Anaphylaxis: An acute hypersensitivity reaction due to exposure to a previously encountered ANTIGEN. The reaction may include rapidly progressing URTICARIA, respiratory distress, vascular collapse, systemic SHOCK, and death.Passive Cutaneous Anaphylaxis: An evanescent cutaneous reaction occurring when antibody is injected into a local area on the skin and antigen is subsequently injected intravenously along with a dye. The dye makes the rapidly occurring capillary dilatation and increased vascular permeability readily visible by leakage into the reaction site. PCA is a sensitive reaction for detecting very small quantities of antibodies and is also a method for studying the mechanisms of immediate hypersensitivity.Food Hypersensitivity: Gastrointestinal disturbances, skin eruptions, or shock due to allergic reactions to allergens in food.Immunoglobulin E: An immunoglobulin associated with MAST CELLS. Overexpression has been associated with allergic hypersensitivity (HYPERSENSITIVITY, IMMEDIATE).Drug Hypersensitivity: Immunologically mediated adverse reactions to medicinal substances used legally or illegally.Insect Bites and Stings: Bites and stings inflicted by insects.SRS-A: A group of LEUKOTRIENES; (LTC4; LTD4; and LTE4) that is the major mediator of BRONCHOCONSTRICTION; HYPERSENSITIVITY; and other allergic reactions. Earlier studies described a "slow-reacting substance of ANAPHYLAXIS" released from lung by cobra venom or after anaphylactic shock. The relationship between SRS-A leukotrienes was established by UV which showed the presence of the conjugated triene. (From Merck Index, 11th ed)Wheat Hypersensitivity: Allergic reaction to wheat that is triggered by the immune system.Peanut Hypersensitivity: Allergic reaction to peanuts that is triggered by the immune system.Mast Cells: Granulated cells that are found in almost all tissues, most abundantly in the skin and the gastrointestinal tract. Like the BASOPHILS, mast cells contain large amounts of HISTAMINE and HEPARIN. Unlike basophils, mast cells normally remain in the tissues and do not circulate in the blood. Mast cells, derived from the bone marrow stem cells, are regulated by the STEM CELL FACTOR.Histamine Release: The secretion of histamine from mast cell and basophil granules by exocytosis. This can be initiated by a number of factors, all of which involve binding of IgE, cross-linked by antigen, to the mast cell or basophil's Fc receptors. Once released, histamine binds to a number of different target cell receptors and exerts a wide variety of effects.Skin Tests: Epicutaneous or intradermal application of a sensitizer for demonstration of either delayed or immediate hypersensitivity. Used in diagnosis of hypersensitivity or as a test for cellular immunity.Urticaria: A vascular reaction of the skin characterized by erythema and wheal formation due to localized increase of vascular permeability. The causative mechanism may be allergy, infection, or stress.Histamine: An amine derived by enzymatic decarboxylation of HISTIDINE. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter.Allergens: Antigen-type substances that produce immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE).Basophils: Granular leukocytes characterized by a relatively pale-staining, lobate nucleus and cytoplasm containing coarse dark-staining granules of variable size and stainable by basic dyes.Bronchial Spasm: Spasmodic contraction of the smooth muscle of the bronchi.Anti-Allergic Agents: Agents that are used to treat allergic reactions. Most of these drugs act by preventing the release of inflammatory mediators or inhibiting the actions of released mediators on their target cells. (From AMA Drug Evaluations Annual, 1994, p475)Cell Degranulation: The process of losing secretory granules (SECRETORY VESICLES). This occurs, for example, in mast cells, basophils, neutrophils, eosinophils, and platelets when secretory products are released from the granules by EXOCYTOSIS.Ant Venoms: Venoms from the superfamily Formicoidea, Ants. They may contain protein factors and toxins, histamine, enzymes, and alkaloids and are often allergenic or immunogenic.Epinephrine: The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.Desensitization, Immunologic: Immunosuppression by the administration of increasing doses of antigen. Though the exact mechanism is not clear, the therapy results in an increase in serum levels of allergen-specific IMMUNOGLOBULIN G, suppression of specific IgE, and an increase in suppressor T-cell activity.Histamine H1 Antagonists: Drugs that selectively bind to but do not activate histamine H1 receptors, thereby blocking the actions of endogenous histamine. Included here are the classical antihistaminics that antagonize or prevent the action of histamine mainly in immediate hypersensitivity. They act in the bronchi, capillaries, and some other smooth muscles, and are used to prevent or allay motion sickness, seasonal rhinitis, and allergic dermatitis and to induce somnolence. The effects of blocking central nervous system H1 receptors are not as well understood.Cromolyn Sodium: A chromone complex that acts by inhibiting the release of chemical mediators from sensitized mast cells. It is used in the prophylactic treatment of both allergic and exercise-induced asthma, but does not affect an established asthmatic attack.Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen.Glafenine: An anthranilic acid derivative with analgesic properties used for the relief of all types of pain.Latex Hypersensitivity: Allergic reaction to products containing processed natural rubber latex such as rubber gloves, condoms, catheters, dental dams, balloons, and sporting equipment. Both T-cell mediated (HYPERSENSITIVITY, DELAYED) and IgE antibody-mediated (HYPERSENSITIVITY, IMMEDIATE) allergic responses are possible. Delayed hypersensitivity results from exposure to antioxidants present in the rubber; immediate hypersensitivity results from exposure to a latex protein.Autacoids: A chemically diverse group of substances produced by various tissues in the body that cause slow contraction of smooth muscle; they have other intense but varied pharmacologic activities.Histamine Antagonists: Drugs that bind to but do not activate histamine receptors, thereby blocking the actions of histamine or histamine agonists. Classical antihistaminics block the histamine H1 receptors only.Hypersensitivity, Immediate: Hypersensitivity reactions which occur within minutes of exposure to challenging antigen due to the release of histamine which follows the antigen-antibody reaction and causes smooth muscle contraction and increased vascular permeability.Arachis hypogaea: A plant species of the family FABACEAE that yields edible seeds, the familiar peanuts, which contain protein, oil and lectins.Ovalbumin: An albumin obtained from the white of eggs. It is a member of the serpin superfamily.Lens Plant: A plant genus of the FABACEAE family known for the seeds used as food.Angioedema: Swelling involving the deep DERMIS, subcutaneous, or submucosal tissues, representing localized EDEMA. Angioedema often occurs in the face, lips, tongue, and larynx.Bee Venoms: Venoms obtained from Apis mellifera (honey bee) and related species. They contain various enzymes, polypeptide toxins, and other substances, some of which are allergenic or immunogenic or both. These venoms were formerly used in rheumatism to stimulate the pituitary-adrenal system.Adrenergic Agonists: Drugs that bind to and activate adrenergic receptors.Neuromuscular Blocking Agents: Drugs that interrupt transmission of nerve impulses at the skeletal neuromuscular junction. They can be of two types, competitive, stabilizing blockers (NEUROMUSCULAR NONDEPOLARIZING AGENTS) or noncompetitive, depolarizing agents (NEUROMUSCULAR DEPOLARIZING AGENTS). Both prevent acetylcholine from triggering the muscle contraction and they are used as anesthesia adjuvants, as relaxants during electroshock, in convulsive states, etc.Antigens, Plant: Substances found in PLANTS that have antigenic activity.Intradermal Tests: Skin tests in which the sensitizer is injected.Ascaris: A genus of nematodes of the superfamily ASCARIDOIDEA whose species usually inhabit the intestine.Guinea Pigs: A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.Arthropod Venoms: Venoms from animals of the phylum Arthropoda. Those most investigated are from scorpions and spiders of the class Arachnidae and from ant, bee, and wasp families of the Insecta order Hymenoptera. The venoms contain protein toxins, enzymes, and other bioactive substances and may be lethal to man.Tryptases: A family of neutral serine proteases with TRYPSIN-like activity. Tryptases are primarily found in the SECRETORY GRANULES of MAST CELLS and are released during mast cell degranulation.Nut Hypersensitivity: Allergic reaction to tree nuts that is triggered by the immune system.Receptors, IgE: Specific molecular sites on the surface of B- and T-lymphocytes which combine with IgEs. Two subclasses exist: low affinity receptors (Fc epsilon RII) and high affinity receptors (Fc epsilon RI).Reagins: Antibodies, especially IGE, that bind to tissue of the same species so that ANTIGENS induce release of HISTAMINE and other vasoactive agents. HYPERSENSITIVITY is the clinical manifestation.Diethylcarbamazine: An anthelmintic used primarily as the citrate in the treatment of filariasis, particularly infestations with Wucheria bancrofti or Loa loa.Platelet Activating Factor: A phospholipid derivative formed by PLATELETS; BASOPHILS; NEUTROPHILS; MONOCYTES; and MACROPHAGES. It is a potent platelet aggregating agent and inducer of systemic anaphylactic symptoms, including HYPOTENSION; THROMBOCYTOPENIA; NEUTROPENIA; and BRONCHOCONSTRICTION.Hymenoptera: An extensive order of highly specialized insects including bees, wasps, and ants.p-Methoxy-N-methylphenethylamine: A potent mast cell degranulator. It is involved in histamine release.Antigens: Substances that are recognized by the immune system and induce an immune reaction.Fagopyrum: A plant genus of the family POLYGONACEAE that is used as an EDIBLE GRAIN. Although the seeds are used as cereal, the plant is not one of the cereal grasses (POACEAE).Methysergide: An ergot derivative that is a congener of LYSERGIC ACID DIETHYLAMIDE. It antagonizes the effects of serotonin in blood vessels and gastrointestinal smooth muscle, but has few of the properties of other ergot alkaloids. Methysergide is used prophylactically in migraine and other vascular headaches and to antagonize serotonin in the carcinoid syndrome.Basophil Degranulation Test: An in vitro test used in the diagnosis of allergies including drug hypersensitivity. The allergen is added to the patient's white blood cells and the subsequent histamine release is measured.

