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Immediate Hypersensitivity Reactions Medication

  • Author: Becky Buelow, MD, MS; Chief Editor: Michael A Kaliner, MD  more...
 
Updated: Feb 09, 2015
 

Medication Summary

Medical therapy varies somewhat depending on which type of allergic reaction is being treated. Some of the drugs and their categories are listed here, but refer to the articles on the specific allergic reaction for more detail.

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Vasopressors

Class Summary

Epinephrine is the first medication that should be used to reverse effects of systemic vasodilation and increased vasopermeability observed with anaphylaxis. Although not the first choice for bronchoconstriction, epinephrine can also relieve some symptoms of bronchospasm and rhinitis. In the past, protocols called for subcutaneous or intravenous administration of epinephrine. However, studies have shown that intramuscular epinephrine leads to higher plasma levels than subcutaneous delivery. Intramuscular administration is now preferred over subcutaneous administration.[45, 46]

Predosed autoinjectable epinephrine is available in at least 3 forms, which include EpiPen, Auvi-Q, and Epinephrine auto-injector. Two doses of each are available (0.3 mg for EpiPen, Auvi-Q, and Epinephrine auto-injector, and 0.15 mg for EpiPen Jr., Auvi-Q, or Epinephrine auto-injector). EpiPen, Auvi-Q, and Epinephrine auto-injectors all come in two-packs (i.e., 2 auto-injectors). Auvi-Q comes with a trainer and is only available in the English language.

Epinephrine (Adrenalin, EpiPen, Auvi-Q, Adrenaclick)

 

Should be administered immediately for anaphylaxis/anaphylactic shock. Multiple preparations allow for delivery SC, IM, IV, or ET. Doses can be repeated q5min prn to maintain blood pressure (and as heart rate allows).

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Bronchodilators

Class Summary

Inhaled bronchodilators are beta-agonists that come in short- and long-acting forms. Short-acting bronchodilators (i.e., albuterol) are used to treat acute bronchospasm. Can also be used prophylactically. For example, a patient with a history of asthma exacerbation in the presence of cats can use a short-acting bronchodilator before exposure to cats. Long-acting bronchodilators (eg, salmeterol) can be used twice daily in conjunction with inhaled glucocorticoids and to help maintain bronchodilation over 12 hours. Long acting beta-agonists are not recommended as monotherapy and their use has been associated with asthma-related death.[47] The FDA has issued a “black box warning” on medications containing long-acting beta-agonists due to this concern. This “black box warning” remains controversial as treatment with an inhaled corticosteroid plus a long acting beta-agonist has been found to be safe and efficacious in the treatment of asthma.[48]

Pirbuterol and formoterol have both short- and long-acting activity. Onset of action is approximately 15 min, but effects last up to 12 hours. Again, these medications should be combined with an inhaled corticosteroid and should be reserved for patients with more frequent or moderate to severe symptoms or lung function. Finally, levalbuterol is the R-enantiomer of albuterol and is available in nebulizer and metered dose inhaler (MDI) forms. Advantage of levalbuterol is that it is less likely to cause paradoxical bronchospasm than racemic albuterol.

Previously, MDIs were made using chlorofluorocarbons (CFCs) as the propellant. However, the use of CFCs has been phased out because of environmental concerns. For this reason, companies are now making MDIs with hydrofluoroalkane-134a (HFA), which is not damaging to the ozone layer. CFC inhalers are no longer available in the United States.

Albuterol (ProAir HFA, Ventolin HFA, Proventil HFA)

 

Sympathomimetic that stimulates beta-2 receptors, leading to bronchodilation. Used for bronchospasm refractory to epinephrine with anaphylaxis. First-line choice for acute bronchospasm associated with asthma.

Salmeterol and fluticasone (Advair)

 

Salmeterol: Selective LABA; stimulates intracellular adenyl cyclase resulting in increased cAMP levels causing bronchial smooth muscle relaxation; also inhibits release of mediators of immediate hypersensitivity from cells, especially from mast cells.

Fluticasone: Trifluorinated corticosteroid with potent anti-inflammatory activity; inhibits multiple cell types (eg, mast cells, eosinophils, basophils, lymphocytes, macrophages, neutrophils) and mediator production or secretion (eg, histamine, eicosanoids, leukotrienes, cytokines) involved in the asthmatic response.

Formoterol and budesonide (Symbicort)

 

Formoterol: Long-acting selective beta2-adrenergic agonist with rapid onset of action; acts locally as bronchodilator; stimulates intracellular adenyl cyclase, which results in increased cyclic adenosine monophosphate levels, causing relaxation of bronchial smooth muscle and inhibition of release of mast cell mediators.

Budesonide: Anti-inflammatory corticosteroid; has potent glucocorticoid activity and weak mineralocorticoid activity.

