Archive for the ‘Tips’ Category

C-reactive protein (CRP) ELISA kit | Lipoprotein(a) [Lp(a)] ELISA kit | Digoxin ELISA Kit

Cardiac Makers Elisa Kits

At DIAGNOSTIC AUTOMATION Inc.   (focusing on ELISA Kits) we take advantage of an influx of new technologies and information incorporating them into novel tests which enables us to offer innovative diagnostic tests every day.  In addition to our 3 in 1 CARDIAC MARKERS TEST (cardiac elisa kits: Troponin I elisa kit, CK-MB elisa kit, myoglobin elisa kit)

http://rapidtest.com/blog/3-in-1-cardiac-markers-rapid-test-troponin-ckmb-myoglobin

Los Angeles-based Diagnostic Automation Inc. is pleased to offer three additional tests in forms of cardiac elisa kits (Cardiac Markers Rapid Tests) to customers around the world available in cassette format. These elisa kit tests are immunochromatography assays for the determination of three biochemical markers: C-reactive protein (CRP) ELISA kit, Lp(a) elisa kit,  and Digoxin ELISA Kit,  simultaneously in human serum or whole blood.

 

1. C-reactive protein (CRP) ELISA kit 

C-reactive protein (CRP): CPR is composed of five protein subunits, produced by the liver and found in blood that plays a key role in the innate immune response.  The gene for this protein is on chromosome 1q21-q23[1].  CRP is a marker for inflammation within the body and has been promoted as a screening test for coronary artery disease [2].  Studies show that elevated levels of CRP are associated with a greater risk of psychological stress and clinical depression.  Elevated levels of CRP may be indicative of elevated levels of certain cytokines, which can increase feelings of stress or depression. On the other hand, it is possible that depression or stress is a cause of elevated level of CRP.  Irrespective of other factors, the study found that healthy people with CRP level above 3mg/liter had two to three fold increased risk of developing depression [3].

Model of C-reactive protein molecular structure [1]

Diagnostic applications: Role in cardiovascular disease

Strong evidence indicates that patients with elevated basal levels of CRP are at an increased risk of hypertension, heart diseases, and diabetes.  C-reactive protein (CRP) is proposed as a screening test for predicting risk and guiding preventive approaches in cardiac diseases [4].  Normal concentration in healthy human serum is usually lower than 10 mg/L, slightly increasing with aging.  Higher levels are found in late pregnant women, mild inflammation and viral infections (10–40 mg/L), active inflammation, bacterial infection (40–200 mg/L), severe bacterial infections and burns (>200 mg/L).  The half-life of CRP is constant, thus, CRP level is mainly determined by the rate of its production.  A level above 2.4 mg/L has been associated with a doubled risk of a coronary event compared to levels below 1 mg/L.  Inflammation can play an important role in atherosclerosis, the process in which fatty deposits build up in coronary arteries. Interest in CRP originated when studies found that patients with unstable angina or chest pain had high levels of this marker.  Researchers found that CRP could be used to predict who would go on to have a heart attack.  Moreover, in a meta-analysis of 20 studies involving 1,466 patients with coronary artery disease, CRP levels were found to be reduced after exercise interventions.  Among those studies, higher CRP concentrations or poorer lipid profiles before beginning exercise were associated with greater reductions in CRP [5].  Other studies have shown that CRP isn’t a predictor of heart attack risk in people without symptoms of heart disease.

(CRP) ELISA kit: At Diagnostic Automation using elisa kit,  CRP level can be measured with a simple blood test .   There are scientific evidences that by treating people with high CRP levels, their likelihood of developing a heart attack or stroke will decrease.

How can CRP values predict potential heart disease?

According to the American Heart Association (AHA) and the Center for Disease Control (CDC), the following guidelines are recommended for the assessment of cardiovascular risk in regards to CRP levels:

CRP is 1 milligram (mg) per liter or less , Low risk for cardiovascular disease

CRP is between 1 and 3 mg per liter, Moderate risk for cardiovascular disease

CRP greater than 3 mg per liter, High risk for cardiovascular disease

CRP level of greater than 10 mg per liter may be seen in an acute plaque rupture such as, a heart attack or stroke, provided there is no other explanation for the elevated level such as other inflammatory or infectious diseases

The CRP level can provide additional information about an individual’s cardiovascular risk in conjunction with other known cardiac risk factors, such as, diabetes mellitus, high blood pressure, high cholesterol, obesity, age, and smoking.  Some experts recommend checking the serum CRP level routinely along with the cholesterol level.  Ideally, for cardiac risk testing, it is advisable to use the average between 2 separate CRP levels drawn 2 weeks part.  According to the American Heart Association checking the CRP level for the entire adult population is not recommended.

