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{{Anaphylaxis}}
{{Anaphylaxis}}


{{CMG}}
{{CMG}}, {{AE}} [[User:Dushka|Dushka Riaz, MD]]


==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.


OR
The progression to [[anaphylaxis]] usually involves an [[IgE]]-mediated or non IgE-mediated response. It is a [[medical emergency]] that involves multiple systems. <ref name="pmid29489197">{{cite journal| author=| title=StatPearls | journal= | year= 2021 | volume=  | issue=  | pages=  | pmid=29489197 | doi= | pmc= | url= }} </ref> The condition involves [[pulmonary]], [[gastrointestinal]], [[cardiovascular]] and [[Integumentary system|integumentary]] systems and can lead to [[cardiorespiratory arrest]]. <ref name="pmid28800865">{{cite journal| author=LoVerde D, Iweala OI, Eginli A, Krishnaswamy G| title=Anaphylaxis. | journal=Chest | year= 2018 | volume= 153 | issue= 2 | pages= 528-543 | pmid=28800865 | doi=10.1016/j.chest.2017.07.033 | pmc=6026262 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28800865  }} </ref>


It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
==Pathophysiology==
 
OR
 
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.


OR
[[Anaphylaxis]] is usually caused by [[food]], particularly [[peanuts]], [[drugs]], and [[insect venoms]]. <ref name="pmid15753908">{{cite journal| author=Sampson HA, Muñoz-Furlong A, Bock SA, Schmitt C, Bass R, Chowdhury BA | display-authors=etal| title=Symposium on the definition and management of anaphylaxis: summary report. | journal=J Allergy Clin Immunol | year= 2005 | volume= 115 | issue= 3 | pages= 584-91 | pmid=15753908 | doi=10.1016/j.jaci.2005.01.009 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15753908  }} </ref> <ref name="pmid12209078">{{cite journal| author=Kemp SF, Lockey RF| title=Anaphylaxis: a review of causes and mechanisms. | journal=J Allergy Clin Immunol | year= 2002 | volume= 110 | issue= 3 | pages= 341-8 | pmid=12209078 | doi=10.1067/mai.2002.126811 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12209078  }} </ref> There have also been cases of idiopathic [[anaphylaxis]]. <ref name="pmid12865776">{{cite journal| author=Lenchner K, Grammer LC| title=A current review of idiopathic anaphylaxis. | journal=Curr Opin Allergy Clin Immunol | year= 2003 | volume= 3 | issue= 4 | pages= 305-11 | pmid=12865776 | doi=10.1097/00130832-200308000-00012 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12865776  }} </ref> <ref name="pmid11895624">{{cite journal| author=Ring J, Darsow U| title=Idiopathic anaphylaxis. | journal=Curr Allergy Asthma Rep | year= 2002 | volume= 2 | issue= 1 | pages= 40-5 | pmid=11895624 | doi=10.1007/s11882-002-0036-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11895624  }} </ref>
[[Anaphylaxis]] arises from [[mast cell]] and [[basophil]] [[degranulation]] after repeated exposure to an [[antigen]]. This results in a [[type 1 hypersensitivity reaction]]. The [[IgE]] then crosslinks and aggregates with receptors resulting in the release of [[histamine]], [[Proteoglycan|proteoglycans]], and [[tryptase]]. This results in [[arachidonic acid]] metabolites being released with further consequences. The reaction as a whole leads to [[vasodilation]], increase [[heart rate]], [[bronchoconstriction]], and [[hypoperfusion]] of vital organs. <ref name="pmid29489197">{{cite journal| author=| title=StatPearls | journal= | year= 2021 | volume=  | issue=  | pages=  | pmid=29489197 | doi= | pmc= | url= }} </ref>


Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
Specifically, [[histamine]] causes [[vasodilation]] and increased [[heart rate]] and permeability which ultimately leads to the [[hypoperfusion]] of various tissues. [[Prostaglandin]] D2 causes [[bronchoconstriction]] of both [[cardiac]] and [[pulmonary]] systems culminating in peripheral [[vasodilation]] and further [[hypoperfusion]] of [[tissues]]. [[Leukotrienes]] and [[platelet activation factor]] also contribute to [[vascular permeability]], along with [[bronchoconstriction]] and [[airway]] remodeling. Finally, [[TNF-alpha]] activate [[Neutrophil|neutrophils]] which increases the synthesis of [[Chemokine|chemokines]]. <ref name="pmid18596587">{{cite journal| author=Peavy RD, Metcalfe DD| title=Understanding the mechanisms of anaphylaxis. | journal=Curr Opin Allergy Clin Immunol | year= 2008 | volume= 8 | issue= 4 | pages= 310-5 | pmid=18596587 | doi=10.1097/ACI.0b013e3283036a90 | pmc=2683407 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18596587  }} </ref> <ref name="pmid29489197">{{cite journal| author=| title=StatPearls | journal= | year= 2021 | volume=  | issue=  | pages=  | pmid=29489197 | doi= | pmc= | url= }} </ref>


OR
[[Anaphylaxis]] can be divided into [[IgE]]-dependent and [[IgE]]-independent mechanisms. [[IgE]] levels are higher in those patients that have [[allergies]]. Once [[IgE]] binds to [[FcεRI]] on [[mast cells]] and [[basophils]] this releases [[histamine]] and other [[inflammatory mediators]]. On repeat exposure to the [[antigen]], these [[IgE]] aggregates lead to [[anaphylaxis]]. <ref name="pmid17438574">{{cite journal| author=Kraft S, Kinet JP| title=New developments in FcepsilonRI regulation, function and inhibition. | journal=Nat Rev Immunol | year= 2007 | volume= 7 | issue= 5 | pages= 365-78 | pmid=17438574 | doi=10.1038/nri2072 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17438574  }} </ref> [[IgE]] levels are even used during the diagnosis of [[allergies]] to determine what [[Allergen|allergens]] a patient is susceptible to. <ref name="pmid20066506">{{cite journal| author=Hamilton RG, MacGlashan DW, Saini SS| title=IgE antibody-specific activity in human allergic disease. | journal=Immunol Res | year= 2010 | volume= 47 | issue= 1-3 | pages= 273-84 | pmid=20066506 | doi=10.1007/s12026-009-8160-3 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20066506  }} </ref> Meanwhile, in [[IgE]]-independent reactions, [[IgG]] mechanisms were also found to lead to [[anaphylaxis]], which has largely been studied in mice. A single episode of [[anaphylaxis]] may also be caused by simultaneous [[IgG]] and [[IgE]]-mediated pathways. <ref name="pmid27130857">{{cite journal| author=Finkelman FD, Khodoun MV, Strait R| title=Human IgE-independent systemic anaphylaxis. | journal=J Allergy Clin Immunol | year= 2016 | volume= 137 | issue= 6 | pages= 1674-1680 | pmid=27130857 | doi=10.1016/j.jaci.2016.02.015 | pmc=7607869 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27130857  }} </ref>


