====== Hypersensitivity Reactions (Types I–IV) ======

Hypersensitivity reactions are exaggerated or misdirected immune responses that result in tissue injury.

Classified by mechanism:

  * Type I – IgE-mediated (Immediate)
  * Type II – Antibody-mediated cytotoxic
  * Type III – Immune complex deposition
  * Type IV – T-cell mediated (Delayed)

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===== Type I – Immediate (IgE-Mediated) =====

Mechanism:
  * Allergen → IgE production
  * IgE binds mast cells
  * Re-exposure → mast cell degranulation

Onset:
  * Minutes

Examples:
  * [[allergy:clinical:allergic_rhinitis|Allergic Rhinitis]]
  * [[allergy:clinical:urticaria_angioedema|Urticaria]]
  * [[allergy:clinical:anaphylaxis|Anaphylaxis]]
  * Atopic asthma

Primary mediators:
  * Histamine
  * Leukotrienes
  * Prostaglandins

See:
  * [[allergy:immunology:type_i_hypersensitivity|Full Type I Pathway]]

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===== Type II – Antibody-Mediated Cytotoxic =====

Mechanism:
  * IgG or IgM binds to cell surface antigen
  * Complement activation
  * Cell destruction

Onset:
  * Hours to days

Examples:
  * Autoimmune hemolytic anemia
  * Immune thrombocytopenia (ITP)
  * Goodpasture syndrome
  * Certain drug-induced cytopenias

Key concept:
  Antibody directed against fixed tissue antigen.

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===== Type III – Immune Complex Disease =====

Mechanism:
  * Antigen–antibody complexes form in circulation
  * Deposit in tissues
  * Activate complement
  * Inflammation and tissue injury

Onset:
  * Days to weeks

Examples:
  * Serum sickness
  * Systemic lupus erythematosus (SLE)
  * Post-infectious glomerulonephritis

Key concept:
  Injury from immune complexes, not direct antibody binding.

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===== Type IV – Delayed (T-Cell Mediated) =====

Mechanism:
  * Sensitized T cells recognize antigen
  * Cytokine release
  * Cytotoxic T-cell–mediated damage

Onset:
  * 48–72 hours or longer

Examples:
  * Contact dermatitis (poison ivy)
  * Tuberculin skin test
  * Stevens-Johnson Syndrome (SJS)
  * Toxic Epidermal Necrolysis (TEN)
  * DRESS syndrome

Key concept:
  No antibodies involved.

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===== Quick Comparison Table =====

^ Type ^ Immune Driver ^ Antibodies? ^ Onset ^ Example ^
| I | IgE + Mast Cells | Yes (IgE) | Minutes | Anaphylaxis |
| II | IgG/IgM vs cell surface | Yes | Hours–Days | Hemolytic anemia |
| III | Immune complexes | Yes | Days–Weeks | Serum sickness |
| IV | T cells | No | 48–72 hr | Contact dermatitis |

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===== Drug Implications =====

Type I:
  * [[allergy:drugs:loratadine|H1 Antihistamines]]
  * [[endocrine:drugs:fluticasone|Corticosteroids]]
  * [[cardio:drugs:epinephrine|Epinephrine]]
  * [[immunology:drugs:omalizumab|Anti-IgE therapy]]

Type II:
  * Immunosuppressants
  * Steroids
  * Plasma exchange (select cases)

Type III:
  * Steroids
  * Immunomodulators

Type IV:
  * Corticosteroids
  * Drug discontinuation
  * Immunosuppressive therapy (severe cases)

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===== High-Yield Differentiation =====

If reaction occurs within minutes → think Type I.

If reaction causes cytopenias → think Type II.

If rash + arthralgias + immune complexes → think Type III.

If delayed blistering rash after drug exposure → think Type IV.

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===== Related Pages =====

  * [[allergy:immunology:type_i_hypersensitivity|Type I Hypersensitivity]]
  * [[allergy:clinical:anaphylaxis|Anaphylaxis]]
  * [[allergy:clinical:urticaria_angioedema|Urticaria & Angioedema]]