gastric ulcer and gastritisgastric ulcer andgastritis gastritis was recorded when the changes were...

Gut, 1971, 12, 639-645

Gastric ulcer and gastritisM. W. L. GEAR1, S. C. TRUELOVE, AND R. WHITEHEAD

From the Nuffield Department of Clinical Medicine and The Department of Morbid Anatomy, RadcliffeInfirmary, Oxford

SUMMARY The gastritis associated with chronic gastric ulcer has been studied by means of biopsyspecimens taken under vision through a fibreoptic gastroscope from four standard sites in thestomach. Observations have been made in patients with untreated gastric ulcer and also in patientsafter medical or surgical treatment of the ulcer. The gastritis is usually widespread in chronic pepticulcer of the body of the stomach, whereas it is commonly more localized in chronic prepyloric ulcer.Superficial or atrophic gastritis has been found to persist or even worsen after healing of the ulcer,whether the treatment was medical or surgical. This finding suggests that gastritis is the basic diseaseprocess and that gastric ulceration is a secondary phenomenon.

Gastric ulcer is frequently associated with chronicgastritis but the relationship between the two iscontroversial. On the one hand, there have beenstudies suggesting that the gastritis is the primarychange with the gastric ulcer supervening (Faber,1935; Hebbel, 1943; Magnus, 1946; Hebbel, 1949;Magnus, 1952). On the other hand, there are studieswhich suggest that the ulcer is the primary lesionand that the gastritis is a zonal change around it(Schindler, 1947; Palmer, 1954; Joske, Finckh, andWood, 1955).The methods employed in all these studies are

open to criticism. Necropsy studies, even when per-formed with fixation immediately after death, are notideal because of agonal changes and autolysis.Gastrectomy specimens suffer from two disadvan-tages: first, only the distal segment of the stomach isavailable for examination and, secondly, operativemanoeuvres have been shown to cause inflammatorychanges in the gastric mucosa (Schindler, Necheles,and Gold, 1939; Sanders and Mecray, 1941). Peroralbiopsy specimens obtained by a Wood's tube orsimilar instrument suffer from the severe dis-advantage that there is little control over the loca-tion of the biopsy site. Radiological examinationhas shown that the biopsy tube usually runs fromthe oesophagus to the greater curve of the stomach,so that the biopsy specimen comes from the greatercurve or close to it. Pyloric mucosa is seldomobtained (Macdonald and Rubin, 1967).The most recent fibreoptic gastroscopes incor-

Received for publication 18 May 1971.'Present address: Gloucestershire Royal Hospital, Southgate Street,Gloucester.

porate facilities for taking multiple biopsy specimensunder direct vision from any part of the stomach.Such an instrument provides the means of studyingthe relationship between gastritis and gastric ulcerin a manner which eliminates most of the objectionsto earlier methods of study. Previous methods ofgastroscopic biopsy, such as those of Kenamore(1940), Benedict (1948), and Hancock and Shiner(1958), suffered from various disadvantages whichprevented their general adoption. In the presentseries we have used the Olympus GFB gastroscopeto make a systematic study of the gastritis associatedwith gastric ulcer.Patients

Ninety-five patients were studied; 35 patients withuntreated chronic gastric ulcer, 19 patients who hadbeen treated medically, 28 who had been treated byvagotomy and pyloroplasty,and 13 treated by partialgastrectomy.The incorporation of facilities for taking biopsy

specimens under vision through a fibreoptic gastro-scope was a new development when the present studybegan. The actual taking of the specimen requiressome skill and experience. For these reasons, in theearly stages, biopsy specimens were obtained fromonly two sites apart from the ulcer itself. As pro-ficiency developed and the safety of this techniqueof gastroscopy with biopsy was demonstrated inover 400 examinations without complication, it wasdecided to obtain biopsy specimens from fourstandard sites. The great majority of the patientsincluded in the present series were examined in thisway.

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Methods

GASTROSCOPY WITH BIOPSYAt gastroscopy, a methodical survey of the stomachwas made. On gastroscopic criteria the gastricmucosa was judged to be normal or to show super-ficial or atrophic gastritis. When the gastritis ap-peared to be zonal or patchy, a description of itsdistribution within the stomach was recorded. If agastric ulcer was seen, photographs were taken andthen cytological and multiple biopsy specimens wereobtained from the ulcer margin to exclude malig-nancy (Gear, Truelove, and Williams, 1969).

