Editing Asthma (section)

===Classification===
{| class="wikitable" style="clear:right; float:right; margin-left:1em; text-align:center"
|+ Clinical classification (≥ 12 years old)<ref name=Yawn2008/>
|-
! scope="col" style="width:6em;" | Severity
! scope="col" style="width:4em;" | Symptom frequency
! scope="col" style="width:4em;" | Night-time symptoms
! scope="col" style="width:4em;" | %FEV<sub>1</sub> of predicted
! scope="col" style="width:4em;" | FEV<sub>1</sub> variability
! scope="col" style="width:4em;" | SABA use
|-
! scope="row" | Intermittent
| ≤2/week
| ≤2/month
| ≥80%
| <20%
| ≤2 days/week
|-
! scope="row" | Mild persistent
| >2/week
| 3–4/month
| ≥80%
| 20–30%
| >2 days/week
|-
! scope="row" | Moderate persistent
| Daily
| >1/week
| 60–80%
| >30%
| daily
|-
! scope="row" | 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 (FEV<sub>1</sub>), and [[peak expiratory flow rate]].<ref name="Yawn2008" /> 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).<ref name="RobbinsCotran2010" /> While asthma is classified based on severity, at the moment there is no clear method for classifying different subgroups of asthma beyond this system.<ref name=Moore2010>{{cite journal | vauthors = Moore WC, Pascual RM | title = Update in asthma 2009 | journal = American Journal of Respiratory and Critical Care Medicine | volume = 181 | issue = 11 | pages = 1181–7 | date = June 2010 | pmid = 20516492 | pmc = 3269238 | doi = 10.1164/rccm.201003-0321UP }}</ref> Finding ways to identify subgroups that respond well to different types of treatments is a current critical goal of asthma research.<ref name=Moore2010/> Recently, asthma has been classified based on whether it is associated with type 2 or non–type 2 inflammation. This approach to immunologic classification is driven by a developing understanding of the underlying immune processes and by the development of therapeutic approaches that target type 2 inflammation.<ref>{{cite book |title=Harrison's principles of internal medicine |date=2022 |publisher=McGraw Hill |isbn=978-1-264-26850-4 |edition=21st |location=New York |pages=2150}}</ref>

Although asthma is a chronic [[obstructive lung disease|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 [[Pneumatosis#Lungs|emphysema]].<ref name="Self, Timothy 2009">{{cite book | veditors = Koda-Kimble MA, Alldredge BK | vauthors = Self T, Chrisman C, Finch C |title=Applied therapeutics: the clinical use of drugs |edition=9th |location=Philadelphia |publisher=Lippincott Williams & Wilkins |year=2009 |chapter=22. Asthma |oclc=230848069 |display-editors=etal}}</ref> Unlike these diseases, the airway obstruction in asthma is usually reversible; however, if left untreated, the chronic inflammation from asthma can lead the lungs to become irreversibly obstructed due to airway remodelling.<ref name=Delacourt2004>{{cite journal | vauthors = Delacourt C | title = [Bronchial changes in untreated asthma] | journal = Archives de Pédiatrie | volume = 11 | issue = Suppl 2 | pages = 71s–73s | date = June 2004 | pmid = 15301800 | doi = 10.1016/S0929-693X(04)90003-6 | trans-title = Bronchial changes in untreated asthma }}</ref> In contrast to emphysema, asthma affects the bronchi, not the [[Pulmonary alveolus|alveoli]].<ref name=Schiffman2009>{{cite web|url=http://www.medicinenet.com/chronic_obstructive_pulmonary_disease_copd/article.htm |title=Chronic obstructive pulmonary disease | vauthors = Schiffman G |date=December 18, 2009 |publisher=MedicineNet |access-date=September 2, 2010 |archive-url=https://web.archive.org/web/20100828011049/http://www.medicinenet.com/chronic_obstructive_pulmonary_disease_copd/article.htm |archive-date= August 28, 2010 |url-status=live}}</ref> The combination of asthma with a component of irreversible airway obstruction has been termed the [[Asthma-COPD overlap|asthma-chronic obstructive disease (COPD) overlap syndrome (ACOS)]]. Compared to other people with "pure" asthma or COPD, people with ACOS exhibit increased morbidity, mortality and possibly more comorbidities.<ref>{{cite journal | vauthors = Gibson PG, McDonald VM | title = Asthma-COPD overlap 2015: now we are six | journal = Thorax | volume = 70 | issue = 7 | pages = 683–691 | date = July 2015 | pmid = 25948695 | doi = 10.1136/thoraxjnl-2014-206740 | s2cid = 38550372 | doi-access = free }}</ref>