Structural determinants of the eosinophil: chemotactic activity of the acidic tetrapeptides of eosinophil chemotactic factor of anaphylaxis. (1/1066)

The acidic tetrapeptides of ECF-A, Ala/Val-Gly-Ser-Glu, exhibit peak in vitro chemotactic activity for human eosinophils at concentrations of 3 X 10(-8) M to 10(-6) M, and rapidly deactivate eosinophils to homologous and other stimuli at concentrations as low as 10(-10) M. The analogue Leu-Gly-Ser-Glu reaches peak activity at 10(-8)M-10(-7)M, while Phe-Gly-Ser-Glu requires 10(-4)M to elicit a peak response. Although inversion of the order of glycine and serine does not alter the eosinophil chemotactic activity of the tetrapeptides, deletion of glycine increases by 10-fold the concentration required for peak chemotactic activity, indicating the critical nature of the spacing between NH2- and COOH-terminal residues. The substituent COOH-terminal tripeptide, which is only marginally chemotactic, irreversibly suppresses eosinophil chemotactic responsiveness at a concentration 10,000-fold higher than concentrations necessary for deactivation by the intact tetrapeptide. The high concentration of tripeptide required for this cell directed effect, which is assumed to be analogous to deactivation, is attributed to the absence of the NH2-terminal residue which would facilitate effective interaction with the eosinophil. A substituent NH2-terminal tripeptide and amides of the NH2-terminal amino acids, which are devoid of chemotactic and deactivating activities, reversibly inhibit the tetrapeptide stimulus in a dose-response fashion. The additional finding that the NH2-terminal tripeptide protects the eosinophil from deactivation by the intact tetrapeptide confirms that the competitive interaction is stimulus specific.  (+info)

The cat lung strip as an in vitro preparation of peripheral airways: a comparison of beta-adrenoceptor agonists, autacoids and anaphylactic challenge on the lung strip and trachea. (2/1066)

1 A new in vitro preparation, the isolated lung strip of the cat, is described for investigating the direct effect of drugs on the smooth muscle of the peripheral airways of the lung. The preparation comprises a thin strip of lung parenchyma which can be mounted in a conventional organ bath for isometric tension recording. Its pharmacological responses have been characterized and compared with the isolated tracheal preparation of the cat. 2 The lung strip exhibited an intrinsic tone which was relaxed by catecholamines, aminophylline and flufenamate. It was contracted strongly by histamine, prostaglandin F2alpha, acetylcholine, compound 48/80, potassium depolarizing solution and alternating current field stimulation. In contrast, the cat trachea was unresponsive to histamine and prostaglandin F2alpha and did not exhibit an intrinsic tone. 3 (-)-Isoprenaline and (-)-adrenaline were much more potent in relaxing the lung strip than the trachea. The potency order of relaxation responses to isoprenaline, adrenaline and (+/-)-noradrenaline in the lung strip was isoprenaline greater than adrenaline greater than noradrenaline but in the trachea was isoprenaline greater than noradrenaline greater than or equal to adrenaline. 4 beta2-Adrenoceptor selective agonists salbutamol and terbutaline were more potent in the lung strip than the trachea, suggesting beta2-adrenoceptors predominated in the lung strip. Propranolol was equipotent in inhibiting isoprenaline relexations of the lung strip and trachea, whereas practolol was much less effective in inhibiting lung strip than trachea, further supporting a predominance of beta2-adrenoceptors in lung strip and beta1-adrenoceptors in trachea. 5 Strong Schultz-Dale type contractions were elicited in both lung strips and trachea by Ascaris lumbricoides antigen in actively sensitized cats. The initial phase of the contractile response of the lung strip following challenge was shown to be due to histamine release and was absent in the trachea. The delayed phase of the contraction which took several minutes to develop in both the mepyramine-treated lung strip and trachea was not due to prostaglandins E1, F2alpha or bradykinin, the probable mediator being slow reacting substance of anaphylaxis (SRS-A). 6 It is concluded that the isolated lung strip of the cat is useful as an in vitro model for investigating the effect of drugs on the smooth muscle of the peripheral airways of the lungs.  (+info)

