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Anaphylaxis is a rapidly progressing, life-threatening allergic reaction.


Anaphylaxis is a type of allergic reaction, in which the immune system responds to otherwise harmless substances from the environment. Unlike other allergic reactions, however, anaphylaxis can kill. Reaction may begin within minutes or even seconds of exposure, and rapidly progress to cause airway constriction, skin and intestinal irritation, and altered heart rhythms. In severe cases, it can result in complete airway obstruction, shock, and death.

Causes and symptoms


Like the majority of other allergic reactions, anaphylaxis is caused by the release of histamine and other chemicals from mast cells. Mast cells are a type of white blood cell and they are found in large numbers in the tissues that regulate exchange with the environment: the airways, digestive system, and skin.
On their surfaces, mast cells display antibodies called IgE (immunoglobulin type E). These antibodies are designed to detect environmental substances to which the immune system is sensitive. Substances from a genuinely threatening source, such as bacteria or viruses, are called antigens. A substance that most people tolerate well, but to which others have an allergic response, is called an allergen. When IgE antibodies bind with allergens, they cause the mast cell to release histamine and other chemicals, which spill out onto neighboring cells.
The interaction of these chemicals with receptors on the surface of blood vessels causes the vessels to leak fluid into surrounding tissues, causing fluid accumulation, redness, and swelling. On the smooth muscle cells of the airways and digestive system, they cause constriction. On nerve endings, they increase sensitivity and cause itching.
In anaphylaxis, the dramatic response is due both to extreme hypersensivity to the allergen and its usually systemic distribution. Allergens are more likely to cause anaphylaxis if they are introduced directly into the circulatory system by injection. However, exposure by ingestion, inhalation, or skin contact can also cause anaphylaxis. In some cases, anaphylaxis may develop over time from less severe allergies.
Anaphylaxis is most often due to allergens in foods, drugs, and insect venom. Specific causes include:
  • Fish, shellfish, and mollusks
  • Nuts and seeds
  • Stings of bees, wasps, or hornets
  • Papain from meat tenderizers
  • Vaccines, including flu and measles vaccines
  • Penicillin
  • Cephalosporins
  • Streptomycin
  • Gamma globulin
  • Insulin
  • Hormones (ACTH, thyroid-stimulating hormone)
  • Aspirin and other NSAIDs
  • Latex, from exam gloves or condoms, for example.
Exposure to cold or exercise can trigger anaphylaxis in some individuals.

Key terms

ACTH — Adrenocorticotropic hormone, a hormone normally produced by the pituitary gland, sometimes taken as a treatment for arthritis and other disorders.
Antibody — An immune system protein which binds to a substance from the environment.
NSAIDs — Non-steroidal antiinflammatory drugs, including aspirin and ibuprofen.
Tracheostomy tube — A tube which is inserted into an incision in the trachea (tracheostomy) to relieve upper airway obstruction.


Symptoms may include:
  • Urticaria (hives)
  • Swelling and irritation of the tongue or mouth
  • Swelling of the sinuses
  • Difficulty breathing
  • Wheezing
  • Cramping, vomiting, or diarrhea
  • Anxiety or confusion
  • Strong, very rapid heartbeat (palpitations)
  • Loss of consciousness.
Not all symptoms may be present.


Anaphylaxis is diagnosed based on the rapid development of symptoms in response to a suspect allergen. Identification of the culprit may be done with RAST testing, a blood test that identifies IgE reactions to specific allergens. Skin testing may be done for less severe anaphylactic reactions.


Emergency treatment of anaphylaxis involves injection of adrenaline (epinephrine) which constricts blood vessels and counteracts the effects of histamine. Oxygen may be given, as well as intravenous replacement fluids. Antihistamines may be used for skin rash, and aminophylline for bronchial constriction. If the upper airway is obstructed, placement of a breathing tube or tracheostomy tube may be needed.


The rapidity of symptom development is an indication of the likely severity of reaction: the faster symptoms develop, the more severe the ultimate reaction. Prompt emergency medical attention and close monitoring reduces the likelihood of death. Nonetheless, death is possible from severe anaphylaxis. For most people who receive rapid treatment, recovery is complete.


Avoidance of the allergic trigger is the only reliable method of preventing anaphylaxis. For insect allergies, this requires recognizing likely nest sites. Preventing food allergies requires knowledge of the prepared foods or dishes in which the allergen is likely to occur, and careful questioning about ingredients when dining out. Use of a Medic-Alert tag detailing drug allergies is vital to prevent inadvertent administration during a medical emergency.
People prone to anaphylaxis should carry an "Epi-pen" or "Ana-kit," which contain an adrenaline dose ready for injection.



