Medication Summary
Various drugs are used for the treatment of upper airway diseases. For allergic rhinitis and conjunctivitis, antihistamine/decongestant and/or intranasal corticosteroid and anticholinergic nose sprays are the treatments of choice. For allergic asthma, short-acting or long-acting bronchodilators, mast-cell stabilizers, antileukotriene agents, corticosteroid inhalers, oral corticosteroids, anticholinergic inhalers, or theophylline may be indicated, depending on the stage of the disease. For allergic fungal sinusitis (AFS), allergic bronchopulmonary aspergillosis (ABPA), allergic bronchopulmonary mycosis (ABPM), and extrinsic allergic alveolitis (EAA), an oral corticosteroid is the treatment of choice; in AFS, it may be supplemented with a corticosteroid inhaler. In ABPA and ABPM, it may be supplemented with a corticosteroid inhaler or theophylline. In EAA, it may be supplemented with a bronchodilator.
Antihistamines, oral
Class Summary
These agents compete with histamine to bind to H1 receptors on the endothelium and smooth muscle. Histamine is a central vasoactive mediator in allergic rhinitis, and prophylactic use of antihistamines typically provides substantial control of symptoms. Dosage of traditional (first-generation) antihistamine classes is limited by the appearance of undesirable adverse effects including sedation, restlessness, dry mouth, urinary retention, constipation, and blurred vision. For this reason, new-generation antihistamines that are mostly free of such adverse effects are welcome options for treatment. Many first-generation antihistamines are available without a prescription, and loratadine, a second-generation antihistamine, is currently available over-the-counter (OTC).
Loratadine (Claritin)
Nonsedating second-generation antihistamine. Fewer adverse effects than first-generation medications. Selectively inhibits peripheral histamine H1 receptors.
Desloratadine (Clarinex)
Relieves nasal congestion and systemic effects of seasonal allergy. Long-acting tricyclic histamine antagonist selective for H1-receptor. Major metabolite of loratadine, which after ingestion is extensively metabolized to active metabolite 3-hydroxydesloratadine.
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 if sedation is a problem.
Levocetirizine (Xyzal)
Histamine1-receptor antagonist. Active enantiomer of cetirizine. Peak plasma levels reached within 1 h and half-life is about 8 h. Available as a 5-mg breakable (scored) tab and 0.5 mg/mL oral solution. Indicated for seasonal and perennial allergic rhinitis.
Fexofenadine (Allegra)
Nonsedating second-generation medication with fewer adverse effects than first-generation medications. Competes with histamine for H1 receptors on GI tract, blood vessels, and respiratory tract, reducing hypersensitivity reactions. Does not sedate. Available in qd and bid preparations.
Antihistamines with decongestants, oral
Class Summary
Antihistamines are most useful for symptoms of itching, sneezing, tearing, or postnasal drip. Decongestants relieve nasal congestion, reducing symptoms of sniffling. Many are available OTC in various combinations of an antihistamine plus pseudoephedrine.
Pseudoephedrine/loratadine (Claritin-D)
Second-generation long-acting antihistamine/decongestant combination with 120 mg or 240 mg pseudoephedrine.
Cetirizine/pseudoephedrine (Zyrtec-D)
Cetirizine 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 if sedation is a problem.
Pseudoephedrine stimulates vasoconstriction by directly activating alpha-adrenergic receptors of the respiratory mucosa. Induces also bronchial relaxation and increases heart rate and contractility by stimulating beta-adrenergic receptors.
Pseudoephedrine/fexofenadine (Allegra-D)
Fexofenadine is a nonsedating second-generation medication with fewer adverse effects than first-generation medications. Competes with histamine for H1 receptors on GI tract, blood vessels, and respiratory tract, reducing hypersensitivity reactions. Does not sedate.
Pseudoephedrine stimulates vasoconstriction by directly activating alpha-adrenergic receptors of the respiratory mucosa. Induces also bronchial relaxation and increases heart rate and contractility by stimulating beta-adrenergic receptors.
Antihistamine nasal sprays
Class Summary
These agents locally relieve nasal symptoms more effectively than oral antihistamines. They are often used with oral antihistamine.
