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Skin reactions are often the first areas in which we see an allergic response. Most of the individuals experiencing anaphylaxis will present with skin reactions (Abbas & Goldin, 2025). Below are some of the clinical manifestations that can occur during anaphylaxis:

Hives (urticaria)

Itching (pruritus)

Flushing

Rash

Angioedema of the face, lips, and tongue.

References:

Abbas, M., & Goldin, J. (2025). Type I hypersensitivity reaction. National Library of Medicine. Retrieved October 9, 2025, from https://www.ncbi.nlm.nih.gov/books/NBK560561/

McLendon, K., & Sternard, B. T. (2023). Anaphylaxis. National Library of Medicine. Retrieved October 9, 2025, from https://www.ncbi.nlm.nih.gov/books/NBK482124/

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Diagnostic Testing for Type I Hypersensitivity

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Diagnostic Testing for Type I Hypersensitivity

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Type I hypersensitivity reactions are IgE-mediated, and diagnostic tests help identify the specific allergen responsible. The most common tests include:

Skin Prick Test (SPT): Small amounts of suspected allergens are placed on the skin and pricked. A raised, red wheal within 15–20 minutes indicates a positive reaction.

Serum-Specific IgE (RAST or ImmunoCAP): A blood test that measures allergen-specific IgE antibodies. Useful when skin testing is contraindicated (such as with severe eczema or antihistamine use).

Intradermal Testing: Injects allergen under the skin for more sensitive detection but carries a higher risk of systemic reaction.

Challenge Tests: Carefully introducing allergens under medical supervision, often for food or drug allergies. Considered the “gold standard” but only done when necessary due to risk of severe reaction.

Clinical Relevance:
These tests confirm the presence of IgE-mediated hypersensitivity, guide patient education on avoidance, and direct treatment (such as immunotherapy or epinephrine use).

References:

1. Abbas, A. K., Lichtman, A. H., & Pillai, S. (2022). Basic immunology: Functions and disorders of the immune system (6th ed.). Elsevier.

2. American Academy of Allergy, Asthma & Immunology (AAAAI). (2023). Allergy testing. https://www.aaaai.org/tools-for-the-public/conditions-library/allergies/allergy-testing

3. Leung, D. Y. M., Sampson, H. A., & Geha, R. S. (2019). Allergic disorders. In J. Loscalzo, A. S. Fauci, D. L. Kasper, S. L. Hauser, D. L. Longo, & J. L. Jameson (Eds.), Harrison’s principles of internal medicine (20th ed., Vol. 2, pp. 2559–2575). McGraw Hill Education.

4. Sicherer, S. H., & Wood, R. A. (2019). Allergy testing in childhood: Using allergen-specific IgE tests. Pediatrics, 143(1), e20183604. https://doi.org/10.1542/peds.2018-3604

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When exposed to a causative agent, respiratory symptoms are often the second response to arise (Abbas & Goldin, 2025). Respiratory symptoms are common when exposed to an oral form (McLendon & Sternard, 2023). Below are some of the signs and symptoms that you will see within the respiratory tract:

Coughing

Wheezing

Shortness of breath (dyspnea)

Chest tightness

"Lump in throat" feeling

Persistent clearing of throat

Oropharyngeal swelling

References:

Abbas, M., & Goldin, J. (2025). Type I hypersensitivity reaction. National Library of Medicine. Retrieved October 9, 2025, from https://www.ncbi.nlm.nih.gov/books/NBK560561/

McLendon, K., & Sternard, B. T. (2023). Anaphylaxis. National Library of Medicine. Retrieved October 9, 2025, from https://www.ncbi.nlm.nih.gov/books/NBK482124/

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Sensitization: Allergen Specific IgE on mast cells/basophils

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Sensitization: Allergen Specific IgE on mast cells/basophils

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On first exposure, antigen-presenting cells activate Th2 cells, which drive B cells to class-switch and produce allergen-specific IgE. That IgE binds high-affinity FcεRI receptors on mast cells and basophils, arming them for future encounters. Sensitized effector cells can persist for months, which explains why re-exposure triggers an immediate reaction. Sensitization itself causes no symptoms, but it sets up the classic Type I pathway.

Source:
McCance & Huether, 2020; Galli & Tsai, 2012.

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Smooth muscle contraction & muscosal edema (airway/GI effects)

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Smooth muscle contraction & muscosal edema (airway/GI effects)

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Leukotrienes and prostaglandins trigger bronchial smooth-muscle contraction and mucosal edema, leading to wheeze/stridor and respiratory distress. In the GI tract, smooth-muscle contraction and secretion cause cramping, vomiting, and diarrhea. These tissue effects explain organ-level findings across airway, skin, cardiovascular, and GI systems during anaphylaxis. Rapid recognition of these patterns supports early epinephrine and airway-first priorities.
Source: AAAAI, n.d.; McCance & Huether, 2020.

