What is safe to take during pregnancy for allergies

Main article: Pathophysiology of asthma

Asthma is the result of chronic inflammation of the conducting zone of the airways (most especially the bronchi and bronchioles), which subsequently results in increased contractability of the surrounding smooth muscles. This among other factors leads to bouts of narrowing of the airway and the classic symptoms of wheezing. The narrowing is typically reversible with or without treatment. Occasionally the airways themselves change.[23] Typical changes in the airways include an increase in eosinophils and thickening of the lamina reticularis.

Chronically the airways’ smooth muscle may increase in size along with an increase in the numbers of mucous glands. Other cell types involved include: T lymphocytes, macrophages, and neutrophils. There may also be involvement of other components of the immune system including: cytokines, chemokines, histamine, and leukotrienes among others.[22]

  1. Figure A shows the location of the lungs and airways in the body. Figure B shows a cross-section of a normal airway. Figure C shows a cross-section of an airway during asthma symptoms.


Signs and symptoms

Wheezing

The sound of wheezing as heard with a stethoscope.


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Asthma is characterized by recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing.[23]Sputum may be produced from the lung by coughing but is often hard to bring up.[24] During recovery from an asthma attack (exacerbation), it may appear pus-like due to high levels of white blood cells called eosinophils.[25] Symptoms are generally worse at night and in the early morning or in response to exercise or freezing air.[26] Some people with asthma rarely experience symptoms, generally in response to triggers, whereas others may react frequently and readily and experience persistent symptoms.[27]

Associated conditions

A number of other health conditions happen more frequently in people with asthma, including gastro-esophageal reflux disease (GERD), rhinosinusitis, and obstructive sleep apnea.[28] Psychological disorders are also more common,[29] with anxiety disorders occurring in between 16–52% and mood disorders in 14–41%.[30] It is not known whether asthma causes psychological problems or psychological problems lead to asthma.[31] Those with asthma, especially if it is poorly controlled, are at increased risk for radiocontrast reactions.[32]


Management

While there is no cure for asthma, symptoms can typically be improved.[135] A specific, customized plan for proactively monitoring and managing symptoms should be created.

This plan should include the reduction of exposure to allergens, testing to assess the severity of symptoms, and the usage of and adjustments to medications.[136] The treatment plan should be written below and advise adjustments to treatment according to changes in symptoms.[137]

The most effective treatment for asthma is identifying triggers, such as cigarette smoke, pets, or aspirin, and eliminating exposure to them. If trigger avoidance is insufficient, the use of medication is recommended. Pharmaceutical drugs are selected based on, among other things, the severity of illness and the frequency of symptoms.

Specific medications for asthma are broadly classified into fast-acting and long-acting categories.[138][139]

Bronchodilators are recommended for short-term relief of symptoms. In those with occasional attacks, no other medication is needed. If mild persistent disease is present (more than two attacks a week), low-dose inhaled corticosteroids or alternatively, a leukotriene antagonist or a mast cell stabilizer by mouth is recommended. For those who own daily attacks, a higher dose of inhaled corticosteroids is used.

In a moderate or severe exacerbation, corticosteroids by mouth are added to these treatments.[7]

People with asthma own higher rates of anxiety, psychological stress, and depression.[140][141] This is associated with poorer asthma control.[140]Cognitive behavioral therapy may improve quality of life, asthma control, and anxiety levels in people with asthma.[140]

Improving people’s knowledge about asthma and using a written action plan has been identified as an significant component of managing asthma.[142] Providing educational sessions that include information specific to a person’s culture is likely effective.[143] More research is necessary to determine if increasing preparedness and knowledge of asthma among school staff and families using home-based and school interventions results in endless term improvements in safety for children with asthma.[144][145][146] School-based asthma self-management interventions, which attempt to improve knowledge of asthma, its triggers and the importance of regular practitioner review, may reduce hospital admissions and emergency department visits.

These interventions may also reduce the number of days children experience asthma symptoms and may lead to little improvements in asthma-related quality of life.[147] More research is necessary to determine if shared-decision-making is helpful for managing adults with asthma[148] or if a personalized asthma action plan is effective and necessary.[149] Some people with asthma use pulse oximeters to monitor their own blood oxygen levels during an asthma attack. However, there is no evidence regarding the use in these instances.[150]

Lifestyle modification

Avoidance of triggers is a key component of improving control and preventing attacks.