Azelastine (Astelin, Astepro)
Aqueous nasal spray to treat seasonal and perennial allergic rhinitis.
Mast-cell stabilizers
Class Summary
These agents prevent mast-cell activation and, thus, degranulation. Degranulation releases mediators (eg, histamine), which causes tissue swelling and chemotactic factors to attract eosinophils to the site. This leads to delayed-phase inflammation. This process is obvious in allergic rhinitis and allergic asthma but may also be involved in other clinical conditions related to mold allergy. Nedocromil may have more anti-inflammatory effect than other agents.
Cromolyn sodium (NasalCrom)
NasalCrom (5.2 mg per spray, nasal solution) used for mast-cell stabilization in allergic rhinitis. Cromolyn sodium nebulizer solution (20 mg/2 mL, nebulizer solution) used to prevent asthma.
Antihistamine and mast cell stabilizer eye drops
Class Summary
Although oral antihistamines are useful for allergic conjunctivitis, ophthalmic drops offer immediate relief of eye symptoms from allergies (eg, itching, tearing, conjunctival swelling). Not indicated to relieve an acute asthma attack.
Olopatadine (Patanol, Pataday)
Ophthalmic antihistamine solution indicated for temporary prevention of ocular itching due to allergic conjunctivitis. Inhibitor of histamine release from mast cells and devoid of effects on serotonin, alpha-adrenergic, muscarinic, and dopamine receptors. Patanol is available as an ophthalmic solution 0.1%. Pataday is available as an ophthalmic solution 0.2%.
Corticosteroid nasal sprays
Class Summary
Corticosteroids are potent anti-inflammatory agents that affect activation of many cells (eg, mast cells, eosinophils, macrophages, lymphocytes) and effect of mediators (eg, histamine, eicosanoids, interleukins [ILs], cytokines) that are important in allergic inflammatory process or hypersensitivity reactions. Therefore, they are important for treatment of the various diseases attributable to mold allergy.
Mometasone (Nasonex)
Demonstrated no mineralocorticoid, androgenic, antiandrogenic, or estrogenic activity in preclinical trials. Decreases rhinovirus-induced up-regulation in respiratory epithelial cells and modulate pretranscriptional mechanisms. Reduces intraepithelial eosinophilia and inflammatory cell infiltration (eg, eosinophils, lymphocytes, monocytes, neutrophils, plasma cells). Available as aqueous nasal spray of 50 mcg per spray.
Fluticasone intranasal (Flonase, Veramyst)
Used to treat allergic rhinitis. Available as aqueous nasal spray. The propionate (Flonase) delivers 50 mcg per actuation, whereas the furoate (Veramyst) delivers 27.5 mcg per actuation. Fluticasone furoate is well tolerated compared with the older propionate version, particularly in children.
Budesonide inhaled (Rhinocort Aqua)
Inhibits bronchoconstriction mechanisms, produces direct smooth muscle relaxation, may decrease number and activity of inflammatory cells, in turn decreasing airway hyperresponsiveness. Has extremely potent vasoconstrictive and anti-inflammatory activity. Alters level of inflammation in airways by inhibiting multiple types of inflammatory cells and decreasing production of cytokines and other mediators. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Used for treatment of allergic rhinitis.
Flunisolide
Inhibits bronchoconstriction mechanisms, produces direct smooth muscle relaxation, may decrease number and activity of inflammatory cells, in turn decreasing airway hyperresponsiveness. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes, and reversing capillary permeability. Does not depress the hypothalamus.
Ciclesonide (Omnaris)
Corticosteroid nasal spray indicated for allergic rhinitis. Prodrug that is enzymatically hydrolyzed to pharmacologic active metabolite C21-desisobutyryl-ciclesonide following intranasal application. Corticosteroids have a wide range of effects on multiple cell types (eg, mast cells, eosinophils, neutrophils, macrophages, lymphocytes) and mediators (eg, histamines, eicosanoids, leukotrienes, cytokines) involved in allergic inflammation. Each spray delivers 50 mcg. Well tolerated in children.
