eMedicine Specialties > Allergy and Immunology > Major Allergic Diseases

Anaphylaxis: Treatment & Medication

Author: Stephen F Kemp, MD, FACP, Professor of Medicine, Associate Professor of Pediatrics, Director of Allergy and Immunology Fellowship Program, Departments of Medicine and Pediatrics, Associate Director of Division of Clinical Immunology and Allergy, Department of Medicine, University of Mississippi Medical Center; Consultant in Allergy and Immunology, Medical Service, G V (Sonny) Montgomery Veterans Affairs Medical Center
Coauthor(s): G William Palmer, MD, Consulting Staff, Shoreline Allergy and Asthma Associates
Contributor Information and Disclosures

Updated: Apr 29, 2009

Treatment

Medical Care

Anaphylaxis is a medical emergency that requires immediate recognition and intervention. Basic equipment and medication should be readily available in the physician's office. Lieberman et al have described this in great detail.29,30

  • For the initial assessment, check the airway closely. If needed, establish and maintain an airway and/or provide ventilatory assistance. Assess the level of consciousness and obtain blood pressure, pulse, and oximetry values.
  • Place the patient in the supine position with legs elevated, and begin supplemental oxygen.
  • Administer intramuscular epinephrine immediately (the thigh muscle is preferable; see Medication).30,14 Epinephrine maintains the blood pressure, antagonizes the effects of the released mediators, and inhibits further release of mediators from mast cells and basophils. Health care professionals are sometimes reluctant to administer epinephrine for fear of adverse effects. However, the use of epinephrine for anaphylaxis has no absolute contraindications. It is the drug of choice and it is usually well tolerated and potentially lifesaving. Anaphylactic deaths correlate with a delay in the administration of epinephrine. The initial dose can be repeated as necessary, depending on the response.
  • Intramuscular administration of epinephrine in the thigh (vastus lateralis) results in higher and more rapid maximum plasma concentrations of epinephrine compared with the intramuscular or subcutaneous administration in the arm (deltoid) of asymptomatic children and adults.31 However, similar studies comparing intramuscular injections to subcutaneous injections in the thigh have not yet been done. Obesity or other conditions that enlarge the subcutaneous fat pad may prevent intramuscular access.
  • Remove the source of the antigen if possible (eg, remove stinger after honeybee sting or stop drug infusion). If anaphylaxis occurs after injection of allergen-specific SCIT, a large local reaction often occurs. Place a tourniquet above the injection site and, after intramuscular epinephrine is administered, inject up to 0.1 mL of epinephrine into the large local reaction site to slow absorbance.
  • The standard treatment of anaphylaxis should also include antihistamines and corticosteroids. However, antihistamines have a much slower onset of action than epinephrine, they exert minimal effect on blood pressure, and they should not be administered alone as treatment.
  • Antihistamine therapy thus is considered adjunctive to epinephrine. Administer both an H1 blocker and an H2 blocker because studies have shown the combination to be superior to an H1 blocker alone in relieving the histamine-mediated symptoms. Diphenhydramine and ranitidine are an appropriate combination. Intravenous administration ensures that effective dosing is not impaired by hemodynamic compromise, which adversely affects gastrointestinal or intramuscular absorption. However, oral or intramuscular administration of antihistamines may suffice for milder anaphylaxis.
  • Establish intravenous access for (1) the administration of adjunctive medications and (2) the administration of intravenous fluids to maintain blood pressure, if needed.
