A Lab Tests

Liver & Kidney Health, General Health & Wellness

Among entities in which AST and ALT increases occur, are therapeutic applications of bovine or porcine heparin. LD (LDH) abnormality with elevation of hepatic fractions was also reported.3In children with acute lymphoblastic leukemia, high ALT activity at diagnosis is associated with rapidly progressive ALL.4A number of drugs, including diphenylhydantoin, heparin therapy and many others, cause ALT increases. Acetaminophen hepatotoxicity may be potentiated in alcoholics, in whom coagulopathy and extremely abnormal aminotransferase levels are described, ALT less than AST.5The hepatitis C virion has been detected by polymerase chain reaction and reverse transcriptase of HCV-RNA sequences in patients with elevated ALT and positive anti-HCV.6

Nutrition & Vitamins, Liver & Kidney Health

Twenty-four hour urine collection to measure protein loss is helpful in work-up of some patients with hypoalbuminemia. Other testsuseful in assessment of nutritional statusinclude TIBC, transferrin, iron, absolute lymphocyte count, and vitamin B12/folate levels.

Liver & Kidney Health, Bone Health

Serum alkaline phosphatase is a member of a family of zinc metalloprotein enzymes that function to split off a terminal phosphate group from an organic phosphate ester. This enzyme functions in an alkaline environment (optimum pH of 10). Active center of ALP enzymes includes a serine residue. Mg and Zn ions are required for minimal activity. Enzyme activity is localized in the brush border of the proximal convoluted tubule of the kidney, intestinal mucosal epithelial cells, hepatic sinusoidal membranes, vascular endothelial cells and osteoblasts of bone. There are distinctive forms of ALP in the placenta and small intestine; hepatic, renal and osteoblast (bone) ALP are similar molecules.Serum ALP activity of intestinal origin occurs only in individuals of ABO blood type O or A. They are secretors of ABH RBC antigens and also carry the Lewis red cell antigen. Serum intestinal ALP level increases in these individuals about two hours following consumption of a fatty meal.Liver alkaline phosphatase is increased in cholestasis and inflammatory liver disease as well as in infiltrative liver disease. The enzyme is sensitive to obstructive biliary processes, even small secondary bile duct obstruction, and thus may be increased in those patients when the bilirubin is normal due to compensatory bilirubin excretion by the rest of the liver. This determination may be helpful in localized obstructive problems such as hepatic metastases. An electrophoretically slow moving isoenzyme with high relative mass may occur in some patients with bile duct obstruction and hepatic metastases and may result in false elevation of CK-MB.7To confirm biliary abnormality, an additional useful test is GT. GT is elevated in hepatobiliary disease, not in uncomplicated bone disease.Serum ALP is increased during pregnancy. Marked decline of high ALP of pregnancy is seen with placental insufficiency and imminent fetal demise.

Liver & Kidney Health, General Health & Wellness

AST has origin from heart, liver, skeletal muscle, kidney, pancreas, spleen, and lung. Very high values, >500 units/L, usually suggest hepatitis or other kinds of hepatocellular necrosis but can also be found with large necrotic tumors, other types of necrosis or extensive hypoxia, congestive failure, and shock. Unexplained AST elevations should first be investigated with ALT and GT. Mitochondrial AST (m-AST) may be useful in the diagnosis of alcoholic liver disease; it is reviewed by Rej.4

Digestive Health

Causes of high serum amylaseinclude acute pancreatitis, pancreatic pseudocyst, pancreatic ascites, pancreatic abscess, neoplasm in or adjacent to pancreas, trauma to pancreas, and common duct stones.Nonpancreaticcauses of hyperamylasemia include inflammatory salivary lesions (eg, mumps), perforated peptic ulcer involving pancreas or not, intestinal obstruction and infarction, afferent loop syndrome, biliary tract disease including stones, aortic aneurysm, peritonitis, acute appendicitis, cerebral trauma, burns and traumatic shock, the postoperative state (with and without pancreatitis), diabetic ketoacidosis, and extrapancreatic carcinomas (especially of esophagus, lung, ovary). Amylase levels more than 25-fold the upper limit of normal are often found when metastatic tumors produce ectopic amylase. Such levels are higher than those usually found in cases of pancreatitis.3In renal insufficiency amylase is usually not more than three times the upper limit of normal. Moderate increases may be reported in normal pregnancy. Increases may be found with tubo-ovarian abscess, ruptured ectopic pregnancy, macroamylasemia, and with a substantial number of drugs, including morphine. Relationships between pancreatitis and hyperlipidemias types I, IV, and V are described. Amylasemia may be associated with hyperparathyroidism.Macroamylaseis a high molecular weight material, normal amylase complexed to high molecular weight protein such as immunoglobulin. It is characterized by high serum amylase and low to normal urine amylase. Macroamylase occurs in normal as well as abnormal subjects.4Other tests:Inpancreatitis, varying percentages of patients have the following other abnormalities in varying combinations: elevation of triglyceride, alkaline phosphatase, AST (SGOT), total bilirubin, white blood cell count, left shift. Calcium levels should be followed in fulminant pancreatitis, since extremely low serum calcium levels can evolve.Serum lipase and two-hour urine amylasemay both be extremely valuable. Although determination of serum methemalbumin has been advocated as a test for acute hemorrhagic pancreatitis, it is cumbersome and is not done in many American laboratories.Isoenzymesof amylase exist: pancreatic and salivary type, as noted under Limitations. They can be separated by polyacrylamide gel or agarose film electrophoresis, isoelectric focusing, ion exchange chromatography, and plant isoamylase inhibitors. A monoclonal antibody approach is described.3,5Amylase isoenzymes are separated in few laboratories. Where available the procedure is an expensive one. It is useful in assessing the decrease of pancreatic function in cystic fibrosis, in children older than five years, who may be candidates for enzyme replacement.

Autoimmune & Inflammation

The indirect immunofluorescent test has three elements to consider in the result:1. Positive or negative fluorescence. A negative test is strong evidence against a diagnosis of SLE but not conclusive.2. The titer (dilution) to which fluorescence remains positive (provides a reflection of the concentration or avidity of the antibody). Many individuals, particularly the elderly, may have low titer ANA without significant disease substantiated after work-up.3. The pattern of nuclear fluorescence (reflecting specificity for various diseases). Homogenous and/or nuclear rim (peripheral) pattern correlates with antibody to native DNA and deoxynucleoprotein and bears correlation with SLE, SLE activity, and lupus nephritis. Homogenous (diffuse) pattern suggests SLE or other connective tissue diseases. Speckled pattern correlates with antibody to nuclear antigens extractable by saline; it is found in many disease states, including SLE and scleroderma. When antibodies to DNA and deoxyribonucleoprotein are present (rim and homogenous pattern), there may be interference with the detection of speckled pattern. Nucleolar pattern is seen in sera of patients with progressive systemic sclerosis and Sjögren's syndrome. Centromere pattern is seen in CREST syndrome.Antinuclear AntibodyANA Pattern IdentificationFound InFollow-up TestsSmooth (homogeneous)SLEAnti-dsDNAAnti-ssDNAAnticardiolipinDrug-induced lupus (DIL) other collagen diseases: chronic active hepatitis systemic sclerodermaAntihistoneAntichromatinRFScl-70SS-A/SS-BImmune complexSpeckledSLEAnti-dsDNAAnti-SmAnticardiolipinSjögren's syndromeAnti-SS-A/SS-BAntihistoneViral or induced lupusMCTDAnti-RNPRARFNucleolarPSS/SclerodermaAnti-RNPScl-70Anti-SS-A/SS-BSjögren's syndromeAnti-SS-A/SS-BSubcutaneous SLEImmune complexSLEAnti-dsDNAAnti-ssDNACentromereSclerodermaSS-A/SS-BScl-70CREST syndromeScl-70Anti-RNPFive percent of the apparently "normal population" demonstrate serum ANA. Low titers of ANA reactivity may be seen in patients with rheumatoid arthritis (40% to 60% of patients), scleroderma (60% to 90%), discoid lupus, necrotizing vasculitis, Sjögren's syndrome (80%), chronic active hepatitis, pulmonary interstitial fibrosis, pneumoconiosis, tuberculosis, malignancy, age over 60 (18%), as well as in SLE, especially if the disease is inactive or under treatment. Titers ≥1:160 usually indicate the presence of active SLE, although occasionally other autoimmune disease may induce these high titers. There are now known groups of "ANA-negative" lupus patients. Such patients often have antibodies to SS-A/Ro antigen (usually when a frozen section substrate is used) and subacute cutaneous lupus. Ten percent of patients with SLE manifest biologic false-positive tests for syphilis; this may even be the initial manifestation. Some other tests used in differentiation of autoimmune states include antibody to double-stranded DNA, rheumatoid factor, antibody to extractable nuclear antigens, total hemolytic complement (C3, C4, etc). Although ANA tests are occasionally ordered on cerebrospinal fluid or synovial fluid, the current assays are not standardized for these fluids and such assays do not add to the diagnostic process.

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

See Thermo Scientific.

Allergy Testing

See Thermo Scientific.

Allergy Testing

See Thermo Scientific.

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

See Thermo Scientific.

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

See Thermo Scientific.

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Blood Disorders

Offered as part of multiple lab tests

Infectious Diseases

Streptolysin is a hemolysin produced by group A streptococci. In an infected individual streptolysin O acts as a protein antigen, and the patient mounts an antibody response. A rise in antibody level begins about one week after infection and peaks two to three weeks later. In the absence of complications or reinfection, the ASO titer will usually fall to preinfection levels within 6 to 12 months. Both clinical and laboratory findings should be correlated in reaching a diagnosis.

