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Home , Bilirubin, Fructosamine, Serology

Basic Laboratory Tests Basic Blood Chemistry Tests

Examples of conditions in Alternative Usual which abnormal values Test Names Units Normal Range occur , Albumin g/dL 3.8-5.2 g/dL Low levels may occur with malnutrition, , malabsorption, kidney disease. Elevated levels are uncommon but may be seen in dehydration. , Total Bili. Total mg/dL 0.2-1.5 mg/dL Liver dysfunction, disease/obstruction, Gilbert’s syndrome (isolated), (isolated) BUN mg/dL 9-25 mg/dL Kidney (renal) disease , serum Creatinine mg/dL 0.7-1.5 mg/dL Kidney (renal) disease LDH (LD) U/L 50-150 U/L Tumors, hemolysis, liver, heart, lung and kidney Protein, Total Tot Protein g/dL 6.1-8.2 g/dL See Albumin and Globulin Aspartate Aminotransferase AST (SGOT) U/L 0-33 U/L Viral , fatty liver, alcohol abuse, , muscle injury, drug reactions, macroenzyme (isolated) Alanine Aminotransferase ALT (SGPT) U/L 0-45 U/L Viral hepatitis, fatty liver, alcohol abuse, cirrhosis, drug reactions Alk. Phos. U/L 30-125 U/L Biliary tract disease, , tumors, drug reactions, bone disease/injury, , growing children/adolescents Gammaglutamyl GGT (GGTP) U/L 0-65 U/L Biliary tract disease, Transpeptidase alcohol abuse, fatty liver, drug reactions Globulin Globulin g/dL 2.1-3.9 g/dL Elevated levels can occur with , , autoimmune diseases and various cancers. Low levels can occur with , inherited abnormalities in globulin production, and in kidney disease. Glucose mg/dL 60-109 mg/dL mellitus, Fructosamine mg/dL 1.2-2.0 mg/dL Diabetes mellitus A1c HbA1c, % 3.0-6.0% Diabetes mellitus Glycosylated Hemoglobin (GHb) Total Cholesterol mg/dL 140-199 mg/dL Familial hyperlipidemia,

HDL Cholesterol HDL mg/dL 35-80 mg/dL hypothyroidism, liver disease, LDL Cholesterol LDL mg/dL 0-129 mg/dL kidney disease, diabetes, Total Cholesterol/HDL Chol/HD No units <5.0 medications, obesity, cigarette Cholesterol ratio L ratio smoking, alcohol consumption LDL Cholesterol/HDL LDL/HD No units 0.9-5.3 Cholesterol ratio (LDLHDL L ratio ratio) Triglycerides mg/dL 0-15 mg/dL Uric Acid UA mg/dL 2-7 mg/dL Gout, renal failure, malignancy

Prostate specific antigen PSA nanograms per 0-4 ng/mL Prostate cancer, milliliter (ng/mL) benign prostate , prostatitis Carbohydrate deficient CDT % 0-2.5% Excessive alcohol consumption, liver disease, Hemoglobin associated HAA micromoles per <10.5 ìmol/L inherited conditions and in acetaldehyde liter (ìmol/L) normal individuals NTproBNP Pro-Brain picograms per <125 pg/mL Various types of heart disease naturetic milliliter (pg/mL) peptide, N terminal fragment C-reactive protein CRP mg/L Low risk <1,2 mg/L Coronary disease, vascular Mod risk 1-2-1.9 disease mg/L High risk >2 mg/L

HIV , serum Non-reactive HIV HIV antibody, Non-reactive HIV infection Hepatitis B surface antigen HBsAg Non-reactive Hepatitis B infection Hepatitis B surface antibody HBsAb Non-reactive Previous Hepatitis B infection, Hepatitis B Hepatitis B core antibody HBcAg Non-reactive Current or previous Hepatitis B infection Hepatitis B “e” antigen HBeAg Non-reactive Current Hepatitis B infection antibody HCVAb Non-reactive Hepatitis C infection