====Asthma exacerbation<span class="anchor" id="Asthma attack"></span>====
<!--"Asthma attack" redirects here.-->
{| class="wikitable" style="clear:right; float:right; margin-left:15px; text-align:center"
|+ Severity of an acute exacerbation<ref name="BTS58" />
|-
! style="border-top:3px solid darkgrey;"| Near-fatal
| colspan="2" style="border-top:3px solid darkgrey;"| High [[Arterial blood gas|PaCO<sub>2</sub>]], or requiring mechanical ventilation, or both
|-
! rowspan="9" style="border-top:3px solid darkgrey;"| Life-threatening<br>(any one of)
|-
! Clinical signs
! Measurements
|-
| Altered [[level of consciousness]]
| [[Peak flow]] < 33%
|-
| Exhaustion
| [[Oxygen saturation]] < 92%
|-
| [[Heart arrhythmia|Arrhythmia]]
| [[Arterial blood gas|PaO<sub>2</sub>]] < 8 kPa
|-
| Low [[blood pressure]]
| "Normal" PaCO<sub>2</sub>
|-
| [[Cyanosis]]
|
|-
| Silent chest
|
|-
| Poor respiratory effort
|
|-
! rowspan="5" style="border-top:3px solid darkgrey;"| Acute severe<br>(any one of)
|-
| colspan="2" | Peak flow 33–50%
|-
| colspan="2" | Respiratory rate ≥ 25 breaths per minute
|-
| colspan="2" | Heart rate ≥ 110 beats per minute
|-
| colspan="2" | Unable to complete sentences in one breath
|-
! rowspan="3" style="border-top:3px solid darkgrey; border-bottom:3 px solid darkgrey;"| Moderate
| colspan="2" style="border-top:3px solid darkgrey;"| Worsening symptoms
|-
| colspan="2" | Peak flow 50–80% best or predicted
|-
| colspan="2" style="border-bottom:3 px solid darkgrey;"| 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]], [[Wheeze|wheezing]], and [[chest tightness]].<ref name=M38/> The wheezing is most often when breathing out.<ref>{{cite book |title=Current Review of Asthma |date=2003 |publisher=Current Medicine Group |location=London |isbn=978-1-4613-1095-2 |page=42 |url=https://books.google.com/books?id=MCEBCAAAQBAJ&pg=PA42 |url-status=live |archive-url=https://web.archive.org/web/20170908184941/https://books.google.com/books?id=MCEBCAAAQBAJ&pg=PA42 |archive-date=September 8, 2017 }}</ref> While these are the primary symptoms of asthma,<ref name=Barnes2008>{{cite book | vauthors = Barnes PJ |chapter=Asthma |title=Harrison's Principles of Internal Medicine |url=https://archive.org/details/harrisonsprincip00asfa |url-access=limited | veditors = Fauci AS, Braunwald E, Kasper DL |location=New York |publisher=McGraw-Hill |date=2008 |edition=17th |isbn=978-0-07-146633-2 |pages=[https://archive.org/details/harrisonsprincip00asfa/page/n1634 1596]–1607 }}</ref> some people present primarily with [[cough]]ing, and in severe cases, air motion may be significantly impaired such that no wheezing is heard.<ref name="BTS58" /> In children, [[Pediatric chest pain|chest pain]] is often present.<ref name="Mac2011">{{cite book |vauthors=McMahon M |title=Pediatrics a competency-based companion |publisher=Saunders/Elsevier |location=Philadelphia |date=2011 |isbn=978-1-4160-5350-7 }}</ref>