 

2. Lipoprotein(a) [Lp(a)] ELISA kit

Lp(a): Lipoprotein (a), also called Lp(a) is a subclass of Lipoprotein consists of an LDL-like particle and the specific apolipoprotein(a) [apo(a)].  Lp(a) plasma concentrations are highly heritable and mainly controlled by the apolipoprotein(a) gene (LPA) positioned on human chromosome 6q26-27.  The protein encoded by this gene is a serine proteinase that inhibits the activity of tissue-type plasminogen activator.  Proteolytically cleaved portion of this protein results in fragments that attach to atherosclerotic lesions and promote thrombogenesis.  Elevated plasma levels of this protein are linked to atherosclerosis [6].

Diagnostic applications:

A strong correlation between elevated level of Lp(a) and heart disease was confirmed by many studies which led to the consensus that Lp(a) is an important independent predictor of heart disease [7].  Evidence from several studies suggest that elevated plasma Lp(a) increases the cardiac diseases risk associated with more traditional risk factors. The clinical use of Lp(a) measurement is to assess the risk of cardiovascular disease.  We use a an elisa kit to measure this specific type of lipoprotein called lipoprotein-a, or Lp(a) in blood.  Normal values are below 30 mg/dL (milligrams per deciliter).  Normal value ranges may vary slightly among different laboratories.  Higher than normal values of Lp(a) are associated with a high risk for atherosclerosis, stroke, and heart attack.  Substantial increases are secondarily observed in nephrotic syndrome and end-stage renal disease, however environmental factors such as diet, and exercise do not have a major impact on the level of Lp(a).  Although Lp(a) is considered a risk factor for heart disease, but the plasma Lp(a) determinations should be limited to either patients at high risk for the development of cardiac diseases or patients at borderline risk for the development of cardiac diseases in whom uncertainty may exist about how aggressively to treat modifiable risk factors such as elevated LDL and cholesterol [8].  Multiple studies have shown that Aspirin and Niacin (Vitamin B3) in high doses, available by prescription known to significantly reduce the level of Lp(a) in some individual with high Lp(a) level

At Diagnostic Automation Lp(a) level can be measured with a simple blood test using Lp(a) ELISA kit with fast and accurate results in 120 minutes.

Model of Lipoprotein, Lp(a) molecular structure [1]

3. Digoxin elisa Kit

Digoxin: Digoxin is a cardiac glycoside which has different products with significant bioavailability and it is used to treat congestive heart failure, atrial fibrillation and paroxysmal atrial tachycardia [9].  Many drugs interact with digoxin, often requiring an adjustment of the digoxin dose [10].  Digoxin is cleared by the kidney and its clearance is low in premature neonates, increases in full term neonates, reaches a maximum in infants and decreases slowly during childhood and adulthood, with an apparent increase in susceptibility to toxicity with age [11, 12]. The circulating half-life is 1 to 1.6 days in patients with normal renal function.  The myocardial concentrations of digoxin to serum levels remain relatively constant during normal renal function.

This distribution ratio of digoxin is approximately 29 to 1 between the heart and serum. Thus, monitoring digoxin therapy by measurement of serum levels is feasible from the pharmacological standpoint, since serum levels are related to tissue levels following post-absorption equilibration.

Recent study has shown that Digoxin has at least 2-compartment behavior. Its pharmacologic and clinical effects correlate not with serum digoxin concentrations but with those in the peripheral non-serum compartment.  Digoxin improves the strength of myocardial contraction and results in the beneficial effects of increased cardiac output, decreased heart size, decreased venous pressure, and decreased blood volume.

Digoxin therapy also results in stabilized and slowed ventricular pulse rate. These therapeutic effects are produced through a network of direct and indirect interactions upon the myocardium, blood vessels, and the autonomic nervous system.  Moreover, recent study show that Digoxin induces calcium uptake into cells by forming transmembrane calcium channels [13].

Digoxin is well absorbed after oral administration and is widely distributed to tissues, especially the heart, kidney, and liver. A number of factors can alter normal absorption, distribution, and bioavailability of the drug, including naturally occurring enteric bacteria in the bowel, presence of food in the gut, strenuous physical activity, ingestion of quinine or quinidine, and concomitant use of a wide range of drugs. Children generally require higher concentrations of digoxin.

After oral administration, there is an early rise in serum concentration. Equilibration of serum and tissue levels reaches at approximately 6 to 8 hours. For this reason, blood specimens for digoxin analysis should be drawn at least 6 to 8 hours after drug administration.  Digoxin is excreted primarily in the urine. The average elimination half-life is 36 to 40 hours, but may be considerably prolonged in those with renal disease, causing digoxin accumulation and toxicity.

Symptoms of digoxin toxicity often mimic the cardiac arrhythmia’s for which the drug was originally prescribed for example, heart block and heart failure.  Other typical symptoms of toxicity include gastrointestinal effects, including anorexia, nausea, vomiting, abdominal pain and diarrhea, and neuropsychologic symptoms, such as fatigue, malaise, dizziness, clouded or blurred vision, visual and auditory hallucination, paranoid ideation, and depression.

 

 

Model of Digoxin molecular structure [1]

 

Diagnostic applications:

A practical and sensitive method of digoxin quantitation in serum is by Digoxin ELISA kit which we offer at Diagnostic Automation.  When digoxin is first prescribed, it takes about 1 or 2 weeks to stabilize in the blood and in the target organ which is heart.  Digoxin first test should be done at around that time, in order to give an accurate reflection of the blood level and correct dosage of digoxin.  Test performed before this period, may not show the correct levels in the blood.