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airway edema + bronchoconstriction diagram

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Basic Review on IgE/FceRl biology

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Airway Changes in anaphylaxis

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Histamine and lipid mediators cause endothelial gap formation, producing capillary leak and interstitial edema (e.g., lips/tongue, airway, skin wheals). Simultaneously, arteriolar vasodilation drops systemic vascular resistance, predisposing to hypotension/shock. Fluid extravasation reduces effective circulating volume, so patients may need aggressive isotonic fluids after epinephrine. These tissue-level changes are the bridge between mast-cell chemistry and bedside signs (angioedema, hives, low BP).
Source: McCance & Huether, 2020; WAO, 2020.

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Smooth muscle contraction & mucosal edema (tissue level)

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Smooth muscle contraction & mucosal edema (tissue level)

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Mast-cell mediators, especially cysteinyl leukotrienes (LTC₄/LTD₄/LTE₄) and prostaglandin D2, cause rapid smooth-muscle contraction and mucosal edema at the tissue level. In the airways, increased bronchial tone plus edema narrows the lumen, raising airway resistance and producing the foundation for wheezing/stridor seen clinically. In the GI tract, these same mediators increase motility and secretion, setting up cramping, nausea, vomiting, and diarrhea. These tissue effects, paired with microvascular leak, explain the swift multi-system progression of anaphylaxis and why IM epinephrine (β2 bronchodilation, α₁ vasoconstriction to shrink edema) is prioritized first.

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Mechanism of Type 1, IgE-Mediated Reactions

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Allergy: IgE-mediated reaction, usually triggered by environmental antigens: pollen, bee stings, nuts, medications.

Primary Exposure: Immunologic Memory

A type I hypersensitivity reaction requires sensitization against an allergen (environmental antigen) prior to producing an anaphylactic reaction. Sensitization is asymptomatic and occurs during the initial antigen-specific exposure. The initial exposure produces antigen-specific memory B and T cells.

Subsequent Exposure: Immediate Hypersensitivity

Sensitized mast cells degranulate, release histamine (+inflammatory mediators) and produce a range of clinical manifestations that vary in severity.

Onset: Immediate, within minutes (up to a few hours)

Physiological Effects:

Tissues that contain numerous mast cells are the most affected: GI, skin, respiratory.

Effects are produced through histamine 1 receptors (H1):

Vasodilation, increased capillary permeability, smooth muscle spasm, mucus secretions, edema.

Source:

Rogers, Julia . MCCANCE & HUETHER’S PATHOPHYSIOLOGY. 9th ed., Elsevier , pp. 255–63, https://pageburstls.elsevier.com/#/books/9780323789905. Accessed 11 Oct. 2025.

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national center for biotechnology information

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World allergy organization anaphylaxis guidance 2020 - PubMed

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Anaphylaxis is the most severe clinical presentation of acute systemic allergic reactions. The occurrence of anaphylaxis has increased in recent years, and subsequently, there is a need to continue disseminating knowledge on the diagnosis and management, so every healthcare professional is prepared ...

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Genetic Predisposition and Extrinsic Risk Factors

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Genetic Predisposition and Extrinsic Risk Factors

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Atopic individuals are genetically predisposed to develop IgE-mediated hypersensitivity

-higher production of IgE

-More Fc receptors (for IgE) on mast cells

-Cytokine (IL-4, IL-3) polymorphism

(Cytokines regulate IgE synthesis)

Family clustering:

1 parent has an allergy -> 40% incidence risk in offspring

BOTH parents have allergies -> up to 80% risk in offspring

Microbiome & Food Allergies:

The microbiota interacts with food antigens and impact immunogenicity. Dysbiosis (imbalance) in the microbiota is linked to activation of B cells, IgE ( in atopic individuals).

Thus, factors such as diet, drugs and comorbidities

have an impact on allergy response. A diet that is low-fiber/high-fat and drugs such as antibiotics, medications can contribute to Dysbiosis.

Hygiene Hypothesis: reduced early exposure to microbes may correlate to increased allergy susceptibility.

-> It's now recommended to introduce peanuts at 4-6 months to reduce risk of peanut allergy development. Previous recommendations was to wait until infant was at least 12 months.

Source:

Abbas M, Goldin J. Type I Hypersensitivity Reaction. [Updated 2025 Aug 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK560561/

Emfietzoglou, Maria. “Atopic Triad.” Osmosis, 11 Aug. 2025, https://www.osmosis.org/answers/atopic-triad.