Signs occurring during an asthma attack include the use of accessory [[muscle]]s of respiration ([[sternocleidomastoid]] and [[scalene muscles]] of the neck), there may be a [[pulsus paradoxus|paradoxical pulse]] (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest.<ref name=Maitre1995>{{cite journal | vauthors = Maitre B, Similowski T, Derenne JP | title = Physical examination of the adult patient with respiratory diseases: inspection and palpation | journal = The European Respiratory Journal | volume = 8 | issue = 9 | pages = 1584–93 | date = September 1995 | doi = 10.1183/09031936.95.08091584 | pmid = 8575588 | s2cid = 30677275 | url = http://erj.ersjournals.com/content/8/9/1584.long | url-status = live | archive-url = https://web.archive.org/web/20150429223309/http://erj.ersjournals.com/content/8/9/1584.long | archive-date = April 29, 2015 | doi-access = free }}</ref> A [[cyanosis|blue colour]] of the skin and nails may occur from lack of oxygen.<ref name=Werner2001>{{cite journal | vauthors = Werner HA | title = Status asthmaticus in children: a review | journal = Chest | volume = 119 | issue = 6 | pages = 1913–29 | date = June 2001 | pmid = 11399724 | doi = 10.1378/chest.119.6.1913 }}</ref>

In a mild exacerbation the [[peak expiratory flow rate]] (PEFR) is ≥200&nbsp;L/min, or ≥50% of the predicted best.<ref name="Shiber2006">{{cite journal | vauthors = Shiber JR, Santana J | title = Dyspnea | journal = The Medical Clinics of North America | volume = 90 | issue = 3 | pages = 453–79 | date = May 2006 | pmid = 16473100 | doi = 10.1016/j.mcna.2005.11.006 }}</ref> Moderate is defined as between 80 and 200&nbsp;L/min, or 25% and 50% of the predicted best, while severe is defined as ≤&nbsp;80 L/min, or ≤25% of the predicted best.<ref name="Shiber2006" />

[[Acute severe asthma]], previously known as status asthmaticus, is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators and corticosteroids.<ref name=Shah2012/> Half of cases are due to infections with others caused by allergen, air pollution, or insufficient or inappropriate medication use.<ref name="Shah2012">{{cite journal | vauthors = Shah R, Saltoun CA | title = Chapter 14: Acute severe asthma (status asthmaticus) | journal = Allergy and Asthma Proceedings | volume = 33 | issue = 3 | pages = 47–50 |year=2012 | pmid = 22794687 | doi = 10.2500/aap.2012.33.3547 }}</ref>

[[Brittle asthma]] is a kind of asthma distinguishable by recurrent, severe attacks.<ref name=BTS58>{{harvnb|British Guideline|2009|p=54}}</ref> 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.<ref name=BTS58/>

====Exercise-induced====
{{Main|Exercise-induced bronchoconstriction}}

Exercise can trigger [[bronchoconstriction]] both in people with or without asthma.<ref name=EIB2012>{{cite journal | vauthors = Khan DA | title = Exercise-induced bronchoconstriction: burden and prevalence | journal = Allergy and Asthma Proceedings | volume = 33 | issue = 1 | pages = 1–6 | date = Jan–Feb 2012 | pmid = 22370526 | doi = 10.2500/aap.2012.33.3507 }}</ref> It occurs in most people with asthma and up to 20% of people without asthma.<ref name=EIB2012/> Exercise-induced bronchoconstriction is common in professional athletes. The highest rates are among cyclists (up to 45%), swimmers, and cross-country skiers.<ref name="Wuestenfeld">{{cite journal | vauthors = Wuestenfeld JC, Wolfarth B | title = Special considerations for adolescent athletic and asthmatic patients | journal = Open Access Journal of Sports Medicine | volume = 4 | pages = 1–7 | date = January 2013 | pmid = 24379703 | pmc = 3871903 | doi = 10.2147/OAJSM.S23438 | doi-access = free }}</ref> While it may occur with any weather conditions, it is more common when it is dry and cold.<ref name=GINA_2011_page17>{{harvnb|GINA|2011|p=17}}</ref> Inhaled beta[[Beta2-adrenergic agonist|<sub>2</sub>]] agonists do not appear to improve athletic performance among those without asthma;<ref name="pmid18394123">{{cite journal | vauthors = Carlsen KH, Anderson SD, Bjermer L, Bonini S, Brusasco V, Canonica W, Cummiskey J, Delgado L, Del Giacco SR, Drobnic F, Haahtela T, Larsson K, Palange P, Popov T, van Cauwenberge P | display-authors = 6 | title = Treatment of exercise-induced asthma, respiratory and allergic disorders in sports and the relationship to doping: Part II of the report from the Joint Task Force of European Respiratory Society (ERS) and European Academy of Allergy and Clinical Immunology (EAACI) in cooperation with GA(2)LEN | journal = Allergy | volume = 63 | issue = 5 | pages = 492–505 | date = May 2008 | pmid = 18394123 | doi = 10.1111/j.1398-9995.2008.01663.x | doi-access =  | others = European Respiratory, Society; European Academy of Allergy and Clinical, Immunology; GA(2)LEN }}</ref> however, oral doses may improve endurance and strength.<ref name="pmid17241101">{{cite journal | vauthors = Kindermann W | title = Do inhaled beta(2)-agonists have an ergogenic potential in non-asthmatic competitive athletes? | journal = Sports Medicine | volume = 37 | issue = 2 | pages = 95–102 |year=2007 | pmid = 17241101 | doi = 10.2165/00007256-200737020-00001 | s2cid = 20993439 }}</ref><ref name="pmid21142283">{{cite journal | vauthors = Pluim BM, de Hon O, Staal JB, Limpens J, Kuipers H, Overbeek SE, Zwinderman AH, Scholten RJ | display-authors = 6 | title = β₂-Agonists and physical performance: a systematic review and meta-analysis of randomized controlled trials | journal = Sports Medicine | volume = 41 | issue = 1 | pages = 39–57 | date = January 2011 | pmid = 21142283 | doi = 10.2165/11537540-000000000-00000 | s2cid = 189906919 }}</ref>