Formoterol and mometasone (Dulera)

 

Mometasone: Glucocorticoid; elicits local anti-inflammatory effects on respiratory tract with minimal systemic absorption.

Formoterol: Long-acting selective beta2-adrenergic agonist with rapid onset of action; acts locally as bronchodilator; stimulates intracellular adenyl cyclase, which results in increased cyclic adenosine monophosphate levels, causing relaxation of bronchial smooth muscle and inhibition of release of mast cell mediators.

Levalbuterol (Xopenex)

 

Used for treatment or prevention of bronchospasm. A selective beta2-agonist agent. Albuterol is a racemic mixture, while levalbuterol contains only the active R- enantiomer of albuterol. The S-enantiomer does not bind to beta2-receptors, but may be responsible for some adverse effects of racemic albuterol, including bronchial hyperreactivity and reduced pulmonary function during prolonged use.

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Corticosteroids

Class Summary

Immunosuppressing agents, such as corticosteroids, can decrease inflammation. They are particularly efficacious in the treatment of skin eruptions and bronchospasm. Additionally, the role of corticosteroids in anaphylactic shock is limited, although believed to help prevent delayed type of anaphylaxis.

Several different formulations are available. Depending on type of corticosteroid, oral, intravenous, and topical forms may be available. In more severe cases of anaphylaxis and asthma, intravenous forms of corticosteroids can be used initially. These can later be switched to oral forms as doses are tapered.

Inhaled corticosteroids are another form of corticosteroids and are key in controlling inflammation of bronchial airways and nasal mucosa. Similarly, topical corticosteroids are useful in treating atopic dermatitis.

Prednisone (Rayos)

 

Believed to ameliorate delayed effects of anaphylactic reactions and may limit biphasic anaphylaxis. Doses below are general guidelines for usage; dosing is highly individualized.

Methylprednisolone (A-Methapred, Medrol, Solu-Medrol, Depo-Medrol)

 

Potent glucocorticoid with minimal to no mineralocorticoid activity.

Modulates carbohydrate, protein, and lipid metabolism and maintenance of fluid and electrolyte homeostasis.

Controls or prevents inflammation by controlling rate of protein synthesis, suppressing migration of polymorphonuclear leukocytes (PMNs) and fibroblasts, reversing capillary permeability, and stabilizing lysosomes at cellular level.

Dexamethasone (Baycadron)

 

Believed to ameliorate delayed effects of anaphylactic reactions and may limit biphasic anaphylaxis.

Prednisolone (Orapred, Millipred, FLo-Pred, Prelone)

 

Glucocorticosteroid; elicits mild mineralocorticoid activity and moderate anti-inflammatory effects; controls or prevents inflammation by controlling rate of protein synthesis, suppressing migration of polymorphonuclear leukocytes (PMNs) and fibroblasts, reversing capillary permeability, and stabilizing lysosomes at cellular level.

Hydrocortisone (A-Hydrocort, Cortef, Solu-Cortef)

 

Glucocorticoid; elicits mild mineralocorticoid activity and moderate anti-inflammatory effects; controls or prevents inflammation by controlling rate of protein synthesis, suppressing migration of polymorphonuclear leukocytes (PMNs) and fibroblasts, and reversing capillary permeability.

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Histamine1-receptor antagonists (antihistamines)

Class Summary

Type 1 histamine-receptor blockers act to block action of histamine on H1 receptor after its release from mast cells and basophils. Most effective when used prophylactically. Sedating first-generation and nonsedating second-generation H1 antihistamines are available. Typically, sedating antihistamines have more adverse anticholinergic effects. Sedating antihistamines include diphenhydramine, hydroxyzine, cyproheptadine, chlorpheniramine, and brompheniramine. The use of sedating antihistamines are discouraged because the nonsedating antihistamines, such as cetirizine and fexofenadine, are highly efficacious with reduced central nervous system side effects. Other nonsedating antihistamines include loratadine (not as efficacious as cetirizine or fexofenadine), levocetirizine, and desloratadine. Intranasal antihistamines azelastine and oloptadine can directly help with nasal congestion. Liquid forms are more rapidly absorbed orally and should be used for immediate treatment of an allergic reactionif intravenous access is not available.

Fexofenadine (Allegra)

 

Selectively inhibits histamine H1 receptor sites in blood vessels, GI tract, and respiratory tract, which in turn inhibits physiologic effects that histamine normally induces at H1 receptor sites. Once-daily dosing is convenient.

Cetirizine (Zyrtec)

 

Selectively inhibits histamine H1 receptor sites in blood vessels, GI tract, and respiratory tract, which in turn inhibits physiologic effects that histamine normally induces at H1 receptor sites. Once-daily dosing is convenient. Bedtime dosing may be useful as sedation occurs in 10-15% of persons using cetirizine.