Biopsy specimens were then obtained from fourstandard sites (Fig. 1). These were: (1) the pre-pyloric region; (2) the middle of the lesser curve justproximal to the incisura; (3) high on the lesser curveabout 1 inches distal to the cardia, and (4) on themiddle of the greater surve at a point opposite thesite of the mid-lesser curve biopsy.

Usually two specimens were obtained from eachsite to ensure having adequate tissue for histologicalexamination.

In order to view the fundal area fully, the patientwas turned into the right lateral positioIn.

Prepyloric Mid lessercurve

Fig. 1 The four standard biol

HISTOLOGYThe gastric biopsy specimeand the four standard sitesto the methods described b

M. W. L. Gear, S. C. Truelove, and R. Whitehead

biopsy specimens were examined again, on thisoccasion 'blind', the pathologist being unaware ofthe name of the patient, the type of treatment, andthe site of the biopsy. The results of the two separategradings for each biopsy correlated almost perfectly.The result of the second examination was taken as themore reliable, as on this occasion all the biopsyspecimens were examined consecutively over a periodof a few days.

TYPES OF MUCOSAL APPEARANCE RECORDEDNormal gastric mucosaThe mucosa was taken to be normal when none ofthe changes described below were seen.

Chronic superficial gastritisIn this grade there is a plasma cell and lymphocyteinfiltrate in the superficial layer of the gastric mucosa.Eosinophils and neutrophils in small numbers arealso seen. There are no histological changes in theepithelium of the glands, but the superficial epith-elium and the epithelium lining the pits frequentlyshows evidence of damage. There is often a loss ofPAS-positivity, the cells appearing flattened andbasophilic and their nuclei somewhat pleomorphic,pyknotic, and palisaded. Occasionally, patches ofintestinal metaplasia were seen in a mucosa whichotherwise showed no signs of atrophic changes.

Chronic active superficial gastritisThis shows similar appearances to those graded as'chronic superficial gastritis', but the cellularinfiltrate is denser and includes a high percentageof polymorphonuclear cells. These acute inflam-matory cells are seen invading and apparently'destroying' the surface epithelium and the epith-elium lining a proportion of the gastric pits.

Chronic atrophic gastritisWhen fully developed the gastric mucosa is de-

Body greater creased in thickness and there is a chronic inflam-gcurve curve matory cell infiltrate involving the whole thickness

Dsy sites of the lamina propria. The superficial epitheliummay show changes similar to those in chronic super-ficial gastritis. There is also atrophy of glands,whether these are of body or pyloric type. Some-times the specialized glands of the body mucosa

.ns from the ulcer edge are replaced by shorter simple tubes lined by awere handled according low columnar epithelium of a simple mucus-yy Whitehead, Gear, and secreting type (pseudopyloric metaplasia).

Truelove (1971).The histological preparations of all the gastric

biopsy specimens (over 500 in all) were examined byone of us (R.W.) and graded according to the scaleoutlined below. The report was filed in the patient'scse notes in the usual way. Some time later all the

Mild, severe, and moderate atrophic gastritisMild atrophic gastritis was recorded when theatrophic changes were slight. Severe atrophicgastritis was recorded when virtually all the normalgland arrangement was lost. Moderate atrophic



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gastritis was recorded when the changes wereintermediate.Intestinal metaplasiaIntestinal metaplasia was recorded quite independ-ently of the degree of gastritis. The epithelium is ofintestinal type with a brush border, and includesgoblet cells and sometimes Paneth cells.Although intestinal metaplasia is almost always

associated with the changes of atrophic gastritis thisis not invariable and this feature has therefore beenconsidered separately.

