Massive release of the histamine-degrading enzyme diamine oxidase during severe anaphylaxis in mastocytosis patients.
anaphylaxis
diamine oxidase
heparin
histamine degradation
mastocytosis
Journal
Allergy
ISSN: 1398-9995
Titre abrégé: Allergy
Pays: Denmark
ID NLM: 7804028
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
15
08
2018
revised:
12
10
2018
accepted:
18
10
2018
pubmed:
13
11
2018
medline:
18
4
2020
entrez:
13
11
2018
Statut:
ppublish
Résumé
Histaminolytic activity mediated by diamine oxidase (DAO) is present in plasma after induction of severe anaphylaxis in rats, guinea pigs, and rabbits. Heparin released during mast cell degranulation in the gastrointestinal tract might liberate DAO from heparin-sensitive storage sites. DAO release during anaphylaxis has not been demonstrated in humans. Plasma DAO, tryptase, and histamine concentrations of four severe anaphylaxis events were determined at multiple serial time points in two patients with systemic mastocytosis. The histamine degradation rates were measured in anaphylaxis samples and in pregnancy sera and plasma with comparable DAO concentrations. Mean DAO (132 ng/mL) and tryptase (304 ng/mL) concentrations increased 187- and 4.0-fold, respectively, over baseline values (DAO 0.7 ng/mL, tryptase 76 ng/mL) during severe anaphylaxis. Under non-anaphylaxis conditions, DAO concentrations were not elevated in 29 mastocytosis patients compared to healthy volunteers and there was no correlation between DAO and tryptase levels in mastocytosis patients. The histamine degradation rate of DAO in plasma from mastocytosis patients during anaphylaxis is severely compromised compared to DAO from pregnancy samples. During severe anaphylaxis in mastocytosis patients, DAO is likely released from heparin-sensitive gastrointestinal storage sites. The measured concentrations can degrade histamine, but DAO activity is compromised compared to pregnancy samples. For accurate histamine measurements during anaphylaxis, DAO inhibition is essential to inhibit further histamine degradation after blood withdrawal. Determination of DAO antigen levels might be of clinical value to improve the diagnosis of mast cell activation.
Sections du résumé
BACKGROUND
Histaminolytic activity mediated by diamine oxidase (DAO) is present in plasma after induction of severe anaphylaxis in rats, guinea pigs, and rabbits. Heparin released during mast cell degranulation in the gastrointestinal tract might liberate DAO from heparin-sensitive storage sites. DAO release during anaphylaxis has not been demonstrated in humans.
METHODS
Plasma DAO, tryptase, and histamine concentrations of four severe anaphylaxis events were determined at multiple serial time points in two patients with systemic mastocytosis. The histamine degradation rates were measured in anaphylaxis samples and in pregnancy sera and plasma with comparable DAO concentrations.
RESULTS
Mean DAO (132 ng/mL) and tryptase (304 ng/mL) concentrations increased 187- and 4.0-fold, respectively, over baseline values (DAO 0.7 ng/mL, tryptase 76 ng/mL) during severe anaphylaxis. Under non-anaphylaxis conditions, DAO concentrations were not elevated in 29 mastocytosis patients compared to healthy volunteers and there was no correlation between DAO and tryptase levels in mastocytosis patients. The histamine degradation rate of DAO in plasma from mastocytosis patients during anaphylaxis is severely compromised compared to DAO from pregnancy samples.
CONCLUSION
During severe anaphylaxis in mastocytosis patients, DAO is likely released from heparin-sensitive gastrointestinal storage sites. The measured concentrations can degrade histamine, but DAO activity is compromised compared to pregnancy samples. For accurate histamine measurements during anaphylaxis, DAO inhibition is essential to inhibit further histamine degradation after blood withdrawal. Determination of DAO antigen levels might be of clinical value to improve the diagnosis of mast cell activation.
Identifiants
pubmed: 30418682
doi: 10.1111/all.13663
pmc: PMC6590243
doi:
Substances chimiques
Histamine
820484N8I3
Amine Oxidase (Copper-Containing)
EC 1.4.3.21
Tryptases
EC 3.4.21.59
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
583-593Informations de copyright
© 2018 The Authors. Allergy Published by John Wiley & Sons Ltd.