  • Racemic epinephrine via a nebulizer can be used to reduce laryngeal swelling, but it does not replace intramuscular administration of epinephrine.
  • Treat bronchospasm that has not responded to intramuscular epinephrine with inhaled beta2-adrenergic agonists such as albuterol.
  • Corticosteroids have no immediate effect on anaphylaxis. However, administer them early to try to prevent a potential late-phase reaction (biphasic anaphylaxis). Patients with asthma or other conditions recently treated with a corticosteroid may be at increased risk for severe or fatal anaphylaxis and may receive additional benefit if corticosteroids are administered to them during anaphylaxis. The authors recommend corticosteroid treatment for all patients with anaphylaxis. If absorption is a concern, intravenous preparations should be used.
  • Maintaining proper blood pressure is important in the treatment of anaphylactic reactions.
    • Hypotension is often the most difficult manifestation of anaphylaxis to treat.
    • Persons with protracted hypotension must be monitored in an intensive care setting.
    • Because hypotension in anaphylaxis is due to a dramatic shift of intravascular volume, the fundamental treatment intervention after epinephrine is aggressive intravenous fluid administration. Large volumes of crystalloid may be required, potentially exceeding 5 L. The exact amount should be individualized and based on blood pressure and urine output. In severe cases, invasive monitoring of central venous pressure and cardiac output may be required.
    • Vasopressors may also be needed to support blood pressure. Intravenous epinephrine (1:10,000 preparation) can be administered as a continuous infusion, especially when the response to intramuscular epinephrine (1:1000) is poor. Dopamine infusion can also be used.
    • Patients with anaphylaxis who are taking a beta-adrenergic blocking agent (eg, for hypertension, migraine prophylaxis) can have refractory anaphylaxis that is poorly responsive to standard measures. Glucagon might be effective in this situation.32 It has both inotropic effects and chronotropic effects on the heart by increasing intracellular levels of cyclic adenosine 3,'5'-monophosphate, independent of the beta-adrenergic receptors. Glucagon can also reverse bronchospasm.
  • Since adequate oxygenation also depends on ventilation, establishing and maintaining an airway or providing ventilatory assistance may be necessary. One of the quickest, easiest, and most effective ways to support ventilation involves a one-way valve facemask with oxygen inlet port (eg, Pocket-Mask [Laerdal Medical Corporation, Gatesville, Tex] or similar device). Artificial ventilation via the mouth-to-mask technique with oxygen attached to the inlet port has provided oxygen saturations comparable to endotracheal intubation. Patients with adequate spontaneous respirations may breathe through the mask.
  • Clinicians proficient in advanced airway management may consider additional intervention, where appropriate. For example, severe laryngeal edema may occur so rapidly during anaphylaxis that endotracheal intubation becomes impossible. Therefore, an endotracheal tube should be inserted promptly if laryngeal edema does not reverse promptly with epinephrine. If intubation fails, cricothyrotomy probably should be attempted next since it is easier to perform than an emergency tracheostomy.
  • Depending on its severity, refractory hypotension may require placement of an invasive cardiovascular monitor (central venous catheter) and arterial line.
  • Treatment of cardiopulmonary arrest is discussed elsewhere.
  • Anti-IgE (eg, omalizumab) complexes circulating (but not receptor-bound) IgE and keeps it from binding to its receptors. It does not remove IgE bound to receptors and takes several months to have a substantial effect. It should not be used in an acute setting and would not be expected to influence IgE-independent or non-immunologic events.

