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Tests
To screen for APC-R associated with venous thromboembolic disorders.

Antinuclear antibodies are associated with rheumatic diseases including Systemic Lupus Erythematous (SLE), mixed connective tissue disease, Sjogren's syndrome, scleroderma, polymyositis, CREST syndrome, and neurologic SLE.


Apolipoprotein A1 (APO A1) has been reported to be a better predictor than HDL cholesterol and triglycerides for Coronary Artery Disease (CAD). Low levels of APO A1 in serum are associated with increased risk of CAD. The measurement of APO A1 may be of value in identifying patients with atherosclerosis. Apolipoprotein B (APO B) has been reported to be a more powerful indicator of CAD than total cholesterol or LDL cholesterol in angiographic CAD and in survivors of myocardial infarction. In some patients with CAD, APO B is elevated even in the presence of normal LDL cholesterol.

BNP is increased in congestive heart failure, left ventricular hypertrophy, acute myocardial infarction, coronary angioplasty, and hypertension. Elevations are also observed in pulmonary hypertension (indicating right ventricular dysfunction), acute lung injury, hypervolemic states, chronic renal failure and cirrhosis. Decreasing levels indicate therapeutic response to anti-hypertensive therapy.

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C-Reactive Protein Cardiac (hs CRP) Useful in predicting risk for cardiovascular disease.


This test determines the subtypes of apoe which will aid in the risk assessment of corornary heart disease (CHD) and hyperlipoproteinemia.

There is a correlation between increased risk of premature heart disease with decreasing size of LDL particles. Ion mobility offers the only direct measurement of lipoprotein particle size and concentration for each lipoprotein from HDL3 to large VLDL.

Cardiolipin antibodies (CA) are seen in a subgroup of patients with autoimmune disorders, particularly systemic lupus erythematosus (SLE), who are at risk for vascular thrombosis, thrombocytopenia, cerebral infarct and/or recurrent spontaneous abortion. Elevations of CA associated with increased risk have also been seen in idiopathic thrombocytopenic purpura, rheumatoid and psoriatic arthritis, and primary Sjögren's syndrome.

A complete blood count is used as a screening test for various disease states including anemia, leukemia and inflammatory processes.

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Test for myocardial infarction and skeletal muscle damage. Elevated results may be due to: myocarditis, myocardial infarction (heart attack), muscular dystrophy, muscle trauma or excessive exercise

Creatine Kinase Isoenzymes is useful in the evaluation of myocardial disease. Isoenzyme MM is found in skeletal muscle whereas isoenzyme MB is increased in recent myocardial (heart) damage.

Clinical Significance

Bacterial sepsis constitutes one of the most serious infectious diseases. The detection of microorganisms in a patient's blood has importance in the diagnosis and prognosis of endocarditis, septicemia, or chronic bacteremia.

Includes

Aerobic culture, anaerobic culture. If culture is positive, identification will be performed at an additional charge (CPT code(s): 87076 or 87106 or 87077 or 87140 or 87143 or 87147 or 87149).
Antibiotic susceptibilities are only performed when appropriate (CPT code(s): 87181 or 87184 or 87185 or 87186).


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To screen for and monitor kidney dysfunction in those with known or suspected kidney disease. Cystatin C is a relatively small protein that is produced throughout the body by all cells that contain a nucleus and is found in a variety of body fluids, including the blood. It is produced, filtered from the blood by the kidneys, and broken down at a constant rate. This test measures the amount of cystatin C in blood to help evaluate kidney function.Cystatin C is filtered out of the blood by the glomeruli, clusters of tiny blood vessels in the kidneys that allow water, dissolved substances, and wastes to pass through their walls while retaining blood cells and larger proteins. What passes through the walls of the glomeruli forms a filtrate fluid. From this fluid, the kidneys reabsorb cystatin C, glucose, and other substances. The remaining fluid and wastes are carried to the bladder and excreted as urine. The reabsorbed cystatin C is then broken down and is not returned to the blood.

Factor V (Leiden) Mutation is a point mutation that causes resistance of Factor V protein degradation by activated protein C (APC). This mutation is associated with increased risk of venous thrombosis.