Retroperitoneal and aortic manifestations of immunoglobulin G4-related disease

Semin Diagn Pathol. 2012 Nov;29(4):212-8. doi: 10.1053/j.semdp.2012.07.003.

Abstract

Retroperitoneal fibrosis is one of the prototypic manifestations of immunoglobulin G4 (IgG4)-related disease (IgG4-RD), but there is growing evidence that the aorta is also involved. These 2 conditions are closely linked, and based on the epicenter of the disease, the clinical manifestations can be classified as retroperitoneal fibrosis, inflammatory abdominal aortic aneurysm (including a combination of the 2), and thoracic aortitis. IgG4-RD is responsible for only a subset (∼50%) of cases of retroperitoneal fibrosis and inflammatory aortic aneurysms. Histological features include an extensive lymphoplasmacytic infiltrate rich in IgG4-positive plasma cells, fibrosis arranged in a storiform pattern, moderate tissue eosinophilia, and partially or completely obliterated veins. Among the 3 layers comprising the aorta, the adventitia is most susceptible to IgG4-related inflammation. The inflammatory process can also disrupt the lamellar elastic fibers in the media, which is seemingly a critical event leading to aneurysmal transformation. Steroid therapy is effective for both retroperitoneal and aortic lesions, as it is for the other manifestations of IgG4-RD. The risk of rupture appears to be low in patients with IgG4-related aortic aneurysms, but immunosuppressive therapy may trigger this critical complication by reducing the wall thickness.

Publication types

  • Review

MeSH terms

  • Aorta / drug effects
  • Aorta / pathology
  • Aortic Aneurysm
  • Autoimmune Diseases / drug therapy
  • Autoimmune Diseases / immunology
  • Autoimmune Diseases / metabolism
  • Autoimmune Diseases / pathology*
  • Eosinophils / pathology
  • Fibrosis
  • Glucocorticoids / therapeutic use
  • Humans
  • Immunoglobulin G / blood*
  • Immunosuppressive Agents / adverse effects
  • Plasma Cells / metabolism
  • Plasma Cells / pathology
  • Retroperitoneal Fibrosis / drug therapy
  • Retroperitoneal Fibrosis / immunology
  • Retroperitoneal Fibrosis / metabolism
  • Retroperitoneal Fibrosis / pathology*
  • Rupture / chemically induced

Substances

  • Glucocorticoids
  • Immunoglobulin G
  • Immunosuppressive Agents