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Atopic Triad: What Is It, Causes, and More | Osmosis

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Atopy refers to the genetic predisposition to developing allergic conditions, such as atopic dermatitis, allergic asthma, allergic rhinitis Learn with Osmosis

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Gastrointestinal symptoms can happen in patients who are experiencing anaphylaxis (McLendon & Sternard, 2023). Below are a some of the symptoms that may present alone or in combination with respiratory and skin symptoms during anaphylaxis.

Nausea/Vomiting

Abdominal Pain

Cramping

Diarrhea

References:

Abbas, M., & Goldin, J. (2025). Type I hypersensitivity reaction. National Library of Medicine. Retrieved October 9, 2025, from https://www.ncbi.nlm.nih.gov/books/NBK560561/

McLendon, K., & Sternard, B. T. (2023). Anaphylaxis. National Library of Medicine. Retrieved October 9, 2025, from https://www.ncbi.nlm.nih.gov/books/NBK482124/

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Anaphylaxis has an impact on the cardiovascular system (Abbas & Goldin, 2025). Below we can see a few of the main symptoms that will present themselves during anaphylaxis:

Hypotension

Tachycardia

Dizziness

References:

Abbas, M., & Goldin, J. (2025). Type I hypersensitivity reaction. National Library of Medicine. Retrieved October 9, 2025, from https://www.ncbi.nlm.nih.gov/books/NBK560561/

McLendon, K., & Sternard, B. T. (2023). Anaphylaxis. National Library of Medicine. Retrieved October 9, 2025, from https://www.ncbi.nlm.nih.gov/books/NBK482124/

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Anaphylaxis is a life-threatening emergency and it requires immediate action (Abbas & Goldin, 2025). Triage will take place during any type of allergic reaction and will be treated with urgency. Maintaining airway is going to be of the upmost importance in addition to ensuring its security. Decontamination will be the next step to make sure that the triggering allergen is thoroughly removed (McLendon & Sternard, 2023). Below we will break down the different types of therapeutic managements that are used to treat anaphylaxis.

1. Epinephrine

This is the most critical step that must be completed with no delay.

It will be administered via intramuscular (IM) injection into the patient's lateral thigh.

Airway constriction will reverse, the blood pressure will increase, edema will decrease, and it will stop the reaction that is occurring.

2. IV fluids & Oxygen

Due to the patients blood pressure dropping, IV fluids will be administered to help with hypotension.

Oxygen will also be given to support breathing.

3. Vasopressors, antihistamines, and bronchodilators.

Vasopressors are used as additional treatment to the hypotension that occurs.

Antihistamines are used to help relieve symptoms of urticaria (hives) and pruritus (itching).

Bronchodilators are used to help relieve the patient of wheezing and general difficulty with breathing.

After experiencing anaphylaxis, patients will be required to stay in the hospital for monitoring of a biphasic reaction (McLendon & Sternard, 2023).

References:

Abbas, M., & Goldin, J. (2025). Type I hypersensitivity reaction. National Library of Medicine. Retrieved October 9, 2025, from https://www.ncbi.nlm.nih.gov/books/NBK560561/

McLendon, K., & Sternard, B. T. (2023). Anaphylaxis. National Library of Medicine. Retrieved October 9, 2025, from https://www.ncbi.nlm.nih.gov/books/NBK482124/

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Case Study Anaphylaxis in Type 1 Hypersensitivity

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Case Study Anaphylaxis in Type 1 Hypersensitivity

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A 21-year-old female with a known peanut allergy accidentally consumes peanut butter at a social event. Within minutes, she experiences itching, facial swelling, shortness of breath, and dizziness. On arrival, EMS notes hypotension, widespread hives, and wheezing. Epinephrine is administered intramuscularly, and she is transported to the emergency department for observation and further care.

This case illustrates the rapid and life-threatening progression of a Type I hypersensitivity reaction, also known as anaphylaxis. The reaction is caused by IgE antibodies binding to mast cells and basophils, leading to the release of histamine and other inflammatory mediators. These substances cause vasodilation, bronchoconstriction, increased vascular permeability, and other systemic effects.

Teaching Points:

Type I hypersensitivity reactions can occur within minutes of allergen exposure and require immediate recognition.

Epinephrine is the first-line treatment and should be administered promptly via intramuscular injection.

Patients should be educated on allergen avoidance, emergency action plans, and proper use of epinephrine auto-injectors.

Observation in a medical setting is necessary following anaphylaxis due to risk of biphasic reactions.