The age or gender of the person being tested, health history, the method used for the test, and many other factors may affect when and how often a lab test is required. The therapeutic range is 0.8 to 2.0ng/mL for those being treated for heart failure and levels >4.0 ng/mL may be potentially life-threatening.  This range for digoxin has been established over time.  Once the dosage level is determined, digoxin levels are monitored routinely, at a frequency determined by the doctor, to verify correct dosage and if any changes occur in drug source, dosage, or other medications taken at the same time.  Recent studies may help to improve patient selection for digoxin therapy, since Digoxin therapy may improve the prognosis of advanced heart failure patients with atrial fibrillation.  However, no benefit of digoxin was demonstrated for patients in with sinus rhythm [15]

Routine measurement of serum digoxin concentration is probably not necessary in stable patients [16].  Laboratory tests may be done for many reasons. Tests are performed for routine health screenings or if a disease or toxicity is suspected.  Lab tests may be used to determine if a medical condition is improving or worsening.  Lab tests may also be used to measure the success or failure of a medication or treatment plan.  Moreover, Digoxin measurement is necessary in the following situations:

To check if  a patient has reached steady state with a new digoxin dose

Following significant change in renal function

Following addition or discontinuation of a potentially interacting drug

Follow up on signs or symptoms consistent with digoxin toxicity

After introduction of any medication which may affect the levels of digoxin in the blood

After  intestinal or stomach illness which also affect the absorption of digoxin

In patients with any kidney problems, which affect the secretion of digoxin

Patients with cancer or thyroid disease who have altered  levels of digoxin in the blood

In patients undergoing therapy with high biotin doses (>5 mg/day), specimens should be drawn at least 8 hours after the last biotin administration. “Digoxin-like” immunoreactive factors may cause falsely-elevated values in some neonates and patients with advanced liver or renal disease.

 

 

 

References:

1.Thompson D, Pepys MB, Wood SP. The physiological structure of human C-reactive protein and its complex with phosphocholine.  Structure . 1999, 7 (2): 169–77

2. Clearfield MB . C-reactive protein: a new risk assessment tool for cardiovascular disease. The Journal of the American Osteopathic Association. 2005, 105 (9): 409–16.

3. Marie Kim Wium-Andersen, David Dynnes Ørsted, Sune Fallgaard Nielsen, MScEE, Børge Grønne Nordestgaard. Elevated C-Reactive Protein Levels, Psychological Distress, and Depression in 73 131 Individuals.  JAMA Psychiatry. 2013;70(2):176-184.

4. Ridker PM. Clinical application of C-reactive protein for cardiovascular disease detection and prevention. Circulation. 2003;107: 363–369

5. Christopher J.K et al. Effect of six months’ exercise training on C-reactive protein levels in healthy elderly subjects.  J Am Coll Cardiol. 2004;44(12):2411-2413.

6. Mahley RW, Weisgraber KH, Bersot TP. Disorders of lipid metabolism. In: Kronenberg HM, Melmed S, Polonsky KS, Larsen PR, eds. Williams Textbook of Endocrinology .  2008:chap 36, 11th ed. Philadelphia, Pa: Saunders Elsevier;

7. Nordestgaard BG, Chapman MJ, Ray K, et al. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J. 2010;31:2844-2853.

8. Kamstrup PR, Tybjærg-Hansen A, Nordestgaard BG. “Lipoprotein(a) and risk of myocardial infarction–genetic epidemiologic evidence of causality”. Scand. J. Clin. Lab. Invest. 2011, 71 (2): 87–93.

9. Jortani SA, Voldew R Jr: Digoxin and its related endogenous factors. Crit Rev Clin Lab Sci 1997;34:225-274

10. Doherty, J.E. and Kane, J.J: Clinical Pharmacology of Digitalis Glycosides. ANN. REV. MED, 1975. 26: 159

11. Butler, V.P. Assays of Digitalis in blood. PROG. CARDOVASC. DIS., 1972. 14:571

12. Lewis RP. Clinical use of serum digoxin concentrations.  Am J Cardiol 1992; 69:97G-107G

13. Kratz A, Ferraro M, Sluss PM, et al: Case records of the Massachusetts General Hospital: laboratory values. N Engl J Med 2004; 351(15):1549-1563

14. Arispe N, Diaz JC, Simakova O, Pollard HB. Heart failure drug digitoxin induces calcium uptake into cells by forming transmembrane calcium channels. Proc Natl Acad Sci U S A. 2008 19;105(7):2610-5

15. Jelliffe RW. Some comments and suggestions concerning population pharmacokinetic modeling, especially of digoxin, and its relation to clinical therapy. Ther Drug Monit.  2012, 34(4):368-77

16. Jorge E et al. Digoxin in advanced heart failure patients: A question of rhythm . Rev Port Cardiol. 2013;32(4):303-10