In some biopsy specimens, mucosa was seen whichwas indistinguishable from the gastric mucosalatrophy seen in pernicious anaemia, with little or noinflammatory infiltrate and with complete intes-tinalization. However, as this was an uncommonfinding, such specimens were classified as showing'severe atrophic gastritis'.Thus, in summary, three separate decisions were

taken about each gastric biopsy: (1) the mucosaltype-antral or body (in severe atrophic gastritisthis was sometimes not possible); (2) the grade ofgastritis; and (3) the presence or absence of intes-tinal metaplasia. The classification of gastritis isdiscussed in greater detail by Whitehead et al (1971).

MEDICAL TREATMENTThe patients in this group were treated conven-tionally with antacids (and carbenoxolone sodiumin some cases) until the symptoms abated andimprovement in the barium meal appearancesoccurred. A few patients in this group were takingpart in a therapeutic trial of an antipepsin compound(Depepsin or SN263).

SURGICAL TREATMENTVagotomy and pyloroplastyMost of the patients treated during this study wereoperated on by one of two surgeons (Mr B. L.Dowling or M.W.L.G.) using an identical techniqueas far as possible. The gastric ulcer was exposed,either through the pyloroplasty incision or througha separate gastrotomy, and wedge segments of theulcer edge were excised and sent for immediatefrozen section histology in order to confirm thebenign nature of the lesion. Either a selective or atruncal vagotomy was then performed, the choiceof procedure being determined randomly. AHeineke-Mikulicz pyloroplasty was always per-formed. The operation was completed by closing thepyloroplasty in two layers, using catgut sutures.Postoperative management was conventional, thepatient usually being allowed home on a normaldiet 10-14 days after operation.The patients treated four or more years earlier

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had been operated on by a variety of surgeons, butin every case a vagotomy and pyloroplasty had beenperformed for gastric ulcer.

Partial gastrectomyThe operation varied somewhat in this group, butin all except two patients, a Billroth I gastrectomywas performed with removal of about half thestomach and gastroduodenal anastomosis. In somecases a vagotomy was added. In two patients, a moreextensive resection necessitated a Polyatype ofgastro-jejunal anastomosis.

Results

GASTRITIS IN UNTREATED GASTRIC ULCERThe 35 patients with untreated gastric ulcer con-sisted of 23 males and 12 females, whose age rangedfrom 26 years to 81 years, with an average of 55years. The length of history varied widely from a fewweeks to many years.

Findings at gastroscopyThe ulcer was well seen in all patients in this seriesand was judged to be benign in appearance. The sizeof the ulcer was judged roughly by using the biopsyforceps or cytology brush as a scale at the side of thecrater when viewed through the gastroscope. Mostprepyloric ulcers were small, about 0.5 to 1 cm indiameter. Ulcers in the body of the stomach weremuch more variable in size, ranging from 1 cm up tolarge craters 3 to 4 cm in diameter.Most of the patients with ulcers in the body of

the stomach showed the changes of superficial oratrophic gastritis (or both) at gastroscopy, whilepatients with prepyloric ulcers often had normalmucosa in the proximal half of the gastric mucosa.The question of the correlation between the

gastroscopic appearances of gastritis and the histo-logical changes in the biopsy specimens is discussedin more detail below.

HistologicalfindingsTwenty-eight (80%) of the 35 patients studied hadone or more biopsy specimens showing atrophicchanges in some degree. The other seven patientsall had at least one biopsy showing superficialgastritis, so no patient in the series had an entirelynormal gastric mucosa.Only two (6%) patients of the 35 studied had the

same grade of gastritis in all four biopsy specimens.In the remainder, there was wide variation from onebiopsy to another, with a tendency for the moresevere atrophic changes to be found distally in theantrum and on the lesser curve, while the greatercurve was least affected.



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Intestinal metaplasia was most commonly seen inbiopsy specimens with severe atrophic gastritis, butfour examples of metaplasia occurred in associationwith superficial gastritis. In general, the distributionof metaplasia in the stomach followed that ofmoderate and severe atrophic gastritis.