Corticosteroid oral inhalers
Class Summary
These are potent anti-inflammatory agents because of their effects on several cell types (eg, mast cells, eosinophils, neutrophils, macrophages, lymphocytes) and on the production and secretion of mediators (eg, histamine, eicosanoids, leukotriene, cytokines) in inflammatory process. Inhalers listed below are valuable for the treatment of mild-to-moderately persistent or severe forms of allergic asthma and are used as supplemental therapy for ABPA, ABPM, and EAA. Oral inhaled corticosteroids allow avoidance of severe adverse effects associated with systemic corticosteroids.
Fluticasone inhaled
Indicated for maintenance and treatment of asthma as prophylaxis; also used in patients requiring long-term systemic corticosteroid treatment to attempt gradual tapering and discontinuation of PO corticosteroids: Available as Flovent MDI (44, 110, 220 mcg per actuation), Flovent Rotadisk (50, 100, 250 mcg per actuation), and dry powder in blister packs for inhalation with inhalation device.
Budesonide inhaled (Pulmicort Flexhaler)
Inhibits bronchoconstriction mechanisms, produces direct smooth muscle relaxation, may decrease number and activity of inflammatory cells, in turn decreasing airway hyperresponsiveness. Has extremely potent vasoconstrictive and anti-inflammatory activity. Alters level of inflammation in airways by inhibiting multiple types of inflammatory cells and decreasing production of cytokines and other mediators. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Used for treatment of allergic rhinitis.
Available as Pulmicort Flexhaler (90 mcg per actuation or 180 mcg per actuation delivers 80 mcg per inhalation or 160 mcg/inhalation); Pulmicort Respules inhalation susp (0.25 mg/2 mL, 0.5 mg/2 mL) inhalation susp
Triamcinolone inhaled (Azmacort)
Indicated for maintenance and treatment of asthma as prophylaxis; also used in patients requiring long-term systemic corticosteroid treatment to attempt gradual tapering and discontinuation of PO corticosteroids. Available as Azmacort (75 mcg per actuation) and MDI with an attached Aerochamber device.
Bronchodilators, short term
Class Summary
Short-term bronchodilators are beta2-agonists that act to relieve bronchospasm by elevating cyclic adenosine monophosphate (AMP) in cells. They are used for acute relief of bronchospasm and for prophylaxis, especially prior to exercise.
Albuterol (Proventil, Ventolin, Proair)
Beta-agonist for bronchospasm refractory to epinephrine. Stimulates adenyl cyclase to convert ATP to cAMP and causes bronchodilation. Relaxes bronchial smooth muscle by action on beta2-receptors with little effect on cardiac muscle contractility. May decrease mediator release from mast cells and basophils and inhibit airway microvascular leakage.
Frequency may be increased. Institute regular schedule in patients on anticholinergic drugs who remain symptomatic.
The following list of albuterol products are for acute relief of asthma in various stages. Most commonly used alone in intermittent asthma or as prophylaxis, especially before exercise.
Available as tab 2 or 4 mg, ER tabs 4 or 8 mg, syrup 2 mg/5 mL, hydrofluoroalkane (HFA) MDI 90 mcg per actuation, and inhalation solution for nebulization 0.083% (0.83 mg/mL, 2.5 mg/3 mL) or 0.5% (5 mg/mL).
Pirbuterol (Maxair)
Directly acts on beta 2-receptors to relax bronchial smooth muscle, relieving bronchospasm and reducing airway resistance.
Levalbuterol (Xopenex)
For acute relief of asthma in various stages. Used alone more commonly in intermittent asthma or as prophylaxis for asthma, especially before exercise.
Inhaled long-acting bronchodilator/corticosteroid combinations
Class Summary
One of the advantages of long-acting beta-agonists is prolonged relief for patients with obstructive lung disease (eg, asthma). They are especially useful for patients with nocturnal cough. However, long-acting beta(2)-adrenergic agonists including salmeterol and formoterol have a black box warning regarding an increase in risk of asthma-related deaths. Because of this risk, salmeterol use is contraindicated without a concomitant long-term asthma control medication such as an inhaled corticosteroid. To ensure compliance with therapy, a fixed-dose combination product containing both an inhaled corticosteroid and LABA is recommended in pediatric and adolescent patients.[22]
Salmeterol/fluticasone inhaled (Advair)
Fluticasone inhibits bronchoconstriction mechanisms, produce direct smooth muscle relaxation, may decrease number and activity of inflammatory cells, in turn decreasing airway hyper-responsiveness. Also has vasoconstrictive activity. Salmeterol relaxes the smooth muscles of the bronchioles in conditions associated with bronchitis, emphysema, asthma, or bronchiectasis, can relieve bronchospasms. Effect may also facilitate expectoration.