Anaphylactic bronchoconstriction in BP2 mice: interactions between serotonin and acetylcholine. (3/1066)

1. Immunized BP2 mice developed an acute bronchoconstriction in vivo and airway muscle contraction in vitro in response to ovalbumin (OA) and these contractions were dose dependent. 2. Methysergide or atropine inhibited OA-induced bronchoconstriction in vivo and airway muscle contraction in vitro. 3. Neostigmine potentiated the OA-induced bronchoconstriction in vivo and airway muscle contraction in vitro of BP2 mice. This potentiation was markedly reduced by the administration of methysergide or atropine and when the two antagonists were administered together, the responses were completely inhibited. 4. Neostigmine also potentiated the serotonin (5-HT)- and acetylcholine (ACh)-induced bronchoconstriction and this potentiation was significantly reversed by atropine. 5. These results indicate that OA provokes a bronchoconstriction in immunized BP2 mice by stimulating the release of 5-HT, which in turn acts via the cholinergic mediator, ACh.  (+info)

Mediators of anaphylaxis but not activated neutrophils augment cholinergic responses of equine small airways. (4/1066)

Neutrophilic inflammation in small airways (SA) and bronchospasm mediated via muscarinic receptors are features of chronic obstructive pulmonary disease in horses (COPD). Histamine, serotonin, and leukotrienes (LTs) are reported to be involved in the exacerbation of COPD, and currently, histamine has been shown to increase tension response to electrical field simulation (EFS) in equine SA. We tested the effects of these mediators and the effects of activated neutrophils on the cholinergic responses in SA. Histamine, serotonin, and LTD4 had a synergistic effect on EFS responses and only an additive effect on the tension response to exogenous ACh or methacholine. Atropine and TTX entirely eliminated the EFS-induced tension response in the presence of all three inflammatory mediators, indicating that augmentation of the EFS response applies only to the endogenous cholinergic response. Neutrophils isolated from control and COPD-affected horses were activated by zymosan, producing 18.1 +/- 2.3 and 25.0 +/- 2.3 nmol superoxide. 10(6) cells-1. 30 min-1, respectively. However, in contrast to the profound effect of mediators, incubation of SA for over 1 h in a suspension of up to 30 x 10(6) zymosan-treated neutrophils/ml did not significantly affect EFS responses of SA isolated from either control or COPD-affected horses. We conclude that in equine SA 1) the endogenous cholinergic responses are subject to strong facilitation by inflammatory mediators; 2) activated neutrophils do not affect cholinergic responses in SA; and 3) in acute bouts of equine COPD, histamine, LTD4, and serotonin (mediators primarily associated with type I allergic reaction) rather than mediators derived from neutrophils most likely contribute to increased cholinergic airway tone.  (+info)

Effect of bolus epinephrine on systemic hemodynamics in canine anaphylactic shock. (5/1066)

OBJECTIVE: Epinephrine (Epi) is considered to be the drug of choice for anaphylactic shock (AS). However, the benefit of this drug on improving systemic hemodynamics in AS has never been shown. We used a canine ragweed model of AS to determine if an intravenous bolus of Epi hastened the recovery of hemodynamics and modified mediator release (Med) compared with no treatment (NT). METHODS: In one protocol (n = 8), the effects on hemodynamics of two intravenous doses of Epi (0.01 and 0.025 mg/kg) were examined for 3 h postshock in respective studies approximately three weeks apart under pentobarbital anesthesia in the same animal. In five other dogs, left ventricular (LV) mechanics were additionally determined by sonomicrometric techniques to determine changes in contractility as defined by the preload recruitable stroke-work (SW) relationship. RESULTS: Compared with NT values, Epi treatments produced only transient increases in mean arterial pressure (MAP) and cardiac output (CO) post-challenge. By 20 min postshock, CO in the Epi studies were generally lower (p < 0.05) and BP was not different from NT values. With Epi treatment, SW was reduced for a given LV end-diastolic volume compared with the control study. Epi treatments also caused relatively higher plasma thromboxane B2 concentrations postshock. CONCLUSION: Our findings indicate that, when given immediately postshock, bolus-Epi did not hasten recovery and caused impairment in LV mechanics in canine AS.  (+info)

Strain-dependent induction of allergic sensitization caused by peanut allergen DNA immunization in mice. (6/1066)