Heart Health & Cardiovascular, General Health & Wellness

In the progressive dystrophies, aldolase levels may be 10 to 15 times normal when muscle mass is relatively intact, as in early stages of the disease. When advanced muscle wasting is present, values decline. In the inflammatory myopathies (eg, dermatomyositis) serum aldolase (as well as CK) levels may be applied to monitoring the response to steroid therapy. They are of particular value in guiding tapering of steroid administration.1No elevation is found in muscular dystrophy secondary to alteration of the nerves or nerve centers.Aldolase is present as a tetramer composed of two of three known subunits designated A, B, and C. Of the four isoenzymes, AAAA is predominant in skeletal muscle, BBBB predominates in liver, and CCCC in brain and other tissue. A hybrid isoenzyme, AAAC is present in tissues but at a lower concentration.2The enzymatic method determines total enzyme activity and thus is not specific for muscle aldolase.Elevated aldolase levels may be found with hepatitis, other liver diseases, myocardial infarction, hemorrhagic pancreatitis, gangrene, delirium tremens, and in some cases of neoplasia. In cases of acute viral hepatitis, increase in serum aldolase tends to parallel ALT (SGPT) levels and is usually up to 20 times the average of normal. Normal results are usually obtained in portal cirrhosis and obstructive jaundice. A small fraction of cases of measles in young adults has been reported to have significant elevations of serum CK and aldolase.3,4Serum aldolase and CK may be elevated in the serum of patients who have taken L-tryptophan and develop eosinophilia-myalgia syndrome.5

Autoimmune & Inflammation

Antibodies to DNA, either single- or double-stranded, are found primarily in systemic lupus erythematosus, and are important, but not necessary or sufficient for diagnosing that condition. Such antibodies are present in 80% to 90% of SLE cases. They are also present in smaller fractions of patients with other rheumatic disorders, and in chronic active hepatitis, infectious mononucleosis, and biliary cirrhosis.In the past, it was considered unnecessary to test for anti-DNA in patients with a negative test for antinuclear antibodies. A group of “ANA-negative lupus” patients has been described with anti-ssDNA and anti-SS-A/Ro and anti-SS-B/La; however, HEp-2 substrate is much more sensitive than frozen section substrates, and it is uncommon for anti-SS-A/Ro to be negative with these newer substrates.This standard dsDNA detects both low- and high-affinity antibodies, providing a very sensitive test for diagnostic purposes; however, it is less predictive for severe nephritis, which is associated with the presence of high-affinity antibodies.Following levels of anti-DNA antibody may be of use in evaluating response to therapy, but should be regarded as a guide rather than a rigid dictator of treatment. Antibody levels correlate particularly well with activity of lupus nephritis.Procainamide and hydralazine may induce anti-DNA antibodies and antihistone antibodies.

Heart Health & Cardiovascular

Offered as part of multiple lab tests

Heart Health & Cardiovascular

Offered as part of multiple lab tests

Liver & Kidney Health

Albumin accounts for approximately 50% of the protein in plasma.2The kidney works to prevent the loss of albumin into the urine through active resorption, but a small amount of albumin can be measured in urine of individuals with normal renal function.The prognostic value of consistently elevated albumin levels is particularly well established in diabetic patients.1Renal disease is a common microvascular complication of diabetes. Without specific interventions, 80% of type I diabetics with repeatedly elevated albumin levels will go on to end-stage renal disease. Twenty percent to 40% of type II diabetics with sustained albuminuria will progress to overt nephropathy.The American Diabetes Association (ADA) recommends that routine urinalysis be performed annually on adults with diabetes.1If the urinalysis is negative for protein, albumin measurement is recommended. The ADA also recommends annual screening of children beginning at puberty or after five years of disease duration. The reference intervals stated above reflect the diagnostic criteria prescribed by the ADA.1

Liver & Kidney Health, Diabetes & Blood Sugar

Albumin accounts for approximately 50% of the protein in plasma.2The kidney works to prevent the loss of albumin into the urine through active resorption, but a small amount of albumin can be measured in urine of individuals with normal renal function.The prognostic value of consistently elevated albumin levels is particularly well established in diabetic patients.1Renal disease is a common microvascular complication of diabetes. Without specific interventions, 80% of type I diabetics with repeatedly elevated albumin levels will go on to end-stage renal disease. Twenty percent to 40% of type II diabetics with sustained albuminuria will progress to overt nephropathy.The American Diabetes Association (ADA) recommends that routine urinalysis should be performed annually on adults with diabetes.1If the urinalysis is negative for protein, albumin measurement is recommended. The ADA also recommends annual screening of children beginning at puberty or after five years disease duration. The reference intervals stated above reflect the diagnostic criteria prescribed by the ADA.1

Liver & Kidney Health, Diabetes & Blood Sugar

This test is used to detect albuminuria by measuring albumin and creatine concentrations in a random (spot) urine sample and calculating the albumin-creatinine ratio (ACR). This test is useful for assessing kidney damage, especially at an early stage, and informing management and prognosis of chronic kidney disease (CKD) [1].Albuminuria, as a marker of kidney damage, provides a more specific and sensitive measurement of glomerular permeability than does proteinuria. An ACR measured from a spot urine sample acquired in the early morning is preferred for initial evaluation of albuminuria. This test can also be used to confirm a positive reagent strip urinalysis result. A moderately increased ACR (≥30 mg/g) for more than 3 months is diagnostic of CKD. The severity of albuminuria is also used for staging and prognosis of CKD [1,2].Albuminuria generally appears before the reduction of glomerular filtration rate in people with diabetic glomerulosclerosis but may appear later in people with hypertensive nephrosclerosis. Albuminuria is independently associated with an increased risk of cardiovascular events and mortality. In individuals with diabetes and/or hypertension, early identification of albuminuria that prompts blood pressure and glycemic control may subsequently reduce the risk of cardiovascular events and CKD progressing to end-stage renal disease. Referral to specialist kidney care services is recommended in individuals with a consistent finding of severely increased ACR (≥300 mg/g) [1-4].Factors that affect urinary ACR include menstrual blood contamination, symptomatic urinary tract infections, exercise, upright posture (orthostatic proteinuria), and other conditions that increase vascular permeability (eg, septicemia). Given the pathological and physiological causes of transient albuminuria, repeating ACR tests twice with early morning urine samples in the next 2 months is recommended. ACR from a timed urine sample can provide a more accurate estimate of albuminuria [1].The results of this test should be interpreted in the context of pertinent clinical and family history and physical examination findings.References1. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease.Kidney Int Suppl. 2013;3(1):1-150.2. Inker LA, et al.Am J Kidney Dis. 2014;63(5):713-735.3. American Diabetes Association. Standards of medical care in diabetes-2020.Diabetes Care. 2020;43(suppl 1):S135-S151.4. Shin JI, et al.Hypertension. 2021;78(4):1042-1052.

Liver & Kidney Health, Digestive Health

Alanine Aminotransferase (ALT) measurements are particularly useful in the diagnosis and management of certain liver diseases, e.g., viral hepatitis and cirrhosis. ALT activity in tissue is generally much lower than aspartate aminotransferase (AST) activity and is found in highest concentrations in the liver. Significant elevations of ALT occur only in diseases of the liver. ALT is often measured in conjunction with AST to determine whether the source of the AST is the liver or the heart. ALT is normally not elevated in cases of myocardial infarction, i.e., a normal ALT, in conjunction with an elevated AST, tends to suggest cardiac disease. However, slight elevations of ALT may occur if an infarct destroys a very large volume of heart muscle.

Autoimmune & Inflammation

Actin antibodies are found in 52% to 85% of patients with autoimmune hepatitis or chronic active hepatitis and in 22% of patients with primary biliary cirrhosis.

Autoimmune & Inflammation

Other abnormalities found in some sarcoidosis patients include elevations of serum alkaline phosphatase, calcium, gamma globulin with polyclonal gammopathy, and hypercalciuria. Serum angiotensin converting enzyme is elevated in 50% of cases of sarcoidosis but not in cases of active tuberculosis or Hodgkin disease. Increases are less frequent when sarcoidosis is inactive.6Some 80% to 90% of patients with demonstrably active sarcoidosis have elevated serum ACE. Angiotensin converting enzyme activity is also increased in sarcoid lymph node homogenate. The diagnosis of sarcoidosis is an histopathologic/clinical complex. Noncaseating granulomas must be proven not to be caused by tuberculosis, histoplasmosis, or other microbiologic entities. Berylliosis is a very rare cause of such granulomas.ACE is a dipeptidyl carboxypeptidase. It functions to split dipeptides from the free carboxy end of a variety of polypeptides including angiotensin I and bradykinin. It is especially known for its generation of the octapeptide angiotensin II by releasing the dipeptide histidyl-leucine from angiotensin I. The major site of ACE production is the pulmonary bed of endothelial cells.Thyroid hormone may modulate ACE activity. Both patients with low T3levels (and clinical hypothyroidism) and patients with anorexia nervosa with associated findings of hypothyroidism may have low serum ACE activity.7,8Monitoring of ACE levels may have application in assessing risk of pulmonary damage due to use of some antineoplastic agents, in particular bleomycin.9Serum ACE is decreased in some patients with bronchogenic carcinoma. With response to chemotherapy/radiation therapy the ACE level has been noted to normalize.10Cerebrospinal fluid ACE is useful in patients with neurosarcoidosis.Elevated serum ACE levels in a case of the uncommon entity, Melkersson-Rosenthal syndrome, probably relate to the sarcoid-like noncaseating granulomas that are found in this condition. ACE levels normalized after successful (clinical management) therapy with methotrexate.11Serum ACE abnormality has been reported in 20% to 30% of alpha1-antitrypsin variants (MZ, ZZ, and MS Pi types) but in only about 1% of individuals with normal MM Pi type.12There is evidence that paraquat poisoning (because of its effect on pulmonary capillary endothelium) is associated with elevated serum ACE.13

Digestive Health, General Health & Wellness

The major sources of amylase are the pancreas and the salivary glands. The most common cause of elevation of serum amylase is inflammation of the pancreas (pancreatitis). In acute pancreatitis, serum amylase begins to rise within 6-24 hours, remains elevated for a few days and returns to normal in 3-7 days. Other causes of elevated serum amylase are inflammation of salivary glands (mumps), biliary tract disease and bowel obstruction. Elevated serum amylase can also be seen with drugs (e.g., morphine) which constrict the pancreatic duct sphincter preventing excretion of amylase into the intestine.

Liver & Kidney Health, Bone Health

Serum alkaline phosphatase levels are of interest in the diagnosis of hepatobiliary disorders and bone disease associated with increased osteoblastic activity. Moderate elevations of alkaline phosphatase may be seen in several conditions that do not involve the liver or bone. Among these are Hodgkin's disease, congestive heart failure, ulcerative colitis, regional enteritis, and intra-abdominal bacterial infections. Elevations are also observed during the third trimester of pregnancy.

Nutrition & Vitamins, Liver & Kidney Health

Serum albumin measurements are used in the monitoring and treatment of numerous diseases involving primarily the liver and kidney. Its main value lies in the follow-up therapy where improvement in the serum albumin level is the best sign of successful medical treatment. There may also be a loss of albumin in the gastrointestinal tract, in the urine by the damaged kidney or direct loss of albumin through the skin. More than 50% of patients with gluten enteropathy have depressed albumin. The only cause of increased albumin is dehydration; there is no naturally occurring hyperalbuminemia.