====Occupational====
{{Main|Occupational asthma}}

Asthma as a result of (or worsened by) workplace exposures is a commonly reported [[occupational disease]].<ref name=Baur2012/> Many cases, however, are not reported or recognized as such.<ref>{{cite book |veditors=Kunnamo I |title=Evidence-based medicine guidelines|url=https://archive.org/details/evidencebasedmed00publ |url-access=limited |year=2005|publisher=Wiley|location=Chichester|isbn=978-0-470-01184-3|page=[https://archive.org/details/evidencebasedmed00publ/page/n250 214]}}</ref><ref>{{cite book |vauthors=Frew AJ |veditors=Castro M, Kraft M |title=Clinical Asthma|url=https://archive.org/details/clinicalasthma0000unse |url-access=registration |year=2008|publisher=Mosby / Elsevier |location=Philadelphia |isbn=978-0-323-07081-2 |chapter=Chapter 42: Occupational Asthma}}</ref> It is estimated that 5–25% of asthma cases in adults are work-related.<!-- <ref name=Baur2012/> --> A few hundred different agents have been implicated, with the most common being [[isocyanates]], grain and wood dust, [[colophony]], [[soldering flux]], [[latex]], animals, and [[aldehydes]].<!-- <ref name=Baur2012/> --> 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.<ref name=Baur2012>{{cite journal | vauthors = Baur X, Aasen TB, Burge PS, Heederik D, Henneberger PK, Maestrelli P, Schlünssen V, Vandenplas O, Wilken D | display-authors = 6 | title = The management of work-related asthma guidelines: a broader perspective | journal = European Respiratory Review | volume = 21 | issue = 124 | pages = 125–39 | date = June 2012 | pmid = 22654084 | doi = 10.1183/09059180.00004711 | others = ERS Task Force on the Management of Work-related, Asthma | pmc = 9487296 | doi-access = free }}</ref>

====Aspirin-exacerbated respiratory disease====
{{Main|Aspirin-exacerbated respiratory disease}}