The most common triggers include allergens, smoke (from tobacco or other sources), air pollution, non selective beta-blockers, and sulfite-containing foods.[151][152] Cigarette smoking and second-hand smoke (passive smoke) may reduce the effectiveness of medications such as corticosteroids.[153] Laws that limit smoking decrease the number of people hospitalized for asthma.[134] Dust mite control measures, including air filtration, chemicals to kill mites, vacuuming, mattress covers and others methods had no effect on asthma symptoms.[56] There is insufficient evidence to propose that dehumidifiers are helpful for controlling asthma.[154]

Overall, exercise is beneficial in people with stable asthma.[155] Yoga could provide little improvements in quality of life and symptoms in people with asthma.[156] More research is necessary to determine how effective weight loss is on improving quality of life, the usage of health care services, and adverse effects for people of every ages with asthma.[157][158]

Medications

Medications used to treat asthma are divided into two general classes: quick-relief medications used to treat acute symptoms; and long-term control medications used to prevent further exacerbation.[138]Antibiotics are generally not needed for sudden worsening of symptoms or for treating asthma at any time.[159][160]

Fast–acting

  1. Older, less selective adrenergic agonists, such as inhaled epinephrine, own similar efficacy to SABAs.[166] They are however not recommended due to concerns regarding excessive cardiac stimulation.[167]
  2. Short-acting beta2-adrenoceptor agonists (SABA), such as salbutamol (albuterolUSAN) are the first line treatment for asthma symptoms.[7] They are recommended before exercise in those with exercise induced symptoms.[161]
  3. Anticholinergic medications, such as ipratropium, provide additional benefit when used in combination with SABA in those with moderate or severe symptoms and may prevent hospitalizations.[7][162][163] Anticholinergic bronchodilators can also be used if a person cannot tolerate a SABA.[96] If a kid requires admission to hospital additional ipratropium does not appear to assist over a SABA.[164] For children over 2 years ancient with acute asthma symptoms, inhaled anticholinergic medications taken alone is safe but is not as effective as inhaled SABA or SABA combined with inhaled anticholinergic medication.[165][162] Adults who get combined inhaled medications that includes short-acting anticholinergics and SABA may be at risk for increased adverse effects such as experiencing a tremor, agitation, and heart beat palpitations compared to people who are treated with SABA by itself.[163]
  4. A short course of corticosteroids after an acute asthma exacerbation may assist prevent relapses and reduce hospitalizations.[168] For adults and children who are in the hospital due to acute asthma, systematic (IV) corticosteroids improve symptoms.[169][170]

Long–term control

  1. Anticholinergic medications such as ipratropium bromide own not been shown to be beneficial for treating chronic asthma in children over 2 years old,[192] but is not suggested for routine treatment of chronic asthma in adults.[193]
  2. Long-acting beta-adrenoceptor agonists (LABA) such as salmeterol and formoterol can improve asthma control, at least in adults, when given in combination with inhaled corticosteroids.[173][174] In children this benefit is uncertain.[173][175][174] When used without steroids they increase the risk of severe side-effects,[176] and with corticosteroids they may slightly increase the risk.[177][178] Evidence suggests that for children who own persistent asthma, a treatment regime that includes LABA added to inhaled corticosteroids may improve lung function but does not reduce the quantity of serious exacerbations.[179] Children who require LABA as part of their asthma treatment may need to go to the hospital more frequently.[179]
  3. Mast cell stabilizers (such as cromolyn sodium) are another non-preferred alternative to corticosteroids.[138]
  4. Corticosteroids are generally considered the most effective treatment available for long-term control.[138] Inhaled forms such as beclomethasone are generally used except in the case of severe persistent disease, in which oral corticosteroids may be needed.[138][171] It is generally recommended that inhaled formulations be used once or twice daily, depending on the severity of symptoms.[172]
  5. Intravenous istration of the drug aminophylline does not provide an improvement in bronchodilation when compared to standard inhaled beta-2 agonist treatment.[189] Aminophylline treatment is associated with more adverse effects compared to inhaled beta-2 agonist treatment.[189]
  6. For children with asthma which is well-controlled on combination therapy of inhaled corticosteroids (ICS) and long-acting beta2-agonists (LABA), the benefits and harms of stopping LABA and stepping below to ICS-only therapy are uncertain.[190] In adults who own stable asthma while they are taking a combination of LABA and inhaled corticosteroids (ICS), stopping LABA may increase the risk of asthma exacerbations that require treatment with corticosteroids by mouth.[191] Stopping LABA probably makes little or no significant difference to asthma control or asthma-related quality of life.[191] Whether or not stopping LABA increases the risk of serious adverse events or exacerbations requiring an emergency department visit or hospitalisation is uncertain.[191]
  7. Leukotriene receptor antagonists (anti-leukotriene agents such as montelukast and zafirlukast) may be used in addition to inhaled corticosteroids, typically also in conjunction with a LABA.[17][138][180][181][182] Evidence is insufficient to support use in acute exacerbations.[183][184] For adults or adolescents who own persistent asthma that is not controlled extremely well, the addition of anti-leukotriene agents along with daily inhaled corticosteriods improves lung function and reduces the risk of moderate and severe asthma exacerbations.[181] Anti-leukotriene agents may be effective alone for adolescents and adults, however there is no clear research suggesting which people with asthma would benefit from anti-leukotriene receptor alone.[185] In those under five years of age, anti-leukotriene agents were the preferred add-on therapy after inhaled corticosteroids by the British Thoracic Society in 2009.[186] A 2013 Cochrane systematic review concluded that anti-leukotriene agents appear to be of little benefit when added to inhaled steroids for treating children.[187] A similar class of drugs, 5-LOX inhibitors, may be used as an alternative in the chronic treatment of mild to moderate asthma among older children and adults.[17][188] As of 2013 there is one medication in this family known as zileuton.[17]
  8. There is no strong evidence to recommend chloroquine medication as a replacement for taking corticosteroids by mouth (for those who are not capable to tolerate inhaled steroids).[194] Methotrexate is not suggested as a replacement for taking corticosteriods by mouth («steroid sparing») due to the adverse effects associated with taking methotrexate and the minimal relief provided for asthma symptoms.[195]