==Genetics==
[[Genes]] involved in the pathogenesis of [[anaphylaxis]] include:<ref name="pmid28780941">{{cite journal| author=Reber LL, Hernandez JD, Galli SJ| title=The pathophysiology of anaphylaxis. | journal=J Allergy Clin Immunol | year= 2017 | volume= 140 | issue= 2 | pages= 335-348 | pmid=28780941 | doi=10.1016/j.jaci.2017.06.003 | pmc=5657389 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28780941  }} </ref> <ref name="pmid18538381">{{cite journal| author=Apter AJ, Schelleman H, Walker A, Addya K, Rebbeck T| title=Clinical and genetic risk factors of self-reported penicillin allergy. | journal=J Allergy Clin Immunol | year= 2008 | volume= 122 | issue= 1 | pages= 152-8 | pmid=18538381 | doi=10.1016/j.jaci.2008.03.037 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18538381  }} </ref> <ref name="pmid15731584">{{cite journal| author=Brown RH, Hamilton RG, Mintz M, Jedlicka AE, Scott AL, Kleeberger SR| title=Genetic predisposition to latex allergy: role of interleukin 13 and interleukin 18. | journal=Anesthesiology | year= 2005 | volume= 102 | issue= 3 | pages= 496-502 | pmid=15731584 | doi=10.1097/00000542-200503000-00004 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15731584  }} </ref> <ref name="pmid20413984">{{cite journal| author=Niedoszytko M, Ratajska M, Chełmińska M, Makowiecki M, Malek E, Siemińska A | display-authors=etal| title=The angiotensinogen AGT p.M235T gene polymorphism may be responsible for the development of severe anaphylactic reactions to insect venom allergens. | journal=Int Arch Allergy Immunol | year= 2010 | volume= 153 | issue= 2 | pages= 166-72 | pmid=20413984 | doi=10.1159/000312634 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20413984  }} </ref> <ref name="pmid18207562">{{cite journal| author=Summers CW, Pumphrey RS, Woods CN, McDowell G, Pemberton PW, Arkwright PD| title=Factors predicting anaphylaxis to peanuts and tree nuts in patients referred to a specialist center. | journal=J Allergy Clin Immunol | year= 2008 | volume= 121 | issue= 3 | pages= 632-638.e2 | pmid=18207562 | doi=10.1016/j.jaci.2007.12.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18207562  }} </ref> <ref name="pmid7479840">{{cite journal| author=Nagata H, Worobec AS, Oh CK, Chowdhury BA, Tannenbaum S, Suzuki Y | display-authors=etal| title=Identification of a point mutation in the catalytic domain of the protooncogene c-kit in peripheral blood mononuclear cells of patients who have mastocytosis with an associated hematologic disorder. | journal=Proc Natl Acad Sci U S A | year= 1995 | volume= 92 | issue= 23 | pages= 10560-4 | pmid=7479840 | doi=10.1073/pnas.92.23.10560 | pmc=40651 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7479840  }} </ref> <ref name="pmid28351784">{{cite journal| author=Gülen T, Ljung C, Nilsson G, Akin C| title=Risk Factor Analysis of Anaphylactic Reactions in Patients With Systemic Mastocytosis. | journal=J Allergy Clin Immunol Pract | year= 2017 | volume= 5 | issue= 5 | pages= 1248-1255 | pmid=28351784 | doi=10.1016/j.jaip.2017.02.008 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28351784  }} </ref> <ref name="pmid16892779">{{cite journal| author=Webb LM, Lieberman P| title=Anaphylaxis: a review of 601 cases. | journal=Ann Allergy Asthma Immunol | year= 2006 | volume= 97 | issue= 1 | pages= 39-43 | pmid=16892779 | doi=10.1016/S1081-1206(10)61367-1 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16892779  }} </ref> <ref name="pmid22335765">{{cite journal| author=Worm M, Edenharter G, Ruëff F, Scherer K, Pföhler C, Mahler V | display-authors=etal| title=Symptom profile and risk factors of anaphylaxis in Central Europe. | journal=Allergy | year= 2012 | volume= 67 | issue= 5 | pages= 691-8 | pmid=22335765 | doi=10.1111/j.1398-9995.2012.02795.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22335765  }} </ref>


[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
*[[Polymorphisms]] in [[IL-10]], [[IL-13]], [[IL-4Rα]] are linked to [[anaphylaxis]] to [[drugs]] and [[latex]].
*[[PAF-AH]] activity levels are correlated inversely with the severity of [[anaphylaxis]].
*Variations in [[angiotensinogen]] MM [[genotype]] with low levels of [[angiotensin]] are linked with high rates of [[hymenoptera]] [[venom allergy]].
*Patients with [[peanut]] [[allergies]] and low serum [[ACE]] levels are linked with high rates of [[pharyngeal edema]].
*Activating [[mutation]] in [[c-KIT]] and [[D816V]] are associated with [[mastocytosis]] and [[hyperresponsivity]] of their [[mast cells]] with resulting increasing [[severity]] of [[anaphylaxis]] rates.
*[[Anaphylaxis]] occurs more commonly in [[women]], though the mechanism is not clear.