The Meck Page. February 20, 1998.


an unusual or exaggerated allergic reaction of an organism to foreign protein or other substances. Substances most likely to cause this include drugs such as antibiotics, local anesthetics, and codeine; drugs prepared from animals, such as insulin, adrenocorticotropic hormone, and enzymes; diagnostic agents, such as iodinated x-ray contrast media; biologicals used to provide immunity, such as vaccines, antitoxins, and gamma globulin; protein foods; the venom of bees, wasps, and hornets; and pollens, molds, and animal dander. The latex in gloves or Foley catheters may cause a reaction in sensitive individuals.
Physiologic Basis. Anaphylaxis is an allergen-reagin reaction brought about by large quantities of IgE antibodies (immunoglobulins) that respond to the presence of foreign agents. Individuals who have an anaphylactoid type of immune response have a familial predisposition to overreact in the presence of an allergen because of their tendency to produce an overabundance of IgE antibodies. When an allergen enters the body reagins (IgE antibodies), which are attached to cells throughout the body, interact with the allergens. This interaction is destructive to some of the body's cells. If the interaction is severe, the outcome can be fatal.

During the interaction mast cells and eosinophils release histamine, slow-reacting substance of anaphylaxis (SRS-A), bradykinin, and enzymes. Histamine brings about bronchospasm, widespread peripheral vasodilation, and increased permeability of the capillaries. SRS-A causes increased constriction of the bronchioles and bronchi. Bradykinin has effects similar to those of histamine. Together they promote collapse of the vascular network by permitting the loss of fluid from the blood vessels into the interstitial fluid compartment.
Clinical Manifestations. If the allergen comes into contact with cell-bound IgE in the respiratory tract, the tissues of the mucosa release chemical mediators that produce the symptoms of asthma and hay fever. An insect bite or sting can produce localized swelling, redness, and itching, or a more severe systemic reaction.

Local anaphylactic reactions usually produce mildly irritating symptoms, which should not be ignored because the reaction can rapidly escalate into a systemic response involving cells throughout the body. The patient may then experience generalized itching, swelling, and urticaria. As the process continues, respiration is impaired because of bronchospasm and laryngeal edema. If an airway is not maintained and supplemental oxygen provided, the person will die of respiratory failure.

Another life-threatening series of events is related to vascular collapse resulting from a shift in body fluid. The symptoms are hypotension, decreasing levels of consciousness, tachycardia, and diminished production of urine. Without effective treatment these symptoms progress to profound shock and death.
Treatment and Patient Care. Mild anaphylaxis can be treated with antihistamines, local applications of cold to minimize swelling, and topical applications of medications to relieve itching and soothe the skin. All anaphylactic reactions require careful assessment and monitoring, and the patient should be instructed to seek additional help if he or she experiences dizziness, heart palpitations, or prolonged or spreading edema anywhere in the body. The drug of choice in the initial treatment of severe anaphylaxis is epinephrine, administered intravenously, subcutaneously, sublingually, or by intermittent positive pressure breathing. The mode of administration is governed by the urgency of the situation and the presenting symptoms. Epinephrine causes bronchodilation, reduces laryngeal spasm, and elevates the blood pressure.

Steroid therapy is initiated to counteract the effects of histamine by decreasing capillary permeability. Acting as antiinflammatory agents, steroids also stabilize mast cells and prevent further release of chemical mediators.

Supportive measures include administration of intravenous fluids and plasma to restore intravascular fluid volume. Pressor agents, such as dopamine, norepinephrine, and isoproterenol, are given to increase and maintain blood pressure.

The best way to control anaphylaxis is by preventing it from happening in the first place, but this is not always possible. A person engaging in normal activities outside the clinical setting can accidentally come in contact with an allergen. An allergic individual should be prepared for such an event by understanding his or her allergy and knowing what actions to take. Those with known atopic allergies should wear a medical identification necklace or bracelet, and those who undergo systemic reactions should carry with them at all times a kit containing diphenhydramine (Benadryl), a syringe and needle, and vials of epinephrine. These kits require a written prescription from a primary health care provider.