Fifty-four per cent of prepyloric and 31 % of mid-lesser curve biopsy specimens showed metaplasia,while only 85% of higlh lesser curve and 11 % ofgreater curve biopsies showed the changes.There were 14 prepyloric (or antral) ulcers, and

21 ulcers in the body of the stomach in the group of35 patients studied. There was a marked differencein the distribution and severity of the gastritis seenwith these two sites of gastric ulcer. In general, thechanges seen were more severe and more extensivein ulcers of the body of the stomach. Thus, 21 % ofbiopsy specimens were normal in patients withprepyloric ulcers, whereas only 2% were normal inthe group of body ulcers. Only 30% of biopsy speci-mens from patients with prepyloric ulcers showedatrophic changes, while 50% were found in patientswith ulcers in the body of the stomach and theatrophic changes were often severe.Only 13% of biopsy specimens in patients with

prepyloric ulcer showed metaplasia, while 36% inpatients with ulcers in the body of the stomachshowed the change.Men were more liable to show severe gastritis

than women, despite the fact that there was a greaterproportion of prepyloric ulcers in men. Men had agreater percentage of biopsy specimens showingatrophic changes, and also almost double theproportion showing chronic active superficialgastritis. The difference is even more striking whenintestinal metaplasia is considered. This change wastwice as frequent in biopsy specimens from men asin those from women.

In view of many previous published reports, itwas somewhat surprising to find that age seemed tohave no effect on the distribution or severity ofgastritis in the group of patients with untreatedgastric ulcer. There were 17 patients aged 55 or lessand 18 aged over 55. In these two groups the per-centages of biopsy specimens showing atrophicgastritis, superficial gastritis, and intestinal meta-plasia were virtually identical.However, the two groups are not entirely compar-

able, as the group over 55 included a dispropor-tionate number of women, with less severe gastritis.The series of 35 patients studied was arbitrarily

divided into two groups: 16 with a short history oftwo years or less and 19 with a long history of morethan two years.There were twice as many patients with ulcers in

the body of the stomach in the group with long his-

tories. The patients with long histories tended tohave a greater number of abnormal biopsy specimensat all grades of gastritis than those with a shorthistory.

Intestinal metaplasia was more than twice asfrequent in biopsies from patients with long historiesthan those with short histories.

GASTRITIS IN MEDICALLY TREATED GASTRICULCERClinical features andfindings at gastroscopyOver the three-year period of the study, 28 patientswho were seen with a gastric ulcer had a gastroscopybefore and after medical treatment. For the reasonsdiscussed earlier, only two biopsy specimens wereobtained at most of the early gastroscopies. Thosepatients from whom four biopsy specimens wereobtained are included in the appropriate untreatedor healed series as well as in the group studied in thissection. The period between the two gastroscopicexaminations was never less than three months, andoften extended to 18 months or two years.One patient aged 42, with a greater curve ulcer,

died some months after the first gastroscopy of anunrecognized perforation of the ulcer with general-ized peritonitis. He had severe bronchitis andemphysema and was admitted in respiratory failure.The perforation was discovered only at postmortemexamination.Of the remaining 27 patients, eight were found to

have a persistent or recurrent gastric ulcer at the timeof the second gastroscopy. However, in two of theeight unhealed ulcers the appearances suggestedpartial healing. Two patients had a vagotomy andpyloroplasty later because of persistence of symp-toms and thus are included in the surgical series.

In patients with a healed ulcer of the body of thestomach, it was common to find persisting gastro-scopic evidence of atrophic gastritis. By contrast,in the patients with a healed prepyloric ulcer, themucosa often looked relatively normal except in theprepyloric region.

HistologicalfindingsIn most cases, the biopsy specimens obtained at

the second examination showed a similar, or worse,grade of gastritis than those from the first examina-tion. In a few instances an improvement occurredwith reversion to normal from superficial gastritis,or to superficial gastritis from mild atrophic changes.On the other hand, patients with severe atrophicgastritis at the first examination never showed im-provement at the second examination.

In the medically treated group, the distributionand severity of the gastritic changes at the fourstandard biopsy sites were similar to those seen in

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unhealed gastric ulcer, with a slightly worse picturein the two proximal biopsy sites. In the majority ofpatients there was no improvement in the gastritiswhen the ulcer had healed. The distribution ofintestinal metaplasia was also similar to that foundin untreated gastric ulcer.VAGOTOMY AND PYLOROPLASTYClinical features and gastroscopic findingsThirty-seven patients were studied, nine at fouryears or more after the operation and 28 with ashort follow up of three to six months.The nine patients who had been studied for more

than four years were part of a series of 45 patientswho had a vagotomy and pyloroplasty for gastriculcer between 1962 and 1965. All the nine patientsstudied were symptomless, except one who wasmildly anaemic and suffered occasional attacks ofdyspepsia. At gastroscopy no sign of an ulcer wasfound but two patients had a slight degree of hour-glass narrowing at the site of the previous ulcer.The appearance of the mucosa was very variable. Intwo patients it appeared virtually normal except inthe immediate vicinity of the pyloroplasty.