Blood Chemistry Tests Indicators of Carbohydrate : Glucose, Glycosylated Hemoglobin (Hemoglobin A1c) and Fructosamine Glucose measurements are made to determine if there is a disorder of carbohydrate metabolism. Such disorders include diabetes mellitus and various forms of hypoglycemia. Diabetes usually results in elevated glucose levels while disorders associated with hypoglycemia may result in low glucose levels. However, normal glucose values do not exclude the possibility that abnormal carbohydrate metabolism may exist. Glucose level rise after meals and fall with fasting so it is important to note when the blood samples were obtained in relation to the last meal. The degree of blood glucose elevation may be an indicator of the severity of diabetes or of how well the diabetes is being controlled. But since glucose levels often vary considerably throughout the day, fructosamine or glycosylated hemoglobin levels may give a better indication of longer-term diabetes control. Improper preparation or delays in analyzing blood samples can result in erroneously low glucose values, a condition termed glycolysis. Glycolysis not only may result in erroneously low glucose values but may also laboratory measurements of creatinine to be erroneously high.

Glycosylated hemoglobin (Hemoglobin A1c). Hemoglobin is the oxygen carrying protein within red blood cells. When hemoglobin comes into prolonged contact with glucose, some glucose may become chemically attached to the hemoglobin molecule resulting in what has become known as glycosylated hemoglobin (GHb) or hemoglobin A1c (HbA1c). Glycosylated hemoglobin levels rise and fall in direct proportion to blood glucose levels. Glycosylated hemoglobin levels reflect average blood glucose levels over the life span of the , about 120 days. Therefore glycosylated hemoglobin concentrations are more useful indicators of long-term diabetes control than are individual blood glucose measurements. The American Diabetes Association recommends that a glycosylated hemoglobin values be kept at 7% or less.

Fructosamine Similar to the way glycosylated hemoglobin is formed, blood glucose may become chemically attached to the protein, albumin, to form fructosamine. As with glycosylated hemoglobin, fructosamine levels rise and fall in direct proportion to blood glucose levels. But because the life-spam of the albumin molecule is shorter than that of the hemoglobin molecule, fructosamine levels reflect average blood glucose concentrations over a shorter period of time, usually thought to be the preceding 3 to 6 weeks.

Indicators of Lipid Metabolism: Total Cholesterol, HDL Cholesterol, LDL Cholesterol, TC/HDL ratio

Cholesterol, Total Cholesterol

Cholesterol is a lipid (fat) that is an essential component of cell membranes and is required for the synthesis of various hormones. Cholesterol is both absorbed from food and synthesized by the liver. Excess amounts of cholesterol may be deposited in arteries resulting in atherosclerosis and predisposing to the risk of heart attack and stroke. Cholesterol circulates in the body bound to various forms of protein. The size and composition of these “lipo- protein” particles determine their potential for causing atherosclerosis.

HDL Cholesterol, LDL Cholesterol, Cholesterol/HDL Ratio The forms of cholesterol commonly measured at the time of insurance underwriting include total cholesterol, high density lipoprotein cholesterol (HDL cholesterol or “HDL”) and low density lipoprotein cholesterol (LDL cholesterol or “LDL”). LDL particles transport cholesterol to the tissues and result in the deposition of cholesterol in arterial walls resulting in atherosclerosis. HDL particles transport cholesterol back to the liver for further metabolism and thereby reduce the risk of atherosclerosis. The total cholesterol/HDL cholesterol ratio (TC/HDL) has been shown to be an important predictor of the risk of atherosclerosis, with lower cholesterol/HDL ratios being associated with less risk. Conversely, elevated LDL levels and lower HDL/LDL ratios are associated with an increased risk of atherosclerosis. In some studies, low total cholesterol levels and total cholesterol levels that are falling without treatment have also been associated with increased mortality risk, primarily cancers and other non-cardiovascular diseases. Total cholesterol, HDL and LDL concentrations vary from day-to-day by up to 13% in a given individual. Ideally, lipid measurements should be made after a 12-hour fast since HDL levels may decrease slightly after meals. However, eating has little effect on total cholesterol levels.