References:

1. Simons, F. E. R., Ardusso, L. R. F., Bilo, M. B., El-Gamal, Y. M., Ledford, D. K., Ring, J., ... & Sheikh, A. (2011). World Allergy Organization anaphylaxis guidelines: 2011 update of the evidence base. International Archives of Allergy and Immunology, 154(3), 195–204. https://doi.org/10.1159/000321343

2. Sicherer, S. H., & Simons, F. E. R. (2017). Epinephrine for first-aid management of anaphylaxis. Pediatrics, 139(3), e20164006. https://doi.org/10.1542/peds.2016-4006

3. Leung, D. Y. M., Sampson, H. A., & Geha, R. S. (2019). Anaphylaxis and other immediate-type hypersensitivity reactions. In J. Loscalzo, A. S. Fauci, D. L. Kasper, S. L. Hauser, D. L. Longo, & J. L. Jameson (Eds.), Harrison’s principles of internal medicine (20th ed., Vol. 2, pp. 2566–2570). McGraw Hill Education.

4. American College of Allergy, Asthma & Immunology (ACAAI). (2022). Anaphylaxis: Symptoms, diagnosis, treatment and management. https://acaai.org/allergies/anaphylaxis

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Primary Organ Systems Involved

1. Respiratory System (Lungs and Airways)
Bronchial smooth-muscle constriction, mucosal edema, and mucus hypersecretion occur.
This leads to bronchospasm, wheezing, dyspnea, and hypoxemia.
Airway obstruction can progress rapidly to respiratory failure.

2. Cardiovascular System (Heart and Vessels)
Systemic vasodilation and capillary permeability cause hypotension, tachycardia, and circulatory collapse, also known as anaphylactic shock.
Decreased venous return reduces cardiac output, worsening tissue hypoxia.

3. Skin and Mucous Membranes
Histamine release leads to urticaria (hives), flushing, and angioedema.
Edema of the lips, tongue, and throat can obstruct the airway.

4. Gastrointestinal System
Smooth-muscle contraction and increased secretions cause nausea, vomiting, abdominal cramps, and diarrhea.i’m

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In type I hypersensitivity widespread release of histamine and other inflammatory mediators causes rapid, systemic effects. In the respiratory system, bronchoconstriction, airway swelling, and mucus secretion lead to shortness of breath, wheezing, and hypoxia. In the cardiovascular system, vasodilation and fluid leakage cause hypotension, tachycardia, and potential shock. The skin and mucous membranes show hives, flushing, and angioedema, which can obstruct the airway, while the gastrointestinal tract may react with nausea, vomiting, or abdominal pain. Overall, anaphylaxis involves multiple organ systems and requires immediate treatment with epinephrine to prevent death.

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People are more likely to develop anaphylaxis if they have prior allergen exposure or a family history of allergies, asthma, or eczema. Parenteral exposure such as injections, IV drugs, or insect stings and high-dose or repeated exposure increase the risk. Common triggers include foods, medications, insect venom, and latex. Individuals with asthma or cardiovascular disease are at higher risk for severe or fatal reactions.

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Huether, S. E., McCance, K. L., & Brashers, V. L. (2020). Understanding pathophysiology (7th ed.). Elsevier.

National Institute of Allergy and Infectious Diseases. (2023). Anaphylaxis: Causes, symptoms, and treatment. U.S. Department of Health and Human Services. https://www.niaid.nih.gov

Osmosis. (2022, June 17). Anaphylaxis: Causes, symptoms, and treatment [Video]. YouTube. https://www.youtube.com/watch?v=8x8kYtH3fAw

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https://www.youtube.com/watch?v=8x8kYtH3fAw

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Type I hypersensitivity, also known as anaphylaxis, involves an overreaction of the immune system that affects multiple organ systems. In the respiratory system, histamine and other inflammatory mediators cause bronchoconstriction, airway swelling, and mucus secretion, leading to wheezing, shortness of breath, and possible respiratory failure. In the cardiovascular system, widespread vasodilation and increased capillary permeability result in low blood pressure, rapid heart rate, and potential circulatory collapse

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The skin and mucous membranes are also affected, with histamine release causing hives, flushing, and swelling of the lips, tongue, or throat, which may block the airway. In the gastrointestinal system, smooth-muscle contractions and increased secretions lead to nausea, vomiting, abdominal cramps, and diarrhea. These symptoms reflect the systemic nature of anaphylaxis and how mast cell degranulation impacts multiple body systems at once.

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Overall, these organ-level changes clearly demonstrate the pathophysiology of Type I hypersensitivity. The reaction is rapid, IgE-mediated, and triggered by exposure to allergens such as food, medication, or insect venom. Immediate treatment with epinephrine is critical to reverse the life-threatening effects of this systemic allergic response.