Bruce

A. Urban,

MD

#{149} Elliot

K. Fishman,

MD

Helicobacter pylon Gastric Carcinoma The abdominal computed tomographic (CT) scans from 61 patients with biopsy-proved Heicobacter (formerly Campy1obactei pylon gastritis were retrospectively reviewed. The CT scans were interpreted on the basis of the original report of the findings at CT examination and without knowledge of the results of biopsy. Of 19 patients (31%) with gastric abnormalities at CT, 14 (74%) had inflammatory changes initially reported as suspicious for gastric malignancy; malignancy was entertained as the primary diagnosis in four of those patients. In five of the 19 abnormal cases (26%), the diagnosis with CT was gastritis. The two major patterns of severe Hpyloni infection identified were (a) circumferential antral wall thickening and (b) thickening of the posterior gastric wall along the greater curvature, with or without evidence of ulceration. Thickening averaged 1.5-2.0 cm in cases suspicious for malignancy. The majority of abnormalities involved the gastric antrum (68%). No cases demonstrated significant adenopathy, obliteration of fat planes, or invasion of adjacent organs. Index

H. Hruban,

MD

Gastritis Mimicking at CT Evaluation’

S

INCE

Warren

and

Marshall’s

(i)

initial description of Helicobacter (formerly Campylobacter) pylon infection in i983, H pylon of the stomach and duodenum has become a wellrecognized probable cause of active, chronic gastritis (2-6). Furthermore, the presence of H pylon infection and histologic gastritis in asymptomatic patients has recently been described (7). Patients with a more acute form of infection can demonstrate severe inflammatory changes, some of which may mimic gastric cancer at endoscopic examination and upper gastrointestinal series (8-i 1). We present histologically proved exampies of severe H pylon gastritis, mitially reported as suspicious for malignancy at computed tomography (CT), and summarize the spectrum of findings of H pylon gastritis detectable with CT. MATERIALS

AND

The records tritis, 1988

METHODS

of H pylon gasconfirmed with biopsy, from June to July 1990 were obtained from The

scans

Radiology

scanning 1 week)

from

trieved

were

65 patients

who

underwent

within 30 days (36 cases within of endoscopic biopsy were reand

reviewed.

suboptimal

distention

and

Four

of the

scans

due to lack of gastric were

dropped

from

the

study.

I From the Departments of Radiology and Radiological Science (B.A.U., E.K.F.) and Pathology (R.H.H.), The Johns Hopkins Hospital, 600 N Wolfe St, Baltimore, MD 21205. From the 1990 RSNA scientific assembly. Received Dccember 4, 1990; revision requested January 23, 1991; revision received February 1 1; accepted February 18. Address reprint requests to E.K.F. © RSNA, 1991

The remaining 61 cases were the focus of this study. There were 33 women (54%) and 28 men (46%) ranging in age from 29 to 80 years (mean, 59 years). CT scanning of the abdomen was performed with a Somatom DR3, DRH, or Plus scanner (Siemens, Iselin, NJ). Standard scanning parameters were 125 kVp, 1-4 seconds, 170-310 mAs, and mm collimation. Patients drank diatrizoate

Winthrop-Breon

approximately 1 hour before the examination and another 250 mL just prior to imaging. Images were routinely obtained at 1.0-cm intervals from the diaphragm through the liver and at 1.5-cm intervals through the remainder of the abdomen. All studies

were

interpreted

by senior

radiologists without prior knowledge of histologic findings. Scan interpretations used for this study were based on the original CT reports. In general, focal gastric wall prominence up to 1 cm was interpreted as compatible with gastritis. A 1-2-cm thickening of the gastric wall was interpreted as compatible with possible malignancy.

and/or

Focal

wall

or

thickness

ulcerating

greater

masses

than

or

equal

to 2 cm were considered highly suspicious for malignancy. Lesion size was determined with use of maximum diameter. The stomach was analyzed for location of lesions in the antrum, body, fundus,

or cardia

(including

the

gastroesoph-

ageal junction). of the abdomen

The remaining portions were examined for secondary signs of malignancy such as adenopathy, obliteration of fat planes, or direct invasion of adjacent organs.

