Fibrosis regression induced by intravenous gammaglobulin treatment. Issue 2 (1st February 2003)

• Record Type: Journal Article
• Authors: Amital, H; Rewald, E; Levy, Y; Bar-Dayan, Y; Manthorpe, R; Engervall, P; Sherer, Y; Langevitz, P; Shoenfeld, Y
• Is Part Of: Annals of the rheumatic diseases. Volume 62:Issue 2(2003)
• Page Start: 175
• Page End: 177
• Publication Date: 2003-02-01
• Subjects: fibrosis -- myelofibrosis -- systemic lupus erythematosus -- systemic sclerosis -- cirrhosis -- intravenous gammaglobulin; GM-CSF, granulocyte macrophage colony stimulating factor -- IFN, interferon -- IL, interleukin -- IVIg, intravenous gammaglobulin -- SLE, systemic lupus erythematosus -- Tsk, tight skin; Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/ard.62.2.175
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Objectives: To review case histories of patients in whom fibrosis played a significant role in the pathogenesis of their disease, and to determine whether intravenous gammaglobulin (IVIg) contributed to the regression of their fibrotic condition. Methods: Eight patients with excess fibrotic reaction in the course of diverse diseases were analysed; a tendency that reverted with different IVIg treatment options. Myelofibrosis was predominant in three patients (a patient with a myeloproliferative syndrome, one with systemic lupus erythematosus, and one with Sjögren's syndrome). Three patients had scleroderma as their main feature, one patient had hepatitis C cirrhosis, and one had idiopathic thrombocytopenic purpura. Results: Fibrotic excess was reduced in all the patients by IVIg treatment. In five patients the disease as a whole benefited from the infusion of immunoglobulins. Conclusion: IVIg may enhance resorption of fibrosis and promote healing in patients with fibrotic associated disorders.