In the clinical setting, all health care personnel should be alert to the need for identifying patients with known allergies and communicating this information to their co-workers. Emergency equipment should be readily available in all places where drugs or diagnostic agents with a risk of provoking anaphylaxis are administered.
active anaphylaxis that produced by injection of a foreign protein.
antiserum anaphylaxis (passive anaphylaxis) that resulting from injection of serum of a sensitized person into a normal person.
passive cutaneous anaphylaxis PCA; localized anaphylaxis passively transferred by intradermal injection of an antibody and, after a latent period (about 24 to 72 hours), intravenous injection of the homologous antigen and Evans blue dye; blueing of the skin at the site of the intradermal injection is evidence of the permeability reaction. Used in studies of antibodies causing immediate hypersensitivity reactions.
reverse anaphylaxis that following injection of antigen, succeeded by injection of antiserum.


An induced systemic or generalized sensitivity; at times the term anaphylaxis is used for anaphylactic shock. The term is commonly used to denote the clinical reaction seen with system IgE-mediated hypersensitivity reaction. Multivalent antigen crosslinks IgE on the surface of tissues mast cells, causing degranulation with release of preformed mediators (for example, histamine). Generation of newly synthesized mediators occurs rapidly. The physiologic manifestations reflect the biologic effects of these mediators. Cutaneous symptoms include pruritus, erythema, urticaria, and angioedema. Respiratory compromise can come from laryngeal obstruction or bronchospasm. Cardiac effects include arrhythmia, hypotension, and shock. The reaction may be fatal if asphyxiation or cardiovascular collapse occurs.
[G. ana, away from, back from, + phylaxis, protection]


/ana·phy·lax·is/ (-fĭ-lak´sis) anaphylactic shock; a manifestation of immediate hypersensitivity in which exposure of a sensitized individual to a specific antigen or hapten results in life-threatening respiratory distress, usually followed by vascular collapse and shock and accompanied by urticaria, pruritus, and angioedema.
active anaphylaxis  that produced by injection of a foreign protein.
antiserum anaphylaxis  passive a.
local anaphylaxis  that confined to a limited area, e.g., cutaneous anaphylaxis.
passive anaphylaxis  that resulting in a normal person from injection of serum of a sensitized person.
passive cutaneous anaphylaxis  PCA; localized anaphylaxis passively transferred by intradermal injection of an antibody and, after a latent period (about 24 to 72 hours), intravenous injection of the homologous antigen and Evans blue dye; blueing of the skin at the site of the intradermal injection is evidence of the permeability reaction. Used in studies of antibodies causing immediate hypersensitivity reaction.
reverse anaphylaxis  that following injection of antigen, succeeded by injection of antiserum.


A sudden, usually systemic allergic reaction, characterized by vasodilation resulting in decreased blood pressure, smooth muscle contraction resulting in shortness of breath, and hives, caused by hypersensitivity induced by a secondary exposure to a foreign substance, such as a drug or protein, after an initial sensitizing exposure.

an′a·phy·lac′tic (-lăk′tĭk), an′a·phy·lac′toid (-toid) adj.
an′a·phy·lac′ti·cal·ly adv.


