Gut, 1991,32,351-354

Congestive gastropathy and Helicobacter pylori: an

endoscopic and morphometric study

P A McCormick, E A Sankey, F Cardin, A P Dhillon, N McIntyre, A K Burroughs

AbstractCongestive gastropathy is a frequent cause ofupper gastrointestinal haemorrhage in patientswith portal hypertension. The pathogenesis isthought to involve venous congestion withgastric. mucosal capillary dilatation. Westudied the relation between gastric mucosalcapillary dilatation, measured morphometri-cally, and endoscopic appearances in 74patients with portal hypertension and 20 con-trol subjects. We also investigated the fre-quency of gastric colonisation withHelicobacter pylorn. Mucosal capillaries inpatients were significantly dilated comparedwith control subjects (p<0.001) but the degreeof dilatation was not related to the severity ofthe endoscopic appearances. H pylori wasidentified in 19 of74 (26%) patients but was notrelated tothe severityofthe endoscopic appear-ances. These results suggest that other factorsin addition to mucosal venous and capillarycongestion are important in the pathogenesisof endoscopic congestive gastropathy and thatgastric colonisation withH pylori is unlikely tobe one of these factors.

Academic DepartmentsofMedicine andHistopathology, RoyalFree Hospital School ofMedicine, LondonP A McCormickE A SankeyF CardinA P DhillonN McIntyreA K BurroughsCorrespondence to:Dr P A McCormick, AcademicDepartment ofMedicine,Royal Free Hospital, PondStreet, LondonNW3 2QG.Accepted for publication21 May 1990

Congestive gastropathy is a frequent endoscopicfinding in patients with portal hypertension andis believed to be responsible for approximately20% of episodes of bleeding in these patients.The pathogenesis of the disorder is, however,controversial. McCormack et al' coined the term'congestive gastropathy' and distinguished ithistologically from inflammatory gastritis. Theysuggested that the endoscopic appearances weredue to venous congestion and capillary dilatationin the gastric mucosa and submucosa. Most,2'but not all,' authors agree that capillary dilata-tion is important in this condition. Morpho-metric analysis of capillary dilatation has rarelybeen performed in biopsy specimens frompatients with portal hypertension. With theexception of a small subgroup of patients withvery severe haemorrhagic gastritis,' the degree ofcapillary dilatation seen in the gastric mucosa hasnot been evaluated with relation to the severity ofthe endoscopic appearances. The aim of thisstudy was to assess the relation between mucosalcapillary dilatation, measured morphometri-cally, and the endoscopic appearances. Ifvenousand capillary congestion are closely related to thegenesis of the endoscopic appearances, onewould expect increased capillary dilatation insubjects with more severe endoscopic appear-ances. Alternatively, if mucosal congestionmakes the mucosa more susceptible to damagefrom other agents6 or reduces its capacity torepair damage, the degree of capillary dilatationmay not necessarily correlate closely with the

endoscopic findings, as the most recent injury isthe critical determinant of the endoscopicappearances.A secondary aim of this study was to deter-

mine the prevalence of Helicobacter pylori colon-isation in our patients. It has been suggested thatthere is a high prevalence ofHpylori colonisationin portal hypertension, particularly in patientswith gastric erosions.7

Patients and methodsSeventy four patients with oesophageal varicesunderwent endoscopy on a total of 93 separateoccasions, and multiple antral biopsy specimenswere taken. Their mean age was 51.5 years(range 18-77 years) and 50 were men. Diagnosesincluded cirrhosis in 67 (30 alcoholic), portalvein block in four, schistosomiasis in two, andcongenital hepatic fibrosis in one. Liver functionwas assessed on each occasion and gradedaccording to Pugh's modification of Child'sgrading system,8 for cirrhotic patients (51% weregrade A, 40% grade B, 9% grade C). Medicationswere also recorded. On 31 occasions patientswere taking H2 antagonists, on 14 occasionssucralfate, on five occasions bismuth, and on oneoccasion antacids. No patients were taking non-steroidal anti-inflammatory agents or P blockers.Fifty nine per cent of patients had previouslybeen treated with endoscopic sclerotherapy.Antral biopsy specimens were also taken from 20control subjects, who had a mean age of 43.9years (range 25-82 years) and of whom 14 werewomen. Control subjects were patients under-going upper gastrointestinal endoscopy whosegastric biopsy specimens were found to be histo-logically normal. They included six patients withmyalgic encephalomyelitis (ME syndrome) whohad gastroscopy and biopsy as part of a researchinvestigation. H pylori was not identified in anyof the control subjects.At each endoscopy the severity of endoscopic