Adverse effects are more likely to occur when administered at high or more frequent doses than recommended. Two delivery mechanisms are available (ie, powder for inhalation [Diskus], metered-dose inhaler [MDI]). Diskus available as combination of salmeterol 50-mcg with fluticasone 100-mcg, 250-mcg, or 500-mcg. MDI available as 21 mcg salmeterol with fluticasone 45-mcg, 115-mcg, or 230 mcg.
Budesonide/formoterol (Symbicort)
Formoterol relieves bronchospasm by relaxing the smooth muscles of the bronchioles in conditions associated with asthma.
Budesonide is an inhaled corticosteroid that alters level of inflammation in airways by inhibiting multiple types of inflammatory cells and decreasing production of cytokines and other mediators involved in the asthmatic response. Available as MDI in 2 strengths; each actuation delivers formoterol 4.5-mcg with either 80-mcg or 160-mcg.
Systemic corticosteroids
Class Summary
These are potent anti-inflammatory agents because of their effects on many cell types (eg, mast cells, eosinophils, neutrophils, macrophages, basophils, lymphocytes) and on the production and secretion of mediators (eg, histamine, eicosanoids, leukotrienes, cytokines) in inflammation. Many conditions related to mold allergy (eg, allergic asthma, ABPA, AFS, ABPM, EAA) require systemic corticosteroids from the onset of disease.
When disease activity decreases, reducing the dose to the lowest effective level and trying to further taper it to an every-other-day schedule are advisable. Also, a oral inhaled corticosteroid may be used to replace a systemic steroid to reduce adverse effects.
For allergic asthma, systemic corticosteroids are indicated when patients have a severe form of asthma resistant to other forms of therapy.
Prednisone
Prednisone remains mainstay PO systemic corticosteroid. Starting doses in each condition or different stages of same disease may differ. Main concerns with systemic corticosteroids, especially with long-term use, are adverse effects, which are more apparent than those of PO inhaled corticosteroids. Various tab strengths and liquids available to customize doses and ease tapering.
Prednisolone (Pediapred, Prelone, Millipred)
Prednisone remains the mainstay PO systemic corticosteroid. Starting doses in each condition or in different stages of the same disease may differ. Main concern with systemic corticosteroids, especially with long-term use, is their adverse effects, which are more apparent than those of PO inhaled corticosteroids. Various tab strengths and liquids are available to enable customized doses and tapering ease.
Leukotriene antagonists/5-lipoxygenase inhibitors
Class Summary
In asthma, leukotriene is an important mediator released in the airway that causes constriction of smooth muscle. This is most apparent in a delayed-phase reaction. Therefore, use of leukotriene antagonists is an important part of treatment to control asthma. These agents are indicated for forms of asthma ranging from mild intermittent to severe. For children, it is a valuable treatment for the night cough or wheeze. Inhibition of lipoxygenase reduces production of leukotriene at peripheral tissue and achieves results similar to those of leukotriene antagonists.
Montelukast (Singulair)
Leukotriene receptor antagonist indicated for long-term treatment of asthma. Available as 4-mg and 5-mg chewable tabs, 4-mg granules, 10-mg PO tabs.
Zafirlukast (Accolate)
Indicated for prophylaxis and long-term treatment of asthma. Leukotriene receptor antagonist.
Zileuton (Zyflo, Zyflo CR)
Indicated for prophylaxis and long-term treatment of asthma. 5-lipoxygenase inhibitor.
Theophylline derivatives
Class Summary
These agents directly relax smooth muscles of bronchial airways and pulmonary blood vessels, acting as bronchodilators and smooth muscle relaxants. They are used to supplement other asthma drugs, typically in moderately severe or severe asthma. Their effects in other forms of pulmonary diseases (eg, ABPA, ABPM, EAA) are unknown, though anecdotal evidence indicates that they have been tried in the chronic stage of the diseases.