of 376 cases

Johns Hopkins Hospital Department of Pathology. Pathologic diagnosis was made by detection of H pylon in the mucosa of the specimens obtained at endoscopic biopsy. Patients with history of prior gastric surgery and/or history of past or present gastric malignancy were excluded from this study. Abdominal CT

terms: Gastritis, 72.291 #{149} Helicobacter infection, 72.202 #{149} Stomach, abnormalities, 72.291 #{149} Stomach, CT, 72.121 1 #{149} Stomach, infection, 72.202 #{149} Stomach, neoplasms, 72.32 1991; 179:689-691

#{149} Ralph

meglumine

4- or

(Hypaque

Laboratories,

8-

500 mL of

3%; New

York)

RESULTS Nineteen of 61 cases (3i%) demonstrated gastric abnormalities. Fourteen of these 19 cases (74%) were reported as suspicious for malignancy. In four of those cases, malignancy was entertained as the primary diagnosis. Two of these four cases were characterized by circumferential thickening of the antral wall. This thickening averaged 2 cm (Fig 1). Two of the four cases demonstrated a 2-cm, masslike thickening of the posterior gastric wail with evidence of ulceration (Fig 2). Ten of the i9 abnormal cases were interpreted as compatible with possible malignancy: seven patients had circumferential thickening of the antral wall, averaging 1.5 cm, with extension into the body of the stomach in one of these patients; two patients had diffuse thickening of the posterior gastric wall averaging i .5 cm, with no evidence of ulceration (Fig 3); one 689

9.. .

Figure 1. demonstrates thickening tric neoplasm

scan of the gastric marked circumferential that is highly suspicious (arrow).

CT

I

*

antru.m for

wall gas-

patient had focal i-cm thickening of the gastroesophageal junction. Five of the 19 abnormal cases (26%) demonstrated minimal focal wall thickening of less than i cm, interpreted as compatible with gastritis: four involved the antrum (Fig 4), and one involved the body of the stomach. Overall, on the basis of the anatomic

location

of the

i9 abnormal

cases, 68% of the lesions involved the antrum, 42% involved the body (greater curvature), and 5% involved the

gastroesophageal

junction.

antrum infected

patients nosis”

and body of the in the majority

in asymptomatic

patients.

In-

in

50%-60% of subjects by age 60 years (13). The precise mechanism of H pylon infection is unclear. The organism

does

produce

urease,

which

in whom of malignancy

ed large intestinal

in approximately patients under-

cidence of infection increases with age, and bacteria can be identified

increases

to the

ty. Wall

of gastric

thickness

is considered

attachment

to surface mucosa has also been postulated as a mechanism of injury (5). H pylon infection responds well to antibiotics and/or bismuth corn#{149} Radiology

greater

abnormal

indistinguishable (18,19). Gastric

690

Antral masses have at upper gastrointes-

detection

age

bacterial

diagprior

folds at upper gastroin 47% of pediatric patients with H pylon infection. Enlargement of gastric folds and thickening of the gastric wall appear to occur due to a combination of mucosal inflammation, submucosal edema, and secondary hypertrophy and hypemplasia of the gastric mucosa. CT has been shown to be sensitive

quate orally

Direct

a “confident was made

gastric series

gastric pH and alters gastric mucus, exposing the underlying mucosa to acid damage. Alternatively, local production of ammonia may play a mole in the development of mucosal darn-

(i4).

changes

tinal series in two adult patients (8,10). Morrison et al (9) demonstrat-

going endoscopic examination (i2). Moreover, Dooley et al (7) recently reported a 32% prevalence of H pylon gastritis

inflammatory

to biopsy (10). been visualized

of patients, but the inflammation tends to be more severe in the antrum (7,11). H pylon gastritis is cornmon-it is present 50% of symptomatic

Severe

may result with acute infection. Masslike changes have been described at endoscopy in three adult

H pylon is a motile, gram-negative rod that is generally accepted as the cause of active, chronic type B gastrithe are

pounds, although infection tends to recur (i5,i6). Diagnosis of H pylon infection is usually made with endoscopic biopsy.