Delivery methods

Medications are typically provided as metered-dose inhalers (MDIs) in combination with an asthma spacer or as a dry powder inhaler.

The spacer is a plastic cylinder that mixes the medication with air, making it easier to get a full dose of the drug. A nebulizer may also be used. Nebulizers and spacers are equally effective in those with mild to moderate symptoms. However, insufficient evidence is available to determine whether a difference exists in those with severe disease.[196]

Salbutamol metered dose inhaler commonly used to treat asthma attacks.

References

1. Ellegard E. Pregnancy rhinitis. Immunol Allergy Clin N Am. 2006;26:119-35. [ Links ]

2.

Franklin KA, Holmgren PA, Jönsson F, Poromaa N, Stenlund H, Svanborg E. Snoring, pregnancy-induced hypertension, and growth retardation of the fetus. Chest. 2000;117: 137-41. [ Links ]

3. Mac Kenzie JN. Irritation of the sexual apparatus as an etiological factor in the production of nasal disease. Am J Med Sci. 1884;87:360-5. [ Links ]

4. Mac Kenzie JN. The physiological and pathological relations between the nose and the sexual apparatus of man. Alien Neurol. 1898;19:219-39. [ Links ]

5. Mohun M. Incidence of vasomotor rhinitis during pregnancy. Arch Otolaryngol. 1943;37:699-709.

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6. Piette V, Daures JP, Demoly P.

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Treating allergic rhinitis in pregnancy. Curr Allergy Asthma Rep. 2006;6:232-8. [ Links ]

7. Orban N, Maughan E, Bleach N. Pregnancy-induced rhinitis. Rhinology. 2013;51:111-9. [ Links ]

8. Ellegard EK. Clinical and pathogenetic characteristics of pregnancy rhinitis. Clin Rev Allergy Immunol. 2004;26:149-59. [ Links ]

9. Namazy JA, Schatz M. Diagnosing rhinitis during pregnancy. Curr Allergy Asthma Rep. 2014;14:458. [ Links ]

10. Ellegard E, Hellgren M, Toren K, Karlsoon T. The incidence of pregnancy rhinitis. Gynecol Obstet Invest. 2000;49:98-101. [ Links ]

11. Shushan S, Sadan O, Lurie S, Evron S, Golan A, Roth Y. Pregnancyassociated rhinitis. Am J Perinatol.

2006;23:431-3. [ Links ]

12. Hamano N, Terada N, Maesako K, Ikeda T, Fukuda S, Wakita J, et al. Expression of histamine recepetors in nasal epithelial cells and endothelial cells — the effect of sex hormones. Int Arch Allergy Appl Immunol. 1998;115:220-7. [ Links ]

13. Schatz M, Zeiger RS. Asthma and allergy in pregnancy. Clin Perinatol.

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1997;24:407-32. [ Links ]

14. Philpott CM, Conboy P, Al-Azzawi F, Murty GE. Nasal physiological changes during pregnancy. Clin Otolaryngol Allied Sci. 2004;29:343-51. [ Links ]

15. Ellegard E, Karlsson G. Nasal congestion during pregnancy. Clin Otolaryngol Allied Sci. 1999;24:307-11. [ Links ]

16. Ellegard E, Karlson G. IgE-mediated reactions and hyperreactivity in pregnancy rhinitis. Arch Otolaryngol Head Neck Surg. 1999;37:50-5.

