LETTERS TO T H E EDITOR degree of acid suppression for healing of duodenal ulcers? Gastroenterology 99:345-351, 1990 5. Dubois A: Gastric emptying of liquids should not be studied independently from gastric secretion. In Functional Disorders of the Gastrointestinal Tract. W Chey (ed). New York, Raven Press, 1983, pp 151-155 6. Fortran JS, Walsh JH: Gastric acid secretion rate and buffer contents of the stomach after eating results in normal subjects and in patients with duodenal ulcer. J Clin Invest 52:645-657, 1973 7. Halter F, Keller M: A comparison between intragastric titration and gastric aspiration under basal conditions and after food or pentagastrin stimulation. Am J Dig Dis 23:723729, 1978 8. Feldman M: Comparison of acid secretion rates measured by gastric aspiration and by in vivo intragastric titration in healthy human subjects. Gastroenterology 76:954-957, 1979 9. Dubois A, Van Eerdewegh P, Gardner JD: Gastric emptying and secretion in Zollinger-Ellison syndrome. J Clin Invest 59:255-263, 1977 10. Go VLW, Hoffman AF, Summerskill WHJ: Simultaneous measurements of total pancreatic, biliary, and gastric outputs in man using a perfusion technique. Gastroenterology 58:321-328, 1970 11. Malagelada JR, Longstreth GF, Summerskill WHJ, Go VLW: Measurement of gastric functions during digestion of ordinary solid meals in man. Gastroenterology 70:203-210, 1976 12. Dubois A: Methods for studying propulsion and retropulsion of the alimentary tract contents. In Techniques in the Life Sciences. DA Titchen (ed). Amsterdam, Elsevier North Holland, 1982, p 202/1-18 13. Dubois A, Natelson BH, Van Eerdewegh P, Gardner JD: Gastric emptying and secretion in the rhesus monkey. Am J Physiol 232:EI86-E192, 1977 14. Batzri S, Harmon JW, Dubois A, Moskowitz D, Weichbrodt R, Rich NM: A new in vivo method for repeatedly studying gastric acid secretion and other secretory parameters in awake guinea pig. J Surg Res 43:398-405, 1987 15. Dorval ED, Mueller GP, Eng RR, Durakovic A, Conklin JJ, Dubois A: Effect of ionizing radiation on gastric secretion and gastric motility in monkeys. Gastroenterol 89:374-380, 1985 16. Hyman PE, Abrams C, Dubois A: Effect of metoclopramide and bethanechol on gastric emptying in infants. Pediatr Res 19:1029-1032, 1985 17. Dubois A, Castell DO: Abnormal gastric emptying response to pentagastrin in duodenal ulcer disease. Dig Dis Sci 26:292-296, 1981 18. Sasaki H, Nagulesparan M, Samloff IM, Straus E, Sievers ME, Dubois A: Low acid output in Pima Indians: A possible cause for the rarity of duodenal ulcer in this population. Dig Dis Sci 29:785-789, 1984 19. Cherner JA, Jensen RT, Dubois A, O'Dorisio TM, Gardner JD, Metcalfe DD: Gastrointestinal dysfunction in systemic mastocytosis. A prospective study. Gastroenterology 95:657-667, 1988


AUTOIMMUNE GASTRITIS: IS Helicobacter pylori A M E R E L Y C O M M E N S A L O R A PATHOGENIC AGENT? To The Editor: We h a v e read with great interest the p a p e r by O r m a n d et al (1) regarding the p r e v a l e n c e of Helicobacter pylori in s o m e specific f o r m s of chronic gastritis (ie, eosinophilic, C r o h n ' s , and M e n e t r i e r ' s gastritis). N o n e of the patients with specific f o r m s o f gastritis s h o w e d evidence o f H. pylori infection c o m p a r e d with the 71% o f the patients with chronic nonspecific gastritis. The authors concluded that the results o f the study " a d d further support to the accumulating evidence that H. pylori plays a pathogenic role in chronic nonspecific gastritis." To determine the p r e v a l e n c e of H. pylori in a further f o r m of specific chronic gastritis, we h a v e evaluated 16 patients (4 males and 12 females; m e a n age 64 years, range 5 5 - 8 0 years) with a u t o i m m u n e gastritis. All patients w e r e diagnosed as having a u t o i m m u n e gastritis on the basis of the p r e s e n c e o f p a r i e t a l cell a n t i b o d i e s , p e n t a g a s t r i n - r e s i s t a n t achlorhydria at gastric analysis, and diffuse fundal a t r o p h y by histological examination in repeated multiple biopsies; no hematological findings consistent with pernicious anemia w e r e detected. E a c h patient u n d e r w e n t u p p e r gastrointestinal endoscopy, and multiple biopsies in fundus, body, and antrum were m a d e (mean four samples, range three to five, in each region) b y separate sterile forceps. Histological specimens were stained with h e m a t o x ylin-eosin to study gastritis and with G i e m s a to search for H. pylori. Twelve patients were found to b e infected b y H. pylori. Biopsies f r o m fundus and b o d y showed the p r e s e n c e of H. pylori in both regions in all cases. The examination of the biopsies f r o m antrum detected chronic atrophic gastritis with H. pylori infection in seven cases and superficial gastritis in the remaining five patients, two of w h o m also showed H. pylori infection. In the four H. pylori-negative patients, the antral specimens revealed chronic atrophic gastritis in two and superficial gastritis in the other two patients. The results are s u m m a r i z e d in Table 1. The results of this study on H. priori infection in a u t o i m m u n e gastritis patients confirm those previously reported b y us in a smaller series (2), showing a p r e v a l e n c e of about 70%. Other authors described a lesser infection rate ranging f r o m 3 to 21% (3-6), nevertheless some others reported a p r e v a l e n c e Digestive Diseases and Sciences, Vol.37, No. 8 (August 1992)