Surgical Care

This is limited to the possible need for surgical intervention to establish airway access.

Consultations

  • Most patients with anaphylaxis should be referred to an allergist-immunologist for further evaluation and treatment. However, the Olmsted County study demonstrated that only 52% of patients were referred for such a consultation,10 and emergency departments fared worse in both civilian and military settings, 12-20% and 29%, respectively.
  • In the case of severe anaphylaxis requiring admission to the intensive care unit, a critical care specialist should be consulted.
  • Prophylaxis for intravenous radiocontrast media (RCM) involves prednisone (or hydrocortisone), diphenhydramine, ranitidine (or another H2 antihistamine), and/or the use of a different low osmolar contrast agent.
    • Use a radiocontrast agent with lower osmolarity.
    • Administer prednisone (50 mg PO) or hydrocortisone (200 mg IV) at 13, 7, and 1 hour before the radiocontrast procedure.
    • Administer diphenhydramine (50 mg PO/IV) and ranitidine (150 mg PO or 50 mg IV) with or without ephedrine (25 mg PO) 1 hour before the procedure. Ephedrine should not be used in patients with hypertension, coronary artery disease (CAD), a strong family history of CAD (for older patients), arrhythmia, thyrotoxicosis, monoamine oxidase inhibitor use, or porphyria.
  • Short-term desensitization procedures can be used for medication allergy in some circumstances in which no therapeutic alternative exists.
    • Published protocols exist for short-term desensitization and are available for various medications. Consult an allergist-immunologist skilled in desensitization procedures to perform these protocols. Most protocols require the patient to be in an intensive care unit setting throughout the procedure and to have established intravenous access and epinephrine at the bedside before the procedure starts. Obtain informed consent prior to the procedure. Anaphylaxis is a potential complication of this procedure.
    • A typical desensitization protocol for beta-lactam antibiotics provides the patient a starting dose that is 6-7 logs below the usual therapeutic dose and increases the dose by 1 log every 20-30 minutes.33
  • Pretreatment protocols do not work for IgE-independent anaphylaxis or cytotoxic dermatitis (erythema multiforme, Stevens-Johnson syndrome, or toxic epidermal necrolysis).
  • Patients should be given epinephrine autoinjectors and should be instructed in the use of the device. Good evidence suggests that physicians underprescribe epinephrine and that patients (or their parents) fail to use epinephrine as quickly as possible.31,34

Diet

The only dietary consideration is the future avoidance of a suspect or culprit food. Clinical trials are presently evaluating short-term oral desensitization for some foods, such as peanuts.

Activity

Once the acute episode of anaphylaxis has resolved, no activity limitations are necessary, except in the case of exercise-induced anaphylaxis.

Medication

The primary medication for acute anaphylaxis is epinephrine. All other therapies are adjunctive, including antihistamines, corticosteroids, and albuterol. Dopamine may be required to maintain blood pressure, and glucagon can be used in patients taking beta-blockers who have refractory anaphylaxis.

Adrenergic agonists

These agents help maintain blood pressure, antagonize effects of released mediators, and prevent further release of mediators.


Epinephrine (Adrenaline, EpiPen, EpiPen Jr, Twinject)

Drug of choice for treating anaphylaxis. Has alpha-agonist effects that include increased peripheral vascular resistance and reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.

Adult

0.2-0.5 mL (0.2-0.5 mg) of 1:1000 solution IM; repeat prn, depending on response
1-2 mL (0.1-0.2 mg) of 1:10,000 preparation (0.1 mg/mL) IV q5-20min prn or continuous IV infusion of 1-4 mcg/min for more critical situations

EpiPen (Dey Laboratories, Napa, CA) autoinjector for adults available with single 0.3-mg (1:1,000 v/v) dose

The Twinject (Verus Pharmaceuticals, San Diego, CA) is pen-sized device containing two 0.3-mg doses of epinephrine; first of two doses in both cases is delivered by autoinjector while second is injected manually

Pediatric

0.01 mg/kg (max. dose 0.3 mg) IM prn
"Rule of 6" calculation for infusion: 0.6 X body weight (kg) = number of milligrams diluted to total 100 mL of saline; then 1 mL/h delivers 0.1 mcg/kg/min IV infusion

EpiPen Jr., with 0.15 mg (1:2,000 v/v) dose, is available for children <30 kg; EpiPen may be used for larger children

Twinject is pen-sized device containing two doses of epinephrine available either as 0.15 or 0.3 mg formulation; first of two doses in both cases is delivered by autoinjector while second is injected manually

Beta-blockers antagonize physiologic effects; increases toxicity of alpha-blocking agents and halogenated inhalational anesthetics; TCAs and MAOIs potentiate effects; digoxin potentiates arrhythmogenic effects

No absolute contraindications in life-threatening anaphylaxis; documented hypersensitivity; cardiac arrhythmias; angle-closure glaucoma; during labor (may delay second stage of labor)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in elderly persons and those with prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, or cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias; adverse effects include anxiety, headache, palpitations, and hypertension

Antihistamines

These agents block effects of released histamine at H1 receptor, thereby treating flushing, urticarial lesions, vasodilation, and smooth muscle contraction in bronchial tree and GI tract.


