6). A zoonotic reservoir is s uggested by higher seroprevalence ra tes in veterinarians (7) and abattoir workers (8) than in controls . Nevertheless, an animal res ervoir has not been identified. and preliminary evidence suggests tha t the prevalence of H pylori infection is s imilar in vegetarians and nonvegetarians (4).

ASSOCIATION WITH SPECIFIC GASTROINTESTINAL CONDITIONS

H pylori is undeniably the cause of hronic ·non specific' gastritis (4.9). a con dition located predomin a nUy in the gastric antrum. There is to dale no correla tion between H pylori infection and nonu lcer dyspepsia (4,8). There is clearly an increased risk of both adenocarcinoma and lymphoma of the stomach with H pylori infection {4,9). although the association does not appear to be causal.

There is strong evidence of causality for H pylori in peptic u lcer disease (4 .9 , 10). The correla tion between H pylor·i infection and duodenal u lcer (ou) is exceed ingly

C AN J INFECT D IS VOL 5 N o 6 N OVEMBER/D ECEMBER 1994

s trong, whereas th e correla tion with gastric ulcer (Gu) is impressive , but not n early as com pelling.

Approximately 95% of ou that are not cau sed by a nonsteroidal anti-inOa mma tory d rugs (NSAIDs) are as ocia led with H pylori infection. Furthermore. when ou is treated sole ly with H2 an tagonist therapy, there is a greater than 70% probability of recurrence within 12

months (11). which is reduced only about 50% by continuing H2 antagonist therapy (1 2) . In con trast, when ou treatm ent includes antimicrobial therapy to eradicate H pylori and wh ere su ch antimicrobial therapy is effective. the one-year relapse rate is less than 10% (4 .9. 10, 13).

The eviden ce linking H pylor i lo peptic u lcer d isease is s o compelling that even the staid United Slates Na tional Institutes of Health (NIII) has acknowledged this association and recommen ds con comitan t a n timicrobial thera py for pa tients with ou in associa tion with H py lori infection (10).

WHAT IS THE BEST REGIMEN FOR TREATING DUODENAL ULCER?

Both the Nll l consensus panel (10) and a recent Can adian report (14) recommen d the addition of a ntimicrobia l ther a py for patients with ou who have H pyl01i infection . However. sin ce at least 95% of patien ts wi th ou n ot pr cipitated by NSAID th erapy will be infected with H pylori. we believe that il is u nnecessary a n d n eedlessly expen s ive to test fo r the p resen ce of H p y lori infection in such individuals. Rather . a ll such individuals should be given antimicrobial therapy d irected against H pylori.

At present. there are inadequate data lo support treatmen t of ou with antimicrobial th erapy alone in the absence of acid-suppressing therapy, although one s tudy found combina tion antimicrobial therapy alone to be successful (15) . As far a s acid-suppressive thera py is concem ed. superior efficacy has been demonstrated with omeprazole plus antimicrobia l thera py compa red with H2 a n tagonists plus antimicrobia l thera py (16) .

The specific antimicrobial regimen and the optimal dura tion of thera py also remain lo be defined. The tra ditional a pproach has been to u se "triple thera py",

257

Infectious disease notes

using a combination of colloidal bismulh (which is nol availab le in Canada) wilh metronidazole a nd eilher tetracycl ine (BMT) or a moxicillin (BAM). These triple ther a py regimens have traditionally been given with ranitidine or another H2 b locker. but more recenlly have a lso been given together with omeprazole.

The optimal duration of treatment h as not been establi sh ed. but a two-week course of omeprazole plus amoxicillin (500 mg qid) is highly effective ( 16). Of interest. th e new macrolide clarithromycin. which has excellent in vitro activity against H pylori. has demons trated significant efficacy as a single agent for the treatment of H pylori infection (17.18) and good results in combination with omeprazole in the treatment of ou ( 19). Further studies of clarithromycin for the treatment of ou are ongoing.

CONCLUSIONS H pylori is now firmly accepted as an important

human pathogen and specifically lhe cause of the vast maj ority of cases of ou that are not due to NSAJD therapy. ll is now recognized thal proper treatment of ou r equires antimicrobial therapy to erad icate H pylori. because eradication of H pylori will markedly reduce the recurrence rate of ou and will obviate the need for long term an tisecretory th erapy in most individuals. Similar recommendations are probably prudent for GU, a lthough the data are less definitive . The optimal drug regimen has not been defined. but a two-week course of omeprazole plus amoxicillin is one effective and s imple regimen. There is inadequate evidence to recommend la rge popula tion screening and treatment for asymptomatic H pylori infection. a lthough this is a n important avenue of clinical research .

