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Invited Commentary

Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania

	Commentary

Top Commentary References

 
The stomach is the most frequent site of gastrointestinal involvement by non-Hodgkin lymphoma, accounting for about one-half of the cases (1). The development of primary gastric lymphoma raises the fascinating question of how a lymphomatous lesion arises in an organ normally devoid of lymphoid tissue. This seeming paradox baffled investigators until the discovery of H pylori by Warren and Marshall in 1983 (2). Since that time, it has been shown that chronic H pylori gastritis causes the lamina propria of the stomach to become inundated with lymphoid aggregates and follicles, also known as mucosa-associated lymphoid tissue (MALT) (3,4). Over a period of time, this lymphoid tissue may degenerate into gastric MALT lymphoma, a low-grade form of B-cell lymphoma considered to be the precursor lesion for most advanced gastric lymphomas (5–7).

Because of the role of H pylori gastritis in the pathogenesis of gastric MALT lymphoma, considerable attention has been focused on the exciting possibility of treating these patients by eradicating H pylori from the stomach without the need for surgery, radiation, or chemotherapy (8,9). However, as already indicated, untreated gastric MALT lymphomas may undergo blastic transformation, eventually leading to the development of more advanced, high-grade forms of gastric lymphoma. This pathologic sequence of events has major implications for patient prognosis; low-grade gastric MALT lymphomas are associated with 5-year survival rates of 75%–91% (10,11), whereas high-grade gastric lymphomas are associated with 5-year survival rates of less than 50% (11).

On the basis of the available data, early diagnosis and treatment of gastric MALT lymphoma could have a substantial effect on patients’ long-term survival. Although MALT lymphomas do not necessarily cause symptoms, affected individuals may nonetheless seek medical attention because of chronic epigastric pain or dyspepsia related to their underlying H pylori gastritis (12). Whatever the explanation, the presence of symptoms in patients with gastric MALT lymphoma provides a remarkable opportunity to detect these tumors at an early and curable stage.

The excellent study by An et al (13) in this issue of RadioGraphics supports earlier observations that gastric MALT lymphoma may be manifested at double-contrast UGI examination by a spectrum of findings, including ulcers, masses, thickened folds, mucosal nodularity, and enlarged areae gastricae (12,14,15). Depending on the predominant morphologic features, it may be difficult to differentiate these tumors from gastric cancer (both early and advanced) or various forms of gastritis with barium studies (12,14,15). However, in the study by An et al (13), nearly 30% of patients with gastric MALT lymphoma had a nodular gastric mucosa. As previously described, this finding is characterized at double-contrast study by multiple rounded, variably sized (2–7 mm in diameter), often confluent nodules with poorly defined borders (12,14). The nodularity is thought to result from focal infiltration and expansion of the lamina propria by proliferating lymphoid aggregates (12). Therefore, early experience indicates that the diagnosis of gastric MALT lymphoma can be suggested on the basis of the radiographic findings in a substantial number of cases.

Other considerations in the differential diagnosis of a nodular gastric mucosa include various forms of gastritis and, less commonly, neoplastic lesions in patients with disseminated metastases or leukemic deposits or even a polyposis syndrome (12). This nodularity must also be differentiated from enlarged areae gastricae, a finding known to be associated with H pylori gastritis (16). However, enlarged areae gastricae tend to be more uniform in size, producing a sharply marginated reticular network. Lymphoid hyperplasia of the stomach has been recognized as another cause of mucosal nodularity resulting from the development of enlarged lymphoid follicles in patients with chronic H pylori gastritis (17). This lymphoid hyperplasia is characterized at double-contrast study by innumerable tiny (1–3 mm in diameter), round, frequently umbilicated nodules that carpet the gastric antrum or the gastric antrum and body (18). In many cases, therefore, the nodules of lymphoid hyperplasia can be differentiated from the nodules of MALT lymphoma by their more discrete borders and smaller and more uniform size. However, endoscopy or biopsy should be performed for a more definitive diagnosis if the radiographic findings are equivocal.