Diphenhydramine (Benadryl)

Widely available with a long history of efficacy and relative safety. FDA indication for anaphylaxis. IV administration provides faster onset of action.

Adult

10-50 mg IV/IM q4h prn; IV rate not to exceed 25 mg/min; not to exceed 400 mg/d
25-50 mg PO q6-8h prn; not to exceed 400 mg/d

Pediatric

12.5-25 mg PO tid/qid or 5 mg/kg/d or 150 mg/m2/d divided tid/qid; not to exceed 300 mg/d
5 mg/kg/d IV/IM or 150 mg/m2/d divided qid; IV rate not to exceed 25 mg/min; daily dose not to exceed 300 mg/d

Potentiates effect of alcohol and other CNS depressants (eg, hypnotics, sedatives, tranquilizers); MAOIs prolong and intensify anticholinergic effects of antihistamines

Documented hypersensitivity; concurrent use of MAOIs

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in breastfeeding and newborns secondary to risk of convulsions and death in the baby; may exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, or urinary tract obstruction; adverse effects include drowsiness, reduced mental alertness, and xerostomia

Histamine2-receptor antagonists

These agents block effects of released histamine at H2 receptors, thereby treating vasodilation, possibly some cardiac effects, and glandular hypersecretion. H2 blockers with H1 blockers have additive benefit over H1 blockers alone in treating anaphylaxis. Ranitidine (Zantac) probably preferred over cimetidine (Tagamet) in anaphylaxis in light of the risk for hypotension with rapidly infused cimetidine and the multiple, complex drug interactions with cimetidine. Famotidine (Pepcid) IV is another good alternative.


Ranitidine (Zantac)

H2 antagonist, which, when combined with an H1 type, may be useful in treating allergic reactions that do not respond to H1 antagonists alone.

Adult

50 mg/dose IV/IM q6-8h
IV bolus administration: Dilute 50 mg in 20 mL NS (concentration of 2.5 mg/mL), inject at rate not >4 mL/min (5 min)
Alternatively, 150 mg PO bid; not to exceed 600 mg/d

Pediatric

<12 years: Not established
>12 years:
1.25-2.5 mg/kg/dose PO q12h; not to exceed 300 mg/d
0.75-1.5 mg/kg/dose IV/IM q6-8h; not to exceed 400 mg/d

May decrease effects of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment; if CrCl is <50 mL/min, maintain 50-mg dose and increase administration interval to 18-24 h; IV administration for >5 d may cause ALT elevations; case reports suggest ranitidine may precipitate acute porphyria

Bronchodilators

These agents stimulate beta2-adrenergic receptors in bronchial smooth muscle, causing bronchodilation.


Albuterol (Proventil, Ventolin)

Beta-agonist for bronchospasm refractory to epinephrine. Relaxes bronchial smooth muscle by action on beta2-receptors, with little effect on cardiac muscle contractility.

Adult

Nebulizer: 2.5-5 mg q4-6h in 2-5 mL sterile NS or water; to make solution, dilute 0.5 mL (2.5 mg) of 0.5% inhalation solution in 1-2.5 mL of NS (more frequent administration can be used for severe bronchospasm)
MDI: 1-2 puffs q4-6h; more frequent administration can be used for severe bronchospasm

Pediatric

Nebulizer
<5 years: 1.25-2.5 mg in 1-2.5 mL q4-6h; to make solution, dilute 0.25-0.5 mL (1.25-2.5 mg) of 0.5% inhalation solution in 1-2.5 mL of NS
>5 years: Administer as in adults
MDI
<12 years: 1-2 puffs qid with tube spacer
>12 years: Administer as in adults

Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation by albuterol; cardiovascular effects may increase with MAOIs, inhaled anesthetics, TCAs, and sympathomimetic agents; may exacerbate diuretic-induced hypokalemia; may decrease digoxin levels

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiovascular disorders (eg, coronary artery disease, cardiac arrhythmias, severe hypertension), hyperthyroidism, diabetes mellitus, and seizure disorder; adverse effects include tremor and mild tachycardia

Corticosteroids

Bind to the intracellular glucocorticoid receptors in inflammatory cells with multiple downstream immunomodulating effects. Glucocorticoids might prevent persistent or biphasic anaphylaxis. Patients with asthma or other conditions recently treated with a corticosteroid may be at increased risk for severe or fatal anaphylaxis and may receive additional benefit if corticosteroids are administered to them during anaphylaxis.


Methylprednisolone (Solu-Medrol)

May help prevent late-phase allergic reactions (biphasic anaphylaxis). No immediate effects.

Adult

Loading: 125-250 mg IV over several min
Maintenance: 0.25-1 mg/kg/dose IV q6h for up to 5 d

Pediatric

Loading: 2 mg/kg IV
Maintenance: Administer as in adults

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin, and rifampin may decrease levels (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics; concomitant use with NSAIDs increases risk of peptic ulcer

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hyperglycemia, edema, osteonecrosis, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use (most are unlikely with short-term use for acute anaphylaxis)

Positive inotropic agents

These agents help maintain blood pressure independent of adrenergic receptors by increasing intracellular levels of cyclic AMP. In addition, stimulate release of endogenous catecholamines.


Glucagon (GlucaGen)

Probably the drug of choice for severe anaphylaxis in patients taking beta-blockers (should be used in addition to epinephrine, NOT as a substitute).

Pancreatic alpha cells of the islets of Langerhans produce glucagon, a polypeptide hormone. Exerts opposite effects of insulin on blood glucose. Elevates blood glucose levels by inhibiting glycogen synthesis and enhancing formation of glucose from noncarbohydrate sources, such as proteins and fats (gluconeogenesis). Increases hydrolysis of glycogen to glucose (glycogenolysis) in liver in addition to accelerating hepatic glycogenolysis and lipolysis in adipose tissue. Also increases force of contraction in heart and has a relaxant effect on GI tract.

Dose used for anaphylaxis is higher than usual dose of 1 mg (1 U) IV/IM/SC used to treat hypoglycemia.

Adult

1-5 mg IV bolus, followed by infusion of 5-15 mcg/min titrated against blood pressure

Pediatric

Hypoglycemia
<20 kg: 0.5 mg (0.5 U) IV/IM/SC or a dose equivalent to 20-30 mcg/kg
>20 kg: 1 mg (1 U) IV/IM/SC
Anaphylaxis: May need higher doses

Effects of anticoagulants may be enhanced (although onset may be delayed); monitor prothrombin activity for signs of bleeding in patients receiving anticoagulants and adjust dose accordingly

Documented hypersensitivity; pheochromocytoma

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adverse effects include nausea, vomiting, sudden and marked increase in blood pressure in patients with pheochromocytoma, and severe rebound hypoglycemia in patients with insulinoma

Vasopressors

These agents are useful as adjunctive therapy to IV fluids to treat refractory hypotension from anaphylaxis.


Dopamine (Intropin)

Considered drug of choice for anaphylaxis-induced refractory hypotension. Stimulates both adrenergic and dopaminergic receptors.

Hemodynamic effect is dependent on dose. Lower doses predominantly stimulate dopaminergic receptors, which, in turn, produce renal and mesenteric vasodilation. Cardiac stimulation and peripheral vasoconstriction produced by higher doses.

More than 50% of patients are satisfactorily maintained on doses <20 mcg/kg/min.