To investigate the potential application of allergen gene immunization in the modulation of food allergy, C3H/HeSn (C3H) mice received i.m. injections of pAra h2 plasmid DNA encoding one of the major peanut allergens, Ara h2. Three weeks following pDNA immunization, serum Ara h2-specific IgG2a, IgG1, but not IgE, were increased significantly in a dose-dependent manner. IgG1 was 30-fold higher in multiply compared with singly immunized mice. Ara h2 or peanut protein injection of immunized mice induced anaphylactic reactions, which were more severe in multiply immunized mice. Heat-inactivated immune serum induced passive cutaneous anaphylaxis, suggesting that anaphylaxis in C3H mice was mediated by IgG1. IgG1 responses were also induced by intradermal injection of pAra h2, and by i.m. injection of pOMC, the plasmid DNA encoding the major egg allergen protein, ovomucoid. To elucidate whether the pDNA immunization-induced anaphylaxis was a strain-dependent phenomenon, AKR/J and BALB/c mice also received multiple i.m. pAra h2 immunizations. Injection of peanut protein into these strains at weeks 3 or 5 following immunization did not induce reactions. Although IgG2a was increased significantly from week 2 in AKR/J mice and from week 4 in BALB/c mice and remained elevated for at least 6 wk, no IgG1 or IgE was detected. These results indicate that the type of immune responses to pDNA immunization in mice is strain dependent. Consequently, models for studying human allergen gene immunization require careful selection of suitable strains. In addition, this suggests that similar interindividual variation is likely in humans.  (+info)

The modified anaphylaxis hypothesis for cot death. Anaphylactic sensitization in guinea-pigs fed cow's milk. (7/1066)

Guinea-pigs on a normal diet, but given cow's milk to drink instead of water, very soon became anaphylactically sensitive to cow's milk and may be fatally shocked following either i.v. injection or intratracheal inhalation of cow's milk.  (+info)

Evidence of anaphylaxy after alteplase infusion. (8/1066)

BACKGROUND AND PURPOSE: Although alteplase, a recombinant tissue plasminogen activator (tPA), is structurally identical to endogenous tPA and therefore should not induce allergy, single cases of acute hypersensitivity reactions have been reported. Until now, specific antibodies against alteplase were not detected in blood samples obtained in these patients. CASE DESCRIPTION: We report an anaphylactic reaction in a 70-year-old white female who was treated with intravenous alteplase for thrombolysis of acute ischemic stroke 160 minutes after onset of a right-sided hemiparesis. Thirty minutes after infusion of alteplase had been started, the patient suffered acute severe sinus tachycardia and hypotension, followed by cyanosis and loss of consciousness. The alteplase infusion was stopped, and following antiallergic therapy, tachycardia and hypotension resolved within 1 hour. The hemiparesis remained unaltered, but additional harm resulting from the hemodynamic complication was not observed. Serum samples analyzed with a radioimmunoprecipitation assay were negative for total antibodies to alteplase, but in a subsequent ELISA, both samples were positive for IgE antibodies to alteplase. CONCLUSIONS: The detection of specific IgE antibodies reactive with alteplase in this patient could provide the first evidence of an anaphylactic-type reaction to alteplase in man. Because previous exposure to alteplase can be excluded, the results suggest that this patient had preexisting antibodies that were cross-reactive with one or more epitopes of alteplase and therefore precipitated the anaphylactic-type reaction.  (+info)