[ Links ]

17. Bende M, Gredmark T. Nasal stuffiness during pregnancy. Laryngoscope. 1999;109:1108-10. [ Links ]

18. Toppozada H, Michaels L, Toppozada M, El-Ghazzawi I, Talaat M, Elwany S. The human respiratory nasal mucosa in pregnancy. J Laryngol Otol. 1982;96:613-26. [ Links ]

19. Wise R, Polito A, Krishnan V. Respiratory physiologic changes in pregnancy. Immunol Allergy Clin North Am. 2006;26:1-12. [ Links ]

20. Namazy JA, Schatz M. Asthma and rhinitis during pregnancy. Mt Sinai J Med. 2011;78:661-70. [ Links ]

21. Peter G. Rhinitis medicamentosa: a review of causes and treatment.

Treat Respir Med. 2005;4:21-9. [ Links ]

22. Savilahti E, Siltanen M, Pekkanen J, Kajossari M. Mothers of extremely low birth weight infants own less atopy than mothers of fullterm infants. Clin Exp Allergy. 2004;34:1851-4.

What is safe to take during pregnancy for allergies

[ Links ]

23. Mattar R, Camano L, Daher S. Recurrent spontaneous abortion and atopy. Rev Bras Ginecol Obstet. 2003;25:331-5. [ Links ]

24. Ellegard E. Special considerations in the treatment of pregnancy rhinitis. Womens Health (Lond Engl). 2005;1:105-14. [ Links ]

25. Rabmurg B. Pregnancy rhinitis and rhinitis medicamentosa. J Am Acad Nurse Pract. 2002;14:527-30. [ Links ]

26. Eccles R. Nasal air flow in health and disease. Acta Otolaryngol. 2000;120:580-95. [ Links ]

27. Federal Register/Vol.

73, No. 104/Thursday, May 29, 2008/Pro-posed Rules. Available from: http://www.fda.gov. [ Links ]

28. Incaudo GA, Takach P. The diagnosis and treatment of allergic rhinitis during pregnancy and lactation. Immunol Allergy Clin North Am. 2006;26:137-54. [ Links ]

29. Aselton P, Jick H, Milunsky A, Hunter JR, Stergachis A. Firsttrimester drug use and congenital disorders. Obstet Gynecol. 1985;65:451-5. [ Links ]

30. Werler MM, Mitchell AA, Shapiro S. First trimester maternal medications use in relation to gastroschisis. Teratology. 1992;45:361-7. [ Links ]

31. Zierler S, Rothman KJ. Congenital heart disease in relation to maternal use of Bendectin and other drugs in early pregnancy.

N Engl J Med. 1985;313:347-52. [ Links ]

32. Rayburn WF, Anderson JC, Smith CV, Appel LL, Davis SA. Uterine and fetal Doppler flow changes from a single dose of a long-acting intranasal decongestant. Obstet Gynecol. 1990;76: 180-2. [ Links ]

33. Yau WP, Mitchell AA, Lin KJ, Werler MM, Hernández-Díaz S. Use of decongestants during pregnancy and the risk of birth defects. Am J Epidemiol. 2013;178:198-208. [ Links ]

34. Torfs CP, Katz EA, Bateson TF, Lam PK, Curry CJ. Maternal medications and environmental exposures as risk factors for gastroschisis. Teratology. 1996;54:84-92. [ Links ]

35.

What is safe to take during pregnancy for allergies

Ellegard E, Hellgren M, Karlsson NG. Fluticasone propionate aqueous nasal spray in pregnancy rhinitis. Clin Otolaryngol. 2001;26:394-400. [ Links ]

36. Norjavaara E, de Verdier MG. Normal pregnancy outcomes in a population-based study including 2968 pregnant women exposed to budesonide. J Allergy Clin Immunol. 2003;111: 736-42. [ Links ]

37. Gluck PA, Gluck JC. A review of pregnancy outcomes after exposure to orally inhaled or intranasal budesonide. Curr Med Res Opin. 2005;21:1075-84. [ Links ]

38. Blaiss MS, Food and Drug istration (U.S.). ACAAI-ACOG (American College of Allergy Asthma, and Immunology and American College of Obstetricians and Gynecologists).

