Quantification of human C1 esterase inhibitor protein using an automated turbidimetric immunoassay.
AAE
HAE
C1 inactivator
C1 inhibitor
C1-INH
Optilite
angioedema
complement
turbidimetric
Journal
Journal of clinical laboratory analysis
ISSN: 1098-2825
Titre abrégé: J Clin Lab Anal
Pays: United States
ID NLM: 8801384
Informations de publication
Date de publication:
Jan 2019
Jan 2019
Historique:
received:
29
05
2018
revised:
02
07
2018
accepted:
03
07
2018
pubmed:
31
7
2018
medline:
16
2
2019
entrez:
31
7
2018
Statut:
ppublish
Résumé
Impaired levels or function of C1 inhibitor (C1-INH) results in angioedema due to increased bradykinin. It is important to distinguish between angioedema related to C1-INH deficiency and that caused by other mechanisms, as treatment options are different. In hereditary (HAE) and acquired (AAE) angioedema, C1-INH concentration is measured to aid patient diagnosis. Here, we describe an automated turbidimetric assay to measure C1-INH concentration on the Optilite Linearity, precision, and interference were established over a range of C1-INH concentrations. The 95th percentile reference interval was generated from 120 healthy adult donors. To compare the Optilite C1-INH assay with a predicate assay used in a clinical laboratory, samples sent for C1-INH investigation were used. The predicate results were provided to allow comparison. The Optilite C1-INH assay was linear across the measuring range at the standard sample dilution. Intra and interassay variability was <6%. The 95th percentile adult reference interval for the assay was 0.21-0.38 g/L. There was a strong correlation between the Optilite concentrations and those generated with the predicate assay (R The Optilite assay allows the automated and precise quantification of C1-INH concentrations in patient samples. It could therefore be used as a tool to aid the investigation of patients with angioedema.
Sections du résumé
BACKGROUND
BACKGROUND
Impaired levels or function of C1 inhibitor (C1-INH) results in angioedema due to increased bradykinin. It is important to distinguish between angioedema related to C1-INH deficiency and that caused by other mechanisms, as treatment options are different. In hereditary (HAE) and acquired (AAE) angioedema, C1-INH concentration is measured to aid patient diagnosis. Here, we describe an automated turbidimetric assay to measure C1-INH concentration on the Optilite
METHODS
METHODS
Linearity, precision, and interference were established over a range of C1-INH concentrations. The 95th percentile reference interval was generated from 120 healthy adult donors. To compare the Optilite C1-INH assay with a predicate assay used in a clinical laboratory, samples sent for C1-INH investigation were used. The predicate results were provided to allow comparison.
RESULTS
RESULTS
The Optilite C1-INH assay was linear across the measuring range at the standard sample dilution. Intra and interassay variability was <6%. The 95th percentile adult reference interval for the assay was 0.21-0.38 g/L. There was a strong correlation between the Optilite concentrations and those generated with the predicate assay (R
CONCLUSION
CONCLUSIONS
The Optilite assay allows the automated and precise quantification of C1-INH concentrations in patient samples. It could therefore be used as a tool to aid the investigation of patients with angioedema.
Identifiants
pubmed: 30058083
doi: 10.1002/jcla.22627
pmc: PMC6430339
doi:
Substances chimiques
Complement C1 Inhibitor Protein
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e22627Informations de copyright
© 2018 The Authors Journal of Clinical Laboratory Analysis Published by Wiley Periodicals, Inc.
Références
World J Gastroenterol. 2010 Oct 21;16(39):4913-21
pubmed: 20954277
Clin Exp Immunol. 2007 Sep;149(3):513-6
pubmed: 17614974
Ann Intern Med. 1976 May;84(5):580-93
pubmed: 1275365
Dtsch Arztebl Int. 2010 Jun;107(23):408-14
pubmed: 20589206
Clin Exp Immunol. 2005 Mar;139(3):379-94
pubmed: 15730382
Allergy Asthma Clin Immunol. 2010 Jul 28;6(1):15
pubmed: 20667118
Clin Exp Immunol. 2014 Jan;175(1):59-67
pubmed: 23786259
J Clin Lab Anal. 2019 Jan;33(1):e22627
pubmed: 30058083
J Clin Pathol. 2002 Feb;55(2):145-7
pubmed: 11865013
Int J Emerg Med. 2017 Dec;10(1):15
pubmed: 28405953
Am J Gastroenterol. 2006 Mar;101(3):619-27
pubmed: 16464219
J Allergy Clin Immunol. 2002 Feb;109(2):195-209
pubmed: 11842287
N Engl J Med. 2002 Aug 22;347(8):621-2
pubmed: 12192030
J Allergy Clin Immunol Pract. 2017 Sep - Oct;5(5):1307-1313
pubmed: 28284781
Allergy Asthma Clin Immunol. 2010 Jul 28;6(1):14
pubmed: 20667117
J Allergy Clin Immunol. 2012 Sep;130(3):692-7
pubmed: 22841766
Allergy Asthma Clin Immunol. 2007 Mar 15;3(1):24-30
pubmed: 20525150
Br J Dermatol. 2009 Nov;161(5):1153-8
pubmed: 19709101
Int Arch Allergy Immunol. 2014;165(2):119-27
pubmed: 25401373
J Investig Allergol Clin Immunol. 2011;21(5):333-47; quiz follow 347
pubmed: 21905496
Lancet. 2012 Feb 4;379(9814):474-81
pubmed: 22305226
Allergy. 2014 May;69(5):602-16
pubmed: 24673465
Am J Manag Care. 2013 Jun;19(7 Suppl):s103-10
pubmed: 23844782
J Clin Invest. 1964 Nov;43:2204-13
pubmed: 14223932
Eur Ann Allergy Clin Immunol. 2013 Feb;45(1):7-16
pubmed: 23678554
J Clin Pathol. 2004 Feb;57(2):213-4
pubmed: 14747456
Ann Allergy Asthma Immunol. 2005 Apr;94(4):498-503
pubmed: 15875532
Medicine (Baltimore). 1992 Jul;71(4):206-15
pubmed: 1518394
Otolaryngol Head Neck Surg. 1999 Sep;121(3):263-8
pubmed: 10471868
Lancet. 1998 Jun 6;351(9117):1693-7
pubmed: 9734886
N Engl J Med. 2008 Sep 4;359(10):1027-36
pubmed: 18768946