  • Anaphylaxis occurs as the result of an allergen response, usually immunoglobulin E-mediated, which leads to mast cell and basophil activation and a combination of dermatologic, respiratory, cardiovascular, gastrointestinal, and neurologic symptoms. (
  • The diagnosis of anaphylaxis is typically made when symptoms occur within one hour of exposure to a specific antigen. (
  • 4 , 5 Patients may arrive at a physician's office remote from an event or with active symptoms, or they may develop anaphylaxis after administration of common treatments used in the clinic. (
  • After an antigen cross-links the IgEs on the membrane of effector cells, a complex intracellular signaling cascade is initiated, which leads cells to release preformed mediators stored in their granules that are responsible for the acute symptoms of anaphylaxis. (
  • While anaphylaxis can have the most serious effect on the heart and lungs, it can actually trigger symptoms throughout the body, Dr. Skomra says. (
  • A more complete description of anaphylaxis and the symptoms associated with it can be viewed in resources , published by the U.S. Department of Health and Human Services' National Institutes of Health. (
  • Food-dependent exercise-induced anaphylaxis is a subtype of anaphylaxis and, although rare, it is an important condition to be familiar with as it can ultimately lead to death. (
  • We present a case of food-dependent exercise-induced anaphylaxis in a 17-year-old white girl due to chickpea. (
  • We hope that this case will serve as an important reminder that although rare, food-dependent exercise-induced anaphylaxis exists and making a diagnosis can lead to life-saving preventative strategies. (
  • Family physicians and patients need to be prepared to recognize and quickly treat anaphylaxis to prevent potentially catastrophic outcomes. (
  • An adrenaline autoinjector should only be prescribed as part of a comprehensive anaphylaxis management plan, which includes an ASCIA Action Plan for Anaphylaxis and education on how to reduce the risk of allergic reactions. (
  • Anaphylaxis was the reason behind about eight per cent of all visits for allergic reactions. (
  • She has taught many nurse practitioner students over the years, and her first lesson for them was always about the recognition and treatment of allergic reactions, especially anaphylaxis, in the clinical setting. (
  • Adrenaline works rapidly to reverse the effects of anaphylaxis and is the first line treatment for anaphylaxis. (
  • In a national survey of school nurses in UK, more than 80% felt confident in the management of respiratory distress, airway obstruction and anaphylaxis, 77% had adrenaline and albuterol available, and 13% had oxygen. (
  • 1 The incidence of anaphylaxis in the United States is 49.8 cases per 100,000 person-years. (
  • ASCIA Action Plans for Anaphylaxis are available from the ASCIA website. (
  • In putting forward the motion, Allison said: "With more awareness, Canadians will become familiar with the risk of anaphylaxis and will hopefully take precautions to limit accidental exposure for those who may be vulnerable. (
  • We found that steroids, which are part of the treatment plan for managing anaphylaxis, can have a negative effect on patient outcomes," says Dr. Ben-Shoshan. (
  • Epinephrine: the drug of choice for anaphylaxis. (
  • Carrying an epinephrine autoinjector and identification regarding the condition is recommended in people with a history of anaphylaxis. (
  • For self-management of patients at risk of anaphylaxis in community settings, they recommend carrying epinephrine auto-injectors and personalized emergency action plans, as well as follow-up with a physician (ideally an allergy/immunology specialist) to help prevent anaphylaxis recurrences. (
  • ICON: Anaphylaxis describes unmet needs in anaphylaxis, noting that although epinephrine in 1 mg/mL ampules is available worldwide, other essentials, including supplemental oxygen, intravenous fluid resuscitation, and epinephrine auto-injectors are not universally available. (
  • Vaccination locations that anticipate vaccinating large numbers of persons (e.g., mass vaccination clinics) should plan adequate staffing and supplies (including epinephrine) for the assessment and management of anaphylaxis. (
  • Persons with a history of anaphylaxis who carry an epinephrine autoinjector could be reminded to bring it to their vaccination appointment. (
  • It is estimated that almost 600,000 Canadians will experience anaphylaxis in their lifetime and that more than half of the individuals who had anaphylaxis were not equipped with life-saving epinephrine. (
  • The team also observed that the majority (80.2%) of anaphylaxis cases were triggered by food, principally peanut and tree nut, and that children who did not receive epinephrine prior to arrival at the ED were more likely to receive multiple (two or more) doses of epinephrine at the hospital. (
  • This is why your doctor will recommend adrenaline (epinephrine) injections in the case of anaphylaxis. (
  • This EBG recommended that children meeting criteria for anaphylaxis receive prompt intramuscular epinephrine and also receive diphenhydramine and a glucocorticoid. (
  • By using clinical criteria that objectively help the clinician discern if a child is likely having anaphylaxis, early intervention with epinephrine, diphenhydramine, and glucocorticoids increases the likelihood of prompt resolution as well as prevention of late-phase reactions. (
  • If you have a history of anaphylaxis, your doctor should coach you and your family members on how to use self-injectable epinephrine. (