Etymology: Gk, ana + phylaxis, protection
an exaggerated, life-threatening hypersensitivity reaction to a previously encountered antigen. It is mediated by antibodies of the E or G class of immunoglobulins and results in the release of chemical mediators from mast cells. The reaction may consist of a localized wheal-and-flare reaction of generalized itching, hyperemia, angioedema, and in severe cases vascular collapse, bronchospasm, and shock. The severity of symptoms depends on the original sensitizing dose of the antigen, the number and distribution of antibodies, and the route of entry and dose of subsequently encountered antigen. Penicillin injection is the most common cause of anaphylactic shock. Insect stings, radiopaque contrast media containing iodide, aspirin, antitoxins prepared with animal sera, and allergens used in testing and desensitizing patients who are hypersensitive also produce anaphylaxis in some individuals. Kinds of anaphylaxis are aggregate anaphylaxis, antiserum anaphylaxis, cutaneous anaphylaxis, cytotoxic anaphylaxis, indirect anaphylaxis, and inverse anaphylaxis. anaphylactic, adj.
observations Manifestations can range from mild to severe. Mild symptoms include queasiness, anxiety, urticaria, itching, flushing, sneezing, nasal congestion, runny nose, cough, conjunctivitis, abdominal cramps, and tachycardia. Moderate reactions include a range of symptoms, including malaise; urticaria; pulmonary congestion, dyspnea, wheezing, and bronchospasm; hoarseness; edema of the periorbital tissue and/or tongue, larynx, and pharynx; dysphagia; nausea; vomiting; diarrhea; hypotension; syncope; and confusion. Severe anaphylaxis presents with pallor and cyanosis, stridor, airway obstruction, and hypoxia. If not treated immediately, respiratory arrest, cardiac arrhythmia, circulatory collapse, seizures, coma, and death rapidly ensue.
interventions Treatment centers on immediate and aggressive management of emerging symptoms. Maintaining the airway and blood pressure is critical. EpINEPHrine and other drugs are used to counteract effects of mediator release and to block further mediator release. Vasoconstrictors are used to maintain blood pressure. Intubation or tracheostomy may be necessary to maintain an airway.
nursing considerations The patient suffering an allergic reaction needs careful monitoring for signs of respiratory distress, hypotension, and decreased circulatory volume. Nursing interventions for anaphylactic shock center on the promotion of adequate ventilation and tissue perfusion. Airway needs are maintained, vital signs are monitored for hypotension, blood gases are monitored for acidosis, ECG is monitored for dysrhythmias, and fluid volume is replaced with IV solutions. Education about prevention of future attacks should include instruction in prophylaxis, such as avoiding known allergens, wearing a Medic Alert bracelet or necklace that identifies allergies, and ensuring that all medical records have allergies highlighted in a prominent place. Those with severe allergic reactions should consider carrying an anaphylaxis kit with preloaded epINEPHrine syringes.
enlarge picture
EpiPen used for anaphylaxis


A brisk immune response resulting from the binding of IgE antibodies to high-affinity IgE receptors on mast cells or basophils, with the release of histamine and tryptase and secretion of leukotrienes and prostaglandins; laryngeal oedema may cause death by asphyxia.
The postmortem examination is often negative; the diagnosis requires history of the terminal events.

Autopsy findings
Cutaneous urticaria and angioedema, pharyngeal or laryngeal spasm, upper airway oedema, lower airways obstruction due to bronchospasm and mucus plugging, hyperinflation of lungs, petechial haemorrhage. Anaphylactic death is quickest with drugs (5 minutes), slower with stings (12 minutes) and slowest with food (30 minutes).

Lab workup
Tissue eosinophilia, serum mast cell tryptase, allergen-specific IgE antibodies.

Adrenaline (with the caveat that too much adrenaline can also kill the patient by causing massive pulmonary oedema).

Fatal anaphylaxis—causative agents
• Peanuts, as well as pecans and other nuts;
• Prawns and other shellfish;
• Acidic fruits (citrus), strawberries;
• Milk and other dairy products.

• Antibiotics—classically penicillin, but increasingly cephalosporins, amoxycillin, ampicillin;
• Anaesthetics—e.g., suxamethonium (succinylcholine), thiopental, acetazolamide, protamine;
• Radiocontrast media—especially ionic media, technitium.

Typically cause death by shock, as well as laryngeal oedema and complete upper airway obstruction, usually accompanied by petechial haemorrhage on mucosal and serosal surfaces (a typical finding in asphyxia).

Chymopapain, platinum compounds, phenylenediamine (used as a hair dye); even skin prick tests can be fatal.

