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Allergy – Inappropriate immune response to normally harmless allergen.
Allergen – Foreign particles which produce an IgE-mediated hypersensitivity reaction in sensitive individuals.
Atopygenetic predisposition to exaggerated immune responses


  • Individuals are said to become ‘sensitized’ after initial exposure to antigen (allowing the development of antigen-specific IgE antibodies), and subsequent exposure will result in an allergic reaction.
  • Antigens can enter the body via the skin or the respiratory or gastrointestinal mucosa.
  • Allergens which enter the body bind to antigen-presenting cells which allow exposure to antigen-specific Th2 cells. These cells produce cytokines which activate mast cells which subsequently release histamine, leukotrienes and prostaglandins.
  • Histamine is responsible for local vessel dilation and increased permeability.
  • Activated Th2 cells also stimulate the production of allergen-specific IgE from B-cells. These antibodies are able to stimulate mast cell degranulation directly once bound to antigen.
  • Prolonged or repeated allergen exposure causes eosinophil activation which enhances local inflammation.


Cellular mechanism and pathology of allergy


  • 30% of the population develop an allergic disorder.
  • The most common allergens include house dust; dust mite faeces; animal dander; pollen (grass or tree); moulds and certain foods.
  • Allergy is more likely if the exposure occurs early, and is likely to improve with age.
  • There is also a genetic component: if one parent affected the risk is 25-40%, if both parents are affected, the risk increases to 50-75%.

Signs and symptoms

These depend on the site of exposure, dose and individual.
Symptoms may include:
o   Urticarial or eczematous rash
o   Asthma
o   Rhinitis
o   Conjunctivitis
o   Diarrhoea and vomiting


  • A careful history may help identify trigger allergens and provide information about attack frequency and changes over time.
  • Family history.
  • Skin prick test – exposure to standardised allergen solution through forearm skin prick. A wheal >2mm larger than the negative (saline) control is a positive result.


  • Avoidance of allergen if possible.
  • Topical treatments: sodium cromoglicate (nasal spray/eye-drops) – stabilises mast cells to prevent degranulation; topical steroids – reduce vessel permeability and cytokine synthesis; emollient cream – reduce itching and water loss through damaged skin; bronchodilators.
  • Oral antihistamines or steroids.
  • Desensitisation therapy can be used in upper airway allergies if symptoms are not controlled on maximal medical therapy.

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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