Lipid Normal/Optimum/Desirable Borderline Increased Risk Total Cholesterol <200 mg/dL 200-239 mg/dL >240 mg/dL HDL Cholesterol >60 mg/dL 40-59 mg/dL < 40 mg/dL LDL Cholesterol <100 mg/dL 100-159 mg/dL >160 mg/dL Total Cholesterol/HDL ratio <3.5 >5 Triglycerides <150 mg/dL 150-199 mg/dL > 200 mg/dL Modified from Hunninghake DB, Pasternak RC, Smith SC, et al: Third Report of the Expert Panel on Detection, Evaluation and Treatment of the High Blood Cholesterol in Adults (Adult Treatment Panel III) Circulation 2004; 110: 227-239

Triglycerides Triglycerides are a major transportation and storage form for lipids. Triglycerides are produced in the intestine after meals and by the liver. Elevated concentrations are risk factors for coronary disease and may be a marker for resistance and pre-diabetes. Triglyceride concentrations above 1,000 mg/dL may cause acute pancreatitis. Triglyceride levels can be markedly elevated after meals. Therefore triglycerides should be measured after a minimum of a 9 hour fast.

Indicators of Kidney (Renal) Function: Glomerular Filtration Rate (GRF), Creatinine, and BUN (Blood Urea Nitrogen) The kidneys’ main functions are to regulate salt and water balance in the body and to filter waste products from protein metabolism. Blood entering the kidneys travel through a myriad of branching arteries until reaching structures called glomeruli that consist of portions of capillaries twisted into what resemble microscopic tufts, each about the size of a pin head. Each kidney contains about 1 million glomeruli. The walls of the glomerular capillaries are very thin and contain pores allowing the fluid portion of the blood to be filtered into collecting tubules which drain into a series of progressively larger tubules, eventually emptying into the ureters and ultimately the bladder. The tubules secrete and reabsorb salts, water and other chemicals to produce urine.

Creatinine A common measure of kidney function is the Glomerular Filtration Rate (GFR), defined as volume of blood filtered by all the glomeruli each minute. Unfortunately, GFR cannot be measured directly. So instead, estimates of GFR (eGFR) are made using calculations based on the volume of blood that is completely filtered (cleared) of a given substance each minute. The most common substance used for this calculation is blood creatinine, a normal product of muscle metabolism. Since blood creatinine is filtered by the glomeruli, deterioration in GFR will result in elevated creatinine levels. But blood creatinine levels are also affected by the amount of muscle mass present and the dietary consumption of meat and protein supplements which are also metabolized into creatinine. Since muscle mass is usually greater in men than women and usually decreases in both sexes with age, blood creatinine concentrations must be interpreted in light of age, gender and build. Finally, the most commonly used analytical method to measure blood creatinine (Jaffe reaction or alkaline picrate method) may be affected by the presence of several factors. Glucose, protein, urea, ascorbic acid (vitamin C) and glycolysis (metabolism of glucose in poorly prepared blood samples) may result in falsely increased creatinine concentrations as determined by the Jaffe reaction.

Estimated GFR (eGFR) Because blood creatinine concentrations may be affected by factors other than GFR, various mathematical equations have been devised to estimated GFR (eGFR) from blood creatinine concentrations after adjusting for many of these other factors. Most equations adjust for age, sex and race. Some adjust for build and other factors. Although some equations perform better than others, all are imperfect. The most commonly used equations are those developed by Levey and used in the Modification of Diet in Renal Disease (MDRD) study and those developed by Rule at the Mayo Clinic. The National Kidney Foundation has defined 5 stages of chronic kidney disease based on GFR estimated from the MDRD equation.