DISCUSSION

tis. Both stomach

Figures 2, 3. (2) CT scan shows a large gastric ulcer arising from the posterior gastric wall (arrow). The ulcer crater does not penetrate beyond the normal gastric lumen, a sign suggestive of ulceration within an intraluminal mass. (3) There is diffuse thickening of the posterior gastric wall along the greater curvature (arrow). This appearance can be seen in gastric adenocarcinoma, lymphoma, or metastasis.

distention administered

than (i7).

i cm Ade-

of the stomach with contrast material

is essential derdistention

for

thickening

of the

ally

abnormali-

CT evaluation, as unproduces apparent

gastric

wall

that

from malignancy adenocarcinoma

demonstrates

focal

ential thickening narrowing of the

of the lumen,

is usu-

or circumfer-

gastric and,

wall, occa-

Figure 4. CT scan shows that the the gastric antrum and duodenum mally thickened (arrow), which is ble with gastritis. The patient had ly undergone cholecystectomy.

sionally,

an

ulceration

lymphoma

wall

(17,20).

typically

thickening

produces

of 4-5

cm.

walls of are minicompatiprevious-

Gastric gastric

Lympho-

ma often involves more than one portion of the stomach, with no site predilection (20,21). Associated bulky adenopathy is more common with lymphoma. Benign leiornyomas produce focal, homogeneous masses that arise from the intramural smooth muscle and range in diameter from 1 to 9 cm (22). Leiomyosarcornas large, exophytic, nonhomogeneous masses

(20,22,23). appearance

averaging

Metastases and

are

12 cm in diameter have a varied

may

involve

the

June

1991

stomach

via direct

lymphatic

extension

extension

(colon),

(esophagus),

and

hematogenous spread (breast). CT is also sensitive in the detection of inflammatory processes in the stomach. Most commonly, this involves benign gastritis or gastric ulcers. Infectious processes such as toxoplasmosis

and

cryptosporidiosis

can cause nonspecific gastric wall thickening (24,25). However, even in the early CT literature, it was recognized that CT has a low specificity in distinguishing inflammatory changes from malignancy (20). Secondary signs such as obliteration of fat planes and evidence of direct cxtension can help differentiate malignant thickening from benign condilions such as prominent rugae and benign ulceration (20,26). The use of intravenously administered contrast material may also help differentiate an enhancing neoplasm from a nonenhancing, edematous gastric wall. To our knowledge, CT findings in H pylon infection have not previousiy been described. In our series, i9 of 6i cases (3i%) imaged over a 2-year period were prospectively interpreted as abnormal. Fourteen of those cases (74%) demonstrated changes reported as suspicious for malignancy. Furthermore,

in four

cases,

maiig-

nancy was entertained as the primary diagnosis. Two major patterns of severe infection were observed: (a) circumferential

antral

wail

and rior

thickening

(b) focal thickening of the postegastric wall along the greater curvature, with or without evidence of ulceration. Wall thickness averaged i.5-2.0 cm in cases suspicious for malignancy. Inflammation invoived both the antrum and body of the stomach, with the majority of cases involving the antrum (68% of abnormal cases). This correlates well with the known site predilection of H pylon for the gastric antrum. No cases demonstrated significant adenopathy, obliteration of fat planes, or direct extension into adjacent organs. In summary, H pylon infection is an increasingly recognized cause of infectious gastritis, even in asympto-

Volume

179

#{149} Number

3

matic individuals. The retrospective nature of this article limits our ability to correlate incidence and prevalence of radiographically detectable H pylori gastritis at CT. Furthermore, without a control series of patients who were without histologic evidence of H pylon infection, we cannot entirely exclude that the findings in this study may only be incidental. However, it is our opinion that the apparent inflammatory changes of H pylon gastritis can be severe enough to mimic gastric malignancy, especially in the antrum and greater curvature. With the increasing use of CT as a screening modality in the evaluation of the abdomen, previously unsuspected gastric masses and gastric wall thickening due to H pylon gastritis will likely be seen with increasing frequency. In most cases, these patients will require endoscopic biopsy and/or follow-up CT scanning for definitive

diagnosis,

ma and gastritis CT evaluation.

as early

can appear U

carcino-

similar

10.

11.

12.

13.

14.

15.

16.

17.

18.

at 19.

References 1.

2.

3.

4.

5.

6.

7.

8.

9.