Theophylline (Theo-24, Theolair)
Wide variety of dosage forms (tab, cap, extended release [ER], sprinkles, liquid) enables ease of dosing. Indicated for treatment of asthma, especially moderate-to-severe form as supplement to other anti-inflammatory drugs.
Monoclonal antibodies
Class Summary
These agents bind selectively to human IgE on the surface of mast cells and basophils.
Omalizumab (Xolair)
Recombinant, DNA-derived, humanized IgG monoclonal antibody that selectively binds to the Fc portion of free IgE and thereby blocks binding to receptors on mast cells and basophils. Reduces mediator release, which promotes allergic response. Indicated for moderate-to-severe persistent asthma in patients who react to perennial allergens in whom symptoms are not controlled by inhaled corticosteroids.
Anticholinergic nasal sprays and oral inhalers
Class Summary
An increase of local production of acetylcholine may cause tissue reaction in the case of hypersensitivity. This is most common in IgE-mediated hypersensitivity. Anticholinergic agents may be useful for allergic rhinitis or allergic asthma.
Ipratropium bromide (Atrovent)
Available as 0.03% (21 mcg per spray) or 0.06% (42 mcg per spray) nasal spray. Suitable for allergic rhinitis. Also available as PO inhaler (18 mcg per actuation) indicated for moderate persistent or severe persistent asthma.
Antova T, Pattenden S, Brunekreef B, et al. Exposure to indoor mould and children's respiratory health in the PATY study. J Epidemiol Community Health. Aug 2008;62(8):708-14. [Medline].
Karvala K, Nordman H, Luukkonen R, et al. Occupational rhinitis in damp and moldy workplaces. Am J Rhinol. Sep-Oct 2008;22(5):457-62. [Medline].
Soeria-Atmadja D, Onell A, Borga A. IgE sensitization to fungi mirrors fungal phylogenetic systematics. J Allergy Clin Immunol. Jun 2010;125(6):1379-1386.e1. [Medline].
Holme J, Hagerhed-Engman L, Mattsson J, Sundell J, Bornehag CG. Culturable mold in indoor air and its association with moisture-related problems and asthma and allergy among Swedish children. Indoor Air. Aug 2010;20(4):329-40. [Medline].
Deger L, Plante C, Goudreau S, et al. Home environmental factors associated with poor asthma control in Montreal children: a population-based study. J Asthma. Jun 2010;47(5):513-20. [Medline].
Fairs A, Agbetile J, Hargadon B, Bourne M, Monteiro WR, Brightling CE, et al. IgE sensitization to Aspergillus fumigatus is associated with reduced lung function in asthma. Am J Respir Crit Care Med. Dec 1 2010;182(11):1362-8. [Medline].
Vesper S, McKinstry C, Haugland R, et al. Development of an Environmental Relative Moldiness index for US homes. J Occup Environ Med. Aug 2007;49(8):829-33. [Medline].
Crameri R, Zeller S, Glaser AG, Vilhelmsson M, Rhyner C. Cross-reactivity among fungal allergens: a clinically relevant phenomenon?. Mycoses. Mar 2009;52(2):99-106. [Medline].
Huang SW, Kimbrough JW. Mold allergy is a risk factor for persistent cold-like symptoms in children. Clin Pediatr (Phila). Dec 1997;36(12):695-9. [Medline].
Manning SC, Vuitch F, Weinberg AG, Brown OE. Allergic aspergillosis: a newly recognized form of sinusitis in the pediatric population. Laryngoscope. Jul 1989;99(7 Pt 1):681-5. [Medline].
[Best Evidence] Cecchi L, D'Amato G, Ayres JG, Galan C, Forastiere F, Forsberg B, et al. Projections of the effects of climate change on allergic asthma: the contribution of aerobiology. Allergy. Sep 2010;65(9):1073-81. [Medline]. [Full Text].
Hamilos DL. Allergic fungal rhinitis and rhinosinusitis. Proc Am Thorac Soc. May 2010;7(3):245-52. [Medline].
