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2010, Volume 26, Number 2, Page(s) 159-161
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DOI: 10.5146/tjpath.2010.01015
“Russell Body” Gastritis: A Case Report
Ahmet MİDİ1, Çiğdem ATAİZİ ÇELİKEL2, Handan KAYA2
1Department of Pathology, Marmara University, Faculty of Medicine, İSTANBUL, TURKEY
2Department of Pathology, Marmara University, Faculty of Medicine, İSTANBUL, TURKEY
Keywords: Russell body, Gastritis, Helicobacter pylori, Mott cells
Abstract
Our case was a 50-year-old female who presented at the outpatients department with dyspeptic symptoms. Microscopical examination of mucosal samples from the corpus and antrum showed widespread Helicobacter pylori within the superficial mucus network, marked neutrophilic cryptitis, widespread reactive/regenerative crypt hyperplasia, intestinal metaplasia, and increased lymphoplasmocytoid cells and plasma cells full of immunoglobulin in the lamina propria. Immunohistochemical staining showed the plasma cells to be CD3 (-), CD20 (-), CD79a (+), CD45 (+), Kappa (+), and Lambda (+).

It is possible for a dense accumulation of Russell bodies to be observed on a background of H. pylori taking into account that Russell bodies contain immunoglobulin aggregates and side products of immunoglobulin synthesis. However, there are only a limited number of articles evaluating this aspect.

We present a case to contribute to the few articles on Helicobacter gastritis characterized by an inflammatory reaction rich in ‘'Russell'' bodies.

Introduction
Johansen A et al have studied the diagnostic significance of Russell body-containing cells in endoscopic biopsies in 19771. However, the term “Russell body gastritis” has first been used by Tazawa K et al2.

Russell bodies occur as a result of a block in the normal pathways of immunoglobulin secretion in plasma cells. Mott cells are plasma cells filled with Russell bodies. Russell bodies have been reported in many types of chronic inflammation and in various B cell lymphocytic neoplasms3-7. Plasma cells are found together with lymphocytes, neutrophils and eosinophils in chronic gastritis. However, only 9 cases of chronic gastritis with plasma cell infiltration where Mott cells are dominant have been reported8-12.

We describe a case in light of the literature as H. pylori gastritis characterized by an inflammatory reaction with widespread distribution of plasma cells full of Russell bodies (Mott cells) in the lamina propria.

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  • Abstract
  • Introduction
  • Case Presentation
  • Disscussion
  • References
  • Case Presentation
    Our case was a 50-year-old female with dyspeptic symptoms.

    Endoscopic Findings: These consisted of hyperemia of fundus and antrum mucosa, prominent submucosal vessel network in the fundus and mucosal irregularity at the posterior wall.

    Microscopic Findings: Mucosal samples of the antrum and corpus showed: H. pylori in the superficial mucus network, neutrophilic cryptitis in the gland and surface epithelium, widespread reactive/regenerative crypt hyperplasia, multifocal atrophy, intestinal metaplasia (Figure 1), plasma cells containing homogenous eosinophilic cytoplasmic globules in the lamina propria (Figure 2).


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    Figure 1: Widespread reactive/regenerative crypt hyperplasia, multifocal atrophy, complete colonic type intestinal metaplasia, and neutrophilic cryptitis in the gland and surface epithelium (H&E, x40).


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    Figure 2: Plasma cells containing homogenous eosinophilic globules in the lamina propria (H&E, x200).

    Immunohistochemistry Panel: CD20 and CD3 (-), and CD45 and CD79a (+) immune reaction in the plasma cells (Figures 3), positive immune reaction in some plasma cells with Kappa and Lambda (Figure 4).


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    Figure 3: CD45 (left, DAB, x100) and CD79a (right, DAB, x200) positive lymphocytes.


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    Figure 4: Positive immune reaction in some plasma cells with kappa (left, DAB, x400) and lambda (right, DAB, x200).

    Pathology Diagnosis: “Russell body” gastritis, multifocal atrophy, intestinal metaplasia, and H. pylori (+)

  • Top
  • Abstract
  • Introduction
  • Case Presentation
  • Disscussion
  • References
  • Discussion
    “Russell body gastritis” has been considered to be a different presentation of Helicobacter pylori gastritis in our case and all other published cases2,8-12. The mechanism may be plasma cell hyperactivation caused by chronic H. pylori infection and the immunoglobulin overproduction leading to Russell body formation. Johansen A et al. reported that Mott cells are found in significantly higher number at the periphery of cancerous samples but they have not mentioned the H. pylori state in their study1. An esophageal and a cervical case characterized by infiltration with plasma cells filled with Russell bodies have also been reported3,4. Such similar lesions outside the stomach indicate that Russell body formation may be associated with Helicobacter pylori or may develop due an antigenic stimulus as a result of chronic infection or some other reason. The disappearance of Mott cells during H. pylori eradication in the stomach also shows that the factor causing Russell body formation is Helicobacter pylori2.

