Long-term follow up of patients with common variable immunodeficiency treated with intravenous immunoglobulin: Reevaluation of intravenous immunoglobulin replacement therapy

Abstract

Five patients with common variable immunodeficiency treated in our hospital between December 1979 and December 1990 were given six kinds of intravenous immunoglobulin preparations (pepsin treated, S-sulfonated, polyethylene glycol treated, pH4 treated, alkylated, and pH4.25 formulation preparation) for replacement therapy. Duration of the therapy ranged from 7.6 to 11 years. Incidences of fever and acute infections were variable among patients, but no significant differences were seen in the incidences among periods given each preparation. Three cases revealed abnormal pulmonary functions in tests. Adverse reactions were rarely seen in our study periods, and no severe reactions were observed. No significant differences were seen in incidences of adverse reactions. Postinfusion levels of serum complement slightly decreased from preinfusion levels. However, the decrease in complement was not related to any adverse reaction. No long-term complications such as transmission of hepatitis have been observed. Our data suggest that no obvious differences exist between the efficacy and safety of each IVIG preparation. Differences of efficacy of IVIG replacement therapy may be due to the variable pathophysiology of each patient.

Sulfonated human immunoglobulin enhances CD16‐linked CD11b expression on human neutrophils

“…Chemical modifications or conformational changes may be induced by SHIG and/or binding to CD16. SHIGbound CD16 appears to have up-regulated CD11b expression in this study; in contrast, the structure of PHIG is essentially that of untreated IG (Motohiro et al, 1985;Mushiake et al, 1993-94), and accordingly PHIG did not affect CD11b expression on neutrophils.…”

Clinical and laboratory aspects of common variable immunodeficiency

“…These studies, describe infections that are commonly associated with T cell deficits and vary from severe infection with viruses such as the cytomegalovirus (CMV), or herpes zoster (CMV) (Kainulainen et al 1999, Linde et al 1988, Mullighan et al 1996, Tarr et al 2001, Witte et al 2000, and also include infection with intracellular parasites like the Toxoplasma gondii or Strongyloides stercorallis (Duarte et al 1990, Naspitz et al 1987, Mushiake et al 1993, Bonilla et al 1997.…”