National Kidney Foundation Stages of Chronic Kidney Disease

Stage Description eGFR (ml/min/1.73 m2) Recommended Actions

— At increased risk ≥60 (with chronic kidney Screening; chronic kidney disease risk reduction disease risk factors)

1 Kidney damage with normal ≥90 Diagnosis and treatment; treatment of comorbid conditions; or increased GFR slowing progression; risk reduction

2 Kidney damage with mild 60–89 Estimating progression decreased GFR

3 Moderately decreased GFR 30–59 Evaluating and treating complications

4 Severely decreased GFR 15–29 Preparation for dialysis or kidney transplantation

Stage Description eGFR (ml/min/1.73 m2) Recommended Actions

5 <15 or dialysis Kidney transplantation or dialysis (if uremia present)

Modified from National Kidney Foundation: K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis 43(5 Suppl 1):S1–290, 2004.

BUN Protein metabolism produces ammonia, a toxic substance that is further metabolized by the liver into urea. Urea is removed from the blood by the kidneys. The laboratory for urea is termed “Blood Urea Nitrogen” or BUN. BUN concentrations rise with reductions in GFR. BUN can also rise with dehydration and upper gastrointestinal bleeding. BUN levels may be reduced in liver disease and by malnutrition.

Liver Function Tests: ALT, AST, Alkaline phosphatase, GGT, Total Bilirubin Five laboratory assays are commonly called (LFTs), although these tests are neither specific to the liver nor true measures of liver function. In most cases, elevated LFTs indicate possible liver cell injury (ALT and AST) or interruption of flow or (ALP, GGT). Only bilirubin, a metabolic breakdown product hemoglobin, is a direct measure of liver function.

Alanine Aminotransferase (ALT or SGPT) and Aspartate Aminotransferase (AST or SGOT) Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are both found within liver cells. When liver cells die or are damaged, these are released into the circulation where they can be measured, allowing them to be considered markers for liver injury. Despite their similarities, they differ somewhat in their specificity for the liver disease. ALT is found in other tissues, including the kidney, lung, , red blood cells and skeletal muscle. However, its concentration is by far highest in the liver and ALT is therefore considered relatively specific for liver disease. AST is also found in many tissues, including the heart, brain, skeletal muscle and kidney. It is more evenly distributed than ALT, so its elevation is considered less specific for liver cell injury. It may also occasionally be occur as a larger-thannormal molecule called a macro-. If this macro-enzyme is present, erroneously high AST levels (sometimes increased many fold) may be reported using conventional assays. There may be substantial overlap between the diseased and non-diseased state when ALT and AST values are mildly elevated. Thus, mild elevations may not necessarily indicate significant disease. However, as ALT and AST levels rise, the likelihood of significant liver dysfunction increases.

Alkaline Phosphatase (Alk. Phos. or ALP) Alkaline phosphatase (Alk. Phos.) is found in a number of tissues. Eighty percent of Alk. Phos. comes from the liver or bone; most of the rest comes from the intestine. Levels may be elevated in normal women during pregnancy due to the Alk. Phos. production by the placenta and in children and adolescents due to Alk. Phos. production by bone growth. Individuals with blood groups B and O have increased intestinal Alk. Phos. levels after fatty meals. Alk. Phos. values normally increase between the ages of 40 and 65, especially in women. In addition, some may interfere with Alk. Phos. assays. In the liver, Alk. Phos. is produced by cells. Obstruction of bile ducts leads to increased Alk. Phos. synthesis. Such obstruction may by caused by hepatitis, drug reactions, gallstones, tumors, scarring (cirrhosis), or other diseases. Gamma-glutamyltransferase (GGT) Gamma-glutamyltransferase (GGT) is the most sensitive marker for biliary tract disease but its specificity is low due to two factors. First, it is found in many tissues including the heart, brain, pancreas, kidney, and seminal vesicles. Second, its production can be increased or induced by substances such as alcohol, barbiturates and phenytoin (Dilantin). Elevated levels due to increased production do not indicate . In addition, GGT levels increase with age, body mass index (BMI) and male sex. This poor specificity limits GGT’s usefulness in diagnosing liver disease. Its principal role in clinical practice is determining whether elevated alkaline phosphatase levels are likely due to liver or biliary tract disorders. If both alkaline phosphatase and GGT levels are elevated, a liver or biliary cause of the alkaline phosphatase elevation is likely; if the GGT level is normal other possible causes for the alkaline phosphatase elevation are more likely. An isolated GGT elevation has not been found to be a good predictor of significant underlying liver disease.