Women's Health

Androstenedione (also known as 4-androstenedione and δ4-androstenedione) is a 19-carbon steroid hormone produced in the adrenal glands and the gonads that is the common precursor in the biochemical pathway that produces the androgen testosterone and the estrogens estrone and estradiol.1-7Androstenedione has approximately one tenth of the androgenic potency of testosterone.1Androstenedione is synthesized by means of two biochemical pathways. The predominant pathway involves conversion of 17-hydroxypregnenolone to dehydroepiandrosterone (DHEA) catalyzed by the enzyme 17,20-lyase, with subsequent conversion of DHEA to androstenedione catalyzed by the enzyme 3-β-hydroxysteroid dehydrogenase. A secondary pathway for androstenedione production involves conversion of 17-hydroxyprogesterone to androstenedione directly by 17,20-lyase. 17,20-lyase is required for both pathways of androstenedione synthesis.The production of adrenal androstenedione is controlled by ACTH, whereas production of gonadal androstenedione is governed by the gonadotropins, luteinizing hormone (LH), and follicle stimulating hormone (FSH). Androstenedione produced in the adrenal gland of both men and women is further converted to testosterone by the enzyme 17-β-hydroxysteroid dehydrogenase.1In women, androstenedione produced by theca cells of the ovary is converted to estrogen by the enzyme aromatase in the granulosa cells of the ovary.5Androstenedione secreted into the plasma by either the adrenal or ovary can be converted to testosterone and estrogens by the same enzymes in peripheral tissues. Androstenedione, largely of ovarian origin, is the only circulating androgen that is higher in premenopausal women than in men.1After menopause, androstenedione production is about halved, primarily due to the reduction of the steroid secreted by the ovary. Nevertheless, androstenedione is the principal steroid produced by the postmenopausal ovary.Congenital adrenal hyperplasia (CAH) is a family of disorders caused by defects in one of the enzymes of the adrenal steroidogenic pathway.1,3,6The most common form of CAH results from mutations in the gene that codes for the 21-hydroxylase enzyme.1,3,6Patients with CAH develop varying degrees of glucocorticoid and mineralocorticoid deficiency due to the inability to produce cortisol and aldosterone, respectively.1,3,6Diminished cortisol levels cause an increase in pituitary adrenocorticotrophic hormone (ACTH) secretion due to a lack of negative feedback. The resultant high levels of ACTH lead to adrenal hyperplasia and dramatically increased production of adrenal steroids proximal to the enzyme block.1,3,6These steroids (progesterone and 17-hydroxyprogesterone) are shunted into the adrenal androgen pathway that leads to increased concentrations of dehydroepiandrosterone and androstenedione.1,3,6These weakly androgenic steroids are then peripherally converted to testosterone that produces the androgenic symptoms frequently associated with CAH.1,3,6The diagnosis and therapeutic monitoring of CAH is based on clinical parameters and the measurement of the concentrations of adrenal steroid products and their metabolites.1,3,6Recent clinical guidelines have recommended the use of 17-hydroxyprogesterone (17OHP) as the primary marker for diagnosis and monitoring of CAH.6Other steroid products--including androstenedione and testosterone--can provide additional clinical information in some circumstances.3,6,8-11There is generally a good correlation between 17OHP, androstenedione, and testosterone concentrations in a single blood sample, suggesting these hormone concentrations are all under similar influences.9Random serum steroid levels in CAH patients tend to fluctuate with time of day and timing relative to glucocorticoid administration.3For this reason, samples for a given patient should be collected at a consistent time before the administration of the morning glucocorticoid dose.3Polycystic ovary syndrome (PCOS) is a syndrome of ovarian dysfunction characterized by hyperandrogenism, menstrual irregularities, and polycystic ovaries.9,12PCOS is associated with an increased risk of diabetes and cardiovascular disease.1The measurement of circulating androstenedione levels has been applied to the diagnosis of PCOS in several studies.6,12-14

Autoimmune & Inflammation

Offered as part of multiple lab tests

Anti-Aging

Adrenocorticotropic hormone (ACTH), or corticotropin, is a peptide hormone consisting of 39 amino acids. It is produced in the anterior pituitary of the brain as part of the precursor molecule pro-opiomelanocortin (POMC). Tissue-specific cleavage results in ACTH and a range of related peptides.1,4ACTH stimulates formation and secretion of glucocorticoids (especially cortisol) by the adrenal cortex. The glucocorticoid production is regulated by various factors.5-8After stimulation (eg, by physical effort or by the internal body clock), the hypothalamus secretes CRH (corticotropin-releasing hormone). CRH acts on the pituitary, which in turn synthesizes and secretes ACTH. Finally, ACTH stimulates secretion of the glucocorticoids by the adrenals. High concentrations of glucocorticoids in the blood inhibit secretion of CRH and ACTH via a negative feedback mechanism.ACTH concentrations show a diurnal variation with high levels in the morning and low levels in the evening; therefore, as with cortisol, it is important to know the collection time of the plasma sample for interpretation of the results.Plasma ACTH measurements are useful in the differential diagnosis of pituitary Cushing's disease (ACTH hypersecretion), autonomous ACTH-producing pituitary tumors (eg, Nelson's syndrome), hypopituitarism with ACTH deficiency, and ectopic ACTH syndrome.9,10In addition to cortisol measurements, ACTH determinations can be used together with functional or stimulation tests to diagnose the origin of glucocorticoid overproduction. Similarly, ACTH measurements can be employed to facilitate differential diagnosis of adrenocortical insufficiency (Addison's disease).ACTH not produced by the pituitary gland is known as ectopic ACTH;11this is often associated with small cell carcinoma of the lung. In rare cases, ectopic ACTH can be caused by thymic tumors, pancreatic adenocarcinomas, or bronchial carcinoids. These tumors often secrete ACTH precursors (POMC and pro-ACTH).

Heart Health & Cardiovascular

The renin-angiotensin system and potassium ion are the major regulators of aldosterone secretion, whereas ACTH and other POMC peptides, sodium ion, vasopressin, dopamine, ANP, α-adrenergic agents, serotonin, and somatostatin are minor modulators.1,2Renin cleaves angiotensinogen, which is synthesized by the liver; to produce angiotensin I. Angiotensin I is, in turn, rapidly cleaved by angiotensin-converting enzyme (ACE) in the lung and other tissues to form angiotensin II. Angiotensin II stimulates aldosterone secretion and vasoconstriction. Factors that decrease renal blood flow, such as hemorrhage, dehydration, salt restriction, upright posture, and renal artery narrowing, increase renin levels which, in turn, raise aldosterone levels. In contrast, factors that increase blood pressure, such as high salt intake, peripheral vasoconstrictors and supine posture, decrease renin and aldosterone levels.3Aldosterone promotes active sodium transport and excretion of potassium.Hypokalemia increases and hyperkalemia decreases renin release.1Potassium also directly increases aldosterone secretion by the adrenal cortex and aldosterone then lowers serum potassium by stimulating its excretion by the kidney. High dietary potassium intake increases plasma aldosterone and enhances the aldosterone response to a subsequent potassium or angiotensin II infusion.3Primary hyperaldosteronism, also referred to as Conn syndrome, is caused by the overproduction of aldosterone by one or both of the adrenal glands.1,2Historically, primary aldosteronism was considered to be an uncommon cause of hypertension. However, recent studies indicate that 10% to 15% of cases are associated with primary hyperaldosteronism.4Secondary hyperaldosteronism is relatively common and can occur as the result of any condition that decreases blood flow to the kidneys (ie, renal artery stenosis), decreases blood pressure, or lowers plasma sodium levels. Secondary hyperaldosteronism may also be seen with cirrhosis, congestive heart failure, and toxemia of pregnancy.Hyperaldosteronism increases reabsorption of sodium and loss of potassium by the kidneys, resulting in an electrolyte imbalance.1,5The condition can be asymptomatic, although muscle weakness can occur if potassium levels are very low. A number of studies have suggested that high-normal aldosterone levels predict development of high blood pressure in normotensive subjects6and that increased aldosterone action contributes to hypertension, cardiovascular fibrosis, and cardiac hypertrophy.5-7

Anti-Aging

The renin-angiotensin system and potassium ion are the major regulators of aldosterone secretion, whereas ACTH and other POMC peptides, sodium ion, vasopressin, dopamine, ANP, α-adrenergic agents, serotonin, and somatostatin are minor modulators.1,2Renin cleaves angiotensinogen, which is synthesized by the liver to produce angiotensin I. Angiotensin I is, in turn, rapidly cleaved by angiotensin-converting enzyme (ACE) in the lung and other tissues to form, angiotensin II. Angiotensin II stimulates aldosterone secretion and vasoconstriction. Factors that decrease renal blood flow, such as hemorrhage, dehydration, salt restriction, upright posture, and renal artery narrowing, increase renin levels which, in turn, raise aldosterone levels. In contrast, factors that increase blood pressure, such as high salt intake, peripheral vasoconstrictors, and supine posture, decrease renin and aldosterone levels.3Aldosterone promotes active sodium transport and excretion of potassium.Hypokalemia increases and hyperkalemia decreases renin release.1Potassium also directly increases aldosterone secretion by the adrenal cortex and aldosterone then lowers serum potassium by stimulating its excretion by the kidney. High dietary potassium intake increases plasma aldosterone and enhances the aldosterone response to a subsequent potassium or angiotensin II infusion.3Aldosterone deficiency conditions typically present with electrolyte abnormalities, including a variable degree of hyponatremia, hyperkalemia, and metabolic acidosis.1,2,4Congenital aldosterone deficiency is characterized by poor growth in childhood and minimal symptoms in adults. Infants typically suffer recurrent dehydration, salt wasting, and failure to thrive. These symptoms are present generally within the first three months of life. A modest uremia with a normal creatinine level reflects dehydration in the presence of intrinsically normal renal function. Plasma renin activity is invariably elevated.Hypoaldosteronism can occur in any condition that causes destruction or dysfunction of the adrenal gland.1,2,4These conditions include primary adrenal insufficiency, congenital adrenal hypoplasia, isolated mineralocorticoid deficiency, acquired secondary aldosterone deficiency (hyporeninemic hypoaldosteronism), and acquired primary aldosterone deficiency. Hyporeninemic hypoaldosteronism is the most common form of isolated hypoaldosteronism and is caused by impaired renin release from the kidney. Congenital hypoaldosteronism caused by inherited enzymatic defects in aldosterone biosynthesis are rare. Corticosterone methyloxidase I (CMO I) deficiency is associated with elevated serum levels of corticosterone and low levels of 18-hydroxy-corticosterone and aldosterone. Corticosterone methyloxidase II (CMO II) deficiency produces high levels of 18-hydroxy-corticosterone, the immediate precursor of aldosterone. Acquired primary hypoaldosteronism can be caused by the administration of heparin. Also, persistently hypotensive, critically ill patients with sepsis, pneumonia, peritonitis, cholangitis, and liver failure can have inappropriately low plasma aldosterone concentrations in relation to elevated plasma renin activity.Primary hyperaldosteronism, also referred to as Conn syndrome, is caused by the overproduction of aldosterone by one or both of the adrenal glands.1,2Historically, primary aldosteronism was considered to be an uncommon cause of hypertension; however, recent studies indicate that 10% to 15% of cases are associated with primary hyperaldosteronism.5Secondary hyperaldosteronism is relatively common and can occur as the result of any condition that decreases blood flow to the kidneys (ie, renal artery stenosis), decreases blood pressure, or lowers plasma sodium levels. Secondary hyperaldosteronism may also be seen with cirrhosis, congestive heart failure. and toxemia of pregnancy.Hyperaldosteronism increases reabsorption of sodium and loss of potassium by the kidneys, resulting in an electrolyte imbalance.1,6The condition can be asymptomatic, although muscle weakness can occur if potassium levels are very low. Several studies have suggested that high-normal aldosterone levels predict development of high blood pressure in normotensive subjects7and that increased aldosterone action contributes to hypertension, cardiovascular fibrosis, and cardiac hypertrophy.6-8