  • One study suggested that patients at risk of food-induced anaphylaxis carry 2 doses of epinephrine. (
  • A 55-year-old woman developed unstable angina following an episode of severe anaphylaxis which was treated with 0.5 mg intramuscular epinephrine (adrenaline). (
  • Four weeks later, she had a second episode of anaphylaxis, and suffered a cardiac arrest after receiving a bolus of intravenous epinephrine. (
  • It highlights the dangers of intravenous epinephrine in treating anaphylaxis outside anaesthetic and intensively monitored settings. (
  • Although epinephrine is the treatment of choice for anaphylaxis, it remains underused. (
  • Severe episodes of anaphylaxis are treated with epinephrine (adrenaline), followed by oral antihistamines and steroids. (
  • Administration of intramuscular epinephrine at the onset of anaphylaxis, before respiratory failure or cardiovascular compromise, is essential. (
  • All patients at risk of recurrent anaphylaxis should be educated about the appropriate use of prescription epinephrine autoinjectors. (
  • Epinephrine (adrenaline) is the medication that is most commonly used to treat anaphylaxis. (
  • As many as 25% of people who have an anaphylactic reaction will experience biphasic anaphylaxis, a recurrence in the hours following the beginning of the reaction, and will require further medical treatment, including additional epinephrine injections. (
  • Epinephrine is the drug of choice and primary therapy in the emergency management of anaphylaxis resulting from insect bites or stings, foods, drugs, latex, or other allergic triggers, and it should be administered immediately. (
  • Anaphylaxis, the most severe form of allergic reaction, will require IV antihistamines (and epinephrine) and blood pressure support with IV fluids. (
  • NASN's Connection Cards are a tool for the school nurse to use to initiate meaningful conversations with students and parents/caregivers on topics related to anaphylaxis and epinephrine. (
  • The Saving Lives at School: Anaphylaxis and Epinephrine handbook is a guide with evidence based information and resources that correspond with the Connection Cards to facilitate their use in school nursing practice. (
  • Included in the epinephrine guidance is the recommendation that if anaphylaxis occurs in a healthcare setting, epinephrine should be given in these doses: 0.01 mg/kg (maximum dose, 0.3 mg) in a prepubescent child, and up to 0.5 mg in a teenager. (
  • Kids with severe allergies can be at risk for a sudden, potentially life-threatening allergic reaction called anaphylaxis . (
  • Anaphylaxis is a severe and potentially life-threatening allergic reaction. (
  • The mission of The Food Allergy & Anaphylaxis Network (FAAN) is to raise public awareness, to provide advocacy and education, and to advance research on behalf of all those affected by food allergies and anaphylaxis (a life-threatening allergic reaction). (
  • Anaphylaxis, known to be a sudden and potentially life-threatening allergic reaction, seems to be increasing among children, according to a new study led by a team at the Research Institute of the McGill University Health Centre (RI-MUHC). (
  • Anaphylaxis is a severe and life-threatening allergic reaction that involves multiple organ systems or the whole body and has an incidence rate of 0.05%-2% [ 1 ]. (
  • Anaphylaxis, a severe life-threatening allergic reaction that can result in death, has a potential health and safety impact for the American workplace. (
  • Anaphylaxis is a life-threatening allergic reaction that can cause your airway to constrict and your blood pressure to drop dangerously low. (
  • The authors of this study show the value of employing a consensus recommendation (in this case, from the National Institute of Allergy and Infectious Diseases on recognition of anaphylaxis and appropriate pharmacologic intervention) as part of an EBG. (
  • Certain medications that a patient is taking may confound the presentation and impede prompt recognition of anaphylaxis (e.g. beta-blockers, antihistamines). (
  • Early recognition of anaphylaxis and the prompt administration of IM adrenaline improves outcomes and decreases mortality. (
  • People who have existing conditions like asthma , allergic rhinitis , etc. may be prone to anaphylaxis from food items. (
  • People suffering from asthma and other atopic diseases are more susceptible to anaphylaxis. (
  • It has been estimated that EIA may represent 5 percent to 15 percent of all cases of anaphylaxis," says Brian Smart, M.D., an allergist and immunologist at the DuPage Medical Group Asthma and Allergy Center in Glen Ellyn, Ill. Although EIA is uncommon, fitness professionals should be aware of this potentially serious condition and its associated variables. (
  • 2 , 3 Compared with that of the general population, the risk of anaphylaxis is doubled in patients with mild asthma and tripled in those with severe disease. (
  • Anaphylaxis may not be recorded, or may be misdiagnosed as something else, for example, asthma. (
  • Patients with asthma and/or cardiovascular disease are at increased risk of mortality in anaphylaxis. (
  • However, there are certain risk factors for more severe reactions, the most important of which is the presence of comorbid asthma: almost all fatal cases of anaphylaxis occur in asthmatics. (
  • We summarized the general patient condition, clinical manifestations during attacks, and factors that influenced the manifestations, including the relationships between gender, age, etiology, and underlying diseases with the laboratory and clinical manifestations of anaphylaxis and among clinical manifestations, the relationship between blood pressure and multisystem involvement. (