Bilirubin Bilirubin is produced when hemoglobin is metabolized. In its native form, bilirubin is insoluble in water. In the liver, molecules are attached (conjugated) to bilirubin to make it water soluble. Conjugated bilirubin is then excreted in the bile. Conjugated bilirubin levels in the serum do not increase until the liver loses half of its functional capacity. However, most mild elevations of total bilirubin in asymptomatic individuals are due to increased levels of unconjugated bilirubin. Insurance laboratories commonly test only for total bilirubin levels and unless specifically asked to do so, do not report results for conjugated and unconjugated bilirubin levels. The most common cause of elevated unconjugated bilirubin levels in asymptomatic individuals is Gilbert’s syndrome, an inherited defect in the enzyme that conjugates bilirubin. Gilberts syndrome is not associated with any significantly increased mortality risk. Other causes of elevated unconjugated bilirubin levels include hemolysis, abnormalities in red blood cell production, and severe liver disease. Elevations in conjugated bilirubin may be caused by liver disease, bile duct obstruction, medications and some inherited disorders.

Proteins: Total Protein, Albumin, Globulin, Albumin to Globulin ratio Although many cells in the body produce proteins that circulate in the blood, the vast majority of proteins are produced by the liver. All proteins are made from building blocks called amino acids. Proteins are the basic components of cells, body tissues, enzymes, hormones, , and clotting factors. The two major classes of circulating proteins are albumin and globulins. Normally, the concentration of albumin is twice that of globulins, i.e. the normal albumin/globulin ratio is 2:1. Low albumin/globulin ratios may be due to low albumin levels or increased globulin levels. Therefore the total protein concentration, albumin concentration and the total globulin concentration must all be considered as well as the ratio of albumin to globulin. Albumin Albumin is the major protein in the blood, comprising about 60% of total blood protein. Albumin is synthesized by the liver and serves three main functions: 1) It is the main contributor to osmotic pressure, the chemical property of solutions that determines the movement of fluid across membranes and maintains fluid balance in blood and tissues. Low albumin levels can result in the leakage of fluid out of blood vessels, producing tissue swelling (edema). 2) Albumin is a major transport protein for many hormones, drugs and other molecules 3) Albumin, because it is a large molecule, 584 amino acids long, serves as a cache for amino acids which can be reused to make other proteins. For that reason, albumin is one of the first proteins to be catabolized (broken down) when malnutrition occurs. Low blood albumin levels may also result from protein malabsorption or impaired synthesis due to liver disease or increased losses of albumin through the kidneys or intestines. Studies have shown that albumin levels of 3.8 mg/dL or less are associated with an increased mortality risk in the elderly. Elevated albumin levels are uncommon but are occasionally seen with dehydration.