Heart Health & Cardiovascular

In 1971, Alaupovic suggested that apolipoproteins should be measured when assessing the relation of lipids and lipoproteins to CHD.2Many patients with CHD were found to have normal serum and cholesterol levels. It was postulated that the chemical composition of the lipoproteins was more important for understanding the process of CHD than their blood levels.Subsequent studies have demonstrated that apolipoproteins are better discriminators than lipids and lipoproteins in patients with CHD and their relatives.A number of studies have shown that apo A-1 and apo B correlate better with evidence of CHD than do lipoprotein measurements alone. In an investigation of first-degree relatives of patients with CHD, serum apo A-1 levels were significantly lower and apo B levels were significantly higher than those of healthy controls. Apo B was a better discriminator between male relatives, and apo A-1 was a better discriminator between female relatives and CHD patients. Furthermore, the percentage of correctly classified subjects increased by 12% when apo A-1 and apo B measurements were added as variables.Avogaro et al found that serum apo A-1 and apo B levels, as well as various ratios using apolipoprotein measurements, were the variables that best discriminated male myocardial infarction survivors from age- and sex-matched controls.3In 1983, Maciejko et al compared apo A-1 and HDL cholesterol measurements for their ability to identify male patients with angiographically assessed CHD.4Analysis of their results indicated that apo A-1 alone misclassified 12.9% of the individuals compared to a misclassification error of 21.3% for HDL cholesterol alone. When apo A-1 and HDL cholesterol were used in combination, a misclassification error of 10.6% resulted. More recent studies have drawn similar conclusions.When apo A-1, apo B, lipids, and lipoprotein cholesterol were measured in school-aged children (mean age of 10 years), apo A-1 and apo B levels were associated with a history of myocardial infarction in their parents. In striking contrast, the levels of serum lipids and lipoprotein-cholesterol values in these children were not related to myocardial infarction in either parent. Although no definite relationship between childhood apolipoprotein levels and adult CHD can be drawn, the results indicate that apolipoprotein measurements are more related to clinical disease than are conventional lipid measurements.5Although the relationship of triglyceride measurements and CHD remains controversial, apolipoprotein measurements may be of benefit in identifying patients with hypertriglyceridemia who are at risk for CHD. Maciejko has suggested that apo B levels are helpful in differentiating primary causes of hypertriglyceridemia, provided that secondary causes (diabetes, alcohol ingestion, uremia, acromegaly, emotional stress or stress from acute illness, and certain drugs such as estrogen or beta blockers) have been ruled out. In familial endogenous hypertriglyceridemia, the apo B concentrations will be low while the patient with hypertriglyceridemia from familial combined hyperlipidemia will have a high apo B level.Apolipoprotein measurements are also useful in the differentiation of familial hyper- or hypolipidemias. As mentioned, apo B may be used to differentiate familial combined hyperlipidemia from familial hypertriglyceridemia. Apo B measurements will also provide laboratory evidence of hyperapobetalipoproteinemia with excess apo B, whereas apo B deficiency states are found in abetalipoproteinemia, hypobetalipoproteinemia, familial hypobetalipoproteinemia with chylomicronemia, and abetalipoproteinemia with normotriglyceridemia. Apo A-1 deficiency states include Tangier disease, hypoalphalipoproteinemia, and HDL deficiency.These studies indicated that apolipoprotein measurements can provide clarification in a variety of clinical states involving dyslipidemias. The Maciejko, Kottke, and Naito studies have concluded that apolipoprotein concentrations have greater discrimination in classifying patients who have or are predisposed to CHD and are more stable parameters than are lipids and lipoproteins.6Lipids and lipoproteins are dynamic molecules whose concentration and composition are continually changing due to normal biologic variation, whereas apo A-1 and apo B levels are less affected, with change reflecting disease rather than biologic variability. In summary, apo A-1 and apo B measurements may be useful in the presence of the following conditions:• Borderline elevations of cholesterol• High cholesterol:HDL ratio with normal cholesterol• Borderline elevations of LDL• Normolipidemic children with a positive family history• Normolipidemic adults with a positive family history• Primary dyslipoproteinemias

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

This allergen-specific IgE antibody test quantifies an individual’s IgE response toAspergillus fumigatus.It is an in vitro quantitative assay that is intended to be used in conjunction with other clinical information to aid in the diagnosis of allergic diseases [1].While allergen-specific serum IgE testing is considered comparable to skin testing in many instances, both the American Academy of Allergy, Asthma, and Immunology and the American College of Allergy, Asthma, and Immunology recognize that allergen-specific serum IgE testing may be preferred in some clinical situations. These include 1) the presence of widespread skin disease, 2) the recent use of antihistamines or other medications that can affect the results of allergy skin tests, 3) uncooperative patients, and 4) medical history suggesting that allergen skin testing would pose a significant risk for a serious allergic reaction [1].A definitive clinical diagnosis of allergy should not be based on the results of any single diagnostic method, but should be made by a trained healthcare provider after all clinical and laboratory findings have been evaluated.More specific information about this allergen can be found athttp://www.phadia.com/en/products/allergy-testing-products/immunocap-allergen-information/molds-and-other-microorganisms/allergens/aspergillus-fumigatus/Reference1. Bernstein IL, et al.Ann Allergy Asthma Immunol.2008;100(Suppl 3):S1-S148.

Allergy Testing

This test quantifies an individual's IgE response to acacia. Allergen-specific serum IgE testing is considered comparable to skin testing and may be preferred in some clinical situations. However, a positive test result only indicates that a patient is sensitized to the allergen of concern. Many IgE-sensitized individuals do not develop any symptoms when exposed to the allergen. A diagnosis of allergy should only be made by a trained medical provider after conducting a thorough clinical evaluation [1].More specific information about this allergen can be found on the following website:https://www.thermofisher.com/phadia/us/en/resources/allergen-encyclopedia.htmlReference1. Bernstein IL, et al.Ann Allergy Asthma Immunol. 2008;100(3 Suppl 3):S1-S148.

Blood Disorders, General Health & Wellness

ABO type and Rh are needed to identify candidates for Rh immune globulin and to assess the risk of hemolytic disease of the newborn.

Allergy Testing

Offered as part of multiple lab tests

Liver & Kidney Health

Albumin excreted in the urine (Microalbumin) is a sensitive marker of nephropathy. It is used to screen for early renal disease in diabetic patients.

Allergy Testing

Offered as part of multiple lab tests

Heart Health & Cardiovascular, General Health & Wellness

Aids in the diagnosis of primary disease of skeletal muscle myocardial infarction and viral hepatitis.

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Digestive Health

AST is widely distributed throughout the tissues with significant amounts being in the heart and liver. Lesser amounts are found in skeletal muscles, kidneys, pancreas, spleen, lungs, and brain. Injury to these tissues results in the release of the AST enzyme to general circulation. In myocardial infarction, serum AST may begin to rise within 6-8 hours after onset, peak within two days and return to normal by the fourth or fifth day post infarction. An increase in serum AST is also found with hepatitis, liver necrosis, cirrhosis, and liver metastasis.

Heart Health & Cardiovascular, Blood Disorders

SeeAntithrombin (AT) Deficiency Profile [015594]for more clinical information.

Digestive Health

Offered as part of multiple lab tests

Autoimmune & Inflammation

This test is useful in evaluating patients presenting with sarcoidosis, Gaucher's disease and lymphangiomyomatosis in that the enzyme is increased in these clinical settings.

Digestive Health

Ammonia is one of the by-products of protein metabolism. Elevated blood ammonia levels have been associated with severe liver dysfunction such as hepatic encephalopathy, coma resulting from cirrhosis, severe hepatitis, Reye's syndrome and drug hepatotoxicity. Also, elevated blood ammonia has been reported in cardiac failure, azotemia, and pulmonary emphysema. Correlation between plasma ammonia and the degree of encephalopathy can be erratic.

Cancer Screening

Elevation of serum AFP above values found in healthy individuals occurs in several malignant diseases, most notably nonseminomatous testicular cancer and primary hepatocellular carcinoma. AFP is not recommended as a screening procedure to detect cancer in the general population.

Liver & Kidney Health

Albumin excreted in the urine (Microalbumin) is a sensitive marker of nephropathy. It is used to screen for early renal disease in diabetic patients.

Autoimmune & Inflammation, General Health & Wellness

This immunofluorescence assay (IFA) is often ordered as part of an initial diagnostic evaluation of individuals with clinical suspicion of autoimmune diseases associated with antinuclear antibodies (ANAs). The American College of Rheumatology (ACR) recommends IFA on human epithelial type 2 (HEp-2) cells as the gold standard method for ANA testing because of its overall high sensitivity [1].ANAs are associated with several autoimmune diseases, such as systemic lupus erythematosus, systemic sclerosis, mixed connective tissue disease, polymyositis, primary biliary cholangitis, rheumatoid arthritis, juvenile rheumatoid arthritis, Sjogren syndrome, and autoimmune hepatitis. The laboratory evaluation for individuals with clinical suspicion of these autoimmune diseases often begins with an ANA screen.Knowing the ANA titer can be helpful in interpreting positive ANA results. A titer of at least 1:40 is considered positive, but low-positive titers are not uncommon in healthy individuals. Higher titers are generally associated with greater likelihood of autoimmune disease [2]. When results are positive, various fluorescent staining patterns observed in the nucleus or the cytoplasm can aid in the differential diagnosis and guide selection of further testing for specific autoantibodies. The International Consensus on Antinuclear Antibody Pattern provides guidance on interpretation and reporting of IFA staining patterns with HEp-2 cells [3].Individuals with negative results on the ANA IFA usually also have negative results on specific ANAs. Therefore, subserology testing is generally not recommended in individuals without positive ANA IFA results and clinical suspicion of relevant autoimmune disease [4]. However, Jo-1 antibody may be detected in ANA IFA-negative patients with some types of myositis, and SSA antibody may be detected in some ANA IFA-negative patients with lupus or Sjogren syndrome [4].The results of this test should be interpreted in the context of pertinent clinical and family history and physical examination findings.References1. Methodology of testing for antinuclear antibodies (position statement). 2009. American College of Rheumatology. Updated December 2019. Accessed May 15, 2023.https://assets.contentstack.io/v3/assets/bltee37abb6b278ab2c/blta48818378bc89445/acr-position-statement-methodology-testing-antinuclear-antibodies.pdf2. Tozzoli R, et al.Am J Clin Pathol. 2002;117(2):316-324.3. Chan EK, et al.Front Immunol. 2015;6:412.4. Yazdany J, et al.Arthritis Care Res (Hoboken). 2013;65(3):329-339.

