Widespread clonal B-cell disorder in Sjogren's syndrome predisposing to Helicobacter pylori-related gastric lymphoma

S. De Vita, G. Ferraccioli, C. Avellini, D. Sorrentino, R. Dolcetti, C. Di Loreto, E. Bartoli, M. Boiocchi, C. A. Beltrami

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Abstract

Helicobacter pylori has been identified as a critical antigenic stimulus to the development of gastric lymphoma, but additional factors should be required for such evolution. This topic is now of major importance to clarify the pathobiology of gastric lymphomagenesis. Peculiar autoimmune diseases, such as Sjogren's syndrome, are well known to predispose to B-cell lymphomas. We report on a patient with Sjogren's syndrome and a widespread B-cell lymphoproliferative disorder. A pathological picture of low-grade lymphoma was observed in the stomach, concomitantly with H. pylori infection. However, the B-cell disorder was definitely nonmalignant in the other tissues involved, i.e., the parotid gland and lymph nodes, which are the characteristic targets of Sjogren's syndrome-associated lymphoproliferation. After H. pylori eradication, a dramatic regression of gastric lymphoma into chronic gastritis was observed, but no amelioration occurred in the parotid and nodal involvement. Multiple molecular analyses showed the expansion of the same B-cell clone in synchronous and metachronous lymph node, parotid, and gastric lesions before and after H. pylori eradication. Thus, H. pylori played a crucial role in the local boosting of B-cell lymphoproliferation, but the underlying B-cell disorder was that associated with the autoimmune disease and was nonmalignant. The comprehensive clinical, pathological, and molecular approach allowed us to then distinguish the role of peculiar individual predisposing factors and of local infection in the pathobiology of mucosa-associated lymphoid tissue-associated lymphoproliferation.

Original languageEnglish
Pages (from-to)1969-1974
Number of pages6
JournalGastroenterology
Volume110
Issue number6
DOIs
Publication statusPublished - 1996

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Sjogren's Syndrome
Helicobacter pylori
B-Lymphocytes
Stomach
Autoimmune Diseases
Lymph Nodes
Lymphoproliferative Disorders
Parotid Gland
Helicobacter Infections
B-Cell Lymphoma
Lymphoid Tissue
Gastritis
Causality
Non-Hodgkin's Lymphoma
Mucous Membrane
Clone Cells
Familial primary gastric lymphoma
Infection

ASJC Scopus subject areas

  • Gastroenterology

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Widespread clonal B-cell disorder in Sjogren's syndrome predisposing to Helicobacter pylori-related gastric lymphoma. / De Vita, S.; Ferraccioli, G.; Avellini, C.; Sorrentino, D.; Dolcetti, R.; Di Loreto, C.; Bartoli, E.; Boiocchi, M.; Beltrami, C. A.

In: Gastroenterology, Vol. 110, No. 6, 1996, p. 1969-1974.

Research output: Contribution to journalArticle

De Vita, S, Ferraccioli, G, Avellini, C, Sorrentino, D, Dolcetti, R, Di Loreto, C, Bartoli, E, Boiocchi, M & Beltrami, CA 1996, 'Widespread clonal B-cell disorder in Sjogren's syndrome predisposing to Helicobacter pylori-related gastric lymphoma', Gastroenterology, vol. 110, no. 6, pp. 1969-1974. https://doi.org/10.1053/gast.1996.v110.pm8964425
De Vita, S. ; Ferraccioli, G. ; Avellini, C. ; Sorrentino, D. ; Dolcetti, R. ; Di Loreto, C. ; Bartoli, E. ; Boiocchi, M. ; Beltrami, C. A. / Widespread clonal B-cell disorder in Sjogren's syndrome predisposing to Helicobacter pylori-related gastric lymphoma. In: Gastroenterology. 1996 ; Vol. 110, No. 6. pp. 1969-1974.
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AU - Avellini, C.

AU - Sorrentino, D.

AU - Dolcetti, R.

AU - Di Loreto, C.

AU - Bartoli, E.

AU - Boiocchi, M.

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AB - Helicobacter pylori has been identified as a critical antigenic stimulus to the development of gastric lymphoma, but additional factors should be required for such evolution. This topic is now of major importance to clarify the pathobiology of gastric lymphomagenesis. Peculiar autoimmune diseases, such as Sjogren's syndrome, are well known to predispose to B-cell lymphomas. We report on a patient with Sjogren's syndrome and a widespread B-cell lymphoproliferative disorder. A pathological picture of low-grade lymphoma was observed in the stomach, concomitantly with H. pylori infection. However, the B-cell disorder was definitely nonmalignant in the other tissues involved, i.e., the parotid gland and lymph nodes, which are the characteristic targets of Sjogren's syndrome-associated lymphoproliferation. After H. pylori eradication, a dramatic regression of gastric lymphoma into chronic gastritis was observed, but no amelioration occurred in the parotid and nodal involvement. Multiple molecular analyses showed the expansion of the same B-cell clone in synchronous and metachronous lymph node, parotid, and gastric lesions before and after H. pylori eradication. Thus, H. pylori played a crucial role in the local boosting of B-cell lymphoproliferation, but the underlying B-cell disorder was that associated with the autoimmune disease and was nonmalignant. The comprehensive clinical, pathological, and molecular approach allowed us to then distinguish the role of peculiar individual predisposing factors and of local infection in the pathobiology of mucosa-associated lymphoid tissue-associated lymphoproliferation.

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