Introduction
Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders.
Uses
Human immunoglobulin G is a purified form of human immunoglobulin G and other proteins used to treat immunodeficiency and a wide variety of autoimmune disorders.
IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases.
Associated Conditions
Pharmacodynamics
Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens.
Mechanism of Action
IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging” or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab′)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components.
Half Life
>20 hours (mammalian reticulocytes, in vitro).
Food Interactions
No interactions found.
Dosage
Children and adults:
- For combined therapy with antibiotics in severe bacterial or viral infections and A-/Hypogammaglobulinemia: The usual dosage for adults and children is 2500-5000 mg and 50-150 mg/kg respectively (as a single dose) by intravenous drip infusion or direct intravenous infusion. In case of intravenous injection, it should be injected very slowly.
- For Idiopathic Thrombocytopenic Purpura: The usual dose is 200-400 mg/kg daily given for 5 consecutive days. The additional doses are discontinued if an adequate response does not occur.
For Kawasaki Syndrome: The usual dosage is 400 mg/kg daily given for 5 consecutive days (approximately) or 2000 mg daily by intravenous drip infusion. It is recommended that the administration start within 7 days from the onset of Kawasaki Syndrome.