Twenty-eight patients with gastric ulcer weretreated by vagotomy and pyloroplasty during thethree-year period of the study. The length of followup varied from three years to a few weeks. All theulcers healed promptly and no patient developed arecurrent ulcer. Nineteen of the 28 had a gastro-scopic examination three months or more aftersurgery, as well as a preoperative gastroscopy.Histological findingsNineteen of the 28 patients treated by vagotomy andpyloroplasty during the period of this study had onlytwo gastric biopsy specimens taken before and afteroperation. In 11 patients, four biopsy specimenswere obtained at the second gastroscopy and these11 are therefore also included in the four biopsystudies.

In general, the histological appearances remainedthe same or became somewhat worse after surgery,but in two cases improvement occurred, withreversion of a mild atrophic change to superficialinflammation.There were 20 patients included in the four biopsy

studies. In general, the mucosal changes appeared tobe worse after surgery despite prompt healing of theulcer. It is interesting to note that the greatestdeterioration occurred in the two proximal biopsysites, high on the lesser curve and on the greatercurve, respectively. The most severe and extensivegastritis was found at the high lesser curve site,almost 90% of specimens showing moderate orsevere atrophic changes. Severe atrophic gastritiswas found equally commonly (30%) at all four

biopsy sites, in contrast to the decreasing frequencyfound in the proximal sites in untreated gastriculcer.

Intestinal metaplasia was frequently found aftersurgical treatment. About 60% of biopsy specimensfrom the prepyloric and two lesser curve sites showedmetaplasia, while 40% of greater curve specimensshowed the change.

Severe atrophic gastritis was three times morefrequent in patients with a long dyspeptic historybefore operation, but the overall incidence of allgrades of atrophic change was not markedly differentin the two groups. Intestinal metaplasia was morefrequent in the group with a history of dyspepsia ofmore than two years.One interesting finding was the occurrence of the

chronic active form of superficial gastritis, especiallyin biopsy specimens taken from the greater curve.This histological appearance was found only in thepatients with a short ulcer history who were re-examined early after operation. It was never seen inpatients with a long ulcer history, or in those whohad had their operation four years or more pre-viously.

Atrophic gastritis was more frequent in biopsyspecimens from the group examined four years ormore after operation, but the difference from thosefollowed for one year was not marked. The findingof biopsy specimens showing chronic active super-ficial gastritis was confined to the patients followedfor less than a year. Intestinal metaplasia was foundin 70%. of biopsy specimens from the long-termgroup, but in only 50% from the short-term group.

In summary, the specimens from patients treatedby vagotomy and pyloroplasty showed a highproportion of moderate or severe atrophic gastritisat all four biopsy sites and a high incidence ofintestinal metaplasia. In those patients studiedbefore and after surgery, the gastritis commonlybecame worse, even over a short period of observa-tion.

It is revealing to compare the findings in the un-treated group of patients with those observed inpatients with the ulcer healed, whether treatedmedically or surgically by vagotomy and pyloro-plasty. This part of the study is confined to patientsexamined by biopsy from all four standard sites.As far as intestinal metaplasia is concerned, this

change was just as frequent in patients whose gastriculcer had healed with medical treatment as it was inthe untreated patients, while it was twice as frequentin the patients whose gastric ulcer had healed aftervagotomy and pyloroplasty.

