As IgM does not cross the placenta, presence of virus
specific IgM in cord blood or neonatal serum is indicative
of congenital infection. IgM levels may be increased
in chronic liver disease, infections, Waldenström’s
macroglobulinemia, and malignant lymphoma. Decreased
levels are observed in immune deficiency states, non-IgM
myeloma, infancy and early childhood lymphoma.
Quantified IgM measurements are useful for the
detection of frequent chronic or acute infections, suspected
immunodeficiency, screening for congenital infections and
can be obtained by using QUANTIA-IgM reagents.
ESTIMATION OF COMPLEMENT C3 IN HUMAN
(Courtesy: Tulip Group of Companies)
Clinically, complement determination helps to detect
whether the complement system has been activated. A
decrease in complement components due to the activation
of complement system or a hereditary deficiency and/
or dysfunction of a complement component is of clinical
significance. C3 is a central component of the complement
system. C3 is the rate-limiting factor for both the alternate
and the classical complement pathways. C3 is often
decreased in active forms of SLE and membranoproliferative
glomerulonephritis. C3 fixation on red cells and on tissue
may result in autoimmune hemolytic disorder or severe
tissue damage. Increased levels of C3 are observed in biliary
obstruction, nephrotic syndrome and during corticosteroid
Information regarding the concentration of C3 can be
obtained by using QUANTIA-C3 reagents.
ESTIMATION OF COMPLEMENT C4 IN HUMAN
(Courtesy: Tulip Group of Companies)
Clinically, complement determination helps to detect
whether the cojmplement system has been activated. A
decrease in complement components due to activation
of complement system or a hereditary deficiency and/or
dysfunction of a complement component is of clinical significance.
C4 is essential for activation of the classical complement
pathway. Most of the conditions, which result in decreased
levels of C3 also, result in decrease of C4. However, in cases
of autoimmune hemolytic anemia (AIHA) and hereditary
angioneurotic edema (HAE), C3 is usually normal while
Information regarding the concentration of C4 can be
obtained by using QUANTIA-C4 reagents.
ESTIMATION OF ANTITHROMBIN III IN
(Courtesy: Tulip Group of Companies)
Antithrombin (AT) formerly referred to as antithrombin
III, a proteinase inhibitor is the most important inhibitor
of the plasma coagulation system. The action of AT III
in presence of heparin is directed against thrombin, Xa
and IX leading to an effective inhibition of coagulation.
Concentration of AT III is useful in differential diagnosis of
congenital AT deficiencies. In type I congenital deficiency,
the AT III concentration is reduced, whereas in type II AT
deficiency the AT III concentration is normal. Estimation of
AT III is useful in diagnosis of disseminated intravascular
coagulation (DIC) and monitoring of the course of
treatment of DIC, monitoring of AT III replacement
therapy and in cases of heparin resistance. Information
regarding the concentration of AT III can be obtained by
using QUANTIA-AT III reagents.
QUANTITATIVE IMMUNOTURBIDIMETRIC
ASSAY FOR ESTIMATION OF FIBRINOGEN
(Courtesy: Tulip Group of Companies)
role in hemostasis. For normal hemostasis to occur
in response to injury or tissue damage, a sufficient
concentration of fibrinogen must be present in plasma.
Low levels of fibrinogen are found in:
¾ Increased fibrinogen consumption due to the prolonged
presence of disseminated intravascular coagulation
¾ Hyperfibrinolysis in patients with neoplasia, acute
promyelocytic leukemias and obstetric complications
such as premature detachment of placenta or abruptio
placentae, amniotic fluid embolism, retention of dead
¾ Dysfibrinogenemia (functionally defective fibrinogen
due to an abnormal molecular form, but the levels
remain normal) found either congenitally or acquired
Studies such as the Framingham study and Northwick
Park Heart Study have demonstrated that an increased
fibrinogen concentration is an independent risk factor for
atherosclerotic diseases, e.g. myocardial infarction or stroke.
Quantia-Fibrinogen is an antigen immunoassay for the
quantitative determination of fibrinogen in human plasma.