Levocetirizine (Xyzal)

 

Selectively inhibits histamine H1 receptor sites in blood vessels, GI tract, and respiratory tract, which in turn inhibits physiologic effects that histamine normally induces at H1 receptor sites.

Desloratadine (Clarinex)

 

Long-acting antihistamine (H1 receptor antagonist). Selectively inhibits receptor sites in blood vessels, GI tract, and respiratory tract, which in turn inhibits physiologic effects that histamine normally induces at H1 receptor sites.

Loratadine (Claritin, Alavert)

 

Long-acting antihistamine (H1 receptor antagonist). Selectively inhibits receptor sites in blood vessels, GI tract, and respiratory tract, which in turn inhibits physiologic effects that histamine normally induces at H1 receptor sites.

Azelastine (Astepro)

 

Effective antihistamine delivered via the intranasal route. Mechanism is similar to oral antihistamines. Systemic absorption occurs and may cause sedation, headache, and nasal burning. Forms complex with histamine for H1-receptor sites in blood vessels, GI tract, and respiratory tract.

Use prn or qd. Use alone or in combination with other medications. Unlike oral antihistamines, has some effect on nasal congestion. Helpful for vasomotor rhinitis. Some patients experience a bitter taste. Systemic absorption may occur, resulting in sedation (reported in approximately 11% of patients).

Olopatadine (Patanase)

 

Effective antihistamine delivered via the intranasal route. Mechanism is similar to oral antihistamines. Systemic absorption occurs and may cause sedation, headache, and nasal burning.

Forms complex with histamine for H1-receptor sites in blood vessels, GI tract, and respiratory tract.

Use prn or qd. Use alone or in combination with other medications. Unlike oral antihistamines, has some effect on nasal congestion. Helpful for vasomotor rhinitis. Some patients experience a bitter taste. Systemic absorption may occur, resulting in sedation (reported in approximately 11% of patients).

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Histamine2- antagonists

Class Summary

Can be administered in addition to H1-receptor blockers for additional control of urticaria and angioedema. Examples include ranitidine, famotidine, and cimetidine. Even though cimetidine has been studied more extensively for this indication than other members of this class, ranitidine and famotidine should be used given the significant drug interactions of cimetidine with other medications.

Ranitidine (Zantac)

 

Multiple formulations are available. Cimetidine was first to be widely used but tends to have more drug interactions than other H2-receptor blockers. If no response to H1-receptor antagonist alone, coadministration with an H2-receptor antagonist can help relieve symptoms of itching and flushing in anaphylaxis, pruritus, and urticaria.

Famotidine (Pepcid, Heartburn Relief Max)

 

Blocks H2 receptors of gastric parietal cells, leading to inhibition of gastric secretions. If no response to H1-receptor antagonist alone, coadministration with an H2-receptor antagonist can help relieve symptoms of itching and flushing in anaphylaxis, pruritus, and urticaria.

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Leukotriene inhibitors

Class Summary

Leukotrienes are synthesized by degranulated mast cells and basophils and likely contribute significantly to symptoms of allergic reactions. Three leukotriene inhibitors are now available in the United States. Montelukast and zafirlukast act as leukotriene D4-receptor blockers, whereas zileuton inhibits 5-lipoxygenase thereby inhibiting the production of all the leukotrienes (leukotrienes B4, C4, D4, and E4). A disadvantage of zileuton is potential liver toxicity; liver enzymes should be drawn before the institution of therapy and periodically thereafter. A sustained release formulation of zileuton is available, permitting q12 h dosing.

Montelukast (Singulair)

 

Leukotriene inhibitors can be a helpful addition to asthma and allergic rhinitis not well controlled with H1-receptor blockers and inhaled corticosteroids.

Zafirlukast (Accolate)

 

Leukotriene pathway inhibitor. Not for use in acute episodes of asthma.

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Immunomodulators

Class Summary

Tacrolimus is a calcineurin inhibitor initially used in oral form as an immunosuppressant for transplantation patients. It has since been developed in topical form (Protopic) and can be used to treat atopic dermatitis that does not respond well to topical corticosteroids. A similar topical agent, pimecrolimus (Elidel), became available in the past few years and is indicated for mild atopic dermatitis. Systemic calcineurin inhibitors have been shown to cause immunosuppression and certain malignancies such as lymphoma. In January 2006, the FDA issued a black box warning for topical tacrolimus and pimecrolimus for these reasons.[43] To date, studies have not shown significant systemic absorption, systemic immunosuppression, or increased risk of malignancy with the topical formulations. Trials are currently underway to assess possible benefit of inhaled tacrolimus for asthma.

Tacrolimus ointment (Protopic)

 

Reduces itching and inflammation by suppressing release of cytokines from T cells. Can be used in patients as young as 2 y. More expensive than topical corticosteroids.