Huang SW, Kimbrough JW. Effect of air cleaner on mold counts in the air and on symptoms of perennial allergic rhinitis. Pediatr Asthma, Allergy & Immunol. 1995;9:205-11.
Gots RE, Layton NJ, Pirages SW. Indoor health: background levels of fungi. AIHA J (Fairfax, Va). Jul-Aug 2003;64(4):427-38. [Medline].
Shah A, Kala J, Sahay S, Panjabi C. Frequency of familial occurrence in 164 patients with allergic bronchopulmonary aspergillosis. Ann Allergy Asthma Immunol. Oct 2008;101(4):363-9. [Medline].
NAEPP. National Asthma Education and Prevention Program. Expert Panel Report 2: Guideline for the Diagnosis and Management of Asthma. NIH Publication No. 97-4051. Available at http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
Asturias JA, Ibarrola I, Ferrer A, et al. Diagnosis of Alternaria alternata sensitization with natural and recombinant Alt a 1 allergens. J Allergy Clin Immunol. Jun 2005;115(6):1210-7. [Medline].
Klote M. Hypersensitive pneumonitis. Allergy and Asthma Proc. 2005;26:493-5.
Stark PC, Celedon JC, Chew GL, et al. Fungal levels in the home and allergic rhinitis by 5 years of age. Environ Health Perspect. Oct 2005;113(10):1405-9. [Medline].
Reponen T, Vesper S, Levin L, et al. High environmental relative moldiness index during infancy as a predictor of asthma at 7 years of age. Ann Allergy Asthma Immunol. Aug 2011;107(2):120-6. [Medline].
van der Ent CK, Hoekstra H, Rijkers GT. Successful treatment of allergic bronchopulmonary aspergillosis with recombinant anti-IgE antibody. Thorax. Mar 2007;62(3):276-7. [Medline].
Fluticasone at different doses for chronic asthma in adults and children. [Best Evidence]. Cochrane Database Syst Rev. Oct 8 2008;(4):CD003534.
Ricketti AJ, Greenberger PA, Patterson R. Serum IgE as an important aid in management of allergic bronchopulmonary aspergillosis. J Allergy Clin Immunol. Jul 1984;74(1):68-71. [Medline].
Greenberger PA. Allergic bronchopulmonary aspergillosis. In: Middleton E, Reed CE, Ellis EF, et al. Allergy: Principles and Practice. 4th ed. Mosby-Year Book; 1998:981-93.
Barnes C, Tuck J, Simon S, Pacheco F, Hu F, Portnoy J. Allergenic materials in the house dust of allergy clinic patients. Ann Allergy Asthma Immunol. May 2001;86(5):517-23. [Medline].
Buckland KF, O'Connor E, Murray LA, Hogaboam CM. Toll like receptor-2 modulates both innate and adaptive immune responses during chronic fungal asthma in mice. Inflamm Res. Aug 2008;57(8):379-87. [Medline].
Bush RK, Portnoy JM, Saxon A, Terr AI, Wood RA. The medical effects of mold exposure. J Allergy Clin Immunol. Feb 2006;117(2):326-33. [Medline].
Casey P, Garrett J, Eaton T. Allergic bronchopulmonary aspergillosis in a lung transplant patient successfully treated with nebulized amphotericin. J Heart Lung Transplant. Nov 2002;21(11):1237-41. [Medline].
Committee on Environmental Health. Spectrum of noninfectious health effects from molds. www.pediatrics.org. Available at http://pediatrics.aappublications.org/content/118/6/2582.full. Accessed December, 2006.
Denning DW, O'Driscoll BR, Powell G, et al. Randomized controlled trial of oral antifungal treatment for severe asthma with fungal sensitization: The Fungal Asthma Sensitization Trial (FAST) study. Am J Respir Crit Care Med. Jan 1 2009;179(1):11-8. [Medline].
Edmondson DA, Nordness ME, Zacharisen MC, Kurup VP, Fink JN. Allergy and "toxic mold syndrome". Ann Allergy Asthma Immunol. Feb 2005;94(2):234-9. [Medline].
