Localized light chain amyloidosis of the stomach that regressed after eradication of Helicobacter pylori over 15 years of follow-up: a case report and new hypothesis.

Abstract

Localized light chain amyloidosis is considered to be a plasmacytic B-cell lymphoproliferative disorder caused by antigenic induction. A hypothesis has been proposed that antigen-induced local plasmacytic B cells produce amyloidogenic proteins that are processed into amyloid fibrils in giant cells leading to amyloid fibril deposition. However, the inciting antigen exposure or immune response that signals plasmacytic B-cell infiltration, activation, and selection, is unknown. A case of localized light chain amyloidosis of the stomach that gradually regressed endoscopically after Helicobacter pylori eradication is presented. Histologically, plasmacytes decreased markedly and macrophages disappeared after eradication, and they are thought to play important roles in amyloid formation. There have been no reports of localized gastric amyloidosis in which the lesion regressed and few reports showing the relationship between localized gastric amyloidosis and Helicobacter pylori infection that evaluated the changes after eradication. Given the review of the latest findings about localized light chain amyloidosis, in addition to circumstantial evidence from the clinical course of this case, we would like to propose a bold new hypothesis that Helicobacter pylori could be one of the antigens inducing localized light chain amyloidosis of the stomach.