Management of rhinitis and asthma in pregnancy. Ann Allergy Asthma Immunol. 2003;90:16-22. [ Links ]

39.

What is safe to take during pregnancy for allergies

Asthma Rocklin RE. asthma medications and their effects on maternal/fetal outcomes during pregnancy. Reprod Toxicol. 2011;32:189-97. [ Links ]

40. Kallen B. Use of antihistamine drugs in early pregnancy and delivery outcomes. J Matern Fetal Neonatal Med. 2002;11:146-52. [ Links ]

41. Gilbey P, McGruthers L, Morency AM, Shrim A. Rhinosinusitisrelated quality of life during pregnancy. Am J Rhinol Allergy. 2012;26:283-6. [ Links ]

Allergic rhinitis is an immunoglobulin E–mediated disease that occurs after exposure to indoor or outdoor allergens, such as dust mites, insects, animal dander, molds, and pollen.

Symptoms include rhinorrhea, sneezing, and nasal congestion, obstruction, and pruritus.1

Optimal treatment includes allergen avoidance and pharmacotherapy. Targeted symptom control with immunotherapy and asthma evaluation should be considered when appropriate.2,3

Symptoms of allergic rhinitis are classified based on the temporal pattern (seasonal, perennial, or episodic), frequency, and severity. Frequency can be divided into intermittent or persistent (more than four days per week and more than four weeks per year, respectively).

Severity can be divided into mild (symptoms do not interfere with quality of life) or severe (symptoms impact asthma control, sleep, sports participation, or school or work performance).3


Diagnosis

While asthma is a well-recognized condition, there is not one universal agreed upon definition.[22] It is defined by the Global Initiative for Asthma as «a chronic inflammatory disorder of the airways in which numerous cells and cellular elements frolic a role. The chronic inflammation is associated with airway hyper-responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing particularly at night or in the early morning.

These episodes are generally associated with widespread but variable airflow obstruction within the lung that is often reversible either spontaneously or with treatment».[23]

There is currently no precise test for the diagnosis, which is typically based on the pattern of symptoms and response to therapy over time.[5][22] A diagnosis of asthma should be suspected if there is a history of recurrent wheezing, coughing or difficulty breathing and these symptoms happen or worsen due to exercise, viral infections, allergens or air pollution.[87]Spirometry is then used to confirm the diagnosis.[87] In children under the age of six the diagnosis is more hard as they are too young for spirometry.[88]

Classification

Severity Symptom frequency Night-time symptoms %FEV1 of predicted FEV1 variability SABA use
Intermittent ≤2/week ≤2/month ≥80% <20% ≤2 days/week
Mild persistent >2/week 3–4/month ≥80% 20–30% >2 days/week
Moderate persistent Daily >1/week 60–80% >30% daily
Severe persistent Continuously Frequent (7/week) <60% >30% ≥twice/day

Asthma is clinically classified according to the frequency of symptoms, forced expiratory volume in one second (FEV1), and peak expiratory flow rate.[12] Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic), based on whether symptoms are precipitated by allergens (atopic) or not (non-atopic).[13] While asthma is classified based on severity, at the moment there is no clear method for classifying diverse subgroups of asthma beyond this system.[95] Finding ways to identify subgroups that reply well to diverse types of treatments is a current critical goal of asthma research.[95]

Although asthma is a chronic obstructive condition, it is not considered as a part of chronic obstructive pulmonary disease, as this term refers specifically to combinations of disease that are irreversible such as bronchiectasis and emphysema.[96] Unlike these diseases, the airway obstruction in asthma is generally reversible; however, if left untreated, the chronic inflammation from asthma can lead the lungs to become irreversibly obstructed due to airway remodeling.[97] In contrast to emphysema, asthma affects the bronchi, not the alveoli.[98]

Alcohol-induced asthma

Main article: Alcohol-induced respiratory reactions

Alcohol may worsen asthmatic symptoms in up to a third of people.[119] This may be even more common in some ethnic groups such as the Japanese and those with aspirin-induced asthma.[119] Other studies own found improvement in asthmatic symptoms from alcohol.[119]

Exercise-induced

Main article: Exercise-induced bronchoconstriction

Exercise can trigger bronchoconstriction both in people with or without asthma.[107] It occurs in most people with asthma and up to 20% of people without asthma.[107] Exercise-induced bronchoconstriction is common in professional athletes.