Women's Health

Offered as part of multiple lab tests

Women's Health

This test is used to detect significant RBC antibodies.

Diabetes & Blood Sugar

Albumin excreted in the urine (Microalbumin) is a sensitive marker of Nephropathy. It is used to screen for early renal disease in diabetic patients.

Hormone Testing, Stress & Fatigue

Determination of ACTH is useful in differentiating between primary and secondary adrenocortical hypo- and hyperfunctional disorders: Addison's Disease, Cushing's Syndrome, Adrenal Carcinoma, Ectopic ACTH Syndrome, Nodular Hyperplasia.

Autoimmune & Inflammation

Myasthenia gravis (MG) is an acquired disorder of neuromuscular transmission that is characterized by skeletal muscle weakness and fatigability on exertion that is exacerbated by repeated muscle activity.2-7This autoimmune disease is caused by antibodies directed toward receptors embedded in the motor endplate of the neuromuscular junction. Progressive weakness of the ocular muscles manifesting as asymmetric ptosis and variable diplopia are the presenting symptoms in 60% of patients.5,7Many patients progress to more generalized weakness of peripheral limb muscles and muscles required for body posture, including facial and neck muscles. Bulbar muscle weakness compromises speaking (dysarthria), chewing and swallowing (dysphagia) and respiratory muscle weakness can lead to a myasthenic crisis where patients need to be ventilated artificially.8Clinical symptoms may be restricted to one muscle group, in particular the eye muscles (ocular MG), or may become generalized (generalized MG).5-8Patients with MG frequently have thymic abnormalities (thymic hyperplasia or thymoma).9Ten to 15 percent of patients with MG patients have thymoma, and up to 50% of thymoma patients develop MG.9It is thought that the thymus plays a role in MG pathogenesis and these patients respond well to the surgical removal of the thymus gland.10Neonatal MG can occur as a result of trans-placental transit of antibodies from an affected mother to the fetus, or in some cases, due to antibody to the fetal form of AChR.11-13In the latter case, the mother may be unaffected. It should be noted that the AChR antibody assays employed by Labcorp contain a mixture of adult and embryonic AChRs allowing for the detection of autoantibodies to both proteins. In most cases affected babies are born with a diminished ability to suck and generalized hypotonia. Decrease in utero feta movement caused by MG can also result in arthrogryposis multiplex congenital, a condition where the neonate suffers from contractures in more than two joints and in multiple body areas.The majority of patients with MG have antibodies to the acetylcholine receptor (AChR) and, less frequently, to the other proteins at postsynaptic membrane of the neuromuscular junction.14-16AChR antibodies impede neuromuscular transmission by a range of pathogenic mechanisms including the alteration of tissue architecture and/or by causing a reduction the density of functionality of AChRs.1,17-21Three functionally different types of antibodies against muscle AChR can be measured.1,21-24• AChR binding antibodies attach to the AChR activate the complement system result in in destruction and focal lysis of the neuromuscular junction leading to the destruction of AChR and AChR-related protein at the end-plate.1,20• AChR blocking antibodies functionally block the binding of the neurotransmitter acetylcholine to the receptor.20These antibodies usually occur in association with AChR-binding antibodies and have a higher prevalence in generalized MG compared with ocular MG.20• AChR modulation antibodies crosslink receptor subunits in such as way as to cause the receptors to be internalized and degraded in a process known as antigenic modulation.20,22,25-27Modulating antibodies are implicated with an increased risk of thymoma and the majority of patients with thymoma have modulating antibodies.28Test for serum autoantibodies are highly sensitive and specific for generalized MG but lack sensitivity when there is pure ocular involvement.1,14,29-30Approximately 85% of patients with generalized MG have detectable muscle AChR antibodies (of one or more types), while fewer patients with ocular MH have the antibodies (50-60%).4,30In general, an elevated level of any one of the AChR-binding antibodies in a patient with compatible clinical features confirms the diagnosis of MG. Approximately 15 percent of individuals with confirmed myasthenia gravis have no measurable AChR binding, blocking, or modulating antibodies. Thirty-five percent of these patients (six percent of all MG patients) will have antibodies directed against a muscle-specific tyrosine kinase (MuSK).10,31Autoantibodies levels do not generally correlate with disease severity. However, in individual patients, serial antibody titers tend to correlate with disease status.18,19,32-34Autoantibodies directed against the contractile elements of striated muscle are found in 30% of adult patients with myasthenia gravis and in 80% of those with thymoma.35-37Striational antibodies are associated with the late-onset MG subgroup and are rarely found in AChR antibody-negative MG.

Heavy Metals & Toxins

Aluminum toxicity has been recognized in many settings where exposure is heavy or prolonged, where renal function is limited, or where a previously accumulated bone burden is released in stress or illness. Toxicity may include:• Encephalopathy (stuttering, gait disturbance, myoclonic jerks, seizures, coma, abnormal EEG)• Osteomalacia or aplastic bone disease (associated with painful spontaneous fractures, hypercalcemia, tumorous calcinosis)• Proximal myopathy• Increased risk of infection• Increased left ventricular mass and decreased myocardial function• Microcytic anemia• With very high levels, sudden deathAluminum is ubiquitous in our environment; it is the third most prevalent element in the earth's crust. The gastrointestinal tract is relatively impervious to aluminum, absorption normally being only about 2%. Aluminum is absorbed by a mechanism related to that for calcium. Gastric acidity and oral citrate favors absorption, and H2-blockers reduce absorption. As is true for several trace elements, transferrin is the primary protein binder and carrier for aluminum in the plasma, where 80% is protein bound and 20% is free or complexed to small molecules such as citrate. Cells appear to take up aluminum from transferrin rather than from citrate. Purified preparations of ferritin from brain and liver have been found to contain aluminum. It is not known if ferritin has a specific binding site for aluminum. Factors regulating the migration of aluminum across the blood-brain barrier are not well understood. Serum aluminum correlates with encephalopathy; red cell aluminum correlates with microcytic anemia;1and bone aluminum correlates with aluminum bone disease. Basal PTH when elevated appears to protect bone and thereby favor CNS toxicity. Other factors favoring one form of toxicity over another are not well understood. Aluminum toxicity has been reported to impair the formation and release of parathyroid hormone. The parathyroid glands concentrate aluminum above levels in surrounding tissues. Treatment of aluminum toxicity in renal failure patients often reactivates hyperparathyroidism, which to a certain extent is helpful for bone remodeling and healing.

Infectious Diseases, Autoimmune & Inflammation

This test is a sensitive test for recentstreptococcalinfection. A rise in ASO begins about one week after infection and peaks two to four weeks later. ASO levels do not rise with cutaneous infections. In the absence of complications or reinfection, the ASO level will fall to preinfection levels within 6 to 12 months. Over 80% of patients with acute rheumatic fever and 95% of patients with acute glomerulonephritis due tostreptococcihave elevated levels of ASO.

Blood Disorders, Nutrition & Vitamins

Offered as part of multiple lab tests

Autoimmune & Inflammation

Offered as part of multiple lab tests

Heart Health & Cardiovascular

Apolipoprotein B (APO B) has been reported to be a powerful indicator of CAD. In some patients with CAD, APO B is elevated even in the presence of normal LDL cholesterol.

Heart Health & Cardiovascular, Diabetes & Blood Sugar

The 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults recommend matching the intensity of statin treatment with the absolute risk of cardiovascular events. However, the standard lipid panel alone does not provide a complete assessment of absolute risk of CVD. Adding advanced CVD markers (ion mobility, apob, lp(a), hs crp and lppla2) in addition to the lipid panel will improve assessment of the CVD risk.

Heart Health & Cardiovascular, Diabetes & Blood Sugar

The advanced lipid profile provides a more comprehensive assessment of dyslipidemia and cardiovascular risk than standard lipid panel measurements.

Sexual Health & STDs

Individuals with the antiphospholipid antibody syndrome (APS) have an increased risk for stroke, myocardial infarction, venous thrombosis, thromboembolism, thrombocytopenia, and/or recurrent miscarriages. In 1999, an international consensus conference found that one criterion for the serologic diagnosis of “definite antiphospholipid syndrome” is the presence of anticardiolipin antibody of IgG and/or IgM isotype, at medium or high titer, on two or more occasions, at least 6 weeks apart.3The presence of ACA of moderate to high titer for IgG is strongly associated with both arterial and venous thrombosis and recurrent pregnancy loss.2,4,5The IgM isotype of ACA has also been shown to be associated with venous thrombosis.4Other studies found that ACA of the IgA isotype at moderate to high titer can also be associated with increased risk of APS.2,6ACA antibodies are quite common in the general population and are not always associated with APS. Studies indicate that there is a higher prevalence of IgM positives than IgG in the general population with these isotypes occurring in 9.4% and 6.5% of the population, respectively.7The incidence of these ACA is even higher in normal pregnancy with detection rates of 17% for IgM and 10.6% for IgG.8Many of these antibodies are transient and not associated with APS. The diagnosis of APS should not be made on the basis of a single ACA result but rather on repeated positive results obtained at least six weeks apart.1The Venereal Disease Research Laboratory (VDRL) agglutination test that has been used for decades in the diagnosis of syphilis is based on the detection of antibodies to cardiolipin.9The first solid-phase immunoassays for ACA were developed in the early 1980s.9These solid-phase assays are at least 100-fold more sensitive than the classical VDRL assay and produce many more positive results. In general, ACA are considered to be more sensitive than lupus anticoagulants (LA) for the detection of APS.4The ACA test is positive in 80% to 90% of patients with APS,10and ACA are implicated in approximately five times more cases of APS than are LA;2however, LA are considered to be more specific for APS than ACA.2,10Due to the heterogeneity of antibodies associated with APS, both LA and ACA testing is recommend when APS is suspected.4,11ACA are frequently observed in patients with other autoimmune disorders and malignancies. Individuals with ACA secondary to these other conditions are at increased risk of developing APS. A variety of therapeutic drugs can induce the production of ACA. These drug-induced antibodies may be clinically significant if they persist.2,12

