Intravenous immunoglobulin

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Intravenous immunoglobulin (IVIG) is a blood product administered intravenously. It contains the pooled IgG immunoglobulins (antibodies extracted from the plasma of over a thousand blood donors). IVIG effect last between 2 weeks and 3 months. It is mainly used as treatment in three major categories:

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[edit] Mechanism of action

IVIG is given as a plamsa protein replacement therapy (IgG) for immune deficient patients which have decreased or abolished antibody production capabilities. IVIG is administered to maintain adequate antibodies levels to prevent infections and confers a passive immunity. Treatment is given every 3-4 weeks.

The precise mechanism by which IVIG suppresses harmful inflammation is believed to be through the Fc Receptor.[1][2]

Additionally, the donor antibody may bind directly with the abnormal host antibody, stimulating its removal. Alternatively, the massive quantity of antibody may stimulate the host's complement system, leading to enhanced removal of all antibodies, including the harmful ones. IVIG also blocks the antibody receptors on immune cells (macrophages), leading to decreased damage by these cells, or regulation of macrophage phagocytosis.

IVIG may also regulate the immune response by reacting with a number of membrane receptors on T cells, B cells, and monocytes that are pertinent to autoreactivity and induction of tolerance to self.[3]

IVIG is useful in some acute infection cases such as in Kawasaki's Disease and pediatric HIV infection.

[edit] IVIG notes

  • IVIG is an infusion of IgG antibodies only. Therefore, peripherial tissues that are defended mainly by IgA antibodies, such as the eyes, lungs, gut and urinary tract are not fully protected by the IVIG treatment.
  • XLA patients are immune to the most virulent adverse effect, anaphylactic shock, as they do not have the antibodies to react against the treatment. Anaphylactic shock has a higher chance to occur in IgA deficient patients which do have other antibody types.
  • In case of reoccurring side effects, it is recommended to slow the pace of the IVIG administration and to reduce the dosage. It is also advisable to change IVIG brand, as some people react against to a specific brand.
  • If the patient is diabetic, he should take into consideration the medium in which the antibodies are solubilized in the IVIG treatment, as some brand solubilize antibodies with high concentrated sugars (such as sucrose and maltose).
  • FDA guidelines for IVIG state the product should be:
    • Prepared out of at least 10,000 different human donors.
    • All four IgG subgroups (1-4) should be present.
    • The IgG should maintain biological activity and lifetime of at least 21 days.
    • Does not contain samples which are HIV, hepatitis B, hepatitis C positive.
    • Screened and treated in a manner that destroys viruses.
  • IVIG is also considered a modulator of the immune system and was shown to be beneficial in treating numerous autoimmune diseases such as rheumatoid arthritis (RH), lupus (SLE), multiple sclerosis (MS), myasthenia gravis, pemphigus, polymyositis (PM), dermatomyositis (DM), granulomatosis (WG), Churg-Strauss syndrome, chronic inflammatory demyelinating polyneuropathy and more.
  • IVIG can be given to pregnant women.
  • IVIG is also used as a treatment for unexplained reoccurring miscarriages. The effectiveness of the therapy is controversial.

[edit] Uses of IVIG

Dosage of IVIG is dependent on indication.

For primary immune dysfunction 100 to 400 mg/kg of body weight every 3 to 4 weeks is implemented.

For neurological and autoimmune diseases 2 grams per kilogram of body weight is implemented for three to six months over a five day course once a month. Then maintenance therapy of 100 to 400 mg/kg of body weight every 3 to 4 weeks follows.

[edit] FDA-approved indications

[edit] Off label uses

[edit] Complications and side effects

Complications of IVIG therapy include

[edit] Brands

The following IVIG preparations are marketed in the United States:

  • Gamunex (Bayer)
  • Gammagard S/D (Baxter/Hyland; Deerfield, Ill)
  • Gammar-IV (Armour; Blue Bell, Pa)
  • Gamimune-N (Miles; Elkhart, Ind; Bayer)
  • Iveegam (Immuno-US; Rochester, NY)
  • Polygam S/D (Baxter/Hyland for American Red Cross; Washington, DC)
  • Sandoglobulin (Sandoz; Vienna, Austria)
  • Venoglobulin-I or Venoglobulin-S (Alpha Therapeutic; Los Angeles, Calif)
  • Carimune/Panglobulin (ZLB Bioplasma/ARC Swiss Red Cross)

[edit] References

  1. ^ [1]James E. Gern, MD. "Antiinflammatory Activity of IVIG Mediated through the Inhibitory FC Receptor" PEDIATRICS Vol. 110 No. 2 August 2002, pp. 467-468
  2. ^ [2] Falk Nimmerjahn and Jeffrey V. Ravetch. "The antiinflammatory activity of IgG: the intravenous IgG paradox". The Journal of Experimental Medicine, Vol. 204, No. 1, 11-15
  3. ^ Bayry J, Thirion M, Misra N, Thorenoor N, Delignat S, Lacroix-Desmazes S, Bellon B, Kaveri S, Kazatchkine MD. Mechanisms of action of intravenous immunoglobulin in autoimmune and inflammatory diseases. Neurol Sci. 2003; 24: S217–S221.

[edit] External Links

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