OR
==Associated Conditions==
Conditions associated with [[anaphylaxis]] include the following and are associated with [[poor prognosis]]: <ref name="pmidhttps://doi.org/10.1186/s13223-018-0283-4">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=https://doi.org/10.1186/s13223-018-0283-4 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10  }} </ref> <ref name="pmid23453138">{{cite journal| author=Lee S, Hess EP, Nestler DM, Bellamkonda Athmaram VR, Bellolio MF, Decker WW | display-authors=etal| title=Antihypertensive medication use is associated with increased organ system involvement and hospitalization in emergency department patients with anaphylaxis. | journal=J Allergy Clin Immunol | year= 2013 | volume= 131 | issue= 4 | pages= 1103-8 | pmid=23453138 | doi=10.1016/j.jaci.2013.01.011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23453138  }} </ref>


The progression to [disease name] usually involves the [molecular pathway].
*[[Asthma]]
*[[Cardiovascular disease]]
*[[Antihypertensive drug|Antihypertensive]] medication use


OR
==Gross Pathology==


The pathophysiology of [disease/malignancy] depends on the histological subtype.
On gross [[pathology]], [[basophil]] and [[mast cell]] [[degranulation]] are characteristic findings of [[anaphylaxis]]. <ref name="pmid29489197">{{cite journal| author=| title=StatPearls | journal= | year= 2021 | volume=  | issue=  | pages=  | pmid=29489197 | doi= | pmc= | url= }} </ref>


==Pathophysiology==
==Microscopic Pathology==
On microscopic [[Histopathology|histopathological]] analysis, [[upper airway]]<nowiki/>s showing [[eosinophils]] due to [[edema]] are characteristic findings of [[anaphylaxis]]. [[Tissue]] sections can also show [[tryptase]], which is an [[enzyme]] specific to [[Mast cell|mast cells]]. <ref name="pmidhttps://doi.org/10.1007/s12024-016-9799-4">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=https://doi.org/10.1007/s12024-016-9799-4 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10  }} </ref>


Anaphylactic shock, the most severe type of anaphylaxis, occurs when an allergic response triggers a quick release from [[mast cell]]s of large quantities of [[immunology|immunological]] mediators ([[histamine]]s, [[prostaglandin]]s, [[leukotriene]]s) leading to systemic [[vasodilation]] (associated with a sudden drop in blood pressure) and [[edema]] of [[bronchial]] [[mucosa]] (resulting in [[bronchoconstriction]] and difficulty breathing).  Anaphylactic shock can lead to death in a matter of minutes if left untreated.
==References==
{{Reflist|2}}


Researchers typically distinguish between true anaphylaxis and pseudo-anaphylaxis.  The symptoms, treatment, and risk of death are identical, but "true" anaphylaxis is always caused directly by [[degranulation]] of [[mast cell]]s or basophils that is mediated by [[immunoglobulin]] E (IgE), and pseudo-anaphylaxis occurs due to all other causes.  The distinction is only important for researchers who are studying mechanisms of allergic reactions. Due to the word "pseudo", it may frustrate patients who feel they are being told that a life-threatening allergic reaction isn't "real".
{{WH}}
{{WS}}
[[Category: (name of the system)]]


==References==
==References==

Latest revision as of 09:47, 15 April 2021

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Dushka Riaz, MD

Overview

The progression to anaphylaxis usually involves an IgE-mediated or non IgE-mediated response. It is a medical emergency that involves multiple systems. [1] The condition involves pulmonary, gastrointestinal, cardiovascular and integumentary systems and can lead to cardiorespiratory arrest. [2]

Pathophysiology

Anaphylaxis is usually caused by food, particularly peanuts, drugs, and insect venoms. [3] [4] There have also been cases of idiopathic anaphylaxis. [5] [6] Anaphylaxis arises from mast cell and basophil degranulation after repeated exposure to an antigen. This results in a type 1 hypersensitivity reaction. The IgE then crosslinks and aggregates with receptors resulting in the release of histamine, proteoglycans, and tryptase. This results in arachidonic acid metabolites being released with further consequences. The reaction as a whole leads to vasodilation, increase heart rate, bronchoconstriction, and hypoperfusion of vital organs. [1]