The highest rates are among cyclists (up to 45%), swimmers, and cross-country skiers.[108] While it may happen with any weather conditions, it is more common when it is dry and cold.[109] Inhaled beta2-agonists do not appear to improve athletic performance among those without asthma,[110] however, oral doses may improve endurance and strength.[111][112]

Occupational

Main article: Occupational asthma

Asthma as a result of (or worsened by) workplace exposures is a commonly reported occupational disease.[113] Numerous cases, however, are not reported or recognized as such.[114][115] It is estimated that 5–25% of asthma cases in adults are work-related.

A few hundred diverse agents own been implicated, with the most common being: isocyanates, grain and wood dust, colophony, soldering flux, latex, animals, and aldehydes.

What is safe to take during pregnancy for allergies

The employment associated with the highest risk of problems include: those who spray paint, bakers and those who process food, nurses, chemical workers, those who work with animals, welders, hairdressers and timber workers.[113]

Asthma exacerbation

Near-fatal High PaCO2, or requiring mechanical ventilation, or both
Life-threatening
(any one of)
Clinical signs Measurements
Altered level of consciousness Peak flow < 33%
Exhaustion Oxygen saturation < 92%
Arrhythmia PaO2 < 8 kPa
Low blood pressure «Normal» PaCO2
Cyanosis
Silent chest
Poor respiratory effort
Acute severe
(any one of)
Peak flow 33–50%
Respiratory rate ≥ 25 breaths per minute
Heart rate ≥ 110 beats per minute
Unable to finish sentences in one breath
Moderate Worsening symptoms
Peak flow 50–80% best or predicted
No features of acute severe asthma

An acute asthma exacerbation is commonly referred to as an asthma attack.

The classic symptoms are shortness of breath, wheezing, and chest tightness.[22] The wheezing is most often when breathing out.[100] While these are the primary symptoms of asthma,[101] some people present primarily with coughing, and in severe cases, air motion may be significantly impaired such that no wheezing is heard.[99] In children, chest pain is often present.[102]

Signs occurring during an asthma attack include the use of accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck), there may be a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest.[103] A blue color of the skin and nails may happen from lack of oxygen.[104]

In a mild exacerbation the peak expiratory flow rate (PEFR) is ≥200 L/min, or ≥50% of the predicted best.[105] Moderate is defined as between 80 and 200 L/min, or 25% and 50% of the predicted best, while severe is defined as ≤ 80 L/min, or ≤25% of the predicted best.[105]

Acute severe asthma, previously known as status asthmaticus, is an acute exacerbation of asthma that does not reply to standard treatments of bronchodilators and corticosteroids.[106] Half of cases are due to infections with others caused by allergen, air pollution, or insufficient or inappropriate medication use.[106]

Brittle asthma is a helpful of asthma distinguishable by recurrent, severe attacks.[99] Type 1 brittle asthma is a disease with wide peak flow variability, despite intense medication.

Type 2 brittle asthma is background well-controlled asthma with sudden severe exacerbations.[99]

Aspirin-induced asthma

Main article: Aspirin-exacerbated respiratory disease

Aspirin-exacerbated respiratory disease (AERD), also known as aspirin-induced asthma, affects up to 9% of asthmatics.[116] AERD consists of asthma, nasal polyps, sinus disease, and respiratory reactions to aspirin and other NSAID medications (such as ibuprofen and naproxen).[117] People often also develop loss of smell and most experience respiratory reactions to alcohol.[118]

Non-atopic asthma

Non-atopic asthma, also known as intrinsic or non-allergic, makes up between 10 and 33% of cases.

There is negative skin test to common inhalant allergens and normal serum concentrations of IgE. Often it starts later in life, and women are more commonly affected than men. Usual treatments may not work as well.[120]

Spirometry

Spirometry is recommended to aid in diagnosis and management.[89][90] It is the single best test for asthma. If the FEV1 measured by this technique improves more than 12% and increases by at least 200 milliliters following istration of a bronchodilator such as salbutamol, this is supportive of the diagnosis. It however may be normal in those with a history of mild asthma, not currently acting up.[22] As caffeine is a bronchodilator in people with asthma, the use of caffeine before a lung function test may interfere with the results.[91]Single-breath diffusing capacity can assist differentiate asthma from COPD.[22] It is reasonable to act out spirometry every one or two years to follow how well a person’s asthma is controlled.[92]

Others

The methacholine challenge involves the inhalation of increasing concentrations of a substance that causes airway narrowing in those predisposed.