Warren JR, Marshall BJ. Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet 1983; 1:12731275. Drumm B, Sherman B, Cutz E, Karmali M. Association of Campylobacter pylon on the gastric mucosa with antral gastritis in children. N Engl J Med 1987; 316:15571561. Blaser MJ. Helicobacter pylon and the pathogenesis of gastroduodenal inflammation. J Infect Dis 1990; 161:626-633. Dooley CP, Cohen H. The clinical significance of Campylobacter pylon. Ann Intern Med 1988; 108:70-79. Goodwin CS, Armstrong JA, Marshall BJ. Campylobacter pyloridis gastritis and peptic ulceration. J Clin Pathol 1986; 39:353-365. Rathbone BJ, Wyatt JI, Heatley RV. Campylobacter pyloridis-a new factor in peptic ulcer disease? Gut 1986; 39:353-365. Dooley CP, Cohen H, Fitzgibbons PL, et at. Prevalence of Helicobacter pylon infection and histologic gastritis in asymptomatic persons. N Engl J Med 1989; 321: 1562-1566. Frommer DJ, Carrick J, Lee A, Hazell SL. Acute presentation of Campylobacter pylon gastritis. Am J Gastroenterol 1988; 83: 1168-1171. Morrison S, Dahms BB, Hoffenberg E, Czinn SJ. Enlarged gastric folds in association with Campylobacten pylon gastritis. Radiology 1989; 171:819-821.

20.

21.

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23.

24.

25.

26.

Hazell SL, Carrick J, Edwards P. Frommer DL, Lee A. Acute infection with Campylobacten pylori can mimic gastric cancer (abstr). Gastroenterology 1988; 94:A178. Yardley JH. Campylobacten pylon and large gastric folds. Radiology 1989; 171: 609-611. Yardley JH, Paull G. Campylobacter pylon: a newly recognized infectious agent in the gastrointestinal tract. Am J Surg Pathol 1988; l2(suppl l):89-99. Perez-Perez GI, Dworkin B, Chodos J, Blaser MJ. Campylobacten pylon-specific serum antibodies in humans. Ann Intern Med 1988; 109:11-17. Sidebotham RL, Baron JH. Hypothesis: Helicobacten pylori, urease, mucus, and gastric ulcer. Lancet 1990; 335:193-195. Marshall BJ, Goodwin CS, Warren JR, et al. Prospective double-blind trial of duodenal ulcer relapse after eradication of Campylobacten pyloni. Lancet 1988; 2:14381442. Coghlan JG, Gilligan D, Humphries H, et al. Campylobacten pyloni and recurrence of duodenal ulcers: a 12-month follow-up study. Lancet 1987; 2:1109-1110. Lee JK, Sagel SS, Stanley RJ. Computed body tomography with MRI correlation. 2nd ed. New York: Raven, 1989; 485-492. Kaye MD, Young SW, Hayward R, Castellino PA. Gastric pseudotumor on CT scanning. AJR 1980; 135:190-193. Komaki S. Normal or benign gastric wall thickening demonstrated by computed tomography. J Comput Assist Tomogr 1982; 6:1103-1107. Balfe DM, Koehler RE, Karstaedt N, Stanley RJ, Sagel SS. Computed tomography of gastric neoplasms. Radiology 1981; 140:431-436. Buy JN, Moss AA. Computed tomography of gastric lymphoma. AJR 1982; 138:859-865. Megibow AJ, Balthazar EJ, Hulnick DH, Naidich DP, Bosniak MA. CT evaluation of gastrointestinal leiomyomas and leiomyosarcomas. AJR 1985; 144:727-731. Scatarige JC, Fishman EK, Jones B, Cameron JL, Sanders RC, Siegelman 55. Gastric leiomyosarcoma: CT observations. J Comput Assist Tomogr 1985; 9:320-327. Smart PE, Weinfeld A, Thompson NE, Dcfortuna SM. Toxoplasmosis of the stomach: a cause of antral narrowing. Radiology 1990; 174:369-370. Soulen MC, Fishman EK, Scatarige JC, Hutchins D, Zerhouni EA. Cryptosporidiosis of the gastric antrum: detection using CT. Radiology 1986; 159:705-706. Komaki S, Toyoshima S. CT’s capability in detecting advanced gastric cancer. Gastrointest Radiol 1983; 8:307-313.

Radiology

#{149} 691

Helicobacter pylori gastritis mimicking gastric carcinoma at CT evaluation.

The abdominal computed tomographic (CT) scans from 61 patients with biopsy-proved Helicobacter (formerly Campylobacter) pylori gastritis were retrospe...
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