Globulins Globulins are the second major class of circulating proteins besides albumin. There are many types of globulins including antibodies, enzymes, and transport proteins. Globulins can be separated by a chemical procedure called electrophoresis. When electrophoresis is performed on blood that is devoid of clotting proteins (serum) it is called “serum protein electrophoresis” (SPEP). SPEP separates serum proteins into an albumin fraction and a globulin fraction which, in turn, is further separated into five globulin subgroups termed alpha1, alpha2, beta, delta and gamma. The gamma fraction consists of antibodies, also called immunoglobulins. Antibodies bind to various components of parasites, and to help fight infections. They can also bind to proteins and other substances, sometimes resulting in inflammation and what has been called “.” Elevated globulin levels can occur with infections, inflammation, autoimmune diseases, multiple myeloma, leukemia, lymphoma and cancers. Low globulin levels can occur with liver disease, inherited abnormalities in globulin production including hyogammaglobulinemia and other immunodeficiencies, and in nephrosis (a type of kidney disease in which protein is lost in the urine).

Tumor markers: Prostate Specific Antigen, Lactate Dehydrogenase (LDH) Prostate specific antigen (PSA) Prostate specific antigen (PSA) is a protein that is produced by prostate tissue. Prostate cancer tissue produces more PSA than normal prostate tissue and PSA testing is done to detect prostate cancer, hopefully at an early stage when a cure is possible. However, besides prostate cancer, elevated PSA levels can also result from an enlarged prostate gland (benign prostatic hypertrophy or BPH), prostate inflammation or infection (prostatitis), and prostate trauma as might occur from a digital prostate examination or from a biopsy. Although higher levels of PSA usually are more suggestive of cancer, the values reached with some benign conditions, particularly prostatitis, can be quite high. The major difficulty in the interpretation of PSA values, especially when PSA elevations are modest, is the great overlap between benign disease (primarily BPH) and prostate cancer. Several factors are often considered to help make this distinction including whether PSA values are increasing or decreasing, the rate of increase in PSA elevations, and estimates of the size of the prostate gland and whether the level of PSA seems appropriate for the gland size. In many cases, a prostate biopsy in necessary to determine whether prostate cancer is the cause of PSA elevations. However, a normal prostate biopsy does not necessarily rule out prostate cancer. A prostate biopsy commonly done by inserting needles into the prostate gland may miss the area where a cancer is located, especially if the biopsy is not done under ultrasound guidance or involves only a small number or samples. Repeated biopsies over a period of time may even be necessary to diagnosis prostate cancer.

Lactate dehydrogenase (LDH) Lactate dehydrogenase (LDH) is an enzyme that is found in virtually all tissues including red blood cells, liver, heart, lung, kidney and muscle. In general, or destruction of tissue will lead to an increase in LDH levels. Five different forms (isoenzymes) of LDH have been identified. The concentration of each isoenzyme varies depending on the organ. Thus, the pattern of isoenzyme elevation may indicate the tissue of origin. Examples of clinical conditions associated with LDH elevations include , hepatitis and muscle injury. Probably the most common cause for increased LDH levels on insurance testing is hemolysis due to red blood cell destruction during collection, transportation or storage of the blood sample. Despite its non-specific nature, an important use of LDH is the evaluation of malignancies. Isolated, unexplained elevations of LDH to more than 2 to 3 times normal are suspicious for a possible malignancy. In general, the degree of LDH elevation is related to the volume of tumor present. Higher LDH levels in patients with cancer are generally associated with a greater tumor burden and poorer prognosis. Any increase in LDH levels above baseline values in an individual with a known or treated malignancy is highly suspicious for recurrent disease.

Uric Acid Uric acid is produced by the liver as a byproduct of the metabolism of purines, compounds that are found in meat and meat products. Elevated uric acid levels () may be due to increased dietary consumption of foods rich in purines or decreased excretion of uric acid in the urine. Other conditions can also cause hyperuricemia, including various malignancies, , psoriasis, renal failure, endocrine disorders, excessive alcohol consumption and some medications. Elevated uric acid levels may result in gout or uric acid kidney stones. There is also evidence that hyperuricemia increases the risk of coronary artery disease.