If negative it means that a person does not own asthma; if positive, however, it is not specific for the disease.[22]

Other supportive evidence includes: a ≥20% difference in peak expiratory flow rate on at least three days in a week for at least two weeks, a ≥20% improvement of peak flow following treatment with either salbutamol, inhaled corticosteroids or prednisone, or a ≥20% decrease in peak flow following exposure to a trigger.[93] Testing peak expiratory flow is more variable than spirometry, however, and thus not recommended for routine diagnosis. It may be useful for daily self-monitoring in those with moderate to severe disease and for checking the effectiveness of new medications.

It may also be helpful in guiding treatment in those with acute exacerbations.[94]

Differential diagnosis

Many other conditions can cause symptoms similar to those of asthma. In children, other upper airway diseases such as allergic rhinitis and sinusitis should be considered as well as other causes of airway obstruction including foreign body aspiration, tracheal stenosis, laryngotracheomalacia, vascular rings, enlarged lymph nodes or neck masses.[121]Bronchiolitis and other viral infections may also produce wheezing.[122] In adults, COPD, congestive heart failure, airway masses, as well as drug-induced coughing due to ACE inhibitors should be considered.

In both populations vocal cord dysfunction may present similarly.[121]

Chronic obstructive pulmonary disease can coexist with asthma and can happen as a complication of chronic asthma. After the age of 65, most people with obstructive airway disease will own asthma and COPD. In this setting, COPD can be differentiated by increased airway neutrophils, abnormally increased wall thickness, and increased smooth muscle in the bronchi. However, this level of investigation is not performed due to COPD and asthma sharing similar principles of management: corticosteroids, long-acting beta-agonists, and smoking cessation.[123] It closely resembles asthma in symptoms, is correlated with more exposure to cigarette smoke, an older age, less symptom reversibility after bronchodilator istration, and decreased likelihood of family history of atopy.[124][125]


Prevention

The evidence for the effectiveness of measures to prevent the development of asthma is weak.[126] The World Health Organization recommends decreasing risk factors such as tobacco smoke, air pollution, chemical irritants including perfume, and the number of lower respiratory infections.[127][128] Other efforts that show promise include: limiting smoke exposure in utero, breastfeeding, and increased exposure to daycare or large families, but none are well supported enough to be recommended for this indication.[126]

Early pet exposure may be useful.[129] Results from exposure to pets at other times are inconclusive[130] and it is only recommended that pets be removed from the home if a person has allergic symptoms to said pet.[131]

Dietary restrictions during pregnancy or when breast feeding own not been found to be effective at preventing asthma in children and are not recommended.[131] Reducing or eliminating compounds known to sensitive people from the work put may be effective.[113] It is not clear if annual influenza vaccinations affects the risk of exacerbations.[132] Immunization, however, is recommended by the World Health Organization.[133] Smoking bans are effective in decreasing exacerbations of asthma.[134]


Causes

Asthma is caused by a combination of complicated and incompletely understood environmental and genetic interactions.[4][33] These influence both its severity and its responsiveness to treatment.[34] It is believed that the recent increased rates of asthma are due to changing epigenetics (heritable factors other than those related to the DNA sequence) and a changing living environment.[35] Asthma that starts before the age of 12 years ancient is more likely due to genetic influence, while onset after age 12 is more likely due to environmental influence.[36]

Medical conditions

A triad of atopic eczema, allergic rhinitis and asthma is called atopy.[72] The strongest risk factor for developing asthma is a history of atopic disease;[59] with asthma occurring at a much greater rate in those who own either eczema or hay fever.[73] Asthma has been associated with eosinophilic granulomatosis with polyangiitis (formerly known as Churg–Strauss syndrome), an autoimmune disease and vasculitis.[74] Individuals with certain types of urticaria may also experience symptoms of asthma.[72]

There is a correlation between obesity and the risk of asthma with both having increased in recent years.[75][76] Several factors may be at frolic including decreased respiratory function due to a buildup of fat and the fact that adipose tissue leads to a pro-inflammatory state.[77]

Beta blocker medications such as propranolol can trigger asthma in those who are susceptible.[78]Cardioselective beta-blockers, however, appear safe in those with mild or moderate disease.[79][80] Other medications that can cause problems in asthmatics are angiotensin-converting enzyme inhibitors, aspirin, and NSAIDs.[81] Use of acid suppressing medication (proton pump inhibitors and H2 blockers) during pregnancy is associated with an increased risk of asthma in the child.[82]

Environmental

See also: Asthma-related microbes

Many environmental factors own been associated with asthma’s development and exacerbation, including, allergens, air pollution, and other environmental chemicals.[37]Smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms.[38] Low air quality from environmental factors such as traffic pollution or high ozone levels[39] has been associated with both asthma development and increased asthma severity.[40] Over half of cases in children in the United States happen in areas when air quality is under the EPA standards.[41] Low air quality is more common in low-income and minority communities.[42]