Drug & Alcohol Testing, Mental Health & Neurological

Amitriptyline is a tricyclic antidepressant that blocks the reuptake of serotonin at nerve endings and possesses high anticholinergic activity and cardiovascular toxicity. The drug is extensively metabolized to many polar compounds, the chief of which is nortriptyline. It is also an antidepressant. Both drugs are prescribed for depression and a range of other disorders.Amitriptyline has a peak serum concentration two to six hours postoral dose, and steady-state is achieved after three to eight days of chronic oral dosing. The half-life is 17 to 40 hours and the usual therapeutic range (predose sample at steady-state) includes nortriptyline and is 80−200 ng/mL. Nortriptyline is administered orally, has a half-life of 15 to 90 hours, and peak serum values two to six hours postoral dose. Steady-state is achieved after 4 to 20 days of chronic dosing. Therapeutic levels of nortriptyline alone are 50−150 ng/mL.All the tricyclic antidepressants have significantdrug interactions. Being potent inducers of hepatic drug-metabolizing enzymes, particularly CYP3A4, CYP1A2, and CYP2C9, the antiepileptic drugs, carbamazepine, phenytoin, phenobarbital, and primidone stimulate the oxidative transformation of concurrently prescribed antidepressants.1This results in decreased drug levels of the antidepressant. To a lesser extent, co-administration of oxcarbazepine, topiramate, and felbamate can also result in decreased antidepressant levels.Other tricyclic antidepressant drug interactions:hydrocortisone, methylphenidate, and phenothiazines increase tricyclic levels; tricyclics impair the antihypertensive effectiveness of clonidine and guanethidine; tricyclics and alcohol produce additive sedative effects, tricyclics and antiparkinsonism agents have potent anticholinergic side effects, and tricyclics and MAO inhibitors should not be co-administered because of the potential for antihypertensive and CNS crises.Tricyclics should be avoided in pregnant and lactating women because these drugs have not been established as safe. Geriatric patients are especially prone to postural hypotension, urinary retention, and sedation.2In general, it has been reported that, “Therapeutic drug monitoring of antidepressants allows us to take into account the influence of factors such as co-medications, diet, smoking habit, impaired organ function, and compliance. Therapeutic drug monitoring and genotyping are thus complementary, and their combined use contributes to improve pharmacotherapy with antidepressants and other drugs.”3

Heart Health & Cardiovascular

The Clinical Guidelines Subcommittee of the Endocrine Society has produced a practice guideline for the detection, diagnosis, and treatment of patients with primary aldosteronism (PA).1Primary aldosteronism (PA) is defined as a group of disorders in which aldosterone production is inappropriately high, relatively autonomous, and nonsuppressible by sodium loading.1This inappropriate production of aldosterone can result in cardiovascular damage, suppression of plasma renin, hypertension, sodium retention, and potassium excretion that can lead to hypokalemia. PA is commonly caused by an adrenal adenoma, by unilateral or bilateral adrenal hyperplasia, or, in rare cases, by the inherited condition of glucocorticoid-remediable aldosteronism (GRA).In the past, clinical guidelines indicated that hypokalemia was required for the diagnosis of PA. As a result, PA was considered to be a relatively uncommon cause of hypertension, accounting for <1% of cases;2,3however, more recent studies have challenged these assumptions. Cross-sectional and prospective studies report PA in >10% of hypertensive patients, both in general and in specialty settings.4-12Only a small subset of these patients with PA (9% to 37%) had hypokalemia.13These studies indicate that normokalemic hypertension constitutes the most common presentation of the disease, with hypokalemia probably present in only the more severe cases. In fact, the presence of hypokalemia has low sensitivity and specificity, and a low positive predictive value for the diagnosis of PA.1The new consensus guideline1recommends that case detection of primary aldosteronism (PA) should be undertaken in patient groups with relatively high prevalence of PA. These include patients with:• Joint National Commission (JNC) stage 2 (>160−179/100−109 mmHg), or stage 3 (>180/110 mmHg) hypertension• Drug-resistant hypertension• Hypertension and spontaneous or diuretic-induced hypokalemia• Hypertension with adrenal incidentaloma• Hypertension and a family history of early-onset hypertension or cerebrovascular accident at a young age (<40 years).The new consensus guideline1also recommends case detection for all hypertensive first-degree relatives of patients with PA. The consensus group went on to recommend the use of the plasma aldosterone:renin ratio (ARR) to detect cases of PA in these patient groups.14-20The ARR is calculated as the ratio of the serum aldosterone (in ng/dL) divided by serum plasma renin activity (in ng/mL/hour). The guideline indicates that the diagnosis of PA provides the opportunity for health benefits provided by curative approaches including surgery or improved control of hypertension through specific medical treatment.The consensus guideline recommended that patients with a positive ARR should proceed to confirmatory testing by any of four confirmatory tests described within the document and listed below to definitively confirm or exclude the diagnosis.11. Oral sodium loading2. Saline infusion3. Fludrocortisone suppression4. Captopril challengeRefer to the consensus document for a more detailed description of the confirmatory test.1

Liver & Kidney Health, Respiratory Health

Alpha-1-Antitrypsin level may be increased in normal pregnancy and in several diseases including chronic pulmonary disease; hereditary angioedema; renal, gastric, liver and pancreatic diseases; diabetes; carcinomas and rheumatoid diseases. Alpha-1-Antitrypsin may be decreased in emphysema, hepatic cirrhosis, respiratory distress syndrome of the newborn, nephrosis, malnutrition and cachexia. If a deficiency is present, aat phenotyping may be considered to confirm heterozygous versus homozygous deficiencies.

Heart Health & Cardiovascular

Apolipoprotein A1 is the primary protein associated with HDL cholesterol. Like HDL cholesterol, increased concentrations are associated with reduced risk of cardiovascular disease.

Allergy Testing

Offered as part of multiple lab tests

Blood Disorders

Offered as part of multiple lab tests

Heavy Metals & Toxins

Individuals undergoing hemodialysis are at risk for aluminum toxicity. Prolonged accumulation may cause anemia, encephalopathy, and vitamin D-resistant osteomalacia. Also, workers exposed to high levels or to long-term low levels of aluminum dust are at increased risk of toxicity.

Heavy Metals & Toxins

Blood levels of arsenic have a short half-life and are useful only for monitoring recent or acute exposure. Urine arsenic measurement is a better measure of arsenic poisoning. In addition to pesticides, rodenticides, weed killers, paint, and wood preservatives contain arsenic.

Hormone Testing, Heart Health & Cardiovascular

Approximately 1-2% of individuals with primary hypertension have primary hyperaldosteronism characterized by hypokalemia (low potassium) and low direct renin. Because serum aldosterone concentrations vary due to dietary sodium intake and body positions, some physicians prefer measurement of 24-hour urine concentrations for aldosterone.

Heavy Metals & Toxins

This assay is used to monitor exposure to arsenic, wellness, and therapy during treatment of chronic myelocytic leukemia.

Autoimmune & Inflammation

Anti-centromere abs are found in 46% of patients with Limited Systemic Sclerosis and 11% in Diffuse Systemic Sclerosis, as well as 12% of patients with primary biliary cirrhosis, and are rarely present in normal individuals. The antibodies are associated with CREST syndrome.

Heart Health & Cardiovascular

Apolipoprotein A1 is the primary protein associated with HDL cholesterol. Like HDL cholesterol, increased concentrations are associated with reduced risk of cardiovascular disease. Apolipoprotein B-100 is the primary protein associated with LDL cholesterol and other lipid particles. Like LDL cholesterol, increased concentrations are associated with increased risk of cardiovascular disease. The ratio of these two apolipoproteins correlates with risk of cardiovascular disease.

Women's Health, Pregnancy & Fertility

Offered as part of multiple lab tests

Drug & Alcohol Testing

Offered as part of multiple lab tests

Women's Health, Pregnancy & Fertility

AMH-MIS may be used in the investigation of ovarian reserve since AMH concentrations in adult women reflect the number of small antral and preantral follicles entering the growth phase of their life cycle. These follicles are proportional to the number of primordial follicles that still remain in the ovary, or the ovarian reserve.AMH decreases throughout a woman's reproductive life, which reflects the continuous decline of the oocyte/follicle pool with age and, accordingly, ovarian aging.

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Drug & Alcohol Testing

Offered as part of multiple lab tests

Infectious Diseases

ADNase B antibodies react against the exoenzyme desoxyribonuclease B produced by streptococci. The detection of these antibodies provides evidence of an existing or past streptococcal infection (rheumatic fever, scarlet fever, tonsillitis, glomerulonephritis, and others). The antibody reaction against streptococcal DNase B starts later than the antibody production against streptolysin O, but it can then be detected on a greater percentage of patients.1An increase in the antistreptolysin concentration rarely occurs with skin infections, while a rise in the ADNase B titer can be observed.1-3

Autoimmune & Inflammation

Anti-Jo-1 antibodies are present in approximately 20% to 30% of patients with adult-onset polymyositis syndromes. They are present in >65% of patients with both myositis and interstitial lung disease. In such patients, the presence of anti-Jo-1 antibodies may be predictive of a response to steroid treatment. Testing for ANAs is not adequate for the detection of anti-Jo-1 antibodies.

Autoimmune & Inflammation

Offered as part of multiple lab tests

Autoimmune & Inflammation

Adrenal Antibody is detected in patients with autoimmune adrenal disease, e.g., Addison's disease.

Hormone Testing, Heart Health & Cardiovascular

Aldosterone is a hormone produced by the adrenal glands. Patients with primary hyperaldosteronism exhibit hypokalemia, hypertension, and low direct renin concentrations.

Liver & Kidney Health, Bone Health

When the Total Alkaline Phosphatase activity is increased, the Isoenzymes are useful in determining the source of the increased activity.

Drug & Alcohol Testing

Amiodarone is an antiarrythmic drug. Therapeutic drug monitoring is useful to monitor compliance and avoid toxicity.

Allergy Testing

Offered as part of multiple lab tests

Hormone Testing, General Health & Wellness

Antidiuretic Hormone (ADH), also known as Arginine Vasopressin (AVP), is a neuropeptide that is secreted from the hypothalamus in response to hypovolemia and elevated plasma osmolality.4-6ADH has two primary functions: to retain water in the body and to constrict blood vessels.5The measurement of ADH has been employed in the differential diagnosis of a variety of disorders related to the physiologic response to changes in plasma osmolality and non-osmotic stress.1,7ADH measurement can aid in the differential diagnosis of conditions including diabetes insipidus (DI) and primary polydipsia.Diabetes insipidus (DI) is a rare disorder of water homeostasis characterized by the excretion of abnormally large volumes of hypotonic urine due to the inability to appropriately concentrate urine in response to volume and osmolar stimuli.8,9The primary causes for DI are decreased ADH production (central DI) or decreased renal response to ADH (nephrogenic DI), both of which lead to hypotonic polyuria which is usually accompanied by polydipsia. Along with these etiologies, the differential diagnosis of hypotonic polyuria includes primary polydipsia.9-11In primary polydipsia, there is no initial compromise in ADH secretion or renal action and instead, excessive fluid intake leads to a drop in plasma osmolality and a suppression of ADH synthesis. Primary polydipsia can be caused by an abnormality in the thirst center (dipsogenic polydipsia) or, more commonly, as the result of one of a number of psychiatric disorders (psychogenic polydipsia).9Historically, the primary diagnostic test for the evaluation of polyuria-polydipsia syndrome has been the standard water deprivation test.12-14In healthy subjects, water deprivation causes the plasma osmolality to rise, leading to the release of ADH into the circulation. In this test, insufficient ADH secretion or effect is revealed by insufficient concentration capacity of the kidneys on osmotic stimulation, which is achieved by a prolonged period of thirsting and followed by assessment of the response to exogenous ADH administration (Desmopressin). Recent studies aimed at validating the classical water deprivation revealed a diagnostic accuracy of only around 70%, with an even lower diagnostic accuracy in patients with primary polydipsia.3,12Direct measurement of ADH upon osmotic stimulation has been proposed as an alternative to measuring 24-hour urine osmolality.15

Autoimmune & Inflammation

Offered as part of multiple lab tests

Hormone Testing, Women's Health

Androstenedione may be useful in evaluating patients with androgen excess and managing patients with congenital adrenal hyperplasia (CAH).

