Russell Body Gastritis Associated with Helicobacter pylori Infection in an HIV-Positive Patient: Case Report and Review of the Literature

Abstract

In 1998 Tazawa and Tsutsumi described for the first time a case of Helicobacter pylori (HP)-related gastritis characterized by the presence of a conspicuous plasma cell infiltrate with Russell bodies, and coined the term Russell body gastritis (RBG). A 59-year-old HIV-positive man complaining of recurrent epigastric pain underwent an upper gastrointestinal endoscopy revealing in the stomach only hyperemia in the antral portion. Histology showed a moderate glandular atrophy associated with an expansion of the lamina propria due to an infiltration of monomorphous cells with eosinophilic cytoplasm inclusions and eccentric nuclei, somewhat resembling plasma cells. A diagnosis of HP-related RBG was made, after excluding, by means of histochemical, immunohistochemical stainings and molecular studies, a neoplastic process. A review of all cases of RBG previously described in the English literature is reported in order to examine the clinical, endoscopic and microscopic features of this histopathological entity and the possible pathogenetic mechanisms.

Russell Body Gastroenteritis: An Aberrant Manifestation of Chronic Inflammation in Gastrointestinal Mucosa

“…The highly pathogenic Helicobacter pylori genotypes vacA and cagA may also be associated with RBG [23]. The disappearance of Russell bodies following successful Helicobacter pylori eradication therapy also supports the etiopathogenic role of the organism in RBG [1, 3, 7, 10, 11, 13, 15]. In 2006, Stewart and Spagnola reported three cases of Helicobacter -associated gastritis with crystalline plasma cell inclusions, which may represent another morphologic manifestation of immunoglobulin accumulation in response to chronic gastritis [24].…”

“…Of the 20 gastric cases, 12 showed evidence of Helicobacter pylori infection; all 4 extragastric (duodenal and esophageal) cases were H. pylori negative. Other associated conditions included HIV infection [9, 11, 16, 20], ethanol abuse [1, 5], gastric carcinoma [14, 19], Barrett esophagus [22], monoclonal gammopathy of uncertain significance [8], and concurrent Hepatitis C infection and insulin-dependent diabetes mellitus [17]. …”

Duodenal localization of plasmablastic myeloma

“…In fact, the presence of neoplastic atypical cells diffusely infiltrating the lamina propria among glandular structures may be easily misdiagnosed as a poorly differentiated carcinoma. Furthermore, even in well differentiated cases with recognizable plasma cells, the issue can be complicated by the presence of numerous Russel bodies - spherical intracytoplasmic eosinophilic immunoglobulin - containing structures, easily detectable by microscopic observation-either in association with neoplastic plasma cell proliferation, in cases of lymphoproliferative disorders displaying a certain degree of plasma cell differentiation, or in non-neoplastic, inflammatory processes characterized by a conspicuous plasma cell infiltrate, such as the so-called Russell body gastritis[3]. In such cases, plasma cells can take on the form of the signet-ring cells of poorly differentiated mucinous carcinoma of the gastrointestinal tract.…”

Rare Gastric Lesions Associated with Helicobacter pylori Infection: A Histopathological Review

“…For example, H. pylori is detected in approximately two-thirds of patients with RBG [8,9,19-21,48,50,52,53,55,57,60,61]. Few other infections that have been reported with RBG include human immunodeficiency virus (three patients) [51,53,59], hepatitis C virus (one patient) [58], and candida esophagitis (one case) [49]. In addition, more than 60% of patients with RBG exhibit lesion regression following H. pylori eradication therapy [19-21,53,60].…”

“…Few other infections that have been reported with RBG include human immunodeficiency virus (three patients) [51,53,59], hepatitis C virus (one patient) [58], and candida esophagitis (one case) [49]. In addition, more than 60% of patients with RBG exhibit lesion regression following H. pylori eradication therapy [19-21,53,60]. Furthermore, it has been reported that highly virulent H. pylori genotypes (vacA and cagA) are associated with the formation of Russell bodies and Mott cells in the antral mucosa [62].…”