ESTIMATION OF LIPOPROTEIN (A) IN HUMAN
(Courtesy: Tulip Group of Companies)
Coronary artery disease (CAD) is emerging as a major
public health problem. Of all the ethnic groups, people
of Indian origin have one of the highest incidences of
Indians at an early stage. The prevalence of premature
Lipoprotein (a) [Lp (a)] is a genetically determined
(a) the distinctive glycoprotein that is homologous
to plasminogen. Lp (a) functions as a dual pathogen
that is highly atherogenic and also prothrombotic. The
Apolipoprotein B-100 part of Lp (a) binds to LDL receptors
and acts as an atherogenic protein. The Apolipoprotein
(a) moiety competes with plasminogen for binding
to fibrinogen and fibrin monomer and thus acts as a
Several studies have demonstrated that Lp (a), is one
of the most powerful and most prevalent independent
risk factors for premature CAD. Early therapeutic
interventions and lifestyle modifications at lower levels
of total cholesterol and LDL cholesterol, particularly in
persons with a family history of premature CAD and in
persons with high Lp (a) levels has been suggested.
The CHD (Coronary heart disease) risk prediction is
high, especially when Lp (a) and LDL concentrations are
elevated simultaneously. Lp (a) elevations have also been
linked to restenosis after angioplasty and progression of
angiographically documented coronary heart disease.
In normolipidemic subjects those with Lp (a) levels
greater than 30 mg/dL may have a risk for myocardial
infarction 1.7 times that of subjects with LP (a) levels below
this level have been documented.
Information regarding the concentration of Lp (a) can
be obtained by using Quantia-Lp (a) reagents.
(Courtesy: Tulip Group of Companies)
The risk of premature atherosclerotic coronary heart
disease (CHD) has direct correlation with plasma
concentration of LDL cholesterol and inverse correlation
with HDL cholesterol. Apolipoprotein A-I (apo A-I) is
the major anti-atherogenic apolipoprotein found in
HDL cholesterol and plays an important role in HDL
metabolism. Apo A-I is an activator of lecithin cholesterol
acyltransferase (LCAT) enzyme present in HDL, which
catalyzes the reaction forming cholesterol esterase (CE).
This CE rich HDL cleans up the cholesterol from peripheral
tissue and transport it to liver [reverse cholesterol
transport (RCT)]. Increased rate of apo A-I production
causes high plasma HDL concentration and may have a
protective effect from premature CAD. Genetic defects
that cause the inability to synthesize apo A-I cause very
low plasma concentrations of HDL-C thereby increasing
the risk of atherosclerotic CHD.
Estimation of apo A-I levels is useful in determining the
cholesterol clearing capacity of the blood in an individual
and thereby predicting the relative risk of CHD. Studies
have demonstrated that in patients with known CAD
on treatment with lipid lowering drugs, levels of apo
A-I and apo B were a significant perdictor for recurrent
cardiovascular events as compared to plasma LDL-C and
TC (Total cholesterol) levels.
Quantia Apo A-I is a turbidimetric immunoassay for
the quantitative determination of apolipoprotein A-I in
(Courtesy: Tulip Group of Companies)
The risk of premature atherosclerotic coronary heart disease
(CHD) has direct correlation with plasma concentration
of LDL cholesterol and inverse correlation with HDL
cholesterol. Apolipoprotein B is a major apolipoprotein of
VLDL and LDL the atherogenic lipoproteins. Apo B helps
in solubilizing the cholesterol within the LDL complex,
which in turn increases the transport capacity of LDL for
subsequent deposition of cholesterol on the arterial wall
thereby promoting heart disease. Only one molecule of
apo B exists per lipoprotein particle. The quantity of apo
B is therefore, a direcct measurement of VLDL and LDL
particles. However, due to wide variations in the amount
of cholesterol in these lipoproteins, measurement of apo
B has better relevance to the concentration of atherogenic
lipoprotein particles than LDL cholesterol or non-HDL
cholestrol levels. Subjects with the greatest risk of mortality
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