Skip to Main Content

++
Table Graphic Jump Location
Favorite Table | Download (.pdf) | Print

Type

Mechanism

Examples

I: Anaphylactic or immediate hypersensitivity

IgE-mediated mast cell degranulation and activation

Anaphylaxis, allergic rhinitis, allergic asthma, acute urticaria, insect sting allergy

II: Antibody-mediated cytolytic reactions

IgM or IgG against antigens bound to cell membrane structures

Autoimmune or drug-induced hemolytic anemia, Goodpasture's disease, Rh hemolytic disease

III: Immune- complex mediated

Complexes of IgM or IgG and circulating antigens

Serum sickness, SLE, vasculitis, poststreptococcal glomerulonephritis

IV: Delayed hypersensitivity

T lymphocytes

Tuberculin skin test reactions, GVHD, contact dermatitis

++

Allergy Testing

++

  • Immediate hypersensitivity skin test (IHST): Stop antihistamines for 5 days before testing. Use the prick technique (introduce antigen intracutaneously via pricking or puncturing). Positive predictive value is good for inhalants, moderate for foods (high rate of false-positive results); negative predictive value is excellent for foods and inhalants.
  • Serum tests: Serum eosinophilia is often present (low diagnostic value); serum IgE is often elevated with atopic dermatitis (low diagnostic value); serum allergen-specific IgE assays (eg, RAST) measure circulating Ag-specific IgE and have similar predictive value to skin testing.

++

Anaphylaxis

++

  • Definition: A serious allergic reaction that is rapid in onset and may cause death
  • Differential Diagnosis:
    • Vasovagal syncope, panic attack, hyperventilation, systemic mastocytosis, scombroid fish poisoning. Rare causes include carcinoid syndrome, pheochromocytoma, and idiosyncratic causes.
    • Anaphylactoid reactions, which have complement activation, but are not IgE mediated.
    • Example: Radiocontrast media, drugs (NSAIDS, opiate), blood products, exercise induced, and idiopathic. Clinical presentation and treatment are the same as for anaphylaxis.
  • Major Trigger: Food (most commonly peanut, tree nuts, shellfish, fish, eggs, milk), insect venom, latex, drugs, immunotherapy
  • Pathophysiology: Production of IgE in a susceptible individual (sensitization)→ IgE-sensitized mast cells and basophils→ exposure of allergen and then allergen binding leads to mast cell degranulation.
  • Clinical Symptoms and PE
    • Variable symptoms: Angioedema, shortness of breath, wheezing, flushing, urticaria, pruritus, hypotension, chest pain, syncope, abdominal pain, vomiting, diarrhea, aura of impending doom.
    • Time pattern: Uniphasic, biphasic (recur up to 8 h later in 3%–20%), or protracted syndrome.
  • Diagnostic Studies
    • Markers of mast cell degranulation, including plasma histamine (only elevated for 1 h after the onset of symptoms), urinary histamine and metabolites (elevated for longer), or serum tryptase level (peaks is 90 minutes and stays elevated for as long as 5 h) may be useful when the diagnosis is uncertain. Undetectable levels do not rule out anaphylaxis (tryptase is positive <50%).
    • In vitro allergen-specific IgE assays or IHST may be used later to confirm. IHST may not be reliably positive in sensitized individuals for up to 4 to 6 weeks after an episode of anaphylaxis. In sensitized individuals, the test should be repeated if results are negative.
  • Treatment
    • Monitor patients with mild reactions limited to flushing, urticaria, angioedema, and mild bronchospasm in the ED for a minimum of 6 to 8 hours. Consider longer observation of patients with mild symptoms who have received epinephrine because epinephrine may have minimized the symptoms.
    • Provide ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.