REFERENCES I. Blaser MJ. GastJic Campylobacler- like orga nisms .

gastritis. and peptic u lcer disease. Gastroenterology 1987:93:371-83.

2. Warren JR. Marshall B. Un identi fi ed curved bacilli on gastJic epitheli um in active chronic gastritis. Lancet 1983:i: 1273.

3 . Goodwin CS. Armstrong JA. Chilvers T. el a l. Transfer of CampyLobacter pyLori and CampyLobacter musteLae lo !-Ieticobacter gen nov as /-Ieticobacter pyLori comb nov and /-Ieticobacter musteLae comb nov . respectively. ln l J System Bacleriol 1989:39:397-405.

4. Hopkins RJ. Morris JG Jr. /-Ielicobacter pylori: lhe missing link in perspective. Am J Med 1994;97:265-77.

258

5. La ngenbergW. Rauws EAJ. OubierJl-1. e tal. Pa tienl-lo-patienl tra ns mission of CampyLobacter pyLori infection by fiberoptic gastroduodenoscopy and biopsy. J Infect Dis 1990: 16 1:507- 11.

6. Kle in PD. Gastrointestinal Physiology Working Group. Graham DY. el a l. Wa ter source as risk factor for /-Ielicobacter pylori infection in Peruvian children . Lancet 199 1:337 :1503-6.

7. Morris A. Nicholson G. Lloyd G. el a l. Seroepidemio!ogy of CampyLobacter pyloridis. NZ Med J 1986:99:657-9.

8. Va ira D. Hollen J. Londei M, et a l. Campylobacter pyLori in aballoir workers: is il a zoonosis? Lancet 1988; ii:725-6.

9 . Veldhuyzen van Zanlen SJO. Sherman PM. !-Ieticobacter pyLori infection as a cause of gastritis. duodenal ulcer. gastJic cancer and nonulcer dyspepsia: a systematic overview. Can Med Assoc J 1994. 150:177-85.

10. NIH Consensu s Development Panel. !-Ielicobacter pyLori in peptic ulcer d isease . JAMA 1994 :272:65-7 1.

11. Boyd EJS, Wilson JA. Wormsley KG. Recurrent u lcer disease. In: Misiesicz JJ. Wood JR. eds . Ranitidine: Therapeutic Advances. Amsterdam: Excerpla Medica . 1984:14:42.

12. Boyd EJS. Penston JG . Johnston DA. Wormsley KG . Does maintenance U1erapy keep duodenal ulce rs healed? Lancel1988;1:1324-7.

13. Forbes GM, Glaser ME. Cullen DJE, e l el. Duodena l ulcer treated with H eticobacter pyLori eradication : seven -year follow-up . Lancet 1994:343:258-60.

14. Veldhuyzen van Zanten SJO, Sherman PM. Indications for treatJnent of /-Ieticobacter pylori infection: a systematic overview. Can Med Assoc J 1994; 150:189-98.

15. Hosking SW, Ling TKW, Chung SCS, et a l. Duodenal u lcer healing by eradication of /-Ieticobacter pyLori without anti-acid treatJnent: randomised contJ·olled trial. Lancet 1994;343:508-10.

16. Labenz J. Gyenes E . Ri.ihl GH, Borsch G. Amoxicillin plus omeprazole versus triple therapy for eradication of !-Ieticobacter pyLori in duodenal ulcer disease: a prospective, randomized, and cont.rolled study. Gul 1993;34:1167-70.

17. Graham DY, Opekun AR, Klein PD. Clarith.romycin for lhe era dication of Heticobacter pylori. J Clin Gastroenterol 1993; 16:292-4.

18. Peterson WL, Graham DY, Marshall B. et al . Cla.rithromycin as monotherapy for eradication of Helicobacter pyLori: a randomized. double-band trial. Am J Gastroenterol 1993:88:1860-4.

19. Logan RPH, Gummell PA, Schaufelberger HD. e l a l. Eradication of /-Ieticobacter pylori with clarith romycin a nd omeprazole . Gu l 1994:35:323-6.

SO Shafran MD FRCPC

Edmonton, Alberta JM Conly MD FRCPC

Toronto, Ontario

CAN J INFECT DIS VOL 5 N o 6 N OVEMBER/DECEMBER 1994

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