  • Uniphasic anaphylaxis - Uniphasic anaphylactic reactions are the most common type, accounting for an estimated 80 to 90 percent of all episodes. (
  • Family physicians and patients need to be prepared to recognize and quickly treat anaphylaxis to prevent potentially catastrophic outcomes. (
  • The cyclodextrin sugammadex and anaphylaxis to rocuronium: is rocuronium still potentially allergenic in the inclusion complex form? (
  • Although anaphylaxis is rare, it is serious and potentially life-threatening. (
  • A rare red meat allergy that starts after being bitten by a lone star tick may cause unexplained cases of recurrent anaphylaxis. (
  • Anaphylaxis: guidelines from the European Academy of Allergy and Clinical Immunology. (
  • ICON: Anaphylaxis provides a unique perspective on the principal evidence-based anaphylaxis guidelines developed and published independently from 2010 through 2014 by four allergy/immunology organizations. (
  • The findings, published this week in the Journal of Allergy and Clinical Immunology (JACI), reveal that the percentage of emergency department (ED) visits due to anaphylaxis doubled over a four-year period based on data collected from the Montreal Children's Hospital of the MUHC (MCH-MUHC). (
  • To evaluate the clinical and allergologic features of anaphylaxis in children referred to the allergology and immunology unit of A. Meyer Children's Hospital (Florence, Italy) from 1994 to 1996. (
  • Hypersensitivity that is caused by secretion of a hormone called progesterone by the body is called catamenial anaphylaxis. (
  • Anaphylaxis is thought to result from antigen-antibody interactions on the surface of mast cells, connective tissue cells that are believed to contain a number of regulatory, or mediator, chemicals. (
  • In addition, it was found that neither mast cells nor basophils were required in mouse models of active systemic anaphylaxis. (
  • Evidence of an underlying clonal mast cell disease has been found in about I in 15 patients with IA in our studies and in about 1 in 12 patientswith venom induced anaphylaxis in a European study. (
  • Thus, a more complete understanding of the prevalence of clonal mast cell disease in those experiencing anaphylaxis and a better understanding of the associated laboratory abnormalities and disrupted molecular signaling pathways will have a substantial impact of the clinical management of patients who present with anaphylaxis. (
  • This protocol thus focuses on determining the prevalence of clonal mast cell disorders in patients with the anaphylaxis, whether unexplained (IA) or associated with exposure to an antigen (SA), and attendant changes in the mast cell compartment. (
  • Many other foods have also been known to trigger anaphylaxis. (
  • Common foods that are known to trigger anaphylaxis vary across the geographic areas of the world. (
  • Exercise is also known to trigger anaphylaxis in the vulnerable group. (
  • Anaphylaxis is the result of the immune system - the body's natural defence system - overreacting to a trigger. (
  • Latex (the liquid that oozes out of plants) from a few plants and is used to manufacture items like hand gloves can trigger anaphylaxis. (
  • This large cohort study shows that age of 65 years or older, medication as a trigger, and presence of comorbid conditions (specifically cardiac and lung disease) were associated with significantly higher odds of severe anaphylaxis. (
  • Other commonly used medications and pain relievers that can trigger anaphylaxis include aspirin, ibuprofen, anesthetics and antibiotics. (
  • Food anaphylaxis. (
  • What is my risk of anaphylaxis to food i've eaten before? (
  • Food allergy is the main cause of anaphylaxis outside of the hospital, according to Food Allergy Research and Education (FARE). (
  • A really good informative website to look at is the Food Allergy & Anaphylaxis Network. (
  • Anaphylaxis often begins within minutes after a person eats a problem food. (
  • The Anaphylaxis Campaign has called for clearer guidelines and greater consistency on food labelling. (
  • Low vitamin D levels -- emerging evidence suggests low vitamin D levels may be associated with risk of anaphylaxis and food allergy. (
  • As mentioned, combining exercise with certain foods-or any food, for some people-can result in anaphylaxis. (
  • Factors associated with increased risk of anaphylaxis include intercurrent infection, concomitant medication/foods (particularly α -blockers, β -blockers, angiotensin-converting enzyme [ACE] inhibitors, non-steroidal anti-inflammatory drugs [NSAIDS], alcohol or spicy food), high ambient temperatures and exercise. (
  • Multiple factors that affect food-induced anaphylaxis are discussed in this review, paying special attention to dietary habits and environmental and genetic conditions. (
  • Food - the leading cause of outpatient anaphylaxis in most surveys. (
  • It has low sensitivity and is often not elevated in food-induced anaphylaxis. (
  • In children, the majority of anaphylaxis is associated with food. (
  • Australia has one of the highest rates of documented food allergy and hospital anaphylaxis admissions in the developed world," write the researchers in Clinical & Experimental Allergy . (
  • For how long should a person who has received emergency treatment for anaphylaxis be observed? (
  • It is recommended that a cluster randomised controlled trial is conducted for people who have received emergency treatment for anaphylaxis. (