    It is reported that plasma cell infiltration increases 2.5 times while the lymphocyte ratio stays constant in atrophic antral gastritis due to H. pylori13. The immunoglobulin response developing against H. pylori is accepted to start first in the gastric mucosa in this disorder. This response is reported to end with an IgA dominant response in the mucosa and an IgG dominant systemic response outside the mucosa14. Taking into account that Russell bodies contain immunoglobulin aggregates or side products of immunoglobulin synthesis, it is normal for Russell bodies to be densely located on a background of H. pylori. However, there are only a limited number of studies on the incidence of plasma cells containing Russell bodies in the gastric mucosa.

    Johansen A et al have compared the peritumoral mucosa in patients with carcinoma (n=315) and gastric biopsies in patients without carcinoma (n=786) for the density of plasma cells containing Russell bodies. The significantly higher density or plasma cells containing Russell bodies in this study led to the statement that these cells could be important for adenocarcinoma development1. We did not see any neoplastic progression in any of the 3 control endoscopies within the last 2 years. Fujiyoshi Y. has defined a Mott cell tumor developing due to the abnormal proliferation of IgG kappa monotypic plasma cells containing Russell bodies on a background of H. pylori6. We thought that this tumor that had metastasized to the perigastric lymph nodes could be the MALT-lymphoma type developing from mucosadependent lymphoid tissue. We found polyclonality with the kappa and lambda immunohistochemistry stain used in our case and did not observe lymphoma development during follow-up.

    Diffuse infiltration of plasma cells with Russell bodies in the gastric mucosa requires differentiating between several diagnoses5,6. Cytokeratin negativity excludes signetring cell carcinoma while the kappa and lambda polyclonal immunoreactive pattern excludes lymphoplasmacytic lymphoma and plasmocytoma. The lesion can be differentiated from mucosa-associated lymphoid tissue (MALT) lymphoma with extreme plasmacytic differentiation with the absence of cytologic atypia, lymphoepithelial lesions, centrocyte-like cells and monocytoid cells.

    Russell body gastritis needs to be kept in mind as it may be difficult to diagnose in biopsies consisting of small fragments.

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  • Abstract
  • Introduction
  • Case Presentation
  • Discussion
  • References
  • References

    1) Johansen A, Sikjär B: The diagnostic significance of Russell bodies in endoscopic gastric biopsies. Acta Pathol Microbiol Scand [A] 1977, 85A:245-250 [ PubMed ]

    2) Tazawa K, Tsutsumi Y: Localized accumulation of Russell bodycontaining plasma cells in gastric mucosa with Helicobacter pylori infection: ‘Russell body gastritis'. Pathol Int 1998, 48:242- 24495894963) Rubio CA: Mott cell (Russell bodies) Barrett's oesophagitis. In Vivo 2005, 19:1097–1100 [ PubMed ]

    4) C.J. Stewart, R. Leake: Reactive plasmacytic infiltration with numerous Russell bodies involving the uterine cervix: ‘Russell body cervicitis', Pathology 2006, 38:177–179 [ PubMed ]

    5) Kurihara K, Sakai H, Hashimoto N: Russell body-like inclusions in oral B-lymphomas, J Oral Pathol 1984, 13:640–649 [ PubMed ]

    6) Fujiyoshi Y, lnagaki H, Tateyama H, Murase T, Eimoto T: Mott cell tumor of the stomach with Helicobacter pylori infection. Pathol Int 2001, 51:43-46 [ PubMed ]

    7) Malik AA, Ganti AK, Potti A, Levitt R, Hanley JF: Role of Helicobacter pylori infection in the incidence and clinical course of monoclonal gammopathy of undetermined significance. Am J Gastroenterol 2002, 97:1371–1374 [ PubMed ]

    8) Ensari A, Savas B, Okcu Heper A, Kuzu I, Idilman R: An unusual presentation of Helicobacter pylori infection: so-called ‘Russell body gastritis'. Virchows Arch 2005, 446:463–466 [ PubMed ]

    9) Pizzolitto S, Camilot D, DeMaglio G, Falconieri G: Russell body gastritis: Expanding the spectrum of Helicobacter pylori – related diseases? Pathol Res Pract 2007, 203:457-460 Epub 2007 Mar 28. [ PubMed ]

    10) Erbersdobler A, Petri S, Lock G: Russell body gastritis: An unusual, tumor-like lesion of the gastric mucosa. Arch Pathol Lab Med 2004, 128:915–917 [ PubMed ]

    11) Drut R, Olenchuk A B: Images in pathology. Russell body gastritis in an HIV-positive patient, Int J Surg Pathol 2006, 14:141–142 [ PubMed ]

    12) Wolkersdörfer GW, Haase M, Morgner A, Baretton G, Miehlke S: Monoclonal gammopathy of undetermined significance and Russell body formation in Helicobacter pylori gastritis. Helicobacter 2006, 11:506-510 [ PubMed ]

    13) Aruin LI, Shatalova OL: Immunoglobulin-secreting stomach cells in peptic ulcer. Arkh Patol 1983, 45:38-45 [ PubMed ]

    14) Schmausser B, Eck M, Greiner A, Lührs H, Vollmers HP, Müller- Hermelink HK: Disparity between mucosal and serum IgA and IgG in Helicobacter pylori infection.Virchows Arch 2002, 441:143-147 [ PubMed ]

  • Top
  • Abstract
  • Introduction
  • Case Presentation
  • Discussion
  • References
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