Adult

2-5 mcg/kg/min IV; after initiating therapy, increase dose by 1-4 mcg/kg/min q10-30min until optimal response obtained; not to exceed 50 mcg/kg/min

Pediatric

Administer as in adults; 6 X body weight (in kg) = No of mg diluted to total 100 mL of saline; then 1 mL delivered 1 mcg/kg/min

Phenytoin, alpha- and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects

Documented hypersensitivity; pheochromocytoma; ventricular fibrillation

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor urine flow, cardiac output, pulmonary wedge pressure, and blood pressure closely during infusion; prior to infusion, correct hypovolemia; monitoring central venous pressure or left ventricular filling pressure may be helpful for detecting and treating hypovolemia; extravasation can cause necrosis of surrounding tissue, which is treated with phentolamine injected at the site

More on Anaphylaxis

Overview: Anaphylaxis
Differential Diagnoses & Workup: Anaphylaxis
Treatment & Medication: Anaphylaxis
Follow-up: Anaphylaxis
References
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Further Reading

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Keywords

anaphylaxis, systemic allergic reaction, anaphylactic reaction, anaphylactoid reaction, allergic reaction, allergies, peanut allergy, latex allergy, shellfish allergy, hypersensitivity reaction, food allergy, insect sting, Hymenoptera venom, wasp sting, bee sting, yellow jacket sting, hornet sting, penicillin allergy, radiocontrast hypersensitivity, cardiovascular collapse, laryngeal edema, atopy, atopic disease, fire ant sting, immunotherapy, platelet activating factor, PAF, anaphylactic shock, EpiPen, epipen, food allergies, bee allergy, bee sting allergy

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Contributor Information and Disclosures

Author

Stephen F Kemp, MD, FACP, Professor of Medicine, Associate Professor of Pediatrics, Director of Allergy and Immunology Fellowship Program, Departments of Medicine and Pediatrics, Associate Director of Division of Clinical Immunology and Allergy, Department of Medicine, University of Mississippi Medical Center; Consultant in Allergy and Immunology, Medical Service, G V (Sonny) Montgomery Veterans Affairs Medical Center
Stephen F Kemp, MD, FACP 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 Federation for Medical Research, American Medical Association, Association of Subspecialty Professors, Joint Council of Allergy, Asthma and Immunology, Mississippi State Medical Association, and Southern Society for Clinical Investigation
Disclosure: Dey LP Honoraria Speaking and teaching; Verus Pharmaceuticals Consulting fee Consulting; Pfizer Consulting fee Endpoint Committee; Intelliject None Consulting

Coauthor(s)

G William Palmer, MD, Consulting Staff, Shoreline Allergy and Asthma Associates
G William Palmer, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology
Disclosure: Nothing to disclose.

Medical Editor

Stephen C Dreskin, MD, PhD, Director of Allergy, Asthma, and Immunology Practice, Professor of Medicine, Departments of Internal Medicine and Immunology, University of Colorado Health Sciences Center
Stephen C Dreskin, MD, PhD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association for the Advancement of Science, American Association of Immunologists, American Association of Neuropathologists, American Association of Ophthalmic Pathologists, American Association of Oral and Maxillofacial Surgeons, American College of Allergy, Asthma and Immunology, Clinical Immunology Society, and Joint Council of Allergy, Asthma and Immunology
Disclosure: Genentech Consulting fee Consulting

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Samuel R Marney, Jr, MD, Director, Associate Professor, Department of Internal Medicine, Division of Allergy and Immunology, Vanderbilt University School of Medicine
Samuel R Marney, Jr, MD 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, and Tennessee Medical Association
Disclosure: Nothing to disclose.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Michael A Kaliner, MD, Clinical Professor of Medicine, George Washington University School of Medicine; Chief, Section of Allergy and Immunology, Washington Hospital Center; 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, and Association of American Physicians
Disclosure: Abbott Consulting fee Consulting; Alcon Consulting fee Consulting; Glaxo Consulting fee Consulting; Greer Consulting fee Consulting; Sanofi Consulting fee Consulting; Schering Consulting fee Consulting; Teva  Consulting; Meda Honoraria Speaking and teaching

 
 
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