Because gastric MALT lymphoma is a curable disease, radiologists should have a low threshold for suggesting this diagnosis when suspicious findings are present at barium study. Although some patients who undergo endoscopy will be found to have gastritis or other benign gastric lesions, it seems reasonable to accept a certain percentage of false-positive diagnoses to detect these tumors at the earliest possible stage. Ultimately, further investigation is needed to better delineate the morphologic features of gastric MALT lymphoma at double-contrast barium study. Nevertheless, an aggressive approach seems warranted for patients with possible radiographic findings of gastric MALT lymphoma because of the important ramifications of early diagnosis of this treatable form of malignant tumor.

	References

Top Commentary References

 

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3. Eidt S, Stolte M. Prevalence of lymphoid follicles and aggregates in Helicobacter pylori gastritis in antral and body mucosa. J Clin Pathol 1993; 46:832-835.[Abstract/Free Full Text]
4. Genta RM, Hamner HW, Graham DY. Gastric lymphoid follicles in Helicobacter pylori infection: frequency, distribution, and response to triple therapy. Hum Pathol 1993; 24:577-583.[Medline]
5. Wotherspoon AC, Ortiz-Hidalgo C, Falzon MR, Isaacson PG. Helicobacter pylori-associated gastritis and primary B-cell gastric lymphoma. Lancet 1991; 338:1175-1176.[Medline]
6. Eidt S, Stolte M, Fischer R. Helicobacter pylori gastritis and primary gastric non-Hodgkin’s lymphomas. J Clin Pathol 1994; 47:436-439.[Abstract/Free Full Text]
7. Chan JKC, Ng CS, Isaacson PG. Relationship between high-grade lymphoma and low-grade B-cell mucosa-associated lymphoid tissue lymphoma (MALToma) of the stomach. Am J Pathol 1990; 136:1153-1164.[Abstract]
8. Bayerdorffer E, Neubauer A, Rudolph B, et al. Regression of primary gastric lymphoma of mucosa-associated lymphoid tissue type after cure of Helicobacter pylori infection. Lancet 1995; 345:1591-1594.[Medline]
9. Roggero E, Zucca E, Pinotti G, et al. Eradication of Helicobacter pylori infection in primary low-grade gastric lymphoma of mucosa-associated lymphoid tissue. Ann Intern Med 1995; 122:767-769.[Abstract/Free Full Text]
10. Cogliatti SB, Schmid U, Schumacher U, et al. Primary B-cell gastric lymphoma: a clinicopathologic study of 145 patients. Gastroenterology 1991; 101:1159-1170.[Medline]
11. Taal BG, Boot H, van Heerde P, de Jong D, Hart AAM, Burgers JMV. Primary non-Hodgkin lymphoma of the stomach: endoscopic pattern and prognosis in low versus high grade malignancy in relation to the MALT concept. Gut 1996; 39:556-561.[Abstract/Free Full Text]
12. Yoo CC, Levine MS, Furth EE, et al. Gastric mucosa-associated lymphoid tissue lymphoma: radiographic findings in six patients. Radiology 1998; 208:239-243.[Abstract/Free Full Text]
13. An SK, Han JK, Kim YH, et al. Gastric mucosa-associated lymphoid tissue lymphoma: spectrum of findings at double-contrast gastrointestinal examination with pathologic correlation. RadioGraphics 2001; 21:000-000.
14. Levine MS, Elmas N, Furth EE, Rubesin SE, Goldwein MI. Helicobacter pylori and gastric MALT lymphoma. AJR Am J Roentgenol 1996; 166:85-86.[Free Full Text]
15. Kim YH, Lim HK, Han JK, et al. Low-grade gastric mucosa-associated lymphoid tissue lymphoma: correlation of radiographic and pathologic findings. Radiology 1999; 212:241-248.[Abstract/Free Full Text]
16. Sohn J, Levine MS, Furth EE, et al. Helicobacter pylori gastritis: radiographic findings. Radiology 1995; 195:763-767.[Abstract/Free Full Text]
17. Sbeih F, Abdullah A, Sullivan S, Merenkov Z. Antral nodularity, gastric lymphoid hyperplasia, and Helicobacter pylori in adults. J Clin Gastroenterol 1996; 22:227-230.[Medline]
18. Torigian DA, Levine MS, Gill NS, et al. Lymphoid hyperplasia of the stomach: radiographic findings in five adult patients. AJR Am J Roentgenol 2001; 177:71-75.[Abstract/Free Full Text]

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