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J Clin Pathol. 2007 September; 60(9): 1071–1072.
PMCID: PMC1972411

Helicobacter pylori‐associated peptic ulcer and florid follicular gastritis mimicking a malignancy

In chronic follicular gastritis the lymphoid follicles are usually localised in the lamina propria.1 In lymphoid hyperplasia associated with a chronic peptic ulcer, numerous lymphoid follicles are sometimes present in the ulcer base, in which the muscularis propria has usually been destroyed and replaced by scar tissue.2 The histology of Helicobacter‐associated chronic gastritis with numerous reactive lymphoid follicles and an indistinct poorly developed marginal zone may closely simulate lymphoma and pose a diagnostic challenge. We present an extreme example of florid follicular gastritis, which mimicked a malignant neoplasm clinically and pathologically. To our knowledge, such florid hyperplasia with reactive lymphoid follicles extending into the muscularis propria and beyond has never been reported.

A 65‐year‐old man presented with intermittent abdominal hunger pain for one month. Endoscopic biopsies revealed a Bormann type II antral ulcer with H pylori infection. Endoscopic findings and image study strongly suggested gastric cancer; a subtotal gastrectomy and regional lymph node dissection were performed. On the lesser curvature side of the antrum, there was a tumour‐like lesion, 4×3×1 cm with ulceration and slightly elevated margins. The cut surface was whitish and firm with effacement of the gastric muscle wall (fig 11).). Microscopically, sections of stomach show ulcerated antral mucosa with an adjacent and underlying intense chronic inflammatory infiltrate comprising reactive germinal centres surrounded by a narrow mantle zone with some peripheral lymphocytes. Beneath the ulcer there was intense scarring with destruction of the muscularis propria, which was preserved lateral to the ulcer margins. The hyperplastic lymphoid follicles extended into the scar tissue, muscularis propria and serosa (fig 22).). Bacilli morphologically typical of H pylori were identified. There were no lymphoepithelial lesions or aggregates of centrocyte‐like atypical lymphocytes to suggest mucosa‐associated lymphoid tissue (MALT) lymphoma. The dissected regional nodes measured up to 2.2 cm in diameter and revealed marked follicular hyperplasia.

figure cp44768.f1
Figure 1 Cut surface of the antral ulcerative lesion is whitish and firm with effacement of the gastric wall.
figure cp44768.f2
Figure 2 Photomicrography shows ulceration in the left upper corner and extensive and transmural lymphoid infiltration (A) with extension through the muscularis propria into the subserosa (C). A higher‐power view shows a germinal centre ...

Immunohistochemistry showed that the germinal centre cells were positive for CD10 and bcl‐6 but not bcl‐2 and they expressed polytypic light chains. The surrounding mantle zone lymphocytes expressed immunoglobulin M (IgM) and IgD without a significant population of IgM‐positive IgD‐negative marginal zone cells. CD3‐positive T‐cells were seen between the follicles. Clonality study using PCR with paraffin‐embedded sections for the framework three region of the Ig heavy chain gene showed polyclonal results.3

Isaacson and Wright proposed the concept of MALT lymphoma in 1983 for a low‐grade gastric B‐cell lymphoma with a distinct indolent clinical course, which is frequently associated with H pylori infection.4 The term “pseudolymphoma” had been used previously to describe lymphoid lesions that show borderline features between hyperplasia and neoplasia or benign tumour‐like enlargement of lymphoid tissue. In a large retrospective morphological and immunophenotypic review of 97 pseudolymphomas, Abbondanzo and Sobin found that the majority (77 cases) were malignant lymphoma, mainly MALT lymphoma, with the remaining 20 cases being reactive lymphoid hyperplasia associated with chronic follicular gastritis (15 cases) or atypical lymphoid infiltrate (5 cases).1 In the 15 cases of chronic follicular gastritis, the reactive germinal centres were localised in the lamina propria, while the remaining five cases (three partial gastrectomies and two endoscopic biopsies) revealed diffuse atypical lymphoid infiltrate that could not be further characterised.

Lymphoid infiltrate with reactive germinal centre formation may be present in follicular gastritis and MALT lymphoma, while dense aggregates of lymphoid follicles may mimic follicular lymphoma. Florid lymphoid hyperplasia in the current case is extremely unusual. Careful histopathological examination and immunohistochemical (and molecular) study revealed the reactive nature of this lesion.

Footnotes

Competing interests: None declared.

References

1. Abbondanzo S L, Sobin L H. Gastric “pseudolymphoma”: a retrospective morphologic and immunophenotypic study of 97 cases. Cancer 1997. 791656–1663.1663 [PubMed]
2. Isaacson P G, Norton A J. Malignant lymphoma of the gastrointestinal tract. In: Isaacson PG, Norton AJ, eds. Extranodal lymphomas. London: Churchill Livingstone, 1994. 35
3. Chuang S S, Lin C N, Shen F C. et al Detecting clonal rearrangement in non‐Hodgkin's lymphomas in Taiwan by polymerase chain reaction. Leuk Lymphoma 2003. 44117–121.121 [PubMed]
4. Isaacson P G, Wright D H. Malignant lymphoma of mucosa‐associated lymphoid tissue. A distinctive type of B‐cell lymphoma. Cancer 1983. 521410–1416.1416 [PubMed]

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