PARTIAL GASTRECTOMYThirteen patients were studied, nine some years after

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operation and four within one year. The types ofoperation were Billroth I (7), Polya (2), and vago-tomy and antrectomy (4). Eleven had suffered fromchronic ulcers of the body of the stomach, the othertwo from prepyloric ulcers. On gastroscopy, evidenceof severe atrophic gastritis was common. Thebiopsy specimens were obtained from three sites:mid lesser curve, high lesser curve, and greater curve.The specimens commonly showed atrophic gastritisevenly distributed over all three biopsy sites. Inview of this, it is somewhat surprising that only twobiopsy specimens (6%) showed intestinal metaplasia.

CORRELATION BETWEEN GASTROSCOPIC ANDHISTOLOGICAL FINDINGSThe appearance of the mucosa was recorded at thetime of gastroscopy and was later correlated withthe histological grade of gastritis. The results areset out in Table I.

Gastroscopic Histological Grade at Corresponding Sites TotalAppearance

Normal Superficial Mixed AtrophicGastritis Superficial Gastritis

andAtrophicGastritis

Normal 4 0 0 2 6Superficialgastritis 1 11 0 14 26Mixed superficialand atrophicgastritis 0 2 29 0 31Atrophic gastritis 0 1 1 17 19

Table I Correlation betweenand histologicalfindings

gastroscopic appearances

When the gastritis appeared at gastroscopy to besuperficial in one part of the stomach and atrophicin another, it was classified as 'mixed'. As can beseen from Table I, most of these cases also had a

'mixed' gastritis on histology, having atrophicchanges in one biopsy and chronic superficialgastritis in another. When the gastroscopy reportmentioned one area particularly as atrophic, thenthe appropriate biopsy site was used in assessing thecorrelation between visual and histological appear-ances. It was unusual to find mucosa which lookednormal and therefore was always noted. Those fewcases where no mention of the state of the mucosawas made in the gastroscopy report were excludedfrom Table I. Thus 82 cases of the total of 87 withbiopsy specimens from four sites were included.

It can be seen from Table I that when 'mixed'superficial and atrophic changes were seen at gastro-scopy, in over 90% of cases the histological findingsagreed. Atrophic gastritis was also correctly diag-

nosed at gastroscopy in 90% of cases. However,when superficial gastritis was diagnosed at gastro-scopy, in half the cases atrophic gastritis was found.There were too few cases with a normal mucosa tomake a satisfactory assessment of the reliability ofthe gastroscopic judgment.

Thus, the signs suggesting atrophic changes atgastroscopy are a reliable guide to the histologicalstate of the mucosa. The signs suggesting superficialgastritis, however, often underestimate the severityof the gastritis. Contact bleeding is probably a fairlyreliable guide to the presence of gastritis, but doesnot differentiate between superficial and atrophicgastritis.

Discussion

The present study has shown that the gastritis asso-ciated with chronic gastric ulcer is regional. Thedistal part of the stomach and mid lesser curve arethe most severely affected both by atrophic changeand by intestinal metaplasia. The distribution ofmetaplasia agrees well with the pattern found byGraham and Schade (1965)'and Stemmermann andHayashi (1968). These findings show that singlebiopsy specimens obtained blind from the greatercurve area may miss large areas of atrophic mucosaor metaplasia in the rest of the stomach. We canconfirm the finding of Joske et al (1955) and of otherworkers that two specimens obtained close togetherfrom the same area of the stomach usually show thesame degree of gastritis, but specimens obtainedfrom the greater curve and lesser curve may showwide variations.

Specimens from the body of the stomach on thegreater curve side are least likely to show gastriticchanges. Conversely, if the greater curve specimenshows severe atrophic gastritis then it is likely thatthe other sites are similarly affected.

Ulcers of the body of the stomach are associatedwith more extensive and more severe gastritis thanulcers of the prepyloric region. Prepyloric ulcers areassociated with gastritis which is localised to thedistal biopsy sites and is often superficial with littleevidence of atrophic changes or metaplasia. Thedifference in gastritis between the two ulcer typespersists after the ulcer has healed, whether treatmentbe medical or surgical.The distribution of gastritic changes in the

stomach after treatment is similar to that found inuntreated gastric ulcer. Severe atrophic gastritisand intestinal metaplasia are found most frequentlyin prepyloric and mid-lesser curve biopsy sites, andtend to spread proximally in treated gastric ulcer,particularly after surgery. The overall frequency ofsevere changes was also increased in the treated

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group, although in a few cases, definite improve-ment occurred after healing of the ulcer.