Alcohol markers: Carbohydrate Deficient Transferrin (CDT) and Hemoglobin Associated Acetaldehyde (HHA)

Carbohydrate deficient transferrin (CDT)

Transferrin is a protein that transports iron. Eight different types of exist. The type of transferrin depends upon the number of carbohydrate chains that are attached to the parent transferrin molecule. In normal serum, most transferrin has four carbohydrate chains, but some normal circulating transferrin molecules have two or three chains and others have five or more chains. In alcoholics, there is an increase in the amount transferrin having zero to three chains. These are called carbohydrate deficient transferrin (CDT) forms. An increase in the amount of CDT has been proposed as a test for chronic excessive alcohol consumption and a number of studies have suggested that CDT can help distinguish alcoholics consuming large amounts of alcohol from light social drinkers and abstainers.

HAA (hemoglobin associated acetaldehyde) Alcohol is metabolized in the liver to acetaldehyde and blood acetaldehyde levels rise following alcohol ingestion. Acetaldehyde is able to chemically bind to various tissue proteins, including hemoglobin. The presence of hemoglobin associated acetaldehyde, or HAA, in the blood has been used as an indicator of chronic excessive alcohol consumption. However it is still not entirely certain what amount and duration of alcohol consumption is necessary to cause elevated HAA levels in the serum. Other factors that either increase the amount of blood acetaldehyde or decrease the metabolism of acetaldehyde may also cause elevated HAA levels.

Markers of Infection: Human Immunodeficiency (HIV), Hepatitis B virus (HBV), and Hepatitis C virus (HCV)

Human Immunodeficiency Virus Antibody Testing (HIV antibody) Infections with the Human Immunodeficiency Virus (HIV) cause the Acquired Immunodeficiency Syndrome (AIDS) in which there is a progressive loss of cells crucial for normal functioning of the immune system. This results in increased susceptibility to multiple other viral, bacterial and protozoan infections and the occurrence of a variety of tumors. Although many medications have been developed to treat HIV infections, HIV infections remain incurable and result in premature death. Two types of HIV viruses have been identified. Most infections are caused by the type 1 virus (HIV-1). A small number are caused by the type 2 virus (HIV-2). Three to six weeks after infection with HIV-1 or HIV-2, antibodies directed against various components of the virus particles are produced in sufficient amounts to be detectable. Sometimes it can take up to 6 months for antibody tests to become positive, however. These antibodies can be detected in whole blood, dried blood spots, urine and oral fluid (saliva). The most common test for HIV antibodies is an enzyme-linked immunosorbent assay (ELISA). Although the false positive results for ELISA HIV testing are uncommon, positive ELISA tests must be confirm ed by another testing method, usually a Western Blot test, before being reported. However Western Blot tests can be inconclusive for the presence of HIV infection and there are several conditions that can produce false positive Western blot tests results. In situations where Western Blot tests are indeterminate or when a false positive Western Blot test is suspected, the presence of HIV infection is usually confirmed with a polymerase chain reaction (PCR) test that detects the actual genetic material (RNA) of the virus.

Hepatitis B Testing The hepatitis B virus consists of an internal core consisting of protein, enzymes and genetic material surrounded by an outer protein coat. The various tests for hepatitis B refer to various components of the virus particle including:

Hepatitis B surface antigen (HBsAg) testing detects material from the outer protein coat. The surface antigen becomes detectable approximately 4 weeks after an individual is infected with the virus. The presence of the antigen indicates an active infection with hepatitis B. The surface antigen disappears with resolution of the infection. Prolonged detection of the surface antigen beyond six months after acute infection indicates a chronic carrier state which may or may be associated with elevated liver function tests.

Hepatitis B surface antibody (anti-HBs, HBs antibody or HBsAb) testing detects antibodies to the outer protein coat of the virus. The surface antibody usually becomes detectable several weeks after the disappearance of the surface antigen. Its presence generally indicates resolution of the infection and development of lifelong . The surface antibody may eventually become undetectable in some individuals with a remote, resolved hepatitis B infection. Individuals who are vaccinated against hepatitis B, and who have an adequate immune response to the vaccine, will also develop a detectable surface antibody test.