Pimecrolimus (Elidel)

 

Calcineurin inhibitor; inhibits T-cell activation; also shown to inhibit release of inflammatory mediators from mast cells.

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Monoclonal antibodies

Class Summary

Omalizumab (Xolair) is a monoclonal anti-IgE antibody indicated for refractory asthma. Has been shown to greatly improve severity of asthma in patients and can be used to help patients dependent on oral steroids to be weaned from steroids. Omalizumab has also been shown to improve urticaria in patients with chronic idiopathic or spontaneous urticaria recalcitrant to standard licensed doses of H1 antihistamines.[49] Additionally, omalizumab has also been shown to decrease allergic response to peanuts in patients with severe peanut allergy[50] , which could be helpful in preventing anaphylaxis from accidental peanut exposure. To date, omalizumab does not have FDA approval for peanut allergy but is approved for asthma and chronic idiopathic urticaria. Patients should undergo a full allergy evaluation prior to starting omalizumab, if needed, because it interferes with prick skin test and in vitro serum specific IgE assay results.

Omalizumab (Xolair)

 

Binds to IgE and thereby prevents IgE from binding to mast cells and basophils.

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5-Lipoxygenase Inhibitors

Class Summary

These agents inhibit leukotriene formation.

Zileuton (Zyflo, Zyflo CR)

 

Inhibitor of 5-lipoxygenase, which inhibits formation of LTB4, LTC4, LTD4, & LTE4

Inhibition of leukotriene formation reduces eosinophil and neutrophil migration, neutrophil and monocyte aggregation, capillary permeability, and smooth muscle contraction.

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Contributor Information and Disclosures
Author

Becky Buelow, MD, MS Instructor, Section of Allergy and Clinical Immunology, Department of Pediatrics, Medical College of Wisconsin

Becky Buelow, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American College of Allergy, Asthma and Immunology, Clinical Immunology Society, Wisconsin Allergy Society

Disclosure: Nothing to disclose.

Coauthor(s)

John M Routes, MD Professor of Pediatrics, Medicine, Microbiology and Molecular Genetics, Chief, Section of Allergy and Clinical Immunology, Department of Pediatrics, Medical College of Wisconsin

John M Routes, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, Clinical Immunology Society, Federation of American Societies for Experimental Biology, American Society for Virology, American Association of Immunologists, American Society for Microbiology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Michael R Simon, MD, MA Clinical Professor Emeritus, Departments of Internal Medicine and Pediatrics, Wayne State University School of Medicine; Professor, Department of Internal Medicine, Oakland University William Beaumont University School of Medicine; Adjunct Staff, Division of Allergy and Immunology, Department of Internal Medicine, William Beaumont Hospital

Michael R Simon, MD, MA is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, Michigan State Medical Society, Michigan Allergy and Asthma Society, American College of Physicians, American Federation for Medical Research, Royal College of Physicians and Surgeons of Canada, Society for Experimental Biology and Medicine

Disclosure: Received ownership interest from Secretory IgA, Inc. for management position; Received ownership interest from siRNAx, Inc. for management position.

Chief Editor

Michael A Kaliner, MD Clinical Professor of Medicine, George Washington University School of Medicine; Medical Director, Institute for Asthma and Allergy

Michael A Kaliner, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association of Immunologists, American College of Allergy, Asthma and Immunology, American Society for Clinical Investigation, American Thoracic Society, Association of American Physicians

Disclosure: Nothing to disclose.

Acknowledgements

Miriam K Anand, MD, FAAAAI, FACAAI Consulting Staff, Department of Allergy/Immunology, Allergy Associates and Lab, Ltd; Clinical Assistant Professor, Midwestern School of Osteopathic Medicine

Miriam K Anand, MD, FAAAAI, FACAAI is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, American College of Physicians-American Society of Internal Medicine, and American Medical Association

Disclosure: TEVA pharmaceuticals Honoraria Speaking and teaching

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Immediate hypersensitivity reactions. Sensitization phase of an immunoglobulin E–mediated allergic reaction.
Table.
Age Step 1 Step 2 Step 3 Step 4 Step 5 Step 6
0-4 years SABA PRN Low-dose ICS Medium-dose ICS Medium-dose ICS plus LABA or montelukast High-dose ICS plus LABA or montelukast High-dose ICS plus LABA or montelukast and oral corticosteroids
5-11 years SABA PRN Low-dose ICS Low-dose ICS plus LABA or LTRA or theophylline Medium-dose ICS plus LABA High-dose ICS plus LABA High-dose ICS plus LABA plus oral corticosteroids
12 years or older SABA PRN Low-dose ICS Low-dose ICS plus LABA or medium-dose ICS Medium-dose ICS plus LABA High-dose ICS plus LABA High-dose ICS plus LABA plus oral corticosteroids
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