Exposure to indoor volatile organic compounds may be a trigger for asthma; formaldehyde exposure, for example, has a positive association.[43]Phthalates in certain types of PVC are associated with asthma in both children and adults.[44][45] While exposure to pesticides is linked to the development of asthma, a cause and effect relationship has yet to be established.[46][47]

The majority of the evidence does not support a causal role between acetaminophen (paracetamol) or antibiotic use and asthma.[48][49] A 2014 systematic review found that the association between acetaminophen use and asthma disappeared when respiratory infections were taken into account.[50] Acetaminophen use by a mom during pregnancy is also associated with an increased risk of the kid developing asthma.[51] Maternal psychological stress during pregnancy is a risk factor for the kid to develop asthma.[52]

Asthma is associated with exposure to indoor allergens.[53] Common indoor allergens include dust mites, cockroaches, animal dander (fragments of fur or feathers), and mold.[54][55] Efforts to decrease dust mites own been found to be ineffective on symptoms in sensitized subjects.[56][57] Feeble evidence suggests that efforts to decrease mold by repairing buildings may assist improve asthma symptoms in adults.[58] Certain viral respiratory infections, such as respiratory syncytial virus and rhinovirus,[22] may increase the risk of developing asthma when acquired as young children.[59] Certain other infections, however, may decrease the risk.[22]

Hygiene hypothesis

The hygiene hypothesis attempts to explain the increased rates of asthma worldwide as a direct and unintended result of reduced exposure, during childhood, to non-pathogenic bacteria and viruses.[60][61] It has been proposed that the reduced exposure to bacteria and viruses is due, in part, to increased cleanliness and decreased family size in modern societies.[62] Exposure to bacterial endotoxin in early childhood may prevent the development of asthma, but exposure at an older age may provoke bronchoconstriction.[63] Evidence supporting the hygiene hypothesis includes lower rates of asthma on farms and in households with pets.[62]

Use of antibiotics in early life has been linked to the development of asthma.[64] Also, delivery via caesarean section is associated with an increased risk (estimated at 20–80%) of asthma – this increased risk is attributed to the lack of healthy bacterial colonization that the newborn would own acquired from passage through the birth canal.[65][66] There is a link between asthma and the degree of affluence which may be related to the hygiene hypothesis as less affluent individuals often own more exposure to bacteria and viruses.[67]

Genetic

Endotoxin levels CC genotype TT genotype
High exposure Low risk High risk
Low exposure High risk Low risk

Family history is a risk factor for asthma, with numerous diverse genes being implicated.[69] If one identical twin is affected, the probability of the other having the disease is approximately 25%.[69] By the finish of 2005, 25 genes had been associated with asthma in six or more separate populations, including GSTM1, IL10, CTLA-4, SPINK5, LTC4S, IL4R and ADAM33, among others.[70] Numerous of these genes are related to the immune system or modulating inflammation.

Even among this list of genes supported by highly replicated studies, results own not been consistent among every populations tested.[70] In 2006 over 100 genes were associated with asthma in one genetic association study alone;[70] more continue to be found.[71]

Some genetic variants may only cause asthma when they are combined with specific environmental exposures.[4] An example is a specific single nucleotide polymorphism in the CD14 region and exposure to endotoxin (a bacterial product).

Endotoxin exposure can come from several environmental sources including tobacco smoke, dogs, and farms. Risk for asthma, then, is sure by both a person’s genetics and the level of endotoxin exposure.[68]

Exacerbation

Some individuals will own stable asthma for weeks or months and then suddenly develop an episode of acute asthma. Diverse individuals react to various factors in diverse ways.[83] Most individuals can develop severe exacerbation from a number of triggering agents.[83]

Home factors that can lead to exacerbation of asthma include dust, animal dander (especially cat and dog hair), cockroach allergens and mold.[83][84]Perfumes are a common cause of acute attacks in women and children.

Both viral and bacterial infections of the upper respiratory tract can worsen the disease.[83] Psychological stress may worsen symptoms – it is thought that stress alters the immune system and thus increases the airway inflammatory response to allergens and irritants.[40][85]

Asthma exacerbations in school‐aged children peak in autumn, shortly after children return to school. This might reflect a combination of factors, including poor treatment adherence, increased allergen and viral exposure, and altered immune tolerance.

There is limited evidence to guide possible approaches to reducing autumn exacerbations, but while costly, seasonal omalizumab treatment from four to six weeks before school return may reduce autumn asthma exacerbations.[86]


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