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Monday, August 11, 2025

Immune globulins


1. Definition and Overview

  • Immune globulins (immunoglobulins) are antibody preparations derived from human plasma containing a broad spectrum of antibodies.

  • Provide passive immunity by supplying exogenous antibodies that neutralize pathogens or toxins.

  • Used for prevention and treatment of infections, immune modulation in autoimmune disorders, and replacement therapy in immunodeficiencies.

  • Available in intravenous (IVIG), subcutaneous (SCIG), and intramuscular (IMIG) formulations.

2. Classification by Use

A. Replacement Therapy

  • Used in primary immunodeficiency (PID) and certain secondary immunodeficiencies.

  • Provides long-term antibody support.

  • Examples: Standard IVIG, SCIG.

B. Immunomodulatory Therapy

  • Used in autoimmune and inflammatory conditions to modulate immune response.

  • Mechanisms include Fc receptor blockade, complement inhibition, and cytokine modulation.

  • Examples: High-dose IVIG in immune thrombocytopenia, Kawasaki disease, Guillain–Barré syndrome.

C. Specific (Hyperimmune) Globulins

  • Contain high titers of antibodies to a specific pathogen or antigen.

  • Produced from donors with high antibody levels after infection or immunization.

  • Examples:

    • Hepatitis B immune globulin (HBIG) – post-exposure prophylaxis.

    • Rabies immune globulin (RIG) – post-exposure prophylaxis.

    • Tetanus immune globulin (TIG) – wound management in non-immunized individuals.

    • Varicella-zoster immune globulin (VZIG) – post-exposure prophylaxis for high-risk contacts.

    • Rho(D) immune globulin – prevention of hemolytic disease of the newborn.

3. Mechanisms of Action

Replacement Therapy

  • Direct pathogen neutralization.

  • Opsonization and promotion of phagocytosis.

  • Complement activation and immune complex clearance.

Immunomodulation

  • Saturation of Fc receptors on macrophages → reduced clearance of autoantibody-coated cells.

  • Suppression of pathogenic autoantibody production.

  • Neutralization of circulating autoantibodies.

  • Modulation of dendritic cell function and T/B-cell activity.

  • Inhibition of pro-inflammatory cytokine release.

Hyperimmune Globulins

  • High-titer specific antibodies bind and neutralize specific pathogen/toxin.

  • Provide immediate but temporary immunity.

4. Therapeutic Indications

Replacement Therapy

  • Primary immunodeficiencies (e.g., X-linked agammaglobulinemia, common variable immunodeficiency).

  • Secondary immunodeficiencies due to B-cell malignancies, post-hematopoietic stem cell transplant.

Immunomodulation

  • Immune thrombocytopenia (ITP).

  • Kawasaki disease.

  • Guillain–Barré syndrome.

  • Chronic inflammatory demyelinating polyneuropathy (CIDP).

  • Myasthenia gravis (acute exacerbations).

Specific Hyperimmune Globulins

  • Post-exposure prophylaxis for hepatitis B, rabies, tetanus, varicella-zoster.

  • Prevention of hemolytic disease of the newborn (Rho(D) immune globulin).

5. Administration Routes and Schedules

Intravenous (IVIG)

  • Administered every 3–4 weeks for replacement therapy.

  • Faster achievement of therapeutic antibody levels.

Subcutaneous (SCIG)

  • Administered weekly or biweekly.

  • Allows home-based self-administration.

  • More stable serum IgG levels, fewer systemic side effects.

Intramuscular (IMIG)

  • Primarily for certain hyperimmune globulins and small-dose prophylaxis.

  • Slower absorption, lower peak levels than IVIG.

6. Contraindications

  • Known hypersensitivity to human immunoglobulins or excipients (e.g., stabilizers like sucrose, maltose).

  • Selective IgA deficiency with anti-IgA antibodies → risk of anaphylaxis.

  • History of severe systemic reaction to immunoglobulin therapy.

7. Adverse Effects

Common

  • Headache, chills, fever, myalgia, fatigue.

  • Infusion site reactions (pain, swelling, erythema in SCIG).

Serious

  • Anaphylaxis (especially in IgA-deficient patients).

  • Thromboembolic events (deep vein thrombosis, myocardial infarction, stroke).

  • Hemolysis (due to anti-A/anti-B antibodies in preparation).

  • Aseptic meningitis.

  • Acute renal failure (more common with sucrose-containing IVIG).

8. Precautions

  • Screen for IgA deficiency prior to therapy if history suggests risk.

  • Ensure adequate hydration before infusion to reduce thromboembolic and renal risks.

  • Use slow infusion rates initially to minimize adverse reactions.

  • Monitor for signs of hemolysis post-infusion in high-dose regimens.

9. Drug Interactions

  • Live attenuated vaccines may have reduced efficacy if given within 3–11 months after immunoglobulin therapy (depending on vaccine).

  • Other immunosuppressive agents may increase infection risk.

  • High-dose IVIG may interfere with certain serologic tests due to passive antibody transfer.

10. Monitoring Parameters

  • Serum IgG levels for replacement therapy to ensure adequate trough concentrations.

  • CBC, renal function tests, liver function tests in long-term therapy.

  • Monitor for infusion-related reactions during and after administration.

  • Monitor disease-specific markers in autoimmune conditions.

11. Key Advantages

  • Provides immediate immune protection in at-risk individuals.

  • Effective in both prophylaxis and treatment of certain conditions.

  • Versatile – covers infectious, autoimmune, and immunodeficiency applications.

12. Limitations

  • Passive immunity is temporary; does not induce immune memory.

  • High cost and limited availability due to dependence on human plasma donations.

  • Requires cold chain storage and careful handling to maintain stability.




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