[[Aspirin-exacerbated respiratory disease]] (AERD), also known as [[aspirin]]-induced asthma, affects up to 9% of asthmatics.<ref>{{cite journal | vauthors = Chang JE, White A, Simon RA, Stevenson DD | title = Aspirin-exacerbated respiratory disease: burden of disease | journal = Allergy and Asthma Proceedings | volume = 33 | issue = 2 | pages = 117–21 |year = 2012 | pmid = 22525387 | doi = 10.2500/aap.2012.33.3541 }}</ref> AERD consists of asthma, nasal polyps, sinus disease, and respiratory reactions to aspirin and other [[NSAID medications]] (such as ibuprofen and naproxen).<ref>{{cite web |url= https://www.aaaai.org/conditions-and-treatments/library/asthma-library/aspirin-exacerbated-respiratory-disease |title= Aspirin Exacerbated Respiratory Disease (AERD) |author= <!--Not stated--> |website= aaaai.org |publisher= American Academy of Allergy Asthma & Immunology |date= August 3, 2018 |access-date= August 2, 2018 |archive-date= September 18, 2018 |archive-url= https://web.archive.org/web/20180918131548/https://www.aaaai.org/conditions-and-treatments/library/asthma-library/aspirin-exacerbated-respiratory-disease |url-status= dead }}</ref> People often also develop loss of smell and most experience respiratory reactions to alcohol.<ref name=Ken2018>{{cite journal | vauthors = Kennedy JL, Stoner AN, Borish L | title = Aspirin-exacerbated respiratory disease: Prevalence, diagnosis, treatment, and considerations for the future | journal = American Journal of Rhinology & Allergy | volume = 30 | issue = 6 | pages = 407–413 | date = November 2016 | pmid = 28124651 | pmc = 5108840 | doi = 10.2500/ajra.2016.30.4370 }}</ref>

====Alcohol-induced asthma====
{{Main|Alcohol-induced respiratory reactions}}

Alcohol may worsen asthmatic symptoms in up to a third of people.<ref name=Adams2013/> This may be even more common in some ethnic groups such as the [[Japanese people|Japanese]] and those with aspirin-exacerbated respiratory disease.<ref name=Adams2013/> Other studies have found improvement in asthmatic symptoms from alcohol.<ref name=Adams2013>{{cite journal | vauthors = Adams KE, Rans TS | title = Adverse reactions to alcohol and alcoholic beverages | journal = Annals of Allergy, Asthma & Immunology | volume = 111 | issue = 6 | pages = 439–45 | date = December 2013 | pmid = 24267355 | doi = 10.1016/j.anai.2013.09.016 }}</ref>

==== Non-atopic asthma ====
Non-atopic asthma, also known as intrinsic or non-allergic, makes up between 10 and 33% of cases.<!-- <ref name=Peter2014/> --> There is negative skin test to common inhalant allergens.<!-- <ref name=Peter2014/>  --> Often it starts later in life, and women are more commonly affected than men.<!-- <ref name=Peter2014/> --> Usual treatments may not work as well.<ref name=Peter2014>{{cite journal | vauthors = Peters SP | title = Asthma phenotypes: nonallergic (intrinsic) asthma | journal = The Journal of Allergy and Clinical Immunology. In Practice | volume = 2 | issue = 6 | pages = 650–652 |year = 2014 | pmid = 25439352 | doi = 10.1016/j.jaip.2014.09.006 }}</ref> The concept that "non-atopic" is synonymous with "non-allergic" is called into question by epidemiological data that the prevalence of asthma is closely related to the serum IgE level standardized for age and sex (P<0.0001), indicating that asthma is almost always associated with some sort of IgE-related reaction and therefore has an allergic basis, although not all the allergic stimuli that cause asthma appear to have been included in the battery of aeroallergens studied (the "missing antigen(s)" hypothesis).<ref>{{cite journal | vauthors = Burrows B, Martinez FD, Halonen M, Barbee RA, Cline MG | title = Association of asthma with serum IgE levels and skin-test reactivity to allergens | journal = The New England Journal of Medicine | volume = 320 | issue = 5 | pages = 271–277 | date = February 1989 | pmid = 2911321 | doi = 10.1056/NEJM198902023200502 }}</ref> For example, an updated systematic review and meta-analysis of population-attributable risk (PAR) of ''Chlamydia pneumoniae'' biomarkers in chronic asthma found that the PAR for ''C. pneumoniae''-specific IgE was 47%.<ref>{{cite journal | vauthors = Hahn DL | title = Chlamydia pneumoniae and chronic asthma: Updated systematic review and meta-analysis of population attributable risk | journal = PLOS ONE | volume = 16 | issue = 4 | pages = e0250034 |year = 2021 | pmid = 33872336 | pmc = 8055030 | doi = 10.1371/journal.pone.0250034 | bibcode = 2021PLoSO..1650034H | doi-access = free }}</ref>