Specifically, histamine causes vasodilation and increased heart rate and permeability which ultimately leads to the hypoperfusion of various tissues. Prostaglandin D2 causes bronchoconstriction of both cardiac and pulmonary systems culminating in peripheral vasodilation and further hypoperfusion of tissues. Leukotrienes and platelet activation factor also contribute to vascular permeability, along with bronchoconstriction and airway remodeling. Finally, TNF-alpha activate neutrophils which increases the synthesis of chemokines. [7] [1]

Anaphylaxis can be divided into IgE-dependent and IgE-independent mechanisms. IgE levels are higher in those patients that have allergies. Once IgE binds to FcεRI on mast cells and basophils this releases histamine and other inflammatory mediators. On repeat exposure to the antigen, these IgE aggregates lead to anaphylaxis. [8] IgE levels are even used during the diagnosis of allergies to determine what allergens a patient is susceptible to. [9] Meanwhile, in IgE-independent reactions, IgG mechanisms were also found to lead to anaphylaxis, which has largely been studied in mice. A single episode of anaphylaxis may also be caused by simultaneous IgG and IgE-mediated pathways. [10]

Genetics

Genes involved in the pathogenesis of anaphylaxis include:[11] [12] [13] [14] [15] [16] [17] [18] [19]

Associated Conditions

Conditions associated with anaphylaxis include the following and are associated with poor prognosis: [20] [21]

Gross Pathology

On gross pathology, basophil and mast cell degranulation are characteristic findings of anaphylaxis. [1]

Microscopic Pathology

On microscopic histopathological analysis, upper airways showing eosinophils due to edema are characteristic findings of anaphylaxis. Tissue sections can also show tryptase, which is an enzyme specific to mast cells. [22]