Bone Health, Nutrition & Vitamins

The bone-specific alkaline phosphatase (BSAP) assay provides a general index of bone formation and a specific index of total osteoblast activity. BSAP and osteocalcin are the most effective markers of bone formation and are particularly useful for monitoring bone formation therapies and antiresorptive therapies.

Heavy Metals & Toxins

Arsenic is widely distributed in the earth's crust. Arsenic is used in some pesticides and industrial applications. Arsenic toxicity can cause skin changes, respiratory illness, nausea and vomiting, and other effects.

Women's Health, Pregnancy & Fertility

Offered as part of multiple lab tests

Autoimmune & Inflammation

Individuals with the antiphospholipid antibody syndrome (APS) have an increased risk for stroke, myocardial infarction, venous thrombosis, thromboembolism, thrombocytopenia, and/or recurrent miscarriages. In 1999, an international consensus conference found that one criterion for the serologic diagnosis of “definite antiphospholipid syndrome” is the presence of anticardiolipin antibody of IgG and/or IgM isotype, at medium or high titer, on two or more occasions, at least six weeks apart.3The presence of ACA of moderate to high titer for IgG is strongly associated with both arterial and venous thrombosis and recurrent pregnancy loss.1,4,5The IgM isotype of ACA has also been shown to be associated with venous thrombosis.4Other studies found that ACA of the IgA isotype at moderate to high titer can also be associated with increased risk of APS.2,6ACA antibodies are quite common in the general population and are not always associated with APS. Studies indicate that there is a higher prevalence of IgM positives than IgG in the general population with these isotypes occurring in 9.4% and 6.5% of the population, respectively.7The incidence of these ACA is even higher in normal pregnancy with detection rates of 17% for IgM and 10.6% for IgG.8Many of these antibodies are transient and not associated with APS. The diagnosis of APS should not be made on the basis of a single ACA result but rather on repeated positive results obtained at least six weeks apart.2The Venereal Disease Research Laboratory (VDRL) agglutination test that has been used for decades in the diagnosis of syphilis is based on the detection of antibodies to cardiolipin.9The first solid-phase immunoassays for ACA were developed in the early 1980s.9These solid-phase assays are at least 100-fold more sensitive than the classical VDRL assay and produce many more positive results. In general, ACA are considered to be more sensitive than lupus anticoagulants (LA) for the detection of APS.4The ACA test is positive in 80% to 90% of patients with APS,10and ACA are implicated in approximately five times more cases of APS than are LA;1however, LA are considered to be more specific for APS than ACA.1,10Due to the heterogeneity of antibodies associated with APS, both LA and ACA testing is recommend when APS is suspected.4,11ACA are frequently observed in patients with other autoimmune disorders and malignancies. Individuals with ACA secondary to these other conditions are at increased risk of developing APS. A variety of therapeutic drugs can induce the production of ACA. These drug-induced antibodies may be clinically significant if they persist.2,12

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

This panel tests for specific IgE antibodies to 5 different stinging insects that are commonly associated with allergies. Allergen-specific serum IgE testing is considered comparable to skin testing and may be preferred in some clinical situations. However, a positive test result only indicates that a patient is sensitized to the allergen of concern. Many IgE-sensitized individuals do not develop any symptoms when exposed to the allergen. A diagnosis of allergy should only be made by a trained medical provider after conducting a thorough clinical evaluation [1].More specific information about allergens included in this panel may be found on the Quest Diagnostics Test Directory.Reference1. Bernstein IL, et al.Ann Allergy Asthma Immunol.2008;100(3 Suppl 3)S1-S148.

Diabetes & Blood Sugar

Adiponectin is the most abundant peptide hormone secreted by adipocytes.1-3Other cell types such as skeletal and cardiac myocytes and endothelial cells can produce lesser amounts of this protein. Adiponectin has a short half-life of 45-75 minutes despite its minimal degradation during circulation. Its clearance is predominantly by the liver but can also bind pancreatic beta cells and certain heart and kidney cell types.1Adiponectin participates in glucose regulation but also exerts anti-inflammatory, anti-atherogenic and cardioprotective effects as well as effects on lipid metabolism and fatty acid oxidation.1,4Adiponectin directly acts on the liver, skeletal muscle, and vasculature through insulin sensitization and anti-inflammatory/anti-atherogenic effects.1Adiponectin increases insulin secretion from the pancreas and mediates insulin sensitivity in skeletal muscle.1,3,5Adiponectin enhances basal glucose and insulin-stimulated glucose uptake in adipose tissues.1,3,4Adiponectin increases insulin sensitivity and down-regulates gluconeogenesis in the liver while activating fatty acid oxidation.1,3Studies have shown that adiponectin decreases inflammation in macrophages, endothelial tissue, muscle, and epithelial cells.3There is evidence that adiponectin prevents the production of reactive oxidative species and promotes down-regulation of inflammation.3Moreover, it has been shown to inhibit CRP secretion and suppression of pathways involving NF-kB signaling and TNF-Alpha.3Obese patients tend to have decreased serum levels of adiponectin. Various cross-sectional studies have established an inverse relationship between adiponectin serum levels and BMI and fat mass.6-8Adiponectin levels are increased in extremely lean patients suffering from conditions such as anorexia nervosa.7Weight loss through means such as diet and exercise and bariatric surgery have resulted in increased plasma levels of adiponectin in patients.7Diminished serum adiponectin levels is a feature in pathologies such as gestational diabetes.7,9Strong genetic associations between adiponectin levels and insulin resistance have also been established5and low levels of it predict future onset of insulin resistance.7,10Adiponectin levels demonstrate an inverse correlation with adiposity and proinflammatory cytokines in patients suffering from metabolic syndrome.11-14Low levels of adiponectin predict a higher incidence of adverse cardiovascular events such as myocardial infarctions and atherosclerosis.14,15Recently, adiponectin has shown to exhibit activity in functions of cell proliferation, where it has been shown to counter cell growth and induce apoptosis.14It is also noteworthy, however, that several recent studies have also demonstrated adiponectin to have anti apoptotic and proliferative roles.14Accumulating evidence suggest that adiponectin is implicated in the pathogenesis of several malignancies.13,16,17Several observational studies showed that low adiponectin levels are associated with higher risk for breast, cervical, endometrial, ovarian and prostate cancer.13,16,17A relationship between adiponectin and the aggressiveness of some of these tumors has also been reported.13,16-18

Liver & Kidney Health

ADH, produced in the supraoptic and paraventricular locations of the hypothalamus, acts on the collecting tubules of the kidney to cause increase in permeability to water and urea. ADH release is triggered by a number of both osmotic and nonosmotic stimuli. Measurement of ADH is useful in separating central diabetes insipidus, which is marked by polydipsia and polyuria and is caused by inadequate ADH production from nephrogenic diabetes insipidus caused by the inability of renal tubules to respond to ADH. In SIADH, release of ADH is disproportionate to a low serum osmolality. SIADH results due to a number of conditions such as pulmonary disease, head trauma, and cancer.

Autoimmune & Inflammation

Antibodies that produce a speckled ANA pattern are usually directed against extractable nucleoprotein complexes found in the nucleus and/or cytoplasm of substrate cells. Included in this group of antigens are RNP, Sm, SS-A, SS-B, Scl-70, and Jo-1.

Men's Health

AMH/MIS may be used in the detection of the onset of puberty in males, in the differential diagnosis of intersex disorders, cryptorchidism, or anorchidism and in the evaluation of male gonadal function in all ages.

Heart Health & Cardiovascular

ADMA and SDMA may be measured in individuals with multiple risk factors for the development of cardiovascular disease.

Diabetes & Blood Sugar

Adipocytes (fat cells) express a variety of proteins that function in the homeostatic control of glucose and lipid metabolism. Insulin regulates the translocation and secretion of many of these proteins in response to changes in energy balance. Adiponectin is a protein whose secretion from adipocytes is enhanced by insulin stimulation. It has been suggested that the development of non-insulin dependent (Type II) diabetes may involve dysregulation of adiponectin secretion. In support of the link between obesity and Type II diabetes, it has been shown that decreased expression of adiponectin correlates with insulin resistance, and that adiponectin appears to be a potent insulin enhancer linking adipose tissue and whole-body glucose metabolism.• Individuals with low adiponectin levels have a 3X greater risk of developing metabolic syndrome [1].• Men with two or more risk factors for metabolic syndrome and high adiponectin levels are half as likely to develop metabolic syndrome as men with low adiponectin levels [2].• Individuals with low levels of adiponectin are up to 9X as likely to develop type 2 diabetes [3].• Individuals with low adiponectin levels have a 2X increase in the prevalence of CAD [4].• Adiponectin levels in the blood can be increased by thiazolidinediones, such as pioglitazone [5].References:1. Chen SJ et al.PLoS ONE. 2012; 7: e45693.2. Kotooka N et al.Int J Cardiol. 2012 Nov 26. pii: S0167-5273(12)01441-6. doi:10.1016/j.ijcard.2012.10.066. [Epub ahead of print].3. Daimon M et al.Diabetes Care. 2003; 26: 2015-2020.4. Kumada M et al.Arterioscler Thromb Vasc Biol. 2003; 23: 35-39.5. McCoy RG et al.Mayo Clin Proc. 2012; 87: 561-570.

