MicroVue™ C1-Inhibitor Plus EIA

The MicroVue C1-lnhibitor EIA measures the amount of functional C1-lnhibitor protein in human plasma or serum.


Product Specifications

Citations 13
Specimen

Serum/EDTA Plasma 10 μL

LLOQ N/A
ULOQ N/A
Assay Time 2 hours
Cross Reactivity

Baboon, Rhesus monkey

Ordering Information

For In Vitro Diagnostic Use.
Catalog Number A037
Catalog Number (CE)  
Size 96 wells/test
Price (USD) $725.00
Price (EURO) 640,00 €

Contact us

US Phone+1 (858) 552 1100
EU Phone+353 (91) 412 474
US Emailcontact-us@quidelortho.com
EU Emailcontact-emea@quidelortho.com

Specifications

Description

The MicroVue C1-lnhibitor EIA measures the amount of functional C1-lnhibitor protein in human plasma or serum.

Size 96 wells/test
Form

96 well plate with 12 eight-well strips in a resealable foil pouch

Specimen Serum/EDTA Plasma 10 μL
Limit of Detection (LOD) N/A
Lower Limit of Quantitation (LLOQ) N/A
Upper Limit of Quantitation (ULOQ) N/A
Intra Assay 3.3–5.4%
Inter Assay 5.7–10%
Standards 5
Controls 2
Sample Values

Normal ≥ 68% mean normal, Equivocal 41–67% mean normal, Abnormal ≤40% mean normal

Assay Time 2 hours
Cross Reactivity

Baboon, Rhesus monkey

Storage

Store the unopened kit at 2°C to 8°C. Refer to Product Insert for additional storage details.

Background

C1-lnhibitor (C1-INH) is a multispecific, protease inhibitor that is present in normal human plasma and serum and that regulates enzymes of the complement, coagulation, fibrinolytic, and kinin-forming systems. The enzymes (proteases) regulated by this protein include the C1r and C1s subunits of the activated first component of complement, activated Hageman factor (factor XIIa), Hageman factor fragments, activated plasma thromboplastin antecedent (PTA or factor XIa), kallikrein (Fletcher factor) and plasmin.2 A deficiency of functionally active C1-INH may lead to life-threatening angioedema. Two major forms of C1-INH deficiency have been reported: the congenital form, termed hereditary angioedema (HAE) and the acquired form, which is associated with a variety of diseases, including lymphoid malignancies. Hereditary angioedema is characterized by transient but recurrent attacks of nonpruritic swelling of various tissues throughout the body. The symptomatology depends upon the organs involved. Intestinal attacks lead to a diversity of symptoms including pain, cramps, vomiting, and diarrhea. The most frequent cause of death in this disease is airway obstruction secondary to laryngeal edema occurring during an attack. There are two types of hereditary angioedema that can be distinguished biochemically. Patients with the more common type (85% of HAE patients) have low levels of functional C1-INH and C1-INH antigen. Patients with the second form (15% of HAE patients) have low levels of functional C1-INH but normal or increased levels of C1-INH antigen, which is associated with a dysfunctional protein. The variable nature of the symptoms at different time-periods during the course of the disease precludes definitive diagnosis based solely on clinical observation. Hereditary or acquired angioedema can only be definitively diagnosed by laboratory tests demonstrating a marked reduction in functional C1-INH levels in a patient’s plasma or serum. Several methods have been reported to measure C1-INH functional or antigenic levels. These methods include enzyme inhibition assays, radial immunodiffusion, immunoelectrophoresis, and inhibition of immune hemolysis. Each of these methods has disadvantages. The enzyme inhibition assay are difficult to set up and conduct on a routine basis, the immunochemical methods which measure total antigen cannot distinguish between functional and nonfunctional C1-INH protein, and the anti-C1r immunodiffusion method, which was developed to measure functional C1-INH activity, is not quantitative. The MicroVue assay is able to measure quantitatively the level of functionally active C1-INH protein present in a patient’s plasma or serum by utilizing a convenient, standardized and reproducible EIA procedure.

Citations

Title Year Applications Sample Species Sample Sample Details

Pharmacokinetics of human recombinant C1-esterase inhibitor and development of anti-drug antibodies in healthy dogs.

2018

ELISA

Canine

Serum

P-I snake venom metalloproteinase is able to activate the complement system by direct cleavage of central components of the cascade.

2013

ELISA

Human

Serum

Bothrops pirajai venom

The role of complement components C1q, MBL and C1 inhibitor in pathogenesis of endometriosis.

2018

ELISA

Human

Peritoneal fluid

Endometriosis

Secreted Phospholipases A2 in Hereditary Angioedema With C1-Inhibitor Deficiency.

2018

ELISA

Human

Plasma

Hereditary Angioedema

Complement C3 and C4, but not their regulators or activated products, are associated with incident metabolic syndrome: the CODAM study.

2018

ELISA

Human

Plasma

Cardiometabolic disease increased risk

Complement levels at admission as a reflection of coronavirus disease 2019 (COVID-19) severity state.

2021

ELISA

Human

Serum

COVID-19

Thromboinflammation Supports Complement Activation in Cancer Patients With COVID-19.

2021

ELISA

Human

Plasma

Cancer, COVID-19

Thromboinflammation Supports Complement Activation in Cancer Patients With COVID-19.

2021

ELISA

Human

Plasma

COVID-19

Depressed activation of the lectin pathway of complement in hereditary angioedema

2008

ELISA

Human

Serum

Hereditary Angioedema

Assessment of endothelium and inflammatory response at the onset of reperfusion injury in hand surgery

2012

ELISA

Human

Serum

A Nationwide Study of Norwegian Patients with Hereditary Angioedema with C1 Inhibitor Deficiency Identified Six Novel Mutations in SERPING1

2015

ELISA

Human

Serum

Hereditary Angioedema

Neutrophil activation during attacks in patients with hereditary angioedema due to C1-inhibitor deficiency

2015

ELISA

Human

Plasma

Venom from Bothrops lanceolatus, a Snake Species Native to Martinique, Potently Activates the Complement System

2018

ELISA

Human

Serum

B. lanceolatus venom