gastropathy was graded using a modification ofthe classification previously employed byMcCormack et al. ' A four point scale was used asfollows:None=normal appearances;Mild=mosaic or snake skin appearance9;Moderate= presence of erythema;Severe=presence of erosions or haemorrhagic

gastritis.The only change from the classification used

by McCormack et al is that we subdivided mildgastropathy into mild and moderate gastropathy.We put the snake skin or mosaic appearance intoa category on its own in the belief that it mayrepresent a less severe form of gastropathy thanthe presence oferythema or erosions and haemor-rhages, or both. Endoscopy was performed using

351

on July 12, 2021 by guest. Protected by copyright.

http://gut.bmj.com

/G

ut: first published as 10.1136/gut.32.4.351 on 1 April 1991. D

ownloaded from

McCormick, Sankey, Cardin, Dhillon, McIntyre, Burroughs

c)

CL)

c).

.)

-o

a)

a

Figure 1: Haematoxylin and eosin stained section ofgastric mucosa showing superficial,middle, and deep layers (original magnification x40).

Olympus K10, Q1O, or XQ20 endoscopes andstandard 5 mm biopsy forceps.Two to four antral biopsy specimens were

taken in each case and stained routinely withhaematoxylin and eosin. Hpylori organisms wereidentified by careful examination of the stainedbiopsy specimens by two independent observersunaware of the endoscopic appearances. Histo-logical gastritis was identified and graded semi-quantitatively using a modification ofWhitehead's criteria.'0 'Mild' gastritis was

defined as superficial chronic gastritis.'Moderate' gastritis was identified as a superficialgastritis with a moderate inflammatory infiltrateofplasma cells and lymphocytes, including smalllymphoid aggregates but with no gland distor-tion. 'Severe' gastritis was defined as superficalactive, or mild atrophic gastritis with a compact(intense) inflammatory infiltrate extendingthrough the mucosa. In addition, neutrophilsmight or might not be present and there could begland neck distortion or evidence of regenera-tion. On each occasion the cross sectional areas of30 well orientated capillaries were measuredusing computer assisted image analysis (LogitecMD 20 densitometric system). Ten consecutivevessels were measured at each of three layers inthe biopsy specimen (10 superficial, 10 middle,

and 10 deep - Fig 1). Values were expressed as

the mean (SEM) in [tm2. Unless otherwise stated,all the figures and percentages refer to numbersof biopsy specimens rather than number ofpatients. The significance of differences betweengroups was tested using Student's t test or theMann-Whitney U test as appropriate. Thedegree of correlation was checked using theSpearman rank correlation coefficient.

Results

ENDOSCOPIC GASTROPATHYOn all but eight occasions there was evidence ofendoscopic gastropathy: mild 6 (6%), moderate61 (66%), severe 18 (19%). The severity ofendoscopic gastropathy did not seem to be relatedto a history of previous endoscopic sclerotherapy(p=0.37) or to drug use: H2 antagonists(p=078), sucralfate (p=0.83). Nor were theendoscopic appearances related to the presenceor degree of histological gastritis (Table I)(coefficient ofcorrelation -0 007 p=0 950). Theseverity of endoscopic gastropathy was similar inpatients with alcoholic cirrhosis compared withthose with portal hypertension of otheraetiologies. Mild, moderate, or severe gastro-pathy was noted at endoscopy in 7%, 70%, and16% ofoccasions in the alcoholics compared with6%, 61%, and 23% of occasions in the non-

alcoholics. A similar pattern seen on histology asmild, moderate, and severe histological gastritiswas noted in 55%, 20%, and 9% of biopsyspecimens from alcoholic patients comparedwith 25%, 37%, and 16% respectively from non-

alcoholic portal hypertensive patients.

CAPILLARY DILATATIONA total of 3140 capillaries were counted in themorphometric analysis. In six biopsy specimensfrom the portal hypertensive group and 13from the control subjects there was insufficientdeep layer mucosa in the specimens for analysisof capillary size in this layer.

