BACKGROUND: Infection by Helicobacter pylori has been linked to monoclonal gammopathy of undetermined significance (MGUS). MGUS is thought to develop due to chronic antigenic stimulation in people with a specific genetic predisposition. METHODS AND RESULTS: We describe a patient presenting with dyspepsia associated with H. pylori-related erosive gastritis. Histopathologic findings revealed infiltration with plasma cells containing accumulated condensed intercisternal immunoglobulins, the so-called 'Russell bodies'. In addition, MGUS was present with total immunoglobulins within the normal range but a significantly decreased serum concentration of IgG subtype 3. Molecular analyses demonstrated IgH formation, T-cell receptor gamma rearrangement, and alterations within the IgHG3 gene sequence. Following H. pylori eradication, gastritis and dyspepsia gradually resolved but MGUS persisted for at least 22 months. CONCLUSIONS: This is the first report to demonstrate that upon infection with H. pylori, an impaired secretory capacity of plasma cells due to specific molecular changes can present as Russell body gastritis. The molecular findings question a pathogenetic link between Russell bodies and H. pylori, but suggest genetic alterations in the immunoglobulin locus as the possible cause for both MGUS and Russell body gastritis.
BACKGROUND: Infection by Helicobacter pylori has been linked to monoclonal gammopathy of undetermined significance (MGUS). MGUS is thought to develop due to chronic antigenic stimulation in people with a specific genetic predisposition. METHODS AND RESULTS: We describe a patient presenting with dyspepsia associated with H. pylori-related erosive gastritis. Histopathologic findings revealed infiltration with plasma cells containing accumulated condensed intercisternal immunoglobulins, the so-called 'Russell bodies'. In addition, MGUS was present with total immunoglobulins within the normal range but a significantly decreased serum concentration of IgG subtype 3. Molecular analyses demonstrated IgH formation, T-cell receptor gamma rearrangement, and alterations within the IgHG3 gene sequence. Following H. pylori eradication, gastritis and dyspepsia gradually resolved but MGUS persisted for at least 22 months. CONCLUSIONS: This is the first report to demonstrate that upon infection with H. pylori, an impaired secretory capacity of plasma cells due to specific molecular changes can present as Russell body gastritis. The molecular findings question a pathogenetic link between Russell bodies and H. pylori, but suggest genetic alterations in the immunoglobulin locus as the possible cause for both MGUS and Russell body gastritis.
Authors: Antonietta Gerarda Gravina; Rocco Maurizio Zagari; Cristiana De Musis; Lorenzo Romano; Carmelina Loguercio; Marco Romano Journal: World J Gastroenterol Date: 2018-08-07 Impact factor: 5.742
Authors: Jung Bin Yoon; Tae Yeong Lee; Jin Sook Lee; Jong Min Yoon; Se Won Jang; Min Jung Kim; Su Jin Lee; Tae Oh Kim Journal: Clin Endosc Date: 2012-11-30