The presence of Hepatitis B core antibody (anti-HBc, HBc antibody or HBcAb) indicates the development of an antibody to the inner core protein of the virus. It usually becomes detectable shortly before elevation of the liver tests and near the time of onset of clinical illness. There are two forms of the core antibody, IgM and IgG. The IgM type indicates an acute infection. This form gradually disappears and is replaced by the IgG variety, usually by about 6 months after an acute infection. The IgG core antibody is an indicator of a prior infection and remains present for life. In individuals with a remote infection who have lost the surface antibody, the core antibody may be the only indicator of previous disease. Those persons who are vaccinated for hepatitis B are not exposed to the core proteins and do not develop the core antibody. Thus, the presence of an isolated hepatitis B surface antibody indicates vaccination as opposed to a prior infection. Hepatitis “e” antigen (HBeAg) is a remnant resulting from the production of new viral particles. During an acute infection it appears later than the surface antigen and its presence is an indicator of active viral production. It is an important marker of active disease and a highly infectious state. HBeAg is an indicator of increased mortality and morbidity risk. Conversely, the absence or disappearance of HBeAg is a good prognostic sign.

Hepatitis C Antibody Testing Hepatitis C antibody (anti-HCV, HCV antibody, or HCVab) develops in response to infection with the hepatitis C virus. The antibody usually takes 4-10 weeks to appear after exposure but may take up to 3 to 6 months to develop. Unlike some other types of antibodies, the hepatitis C antibody does not eliminate the virus. Since 75-85% of individuals with hepatitis C develop persistent disease, the presence of the antibody is usually an indicator of chronic infection. However, a minority of individuals may clear the virus from their system without treatment. In resolved infections, the levels may gradually diminish over time and disappear after many years. In addition, some individuals may have a false positive screening test for Hepatitis C. Additional specialized testing may be necessary to differentiate those persons with a positive hepatitis C antibody test who are actively infected from those who have a false positive test or those who have cleared the virus and are no longer infected.

Other markers of heart and vascular diseases: hs-CRP and NTproBNP hsCRP C-reactive protein (CRP) is a protein produced by the liver in response to a variety of inflammatory conditions. Tests for CRP have traditionally been used to assess disease activity in a variety of inflammatory conditions such as infections, rheumatoid arthritis and appendicitis. There is also some evidence to suggest that CRP may play a part in causing atherosclerosis. More recently the test for CRP has been modified to detect smaller CRP elevations previously considered to be within the normal range. This modified test is known as highly sensitive C-reactive protein (hs-CRP) test. Some studies have shown that low levels of inflammation, detectable by hsCRP elevations, are associated with increased death rates in individuals with and without a prior diagnosis of coronary artery disease. For this reason hsCRP is sometimes used to assess the risk of coronary artery disease.

NTproBNP B-type natriuretic peptide (BNP) is a protein that is released by the heart muscle in response to pressure overload or cardiac muscle stretching. BNP stimulates the kidneys to eliminate salt and water and causes blood vessels to dilate and blood pressure to fall. BNP is formed in the heart muscle cells as part of a larger protein called proBNP. ProBNP is then cleaved into two parts: an inactive fragment called NTproBNP and the active form, BNP. Both BNP and NTproBNP are useful laboratory tests to screen for a variety of heart problems including congestive heart failure, coronary artery disease, left ventricular hypertrophy, valvular heart disease, and . Because NTproBNP is more stable in blood specimens than BNP, NTproBNP is preferred for insurance laboratory testing. BNP and NTproBNP levels are higher in women than men and increase with age and in kidney disease. Studies have shown an increased risk mortality risk in individuals having elevated BNP or NTproBNP levels.