TABLE I Prevalence ofHelicobacter pylori (HP) inrelation to the degree ofhistological gastritis in biopsyspecimensfrom patients with portal hypertension

Histological gastritis

None Mild Moderate Severe

Capillary areas ([tm2) 214 (21) 179 (10) 197 (14) 203 (25)Mean (SEM)No HP +ve/total 0/13 2/41 11/27 9/12(%) (0) (5) (41) (75)Endoscopic gastropathy:No (%)None 1/13 2/41 3/27 1/12

(8) (5) (1 1) (8)Mild 0/13 2/41 2/27 2/12

(0) (5) (7) (17)Moderate 11/13 28/41 17/27 5/12

(84) (68) (63) 42)Severe 1/13 9/41 5/27 4/12

(8) (22) (19) (33)

Presence ofH pylori correlated with the severity of histologicalgastritis (Spearman correlation coefficient 0 57; p<0001).Severity of histological gastritis was not correlated with severity ofendoscopic gastropathy (Spearman correlation coefficient-0 007; p=0-95) and did not significantly influence the degree ofcapillary dilatation in portal hypertensive patients. Severitv ofhistological gastritis did not significantly influence capillarydilatation.

352

on July 12, 2021 by guest. Protected by copyright.

http://gut.bmj.com

/G

ut: first published as 10.1136/gut.32.4.351 on 1 April 1991. D

ownloaded from

Congestive gastropathy and Helicobacter pylori: an endoscopic and morphometric study

450-

N 400E

cu 350-00

E13E 300.C.2.5 250-

M-

1200-

a,.o 1 50-.E

cO 100 -

50-

0-

l@Sll@00~ ~ ~ ~ ~

0

0

0

00

:00

Control None Mild Moderate Severesubjects

Endoscopic gastntis gradeportal hypertensive patients

Figure 2: Mean capillary areasfor individual patients in thesuperficial mucosal layer in controls and portal hypertensivepatients. Capillary areas were significantly greater infourgroups ofportal hypertensive patients compared with controls(p<0o001).

A summary of the results of the morphometricanalysis is given in Table II. Superficial capil-laries were significantly dilated in portal hyper-tensive patients with all grades of endoscopicappearance compared with control subjects: con-trol subjects (mean (SEM) 87 (4) p.m2); portalhypertensive patients with normal endoscopicappearances (186 (33) [tm2; p<0 001), with mildgastropathy (210 (22) 1km2; p<0 001), withmoderate gastropathy (194 (9) 1km'; p<0 001),and with severe gastropathy (174 (32) pm';p<0o001).

Individual results for mean capillary size in thesuperficial mucosa are shown in Figure 2. This isthe layer which is most visible to the endoscopist.A similar pattern was seen in the middle mucosallayer but there was no significant differencebetween biopsy specimens from control subjectsand patients with portal hypertension in the deeplayer. There was no significant difference incapillary size between different grades of severity

TABLE II Capillary areas (tm' values mean (SEM))forcontrol subjects and patients with portal hypertensionaccording to endoscopic grade

Endoscopic gastropathyMucosallayer Control None Mild Moderate Severe

Superficial 87 (4) 186 (33)* 210 (22)* 194 (9)* 174 (32)*Middle 125 (8) 264 (42)* 203 (16)* 253 (14)* 239 (21)*Deep 235 (39) 293 (48) 239 (36) 333 (28) 343 (61)

*p<0-01 compared with control values.

TABLE III Prevalence ofHelicobacter pylori (HP) inrelation to the degree ofendoscopic gastropathy

Endoscopic gastropathy

None Mild Moderate Severe

HP +ve/total 3/8 3/6 12/61 4/18(%) (38) (50) (20) (22)

There is no significant correlation between the presence ofH pyloriand the severity of endoscopic gastropathy (Spearman correlationcoefficient -0-12; p=0 25).

of endoscopic gastropathy in portal hypertensivepatients at any ofthe three levels in the specimen.To allow for the possibility that the presence ofhistological gastritis may contribute to capillarydilatation, we compared mean capillary size inportal hypertensive patients with and withouthistological gastritis. The presence or severity ofhistological gastritis did not seem to influence thedegree of capillary dilatation in any of the threemucosal layers. Figures for the superficialmucosal layer are summarised in Table I.