Références
Inflamm Res. 1998;47 Suppl 1:S60-1
pubmed: 9561417
Scand J Clin Lab Invest. 1970 Jan;25(1):33-9
pubmed: 4986449
J Clin Invest. 1973 Aug;52(8):1985-93
pubmed: 4198195
Naunyn Schmiedebergs Arch Exp Pathol Pharmakol. 1966 Jan 5;252(4):332-8
pubmed: 4222841
Acta Med Scand. 1966 Nov;180(5):533-6
pubmed: 4958839
N Engl J Med. 1987 Jun 25;316(26):1622-6
pubmed: 3295549
Allergy. 2019 Mar;74(3):583-593
pubmed: 30418682
Clin Biochem. 2017 May;50(7-8):444-451
pubmed: 28041932
Emerg Med Australas. 2018 Jun;30(3):366-374
pubmed: 29094472
J Allergy Clin Immunol. 1988 Sep;82(3 Pt 1):425-32
pubmed: 3170991
Biochem J. 1987 Dec 15;248(3):821-7
pubmed: 2449172
Clin Appl Thromb Hemost. 2008 Jul;14(3):360-4
pubmed: 18160568
J Allergy Clin Immunol. 1988 Oct;82(4):646-54
pubmed: 2459179
Acta Physiol Scand. 1968 Dec;74(4):533-42
pubmed: 4981028
J Allergy Clin Immunol. 2009 Oct;124(4):786-92.e4
pubmed: 19767073
J Allergy Clin Immunol. 2010 Dec;126(6):1099-104.e4
pubmed: 21035176
Am J Obstet Gynecol. 1964 May 15;89:199-203
pubmed: 14144412
Agents Actions. 1988 Apr;23(3-4):361-5
pubmed: 3134804
J Allergy. 1967 Oct;40(4):207-14
pubmed: 4167844
J Physiol. 1929 Jun 7;67(3):256-63
pubmed: 16994028
Int Arch Allergy Immunol. 2002 Jun;128(2):136-41
pubmed: 12065914
Am J Hematol. 2003 May;73(1):18-25
pubmed: 12701115
J Allergy Clin Immunol Pract. 2017 Jan - Feb;5(1):58-62.e5
pubmed: 28065342
Clin Exp Allergy. 2011 Dec;41(12):1777-83
pubmed: 22092437
Int Arch Allergy Immunol. 2013;160(2):192-9
pubmed: 23018683
Allergol Immunopathol (Madr). 2014 Nov-Dec;42(6):544-52
pubmed: 25224360
Clin Chem Lab Med. 2010 May;48(5):701-6
pubmed: 20178448
J Biol Inorg Chem. 2002 Jun;7(6):565-79
pubmed: 12072962
Sci Rep. 2018 Apr 20;8(1):6342
pubmed: 29679053
Immunol Allergy Clin North Am. 2006 Aug;26(3):451-63
pubmed: 16931288
Proc Soc Exp Biol Med. 1961 Jul;107:466-9
pubmed: 13763166
Allergy. 2013 Apr;68(4):417-24
pubmed: 23409940
Int Arch Allergy Appl Immunol. 1971;40(3):340-50
pubmed: 4993764
Proc Soc Exp Biol Med. 1952 Mar;79(3):379-81
pubmed: 14920435
Anesthesiology. 2014 Aug;121(2):272-9
pubmed: 24787350
Br J Anaesth. 1990 Dec;65(6):833-6
pubmed: 2265056
Am J Surg Pathol. 2014 Jun;38(6):832-43
pubmed: 24618605
J Allergy Clin Immunol. 2004 Jul;114(1):3-11; quiz 12
pubmed: 15241337
Gastroenterology. 1988 Dec;95(6):1503-9
pubmed: 3141238
Gastroenterology. 1990 Jun;98(6):1493-501
pubmed: 2110916
J Allergy Clin Immunol. 2014 Dec;134(6):1448-1450.e3
pubmed: 25086867
J Allergy Clin Immunol. 2004 Jun;113(6):1086-92
pubmed: 15208589
Comp Biochem Physiol C Comp Pharmacol. 1980;67C(2):187-90
pubmed: 6108183
Int Arch Allergy Appl Immunol. 1970;39(5-6):449-58
pubmed: 4099443
Q J Exp Physiol Cogn Med Sci. 1967 Jul;52(3):319-30
pubmed: 5182414
Obstet Gynecol. 1972 Mar;39(3):426-30
pubmed: 4623064
Clin Exp Allergy. 2011 Dec;41(12):1660-2
pubmed: 22107141
J Investig Allergol Clin Immunol. 2010;20(6):540-1
pubmed: 21243944
Blood. 2017 Mar 16;129(11):1420-1427
pubmed: 28031180
Blood. 2008 Aug 15;112(4):946-56
pubmed: 18684881
J Physiol. 1930 Dec 4;70(4):349-72
pubmed: 16994147
Nat Genet. 2016 Dec;48(12):1564-1569
pubmed: 27749843
J Physiol. 1961 Apr;156:207-16
pubmed: 13694247
J Allergy Clin Immunol. 1992 Jul;90(1):110-8
pubmed: 1629497
Allergy. 2016 Feb;71(2):135-6
pubmed: 26381421
Inflamm Res. 2000 Apr;49 Suppl 1:S53-4
pubmed: 10864420
J Clin Pathol. 2000 Nov;53(11):858-62
pubmed: 11127270
Biochemistry. 2009 Oct 20;48(41):9810-22
pubmed: 19764817