References

  1. ↑ 1.0 1.1 1.2 1.3 "StatPearls". 2021. PMID 29489197.
  2. ↑ LoVerde D, Iweala OI, Eginli A, Krishnaswamy G (2018). "Anaphylaxis". Chest. 153 (2): 528–543. doi:10.1016/j.chest.2017.07.033. PMC 6026262. PMID 28800865.
  3. ↑ Sampson HA, Muñoz-Furlong A, Bock SA, Schmitt C, Bass R, Chowdhury BA; et al. (2005). "Symposium on the definition and management of anaphylaxis: summary report". J Allergy Clin Immunol. 115 (3): 584–91. doi:10.1016/j.jaci.2005.01.009. PMID 15753908.
  4. ↑ Kemp SF, Lockey RF (2002). "Anaphylaxis: a review of causes and mechanisms". J Allergy Clin Immunol. 110 (3): 341–8. doi:10.1067/mai.2002.126811. PMID 12209078.
  5. ↑ Lenchner K, Grammer LC (2003). "A current review of idiopathic anaphylaxis". Curr Opin Allergy Clin Immunol. 3 (4): 305–11. doi:10.1097/00130832-200308000-00012. PMID 12865776.
  6. ↑ Ring J, Darsow U (2002). "Idiopathic anaphylaxis". Curr Allergy Asthma Rep. 2 (1): 40–5. doi:10.1007/s11882-002-0036-8. PMID 11895624.
  7. ↑ Peavy RD, Metcalfe DD (2008). "Understanding the mechanisms of anaphylaxis". Curr Opin Allergy Clin Immunol. 8 (4): 310–5. doi:10.1097/ACI.0b013e3283036a90. PMC 2683407. PMID 18596587.
  8. ↑ Kraft S, Kinet JP (2007). "New developments in FcepsilonRI regulation, function and inhibition". Nat Rev Immunol. 7 (5): 365–78. doi:10.1038/nri2072. PMID 17438574.
  9. ↑ Hamilton RG, MacGlashan DW, Saini SS (2010). "IgE antibody-specific activity in human allergic disease". Immunol Res. 47 (1–3): 273–84. doi:10.1007/s12026-009-8160-3. PMID 20066506.
  10. ↑ Finkelman FD, Khodoun MV, Strait R (2016). "Human IgE-independent systemic anaphylaxis". J Allergy Clin Immunol. 137 (6): 1674–1680. doi:10.1016/j.jaci.2016.02.015. PMC 7607869 Check |pmc= value (help). PMID 27130857.
  11. ↑ Reber LL, Hernandez JD, Galli SJ (2017). "The pathophysiology of anaphylaxis". J Allergy Clin Immunol. 140 (2): 335–348. doi:10.1016/j.jaci.2017.06.003. PMC 5657389. PMID 28780941.
  12. ↑ Apter AJ, Schelleman H, Walker A, Addya K, Rebbeck T (2008). "Clinical and genetic risk factors of self-reported penicillin allergy". J Allergy Clin Immunol. 122 (1): 152–8. doi:10.1016/j.jaci.2008.03.037. PMID 18538381.
  13. ↑ Brown RH, Hamilton RG, Mintz M, Jedlicka AE, Scott AL, Kleeberger SR (2005). "Genetic predisposition to latex allergy: role of interleukin 13 and interleukin 18". Anesthesiology. 102 (3): 496–502. doi:10.1097/00000542-200503000-00004. PMID 15731584.
  14. ↑ Niedoszytko M, Ratajska M, Chełmińska M, Makowiecki M, Malek E, Siemińska A; et al. (2010). "The angiotensinogen AGT p.M235T gene polymorphism may be responsible for the development of severe anaphylactic reactions to insect venom allergens". Int Arch Allergy Immunol. 153 (2): 166–72. doi:10.1159/000312634. PMID 20413984.
  15. ↑ Summers CW, Pumphrey RS, Woods CN, McDowell G, Pemberton PW, Arkwright PD (2008). "Factors predicting anaphylaxis to peanuts and tree nuts in patients referred to a specialist center". J Allergy Clin Immunol. 121 (3): 632–638.e2. doi:10.1016/j.jaci.2007.12.003. PMID 18207562.
  16. ↑ Nagata H, Worobec AS, Oh CK, Chowdhury BA, Tannenbaum S, Suzuki Y; et al. (1995). "Identification of a point mutation in the catalytic domain of the protooncogene c-kit in peripheral blood mononuclear cells of patients who have mastocytosis with an associated hematologic disorder". Proc Natl Acad Sci U S A. 92 (23): 10560–4. doi:10.1073/pnas.92.23.10560. PMC 40651. PMID 7479840.
  17. ↑ Gülen T, Ljung C, Nilsson G, Akin C (2017). "Risk Factor Analysis of Anaphylactic Reactions in Patients With Systemic Mastocytosis". J Allergy Clin Immunol Pract. 5 (5): 1248–1255. doi:10.1016/j.jaip.2017.02.008. PMID 28351784.
  18. ↑ Webb LM, Lieberman P (2006). "Anaphylaxis: a review of 601 cases". Ann Allergy Asthma Immunol. 97 (1): 39–43. doi:10.1016/S1081-1206(10)61367-1. PMID 16892779.
  19. ↑ Worm M, Edenharter G, Ruëff F, Scherer K, Pföhler C, Mahler V; et al. (2012). "Symptom profile and risk factors of anaphylaxis in Central Europe". Allergy. 67 (5): 691–8. doi:10.1111/j.1398-9995.2012.02795.x. PMID 22335765.
  20. ↑ Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID https://doi.org/10.1186/s13223-018-0283-4 Check |pmid= value (help).
  21. ↑ Lee S, Hess EP, Nestler DM, Bellamkonda Athmaram VR, Bellolio MF, Decker WW; et al. (2013). "Antihypertensive medication use is associated with increased organ system involvement and hospitalization in emergency department patients with anaphylaxis". J Allergy Clin Immunol. 131 (4): 1103–8. doi:10.1016/j.jaci.2013.01.011. PMID 23453138.
  22. ↑ Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID https://doi.org/10.1007/s12024-016-9799-4 Check |pmid= value (help).

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References

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