In addition, there were no significant dif-ferences in the degree of capillary dilatation inany of the three mucosal layers between patientswho had and those who had not been treatedpreviously with endoscopic sclerotherapy. Therelevant figures, for the sclerosis and non-sclerosis groups respectively were mean (SEM)196 (10) rim' v 187 (11) ,tm' (p=0 85) for super-ficial mucosa; 255 (14) Itm2 v 243 (15) Im2(p=091) for middle mucosa; and 338 (20) [im2 v329 (40) [tm2 (p=0.72) for deep mucosa. Thedegree of capillary dilatation was similar inpatients with alcoholic cirrhosis compared withsubjects with other causes ofportal hypertension.The figures for the superficial mucosa layer weremean (SEM) 188 (10) .tm2 for biopsy specimensfrom alcoholic cirrhotic patients compared with195 (11) [tm2 for specimens from non-alcoholicpatients.

PREVALENCE OF HELICOBACTER PYLORIH pylori was identified in 22 of 93 biopsyspecimens (23.7%) and in 19 of 74 patients(26%). The presence ofH pylon was associatedwith histological gastritis (Table II), beingabsent in 13 biopsy specimens without histo-logical gastritis and present in 9 of 12 specimens(75%) showing severe histological gastritis (co-efficient of correlation 0.57 p<0-001). In con-trast, the presence of H pylon was not closelyassociated with the severity ofendoscopic gastro-pathy (Table III) (coefficient of correlation-0.12, p=0.25).Hpyloriwas identified in 38% ofspecimens from patients with normal endoscopicappearances and in 22% of those with severeendoscopic gastropathy.

DiscussionOur study confirms that gastric mucosal capil-lary dilatation is present in patients with portalhypertension as compared with control subjects.The degree of capillary dilatation did not seem tobe influenced by the presence or absence ofgastritis. Neither was the degree of capillarydilatation related to the severity of endoscopicappearances. Moreover the degree of endoscopicgastropathy and the degree of capillary dilatationdid not seem to be influenced by prior sclero-therapy, as had been suggested previously. 'These findings suggest that factors other than thedegree of mucosal congestion may be importantin the pathogenesis of the endoscopic changes.

Although the endoscopic appearances of con-gestive gastropathy are usually more noticeablein the fundus of the stomach,'9 we chose to takeantral biopsy specimens to avoid inadvertentbiopsy of gastric varices and also to maximise the

353

.

on July 12, 2021 by guest. Protected by copyright.

http://gut.bmj.com

/G

ut: first published as 10.1136/gut.32.4.351 on 1 April 1991. D

ownloaded from

354 McCormick, Sankey, Cardin, Dhillon, McIntyre, Burroughs

detection ofH pylon colonisation. We suspectedinitially that colonisation with H pylori might berelated to the severity of the endoscopic changes.Our results do not, however, support thishypothesis. Hpylori was identified in 26% of ourpatients, but was not related to the presence ofendoscopic gastropathy. To identify H pylori weused routine haematoxylin and eosin stainedbiopsy specimens. In our experience and that ofothers," 12 90% of H pylori are detected by thismethod. The use of special stains might haveincreased the yield slightly" but would not havealtered the results significantly. The question asto whether H pylon should be treated whenidentified has not been resolved in patients withpeptic ulcer disease,'3 and has not been evaluatedin patients with portal hypertension. Given thatthe presence of H pylori is unrelated to theendoscopic appearances, we treat only patientswho also have dyspeptic symptoms.We feel that the most likely explanation for the

pathogenesis of the endoscopic changes in thegastric mucosa of patients with varices is thatmucosal congestion may render the mucosa moreprone to injury or reduce its capacity to repairinjury. Support for this suggestion comes fromwork in animals showing an increased suscepti-bility of the portal hypertensive mucosa to injuryfrom agents such as bile acids, aspirin, oralcohol.6 It is not known, however, whetherresults from the animal model used in thesestudies can be extrapolated to human portalhypertensive gastropathy'4 and more work in thisarea is required. If the human portal hyperten-sive gastric mucosa is more prone to injury thiswould suggest that treatment could be aimed atthe two mechanisms involved; either by reduc-ing portal pressure with drugs'" or surgery16 or bytrying to reduce gastric mucosal injury. Themechanisms of gastric injury in patients withportal hypertension must be more clearly eluci-dated in order to justify drug therapy in clinicalpractice. Trials of cytoprotective agents such asmisoprostol may be worthwhile.

