see also:

• immunology
• histamine physiology, receptors and antihistamines
• antihistamines (H1)
• anaphylaxis
• allergens
• illness after eating seafood
• Stevens-Johnson syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)
• urticaria
• hereditary angioedema (HAE)
• radiologic contrast media precautions and adverse reactions
• eosinophilia
• allergic rhinitis
• asthma
• tick-induced mammalian red meat allergy (MMA) / alpha-gal syndrome
• pork-cat syndrome
• Aust. Prescriber 2012 - Safe use of adrenaline autoinjectors

• see anaphylaxis

• antigen binds to Antigen presenting Cell (APC) ⇒ activates T Helper cell ⇒ IL-4 production ⇒ B IgE type ⇒ IgE production

• mast cell degranulation due to either:
  • IgE from priming event binds antigen complex
    • it appears a protein, neuritin, prevents the over-production of IgE and thus allergies, anaphylaxis, asthma and many auto-immune conditions could be the result of a deficiency of neuritin according to researchers at the Australian National University (ANU) in 2021
  • direct degranulation via C3alpha/C5alpha, morphine, codeine;
• ⇒ immediate granule release (~20 min)
  • histamine, etc
  • ⇒ H1 effector ⇒ increased permeability; urticaria; asthma;
  • ⇒ H2 feedback ⇒ down-regulation
  • ⇒ decreased mast cell degranulation
  • ⇒ decreased PMNL activity, etc;
  • ⇒ activation phospholipase A2 (slow ~8 hrs, inhib. by NSAID/steroids)
  • ⇒ PG, thromboxane, SRS-A, leukotriene production;

• strict avoidance of precipitant - may need allergy testing to ascertain
• patient to have an EpiPen on hand at all times
• patient and famiy education
• in Victoria, there is mandatory reporting of food allergies to the government in an attempt to reduce fatalities at schools, etc
• consider desensitisation immunotherapy to develop tolerance
  • eg. peanut oral immunotherapy
    • peanut allergy occurs in ~2% of children in Western countries
    • initial oral dosing with supervision, then using 30mg or 300mg maintenance doses generally develops tolerance to accidental exposures and the 30mg dose appears to be as effective with less side effects than the standard 300mg dose of peanut ¹⁾

• Ab + Ag (assoc. with or part of a cell/tissue) ⇒ complement activation
  • ⇒ lytic action on cell memb. via complement/effector cell products
• eg. Goodpasture's disease; Rh isoimmunisation disease of pregnancy; autoimmune haemolyticanaemia;
• eg. myasthenia gravis (not lytic though only Ig bind Ach receptors)

• Ab-Ag complexes in circulation in ratio 1-2:1 may cause deposition onto cell membranes activating complement 
  • ⇒ local inflammation including urticaria with joint effusions
• eg. serum sickness (such as due to 1-2wks after taking cefaclor)
• if Ab»Ag, then v.large complexes which are taken up by phagocytes & hence no serum sickness;

• cell mediated

• hapten on/in epidermis activates Langerhan's ⇒ LN T cells
  • ⇒ local mainly epidermal inflammatory response
    • ⇒ spongiosis/blisters with initially lymphocytic infiltration & later macrophages;
• eg. poison oak; nickel;

• soluble transient hapten in dermis activates macrophages
  • ⇒ dermal response ⇒ papule with monocytic infiltrate & some macrophages;

• continuous Ag stimulation ⇒ macrophage activation;