gastrostomy. I would like to report three recent cases of ad­verse effects after insertion of the Bard gastrostomy button.The procedure was planned in advance. All three patientshad a conventional Bower 20F gastrostomy tube (BowerPEG, E. Merck Ltd., Hampshire, u.K.) inserted 2 monthsbefore the change to the Bard 18F gastrostomy button (BardLtd., Essex, u.K.). The procedure was carried out success­fully and uneventfully in each case. However, in one of thesecases, the button had to be removed within 72 hours becauseinfusion through the button caused intense pain. Subse­quent contrast radiologic examination failed to show anycommunication between the button and the gastric lumen.Fortunately, the patient was never harmed by the mishap.After the event, he preferred his old fine-bore nasogastrictube to another Bower gastrostomy tube. The other twocases were complicated by severe contact dermatitis, prob­ably the result of reflux of gastric juice around the looselyfitted gastrostomy button stem. Further damage could notbe prevented by regular administration of an H2 antagonistand metoclopamide. A variety of barrier creams failed toprotect the peri-stomal area. Both patients had a great dealof pain and discomfort and eventually requested to havetheir button removed and changed back to the Bower 20Fgastrostomy device via the same tract. Their contact derma­titis healed, and they have now been followed-up for morethan 3 months without further problem.

As far as I am aware, the Bard gastrostomy button onlycomes in three sizes, the 18F, 24F, and 28F. The latter twoare obviously too big for the fistula tract created by a 20Ftube. Therefore, I have always chosen the smaller size but­ton to replace the usual Bower 20F gastrostomy tube, whichhappens to be my favorite device. Although these three ad­verse events were unpleasant, they did not deter my furtherefforts because most other patients had in fact benefitedfrom the skin level gastrostomy device. I totally agree withShike's advice that safety should come before simplicity.After all, the procedure is aimed at improving and notadversely affecting the patient's quality of life. In view of the"acid reflux" problem that I have encountered, I would urgethe company that produces the gastrostomy button to man­ufacture a wider range of sizes that would accommodate thedifferent kinds ofgastrostomy tubes available on the market.

Chi K. Ching, MDCity Hospital

Nottingham, United Kingdom

REFERENCES1. McQuaid KR, Little TE. Two fatal complications related to

gastrostomy "button" placement. Gastrointest Endosc 1992;38:601-3.

2. Shike M. Safety first, simplicity second [Editorial]. GastrointestEndosc 1992;38:628-9.

Does gastro-duodenal dyspepsia correlatewith (neutrophilic) gastro-duodenitis?

To the Editor:

Correlating symptoms with histologic gastro-duodenitis isdifficult because of multiple variables, and, as a result, theliterature abounds with controversial results. I would like to

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discuss the method of study and the findings in the recentarticle by Schubert et aLl

The authors address my hypothesis that non-ulcer dys­pepsia is a result of an "active" gastritis (neutrophilic infil­trate). They conclude that their findings fail to substantiatethis concept because their study demonstrates that, contraryto the "DeLuca hypothesis," no greater incidence of symp­toms occurred with "active" gastritis as compared to pa­tients with normal histologic findings or with chronic gastri­tis. The study is well conducted, with a listing of clinical andhistologic criteria, and a large population base of 474patients. I would like to comment on their symptom criteria,their histologic classification, and their histologic results.

The bases for my hypothesis were the findings resultingfrom the study of patients with dyspepsia performed in the1970s2,3 and the additional findings resulting from an ongo­ing study of the same population, the preliminary results ofwhich were published in a recent abstract.4 In our originalstudy we separated symptoms from the esophagus fromthose of the stomach and duodenum. The latter were givenin more detail and divided into classic and atypical-like ul­cer symptoms.2, 3 In our recent publication4 we placed thelatter group of symptoms in a category we introduced called"gastro-duodenal dyspepsia." Patients placed in this cate­gory have symptoms most likely attributable to the stomachand duodenum, and usually can be separated from thosearising from other gastrointestinal organs, for example, theesophagus or colon. The Schubert division of epigastric pain,separate from esophageal symptoms, is good, but I do notbelieve that only one symptom, epigastric pain,5 is sufficientto categorize the group with classic ulcer-like symptoms.Most of the remainder of his symptoms do fit into our atyp­ical category of gastro-duodenal dyspepsia.

Schubert's classification of gastritis with Helicobacterinfiltration is not unlike our classification; however, althoughthey do score Helicobacter pylori by 0, 1 and 2, there is nodegree of scoring of the gastritis classification. One can onlypresume that a correlation exists between grades of Helico­bacter pylori infiltration and grades of neutrophilic invasion.The lack of gastritis scoring makes it difficult to relate dys­pepsia with degree of "active" gastritis. In our recent study4we also introduced the term "neutrophilic gastritis" toreplace the terms "active" and "acute" and the terms "lym­phoplasmacytic" gastritis to replace the term "chronic." Us­ing the cell type to classify inflammatory gastritis is morespecific, tells us exactly what is happening histologically, andis better than using terms that often have multiple connota­tions.

