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.
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 neoplasms[3-7]. 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 reported[8-12].
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.
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).
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).
Figure 3: CD45 (left, DAB, x100) and CD79a (right, DAB, x200) positive lymphocytes.
Pathology Diagnosis: “Russell body” gastritis, multifocal atrophy, intestinal metaplasia, and H. pylori (+)
It is reported that plasma cell infiltration increases 2.5 times while the lymphocyte ratio stays constant in atrophic antral gastritis due to H. pylori[13]. 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 mucosa[14]. 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 development[1]. 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. pylori[6]. 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 diagnoses[5,6]. 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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