Patients (N) H. pylori + pts Superificial gastritis Atrophic gastritis



16 12

16 12

16 (12)

16 (12)


16 9 7 (2) 9 (7)

*Numbers in parentheses are relative number of H. pyloripositive patients with antral superficial or atrophic gastritis.

similar to ours (7). The reasons for this wide distribution of prevalence is still unclear, even if subgroups with different diatheses to infection and possible underestimation of the bacterium due to patchy localization (the detection relating with the biopsy number) are to be considered. In the majority of our autoimmune gastritis patients, H. pylori was found to colonize fundic and body atrophic mucosa. It is widely accepted that the atrophy in these gastric sites is induced by specific autoantibodies. Consequently, the H. pylori in these regions seems to be interpreted as a merely commensal. It is more difficult to try to establish the role of the organism in this type of patient with antrum affected by gastritis (superficial in two cases and atrophic in seven), the cause of which is not yet well defined. Taking into consideration that H. pylori has been recognized, even if not universally, to play an etiological role in the development of chronic nonspecific antral gastritis (type B) (8), it is reasonable to suggest that the pathological involvement of the antrum in these patients might be the result of H. pylori infection. Whether our data will be supported in a larger series of patients, H. pylori could be thought of as playing a double role. G. CARIANI, MD A. VANDELLI, MD G. FONTANA, MD

Department of Emergency Medicine St. Orsola Hospital Bologna, Italy G. BONORA, MD

Department of Internal Medicine and Gastroenterology St. Orsola Hospital Bologna, Italy G. MAZZOLENI, MD

Department of Pathology St. Orsola Hospital Bologna, Italy Digestive Disease~ and Sciences, Vol. 37, No. 8 (August 1992)

REFERENCES 1. Ormand JE, Talley NJ, Shorter RJ, Conley CR, Carpenter HA, Fick A, Wilson WR, Phillips SF: Prevalence of Helicobacter pylori in specific forms of gastritis. Further evidence supporting a pathogenic role for H. priori in chronic nonspecific gastritis. Dig Dis Sci 36:142-145, 1991 2. Vandelli A, Cariani G, Bonora G, Mazzoleni G, Fontana G: Type A chronic atrophic gastritis: Antral involvement and Helicobacter-like organisms status. Gastroenterology 100:A179, 1991 3. Fong T-L, Dooley CP, Dehesa M, Cohen H, Carmel R, Fitzgibbons P, Perez-Perez GI, Blaser MJ: Helicobacter pylori infection in pernicious anemia: A prospective controlled study. Gastroenterology 100:328-332, 1991 4. O'Connor HJ, Axon ATR, Dixon MF: Campylobacter-like organisms unusual in type A (pernicious anemia) gastritis. Lancet 2:1091, 1984 (letter) 5. Gonzales JD, Sancho FJ, Siantz S, Such J, Fernandez M, Mones Xiol J: Campylobacter pylori and pernicious anemia. Lancet 1:57, 1988 (letter) 6. Flejou J-F, Bahame P, Smith AC, Stockbrugger RW, Rode J, Price AB: Pernicious anemia and Campylobacter-like organisms: Is the gastric antrum resistant to colonization? Gut 30:60-64, 1989 7. Faisal MA, Russel RM, Samloff IM, Holt PR: Helicobacter pylori infection and atrophic gastritis in the elderly. Gastroenterology 99:1543-1544, 1990 (letter) 8. Dooley CP, Cohen H: The clinical significance of Campylobacter pylori. Ann Intern Meal 108:70-79, 1988


To The Editor: We read with interest in the January issue the review article and a report on antroduodenal manometry by Dr. E.M.M. Quigley and his colleagues (1, 2). While agreeing with several points that Dr. Quigley makes, we feel that additional comment may place some of his remarks in better perspective for your readers. Thus, our experience covers I5 years of research in manometry of the upper gut, and l0 years and 2000 clinical studies of gastroduodenojejunal manometry. Firstly, regarding the report of his own work (2). We were struck with the variable technical success among the different patient subgroups. Unsuccessful intubation in 38% of healthy controls is most unusual, even if these persons were "tube-naive." From our own rather considerable experience with these techniques, 10% or less failures would be an acceptable figure. On the other hand, Quigley achieved success to this degree (90%) in a population that is not always tolerant of intubation, namely patients with irritable bowel syndrome. It would be of interest to know in what sequence the subjects were studied by his coworkers. Not only is


Autoimmune gastritis: is Helicobacter pylori a merely commensal or a pathogenic agent?

LETTERS TO T H E EDITOR degree of acid suppression for healing of duodenal ulcers? Gastroenterology 99:345-351, 1990 5. Dubois A: Gastric emptying of...
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