transfusion reaction

Blood transfusion reaction, incompatibility reaction Transfusion medicine Any untoward response to the transfusion of non-self blood products, in particular RBCs, which evokes febrile reactions that are either minor–occurring in 1:40 transfusions and attributed to nonspecific leukocyte-derived pyrogens, or major–occurring in 1:3000 transfusions and caused by a true immune reaction, which is graded according to the presence of urticaria, itching, chills, fever and, if the reaction is intense, collapse, cyanosis, chest and/or back pain and diffuse hemorrhage Note: If any of above signs appear in a transfusion reaction, or if the temperature rises 1ºC, the transfusion must be stopped; most Pts survive if < 200 ml has been transfused in cases of red cell incompatibility-induced transfusion reaction; over 50% die when 500 ml or more has been transfused; TF mortality is ± 1.13/105 transfusions Clinical Flank pain, fever, chills, bloody urine, rash, hypotension, vertigo, fainting
Transfusion reactions
Immune, non-infectious transfusion reactions  
• Allergic Urticaria with immediate hypersensitivity
• Anaphylaxis Spontaneous anti-IgA antibody formation, occurs in ± 1:30 of Pts with immunoglobulin A deficiency, which affects 1:600 of the general population–total frequency: 1/30 X 1/600 = 1/18,000
• Antibodies to red cell antigens, eg antibodies to ABH, Ii, MNSs, P1, HLA
• Serum sickness Antibodies to donor's immunoglobulins and proteins
Non-immune, non-infectious transfusion reactions  
• Air embolism A problem of historic interest that occurred when air vents were included in transfusion sets
• Anticoagulant Citrate anticoagulant may cause tremors and EKG changes
• Coagulation defects Depletion of factors VIII and V; this 'dilutional' effect requires massive transfusion of 10 + units before becoming significant
• Cold blood In ultra-emergent situations, blood stored at 4º C may be tranfused prior to reaching body temperature at 37º C; warming a unit of blood from 4 to 37º C requires 30 kcal/L of energy, consumed as glucose; cold blood slows metabolism, exacerbates lactic acidosis, ↓ available calcium, ↑ hemoglobin's affinity for O2 and causes K+ leakage, a major concern in cold hemoglobinuria
• Hemolysis A phenomenon due to blood collection trauma, a clinically insignificant problem
• Hyperammonemia and lactic acid Both molecules accumulate during packed red cell storage and when transfused, require hepatorenal clearance, of concern in Pts with hepatic or renal dysfunction, who should receive the freshest units possible
• Hyperkalemia Hemolysis causes an ↑ of 1 mmol/L/day of potassium in a unit of stored blood, of concern in Pts with poor renal function, potentially causing arrhythmia
• Iron overload Each unit of packed RBCs has 250 mg iron, potentially causing hemosiderosis in multi-transfused Pts
Microaggregates Sludged debris in the pulmonary vasculature causing ARDS may be removed with micropore filters
Pseudoreaction Transfusion reaction mimics, eg anxiety, anaphylaxis related to a drug being administered at the same time as the transfusion
Infections transmitted by blood transfusion
• Viruses B19, CMV, EBV, HAV, HBV, HCV, HDV, HEV, Creutzfeldt-Jakob disease, Colorado tick fever, tropical viruses–eg Rift Valley fever, Ebola, Lassa, dengue, HHV 6, HIV-1, HIV-2, HTLV-I, HTLV-II
• Bacteria Transmission of bacterial infections from an infected donor is uncommon and includes brucellosis and syphilis in older reports; more recent reports include Lyme disease and Yersinia enterocolitica  Note: Although virtually any bacteria could in theory be transmitted in blood, the usual cause is contamination during processing rather than transmission from an infected donor
• Parasites Babesiosis, Leishmania donovani, L tropica, malaria, microfilariasis–Brugia malayi, Loa loa, Mansonella perstans, Mansonella ozzardi, Toxoplasma gondii, Trypanosoma cruzi


The immediate, transient Type 1 immunologic (allergic) reaction characterized by contraction of smooth muscle and dilation of capillaries due to release of pharmacologically active substances (histamine, bradykinin, serotonin, and slow-reacting substance), classically initiated by the combination of antigen (allergen) with mast-cell-fixed, cytophilic antibody (chiefly IgE); the reaction can be initiated, also, by relatively large quantities of serum aggregates (antigen-antibody complexes, and others) that seemingly activate complement leading to production of anaphylatoxin, a reaction sometimes termed "aggregate anaphylaxis."
Compare: anaphylactoid shock
[G. ana, away from, back from, + phylaxis, protection]


A severe, often fatal, form of hypersensitivity allergic reaction most commonly provoked by drugs such as penicillin, intravenous iron or procainamide, but also brought on by allergy to foods, vaccines, insect bites or snake bites and contact with latex rubber. There is always a history of a previous reaction to the ALLERGEN. The effects are a drop in blood pressure (hypotension), local swelling of the skin (angio-oedema) and mucous membranes, narrowing of the air tubes (bronchi), itching, vomiting and abdominal pain. The sooner the onset after exposure to the allergen, the more severe the reaction. Anaphylactic shock is a serious, widespread allergic attack which may cause death by AIRWAY obstruction from swelling of the lining of the LARYNX.


a hypersensitive reaction that can occur after a second exposure to an ANTIGEN. Such anaphylactic ‘shock’ responses are varied, ranging from reddening and itching of the skin through to respiratory failure and death.