A major criticism of Schubert's study is that the correla­tion of symptoms to histologic findings is limited only to an­tral biopsies, excluding the possibility that these patientsmay have inflammation (neutrophilic or lymphoplasma­cytic) of the fundus or duodenum as possible causes ofsymptoms. In our original study,l we did correlate symptomswith biopsies of the fundus, antrum, and duodenum (Table1). It is clear from our results that the correlation of classiculcer symptoms with the endoscopic diagnosis of peptic ul­cer is excellent. However, the correlation of symptoms withhistologic inflammatory types of gastritis, although best forthe neutrophilic forms, still remains unimpressive. The pre­liminary results of our follow-up study of these patients overthe past 12 years showed a similar relationship.4

GASTROINTESTINAL ENDOSCOPY

Modified from Greenlaw et al. Dig Dis Sci 1980;25:660-72

Table 1.Correlation of symptoms with histologic gastritis

Gastroduodenal dyspepsia

EndoscopicPeptic ulcer 25 96 4

(duodenal/gastric)Histologic

Acute (neutrophilic) 39 64 36gastro-duodenitis

Chronic (lymphoplas- 20 50 50macytic) gastro-duodenitis

Normal 12 8 92Excluded 4

The impressions gained from these studies resulted in thehypothesis of "no acid, no polyps-no active gastritis, nodyspepsia."2 The hypothesis presented in this paper,2 Iagree, requires additional study before it can be consideredas more established fact. In future studies testing thishypothesis, more conclusive correlations will be obtained ifinvestigators are more specific about identifying symptomsmost attributable to the stomach and duodenum, andexclude esophageal dyspepsia and irritable bowel syndrome(flatulence, for example). In addition, there should be a moredetailed description of histologic findings. The type ofinflammation, neutrophilic or lymphoplasmacytic, should bespecified, and the degree of inflammation, for example, 0, 1,2 or 3, should be estimated. Most importantly the fundus, theantrum, and the duodenum, should be involved in attemptsto correlate histologic findings with gastro-duodenal dys­pepsia.

Timothy SchubertTacoma, Washington

tial finding of our study was that acute (neutrophilic) gastri­tis and high-grade Helicobacter pylori were as common inpatients endoscoped for esophageal dysphagia or non-ulcergastrointestinal bleeding as in patients with "gastro-duode­nal-dyspepsia" and failed to correlate with particular symp­toms of "gastro-duodenal-dyspepsia" any more stronglythan with symptoms of esophageal dyspepsia of irritablebowel syndrome. I

Several issues raised by Dr. DeLuca require further clar­ification. Among patients with epigastric pain Dr. DeLucaappears to be able to distinguish by symptoms those withulcers and those without. We found the opposite. Amongpatients referred for endoscopy with epigastric pain wefound only male gender and prior history of ulcer predictorsof ulcer presence.2Symptoms were useful only in that thosewith "esophageal dyspepsia" had a low risk of ulcers. Noparticular symptom of "gastro-duodenal-dyspepsia" corre­lated with ulceration.

We previously have shown a correlation between antralHelicobacter pylori concentration and grade of neutrophilicinfiltration.3 Similar grading of neutrophilic infiltration andgrading of symptom severity was performed for our studypopulation, and review of that data shows that no correlationexists. For this study we chose antral biopsies because inmost instances non-autoimmune gastritis inflammation ismost severe in the antrum.

It is clear that further studies, especially blinded treat­ment trials with long-term follow-up, are necessary toestablish definitively whether Helicobacter pylori and neu­trophilic gastritis cause non-ulcer dyspepsia. Nevertheless,our findings suggest the answer to non-ulcer dyspepsia liessomewhere other than with neutrophilic gastritis and Heli­cobacter pylori.

REFERENCES

Atypicalulcer(%)

Classiculcer(%)

No. of Patients

Vincent A. DeLuca, Jr., MDGriffin Hospital

Derby, Connecticut

REFERENCES1. Schubert T, Schubert A, Chan K. Non-ulcer dyspepsia, gastri­

tis, and Helicobacter pylori in patients referred for endoscopy.Gastrointest Endosc 1992;38:357-60.

2. Greenlaw R, Sheahan DG, DeLuca VA, et al. Gastroduodenitis:a new concept: clinical pathological correlation [Abstract]. Gas­troenterology 1976;70:891.

3. Greenlaw R, Sheahan DG, DeLuca VA, Miller D, Myerson D,Myerson P. Gastro-duodenitis: a broader concept of peptic ul­cer disease. Dig Dis Sci 1980;25:660-72.

4. Haque S, Ciarolla D, Wain S, DeLuca V Jr. Helicobacter pylori:the stomach and progression of gastritis: a 14-year follow-up[Abstract]. Gastroenterology 1992;102:A79.

5. Talley NJ, McNeil D, Piper DW. Discriminate value of dyspep­tic symptoms: a study ofthe clinical presentation of 221 patientswith dyspepsia of unknown cause, peptic ulceration, and chole­lithiasis. Gut 1987;28:40-6.

Response

We greatly appreciate Dr. DeLuca's interest in our article,and he makes a number of cogent observations. The essen­VOLUME 39, NO.3, 1993

1. Reference 1 above.2. Schubert T, Bologna S, Schubert A, Mascha E, Ma C. Ulcer risk

factors interactions between Helicobacter pylori infection,nonsteroidal use and age. Am J Med 1993, in press.

3. Alam K, Schubert T, Bologna S, Ma C. Increased density ofHelicobacter pylori on antral biopsy is associated with severityof acute and chronic inflammation and likelihood of duodenalulceration. Am J Gastroenterol 1992;87:424-8.

Effect of intravenous erythromycin ongastric emptying

To the Editor:

We read with interest the letter to the editor by Chaussadeet al. l that described patients with idiopathic or diabeticgastroparesis in whom there was presence of retained food atendoscopy. A 150-mg dose of intravenous erythromycin af­fected rapid emptying of the stomach as evaluated on a fol­low-up endoscopy performed promptly after the erythro­mycin was given.

We would like to describe the case of a 42-year-old manwho had a Billroth I gastrectomy performed in 1980 for re­fractory peptic ulcer disease, recurrent episodes of gastricbezoar formation, and episodes of reflux. The patient hadnausea and worsening of reflux symptoms and underwent an

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