==== Infectious asthma ====
Infectious asthma is an easily identified clinical presentation.<ref>{{cite journal | vauthors = Hahn DL, Schultek NM  | title = Infectious Asthma: An Easily Identified Clinical Presentation with Implications for Diagnosis, Prognosis, Treatment, and Prevention of Asthma | journal = Journal of Asthma and Allergy | volume = 15 | pages = 1269–1272 |year = 2022 | pmid = 36164333 | pmc = 9508995 | doi = 10.2147/JAA.S379890 | doi-access = free }}</ref> When queried, asthma patients may report that their first asthma symptoms began after an acute lower respiratory tract illness. This type of history has been labelled the "infectious asthma" (IA) syndrome,<ref name="Infectious asthma: a reemerging cli">{{cite journal | vauthors = Hahn DL | title = Infectious asthma: a reemerging clinical entity? | journal = The Journal of Family Practice | volume = 41 | issue = 2 | pages = 153–157 | date = August 1995 | pmid = 7636455 }}</ref> or as "asthma associated with infection" (AAWI)<ref>{{cite journal | vauthors = Hahn DL, Peeling RW, Dillon E, McDonald R, Saikku P | title = Serologic markers for Chlamydia pneumoniae in asthma | journal = Annals of Allergy, Asthma & Immunology | volume = 84 | issue = 2 | pages = 227–233 | date = February 2000 | pmid = 10719781 | doi = 10.1016/S1081-1206(10)62760-3 }}</ref> to distinguish infection-associated asthma initiation from the well known association of respiratory infections with asthma exacerbations. Reported clinical prevalences of IA for adults range from around 40% in a primary care practice<ref name="Infectious asthma: a reemerging cli" /> to 70% in a speciality practice treating mainly severe asthma patients.<ref name="Outcomes of Antibiotics in Adults w">{{cite journal | vauthors = Wagshul FA, Brown DT, Schultek NM, Hahn DL | title = Outcomes of Antibiotics in Adults with 'Difficult to Treat' Asthma or the Overlap Syndrome | journal = Journal of Asthma and Allergy | volume = 14 | pages = 703–712 |year = 2021 | pmid = 34163182 | pmc = 8216074 | doi = 10.2147/JAA.S313480 | doi-access = free }}</ref> Additional information on the clinical prevalence  of IA in adult-onset asthma is unavailable because clinicians are not trained to elicit this type of history routinely, and recollection in child-onset asthma is challenging. A population-based incident case-control study in a geographically defined area of Finland reported that 35.8% of new-onset asthma cases had experienced acute bronchitis or pneumonia in the year preceding asthma onset, representing a significantly higher risk compared to randomly selected controls ([[odds ratio]] 7.2, 95% confidence interval 5.2–10).<ref>{{cite journal | vauthors = Rantala A, Jaakkola JJ, Jaakkola MS  | title = Respiratory infections precede adult-onset asthma | journal = PLOS ONE | volume =  6| pages = e27912 |year = 2011 | issue = 12 | pmid = 22205932 | pmc = 3244385 | doi = 10.1371/journal.pone.0027912 | bibcode = 2011PLoSO...627912R | doi-access = free }}</ref>

==== Phenotyping and endotyping ====
{{Main|Asthma phenotyping and endotyping}}

Asthma phenotyping and endotyping has emerged as a novel approach to asthma classification inspired by [[precision medicine]] which separates the clinical presentations of asthma, or asthma phenotypes, from their underlying causes, or asthma endotypes. The best-supported endotypic distinction is the type 2-high/type 2-low distinction. Classification based on type 2 inflammation is useful in predicting which patients will benefit from targeted [[biologic therapy]].<ref>{{cite journal | vauthors = Kuruvilla ME, Lee FE, Lee GB | title = Understanding Asthma Phenotypes, Endotypes, and Mechanisms of Disease | journal = Clinical Reviews in Allergy & Immunology | volume = 56 | issue = 2 | pages = 219–233 | date = April 2019 | pmid = 30206782 | pmc = 6411459 | doi = 10.1007/s12016-018-8712-1 }}</ref><ref>{{cite journal | vauthors = Ray A, Camiolo M, Fitzpatrick A, Gauthier M, Wenzel SE | title = Are We Meeting the Promise of Endotypes and Precision Medicine in Asthma? | journal = Physiological Reviews | volume = 100 | issue = 3 | pages = 983–1017 | date = July 2020 | pmid = 31917651 | pmc = 7474260 | doi = 10.1152/physrev.00023.2019 }}</ref>