An induced systemic or generalized sensitivity; at times the term anaphylaxis is used for anaphylactic shock. The physiologic manifestations reflect the biologic effects of these mediators. Cutaneous symptoms include pruritus, erythema, urticaria, and angioedema. Respiratory compromise can come from laryngeal obstruction or bronchospasm. Cardiac effects include arrhythmia, hypotension, and shock. The reaction may be fatal if asphyxiation or cardiovascular collapse occurs.
[G. ana, away from, back from, + phylaxis, protection]


an unusual or exaggerated allergic reaction of an animal to foreign protein or other substances. Anaphylaxis is an immediate or antibody-mediated hypersensitivity reaction (type I) produced by the release of vasoactive agents such as histamine and serotonin. Release is a consequence of the binding of IgE antibodies to Fc receptors on the surface of particularly mast cells and basophils. Antigen binding to two adjacent IgE molecules causes perturbation of the cell membrane leading to the release of vasoactive substances. Anaphylaxis may be localized, usually cutaneous, or generalized. Called also anaphylactic shock.
Substances most likely to produce anaphylaxis include drugs, particularly antibiotics and local anesthetics; drugs prepared from animals, such as insulin, adrenocorticotropic hormone and enzymes; diagnostic agents, such as iodinated x-ray contrast media; biologicals used to provide immunity, such as vaccines, antitoxins and gamma globulin; protein foods; the venom of bees, wasps and hornets; and pollens and molds. See also hypersensitivity, anaphylactic.

acquired anaphylaxis
that in which sensitization is known to have been produced by administration of a foreign antigen.
active anaphylaxis
see acquired anaphylaxis (above).
aggregate anaphylaxis
caused by large amounts of antibody-antigen complexes that activate complement and resulting in degranulation of mast cells.
antiserum anaphylaxis
passive anaphylaxis.
cutaneous anaphylaxis
a localized form of anaphylaxis, which follows the injection of antigen into the skin.
cytotoxic anaphylaxis
a form of anaphylaxis triggered by antibodies against self antigens. Blood transfusion reactions and Rh reactions are examples.
cytotropic anaphylaxis
refers to binding of IgE to Fc receptors.
heterologous anaphylaxis
passive anaphylaxis induced by transfer of serum from an animal of a different species.
homologous anaphylaxis
passive anaphylaxis induced by transfer of serum from an animal of the same species.
indirect anaphylaxis
that induced by an animal's own protein modified in some way.
passive anaphylaxis
that resulting in a normal animal from injection of serum of a sensitized animal.
passive cutaneous anaphylaxis (PCA)
localized anaphylaxis passively transferred by intradermal injection of an antibody and, after a latent period (about 24 to 72 hours), intravenous injection of the homologous antigen and Evans blue dye; blueing of the skin at the site of the intradermal injection is evidence of PCA.
reverse passive cutaneous anaphylaxis
antigen is injected first, succeeded by the injection of antiserum.
systemic anaphylaxis
a generalized anaphylactic reaction most often observed when the antigen is injected intravenously but may also be produced after local administration of antigen. The main shock organs in cattle and sheep are the lungs, in the horse, cat and pig the lungs and intestines, and in dogs the liver, specifically the hepatic veins.
References in periodicals archive ?
Given that these drugs are histamine releasers, that many anaphylactoid reactions caused by direct release of inflammatory mediators may show some features of a true IgE-antibody-mediated anaphylactic response and that skin testing with known histamine releasers is often uncertain and requires careful attention to the dilutions employed, it seems likely that some reactions due to direct release of mediators as well as some true immediate allergic reactions to opioid analgesics are misdiagnosed.
Immediate hypersensitivity can be divided into three types or syndromes: allergy, anaphylaxis, and anaphylactoid reaction.
There are many agents that can cause anaphylaxis or anaphylactoid reactions.
41) Before Zomax was taken FDA also failed to analyze data it had that strongly intimated that Zomax was associated with a higher incidence of anaphylactoid reactions than other drugs in its class.
metobolic food disorders, anaphylactoid reactions, food idiosyncrasies, and histamine poisoning) that many consumers and some physicians often confuse with food allergies.
Anaphylactoid reactions during anaesthesia, seven years of experience of intradermal testing.
Anaphylactoid reactions are indistinguishable from anaphylaxis and for all practical purposes are treated in a similar way.
Incidence of anaphylactoid reactions to isosulfan blue dye during breast carcinoma lymphatic mapping in patients treated with preoperative prophylaxis.
data from 1976 through 1996 showed a total of 196 serious anaphylactoid reactions and 31 deaths related to the use of this compound.