In summary, this study shows that the severityof the endoscopic appearances of congestivegastropathy in patients with varices does not

correlate with either the degree of mucosalcapillary dilatation or histological gastritis. Thissuggests that mucosal congestion is a necessarybut not sole prerequisite for the development ofthe endoscopic appearances of congestive gastro-pathy. Other factors may play a role in thepathogenesis of gastric injury but colonisationwithH pylori is unlikely to be one of these.

We would like the thank Miss Doris Elliott for secretarialassistance. Dr Cardin was supported by the R Farimi Foundationfor Gastroenterological Research.

1 McCormack TT, Sims J, Eyre-Brook I et al. Gastric lesions inportal hypertension: inflammatory gastritis or congestivegastropathy? Gut 1985; 26: 1226-32.

2 Foster PN, Wyatt JI, Bullimore DW, Losowsky MS. Gastricmucosa in patients with portal hypertension: prevalence ofcapillary dilatation and Campylobacter pylon. .7 Clin Pathol1989; 42: 919-21.

3 Quintero E, Pique JM, Bombi JA et al. Gastric mucosalvascular ectasias causing bleeding in cirrhosis. A distinctentity associated with hypergastrinaemia and low serumlevels of pepsinogen 1. Gastroenterology 1987; 93: 1054-61.

4 Hashizume M, Tanaka K, Inokuchi K. Morphology of gastricmicrocirculation in cirrhosis. Hepatology 1983; 3: 1008-12.

5 Corbishley CM, Saverymuttu SH, Maxwell JD. Use ofendoscopic biopsy for diagnosing congestive gastropathy..7Clin Pathol 1988; 41: 1187-90.

6 Sarfeh IJ, Somiman H, Waxman K et al. Impaired oxygena-tion of gastric mucosa in portal hypertension. The basis forincreased susceptibility to injury. Dig Dis Sci 1989; 34:225-8.

7 Paoluzi P, Piatroisuti A, Marchaggiano et al. Prevalence ofCampylobacter pylon in cirrhotic patients with gastricerosions. Gastroenterology 1988; 94: A342 (abstract).

8 Pugh RNH, Murray-Lyon IM, Dawson JL et al. Transectionof the oesophagus for bleeding oesophageal varices. BrJSurg 1973; 60: 646-9.

9 Papazian A, Braillon A, Dupas JL, Sevenet F, Capron JP.Portal hypertensive gastric mucosa; an endoscopic study.Gut 1986; 27: 1199-1203.

10 Whitehead R, Truelove SC, Gear MWL. The histologicaldiagnosis ofchronic gastritis in fibreoptic gastroscope biopsyspecimens.JI Clin Pathol 1972; 25: 1-11.

11 Hamilton-Dutoit SJ, Szeto ML, Dhillon AP, Pounder REP.The detection of Campylobacter pyloridis (CP) in gastricbiopsies: a comparative study of histology and the 'CLOtest'.J Pathol 1988; 154: 86A (abstract).

12 Schnell GA, Schubert TT. Usefulness of culture, histologyand urease testing in the detection of Campylobacter pylon'.AmJ Gastroenterology 1989; 84: 133-7.

13 Preston WL. Antibiotic therapy of duodenal ulcer? Hold offfor now. Gastroenterology 1989; 97: 508-10.

14 Groszmann RJ, Colombata LA. Gastric vascular changes inportal hypertension. Hepatology 1988; 8: 1708-10.

15 Hosking SW, Kennedy HJ, Seddon E, Triger DR. The role ofpropranolol in congestive gastropathy ofportal hypertension.Hepatology 1987; 7: 437-41.

16 Sarfeh IJ, Juler GL, Stemmer EA et al. Results of surgicalmanagement of haemorrhagic gastritis in patients withgastro-oesophageal varices. Surg Gynaecol Obstet 1982; 155:167-70.

on July 12, 2021 by guest. Protected by copyright.

http://gut.bmj.com

/G

ut: first published as 10.1136/gut.32.4.351 on 1 April 1991. D

ownloaded from