Gruchalla RS, Pongracic J, Plaut M, et al. Inner City Asthma Study: relationships among sensitivity, allergen exposure, and asthma morbidity. J Allergy Clin Immunol. Mar 2005;115(3):478-85. [Medline].
Hamilos DL. Chronic sinusitis. J Allergy Clin Immunol. Aug 2000;106(2):213-27. [Medline].
Huang SW. The risk of sinusitis in children with allergic rhinitis. Allergy Asthma Proc. Mar-Apr 2000;21(2):85-8. [Medline].
Huang SW. Treating pediatric perennial allergic rhinitis. Pract Allergy Immunol. 1995;10:193-8.
Huang SW, Giannoni C. The risk of adenoid hypertrophy in children with allergic rhinitis. Ann Allergy Asthma Immunol. Oct 2001;87(4):350-5. [Medline].
Jaakkola JJ, Hwang BF, Jaakkola N. Home dampness and molds, parental atopy, and asthma in childhood: a six-year population-based cohort study. Environ Health Perspect. Mar 2005;113(3):357-61. [Medline].
Jacob B, Ritz B, Gehring U, et al. Indoor exposure to molds and allergic sensitization. Environ Health Perspect. Jul 2002;110(7):647-53. [Medline].
Knutsen AP. When to suspect allergic bronchopulmonary aspergillosis. J Respir Dis. March 2006;27:123-34.
Knutsen AP, Vijay HM, Kumar V, et al. Mold-sensitivity in children with moderate-severe asthma is associated with HLA-DR and HLA-DQ. Allergy. Nov 2010;65(11):1367-75. [Medline].
Krieger JK, Takaro TK, Allen C, et al. The Seattle-King County healthy homes project: implementation of a comprehensive approach to improving indoor environmental quality for low-income children with asthma. Environ Health Perspect. Apr 2002;110 Suppl 2:311-22. [Medline].
Meklin T, Potus T, Pekkanen J, Hyvarinen A, Hirvonen MR, Nevalainen A. Effects of moisture-damage repairs on microbial exposure and symptoms in schoolchildren. Indoor Air. 2005;15 Suppl 10:40-7. [Medline].
Myatt TA, Minegishi T, Allen JG, Macintosh DL. Control of asthma triggers in indoor air with air cleaners: a modeling analysis. Environ Health. Aug 6 2008;7:43. [Medline].
[Guideline] NHLBI. Guideline for the diagnosis and management of asthma-expert panel 11 report. NIH. 1997.
Salvaggio JE, Hendrick DJ. Extrinsic allergic alveolitis. In: Allergy. 2nd ed. 2000:37-53.
Santilli J, Rockwell W. Fungal contamination of elementary schools: a new environmental hazard. Ann Allergy Asthma Immunol. Feb 2003;90(2):203-8. [Medline].
Schneider D, Freeman NC, McGarvey P. Asthma and respiratory dysfunction among urban, primarily Hispanic school children. Arch Environ Health. Jan 2004;59(1):4-13. [Medline].
Selman M, Lacasse Y, Pardo A, Cormier Y. Hypersensitivity pneumonitis caused by fungi. Proc Am Thorac Soc. May 2010;7(3):229-36. [Medline].
[Best Evidence] [Guideline] Selman M, Lacasse Y, Pardo A, et al. Hypersensitive pneumonitis caused by fungi. Proc Am Thorac Soc. May/2010;7:229-236. [Medline].
Solomon WR. Pollen and fungi. Aerobiology and inhalant allergens. In: Middleton E, Reed CE, Ellis EF, et al. Allergy: Principles and Practice. 5th ed. Mosby-Year Book; 1998:367-93.
Suzuki K, Iwata S, Iwata H. Allergic bronchopulmonary aspergillosis in a 9-year-old boy. Eur J Pediatr. Jul 2002;161(7):408-9. [Medline].
Virant FS. Allergic rhinitis. Pediatr Rev. Sep 1992;13(9):323-8. [Medline].
Wiszniewska M, Swierczynska-Machura D, Cezary P, Walusiak-Skorupa J. [Fungal allergy among art conservators: prevalence, risk factors and clinical symptoms]. Med Pr. 2010;61(2):133-41. [Medline].
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