There has been a great deal of controversy aboutthe gastroscopic diagnosis of gastritis. The earlygastroscopists like Schindler recognized three types:hypertrophic, superficial, and atrophic gastritis.Palmer (1954) felt that atrophic gastritis could bediagnosed reliably at gastroscopy, but that super-ficial gastritis and normal mucosa could not be dis-tinguished in many cases. Joske et al (1955) wentfurther and stated that gastroscopy was too un-reliable to be of any value in the diagnosis of anygrade of gastritis. However, they based their viewson specimens obtained by blind biopsy techniques.The present study, with biopsy under direct vision,has confirmed Palmer's view that atrophic gastritiscan be diagnosed reliably at gastroscopy.

In conclusion, the present study suggests thatgastritis is the basic disease process and gastriculceration is a secondary phenomenon. The gastritisis widespread in association with chronic peptic ulcerof the body of the stomach, whereas it is commonlymore localized with chronic prepyloric ulcer. Super-ficial or atrophic gastritis has been found to persistor even worsen after healing of the ulcer, whethertreatment be medical or surgical. This finding dis-poses of the idea that the gastritis associated withgastric ulcer is simply a zonal gastritis secondary tothe ulcer.

We wish to thank the Nuffield Committee for mak-ing a research grant to one of us (M.W.L.G.).

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11, 281-283.Faber, K. (1935). Gastritis and Its Consequences. Oxford University

Press, London.Gear, M. W. L., Truelove, S. C., Williams, D. G., Massarella, G. R.,

and Boddington, M. M. (1969). Gastric cancer simulatingbenign gastric ulcer. Brit. J. Surg., 56, 739-742.

Graham, R. I., and Schade, R. 0. K. (1965). The distribution ofintestinal metaplasia in macroscopic specimen, demonstratedby a histochemical method. Acta path. microbiol. scand., 65,53-59.

Hancock, P. E. T., and Shiner, M. (1958). Combined gastroscopy andgastric biopsy under direct vision. Lancet, 1, 1204-1205.

Hebbel, R. (1943). Chronic gastritis: its relation to gastric andduodenal ulcer and to gastric carcinoma. Amer. J. Path., 19,43-71.

Hebbel, R. (1949). The topography of chronic gastritis in otherwisenormal stomachs. Amer. J. Path., 25, 125-141.

Joske, R. A., Finckh, E. S., and Wood, I. J. (1955). Gastric biopsy: astudy of 1,000 consecutive successful gastric biopsies. Quart.J. Med., 24, 269-294.

Kenamore, B. (1940): A biopsy forceps for the flexible gastroscope.Amer. J. dig. Dis., 7, 539.

Macdonald, W. C., and Rubin, C. E. (1967). Gastric biopsy: a criticalevaluation. Gastroenterology, 53, 143-170.

Magnus, H. A. (1946). The pathology of simple gastritis. J. Path.Bact., 58, 431-439.

Magnus, H. A. (1952). Gastritis. In Modern Trends in Gastro-enterology.1st series, edited by F. H. Jones, pp. 323-351. Butterworth,London.

Palmer, E. D. (1954). Gastritis: A revaluation. Medicine (Baltimore),33, 199-290.

Sanders, G. B., and Mecray, P. M. (1941). Pseudogastritis of operativeorigin. Ann. Surg., 114, 986-996.

Schindler, R. (1947). Gastritis. Heineman, London.Schindler, R., Necheles, H., and Gold, R. (1939). Surgical gastritis:

a study on the genesis of gastritis found in resected stomachswith particular reference to so-called 'antral gastritis' asso-ciated with ulcer. Surg. Gynec. Obstet., 69, 281-286.

Stemmermann, G. N., and Hayashi, T. (1968). Intestinal metaplasia ofthe gastric mucosa: a gross and microscopic study of itsdistribution in various disease states. J. nat. Cancer Inst., 41,627-634.

Whitehead, R., Gear, M. W. L., and Truelove, S. C. (1971). The histo-logical diagnosis of chronic gastritis in fibreoptic gastroscopebiopsy specimens. J. clin. Path. In Press.



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