Infectious Diseases, Liver & Kidney Health

Hepatitis A virus (HAV) is a picovirus primarily transmitted via the fecal-oral route. HAV replicates in the liver and is shed in high concentrations in feces from 2-3 weeks before to 1 week after the onset of clinical illness. IgM antibody develops within a week of symptom onset, peaks around three months, and is usually no longer detectable after six months. The presence of IgM antibody to HAV is diagnostic of acute HAV infection.Hepatitis B surface antigen (HBsAg) is a distinctive serological marker of acute or chronic hepatitis B infection. HBsAg is the first antigen to appear following infection with HBV and is generally detected 1-10 weeks after the onset of clinical symptoms. HBsAg assays are routinely used to diagnose suspected HBV infection and monitor the status of infected individuals to determine whether the infection has resolved or the patient has become a chronic carrier of the virus. In patients that recover from HBV infection, HBsAg is undetectable 3-5 months after the onset of infection. In patients with chronic infection, HBsAg remains detectable for life.Anti-HBc IgM increases rapidly, peaks during the acute infection stage of HBV infection, and then falls to a relatively low level as the patient recovers or becomes a chronic carrier. Anti-HBc IgM is useful in the diagnosis of acute HBV infection even when HBsAg concentrations are below the sensitivity of the diagnostic assay.Detection of both HCV antibody and HCV RNA indicates current HCV infection. Detection of HCV antibody in the absence of HCV RNA is consistent with the absence of current HCV infection. Repeat HCV RNA testing is recommended if the person tested is suspected to have had HCV exposure within the past 6 months or has clinical evidence of HCV disease.

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Autoimmune & Inflammation

Offered as part of multiple lab tests

Autoimmune & Inflammation

Scl-70 antibody is seen in 20% of patients with scleroderma, and in some patients with CREST syndrome (calcinosis, Raynaud, esophageal dysfunction, sclerodactyly, telangiectasia). These syndromes are also associated with a high frequency of speckled pattern immunofluorescent antinuclear antibody tests. Scl-70 may identify a subset of scleroderma patients with severe skin, joint, and lung disease. In addition, the presence of Scl-70 in Raynaud phenomenon may indicate a poor prognosis.

Allergy Testing

This panel tests for specific IgE antibodies to 6 molds that are commonly associated with allergies. Allergen-specific serum IgE testing is considered comparable to skin testing and may be preferred in some clinical situations. However, a positive test result only indicates that a patient is sensitized to the allergen of concern. Many IgE-sensitized individuals do not develop any symptoms when exposed to the allergen. A diagnosis of allergy should only be made by a trained medical provider after conducting a thorough clinical evaluation [1].More specific information about allergens included in this panel may be found on the Quest Diagnostics Test Directory.Reference1. Bernstein IL, et al.Ann Allergy Asthma Immunol. 2008;100(3 Suppl 3):S1-S148.

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

This in vitro allergen-specific IgE panel is used to quantitatively measure an individual's IgE response to 5 different cereals that are commonly associated with allergies. These cereals include barley, buckwheat, gluten, rice, and rye. This IgE panel is intended to be used in conjunction with other clinical information to aid in the diagnosis of food allergies [1].While allergen-specific serum IgE testing is considered comparable to skin testing in many instances, both the American Academy of Allergy, Asthma, and Immunology and the American College of Allergy, Asthma, and Immunology recognize that allergen-specific serum IgE testing may be preferred in some clinical situations. These include (1) the presence of widespread skin disease, (2) the recent use of antihistamines or other medications that can affect the results of allergy skin tests, (3) uncooperative patients, and (4) medical history suggesting that allergen skin testing would pose a significant risk for a serious allergic reaction [1].Food-specific IgE tests are extremely sensitive. However, a positive test result only indicates that a patient is IgE-sensitized to the food of concern. Many IgE-sensitized individuals do not develop any symptoms when the food is ingested. A diagnosis of food allergy should only be made by a trained medical provider after conducting a thorough clinical evaluation [2,3]. While food-specific IgE test results may contribute to that evaluation, they cannot replace it. Moreover, several forms of food hypersensitivity are not associated with the presence of food-specific IgE in serum.The results of this panel should be interpreted in the context of pertinent clinical and family history and physical examination findings. More specific information about each allergen included in this panel may be found on the Quest Diagnostics Test Directory.References1. Bernstein IL, et al.Ann Allergy Asthma Immunol.2008;100(3 Suppl 3)S1-S148.2. Sampson HA, et al.J Allergy Clin Immunol. 2014;134(5):1016-1025.3. NIAID-Sponsored Expert Panel, Boyce JA, et al.J Allergy Clin Immunol.2010;126(6 Suppl):S1-S58

Allergy Testing

This panel tests for specific IgE antibodies to 7 nuts that are commonly associated with allergies. Allergen-specific serum IgE testing is considered comparable to skin testing and may be preferred in some clinical situations. However, a positive test result only indicates that a patient is sensitized to the allergen of concern. Many IgE-sensitized individuals do not develop any symptoms when exposed to the allergen. A diagnosis of allergy should only be made by a trained medical provider after conducting a thorough clinical evaluation [1].More specific information about allergens included in this panel may be found on the Quest Diagnostics Test Directory.⁠⁠⁠⁠⁠⁠⁠Reference1. Bernstein IL, et al.Ann Allergy Asthma Immunol. 2008;100(3 Suppl 3):S1-S148.

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Hormone Testing, Heart Health & Cardiovascular

The Aldosterone-renin ratio is used to screen for primary aldosteronism.

Allergy Testing

This in vitro allergen-specific IgE panel is used to quantitatively measure an individual's IgE response to 4 different shellfish that are commonly associated with allergies. These shellfish include clam, crab, lobster, and shrimp. This IgE panel is intended to be used in conjunction with other clinical information to aid in the diagnosis of food allergies [1].While allergen-specific serum IgE testing is considered comparable to skin testing in many instances, both the American Academy of Allergy, Asthma, and Immunology and the American College of Allergy, Asthma, and Immunology recognize that allergen-specific serum IgE testing may be preferred in some clinical situations. These include (1) the presence of widespread skin disease, (2) the recent use of antihistamines or other medications that can affect the results of allergy skin tests, (3) uncooperative patients, and (4) medical history suggesting that allergen skin testing would pose a significant risk for a serious allergic reaction [1].Food-specific IgE tests are extremely sensitive. However, a positive test result only indicates that a patient is IgE-sensitized to the food of concern. Many IgE-sensitized individuals do not develop any symptoms when the food is ingested. A diagnosis of food allergy should only be made by a trained medical provider after conducting a thorough clinical evaluation [2,3]. While food-specific IgE test results may contribute to that evaluation, they cannot replace it. Moreover, several forms of food hypersensitivity are not associated with the presence of food-specific IgE in serum.The results of this panel should be interpreted in the context of pertinent clinical and family history and physical examination findings. More specific information about each allergen included in this panel may be found on the Quest Diagnostics Test Directory.References1. Bernstein IL, et al.Ann Allergy Asthma Immunol.2008;100(3 Suppl 3)S1-S148.2. Sampson HA, et al.J Allergy Clin Immunol. 2014;134(5):1016-1025.3. NIAID-Sponsored Expert Panel, Boyce JA, et al.J Allergy Clin Immunol.2010;126(6 Suppl):S1-S58

Allergy Testing

This in vitro allergen-specific IgE panel is used to quantitatively measure an individual's IgE response to 6 different seafood that are commonly associated with allergies. These shellfish include codfish, crab, lobster, salmon, shrimp, and tuna. This IgE panel is intended to be used in conjunction with other clinical information to aid in the diagnosis of food allergies [1].While allergen-specific serum IgE testing is considered comparable to skin testing in many instances, both the American Academy of Allergy, Asthma, and Immunology and the American College of Allergy, Asthma, and Immunology recognize that allergen-specific serum IgE testing may be preferred in some clinical situations. These include (1) the presence of widespread skin disease, (2) the recent use of antihistamines or other medications that can affect the results of allergy skin tests, (3) uncooperative patients, and (4) medical history suggesting that allergen skin testing would pose a significant risk for a serious allergic reaction [1].Food-specific IgE tests are extremely sensitive. However, a positive test result only indicates that a patient is IgE-sensitized to the food of concern. Many IgE-sensitized individuals do not develop any symptoms when the food is ingested. A diagnosis of food allergy should only be made by a trained medical provider after conducting a thorough clinical evaluation [2,3]. While food-specific IgE test results may contribute to that evaluation, they cannot replace it. Moreover, several forms of food hypersensitivity are not associated with the presence of food-specific IgE in serum.The results of this panel should be interpreted in the context of pertinent clinical and family history and physical examination findings. More specific information about each allergen included in this panel may be found on the Quest Diagnostics Test Directory.References1. Bernstein IL, et al.Ann Allergy Asthma Immunol.2008;100(3 Suppl 3)S1-S148.2. Sampson HA, et al.J Allergy Clin Immunol. 2014;134(5):1016-1025.3. NIAID-Sponsored Expert Panel, Boyce JA, et al.J Allergy Clin Immunol.2010;126(6 Suppl):S1-S58

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Genetic Testing, Mental Health & Neurological

Offered as part of multiple lab tests

Allergy Testing

Offered as part of multiple lab tests

Autoimmune & Inflammation

Offered as part of multiple lab tests

Autoimmune & Inflammation

Myasthenia Gravis (MG) is an autoimmune neuromuscular disorder characterized by muscle weakness, most commonly due to autoantibody-mediated loss of functional acetylcholine receptors (AChR) in the neuromuscular junction. AChR binding autoantibodies are diagnostic of MG, and are found in 85-90% of MG patients. This assay aids in the differential diagnosis of conditions with MG-like muscle weakness and in monitoring therapeutic response. If binding antibodies are negative, assays for modulating and blocking antibodies should be considered.

Autoimmune & Inflammation

Offered as part of multiple lab tests

Hormone Testing

Alpha MSH is a 13 amino acid peptide (1665 kD) with serine at the N terminal end and amidated valine at the C terminal end. Alpha MSH is derived from pro-opiomelanocorticotropin, a precursor protein which contains within its structure, the sequence of ACTH, beta MSH and gamma MSH. The amino acid sequence of alpha MSH is identical to ACTH 1-13 in humans. Alpha MSH stimulates melanosome dispersion within dermal melanocytes and melanin biosynthesis within epidermal melanocytes. It also stimulates aldosterone synthesis. Plasma alpha MSH increases in humans with high fever due to endotoxin. Average plasma alpha MSH has been found higher in AIDS patients and also in obese men with insulin resistance.

Blood Disorders

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

Allergy Testing

This panel tests for specific IgE antibodies to 5 different molds that are commonly associated with allergies. Allergen-specific serum IgE testing is considered comparable to skin testing and may be preferred in some clinical situations. However, a positive test result only indicates that a patient is sensitized to the allergen of concern. Many IgE-sensitized individuals do not develop any symptoms when exposed to the allergen. A diagnosis of allergy should only be made by a trained medical provider after conducting a thorough clinical evaluation [1].More specific information about allergens included in this panel may be found on the Quest Diagnostics Test Directory.Reference1. Bernstein IL, et al.Ann Allergy Asthma Immunol.2008;100(3 Suppl 3)S1-S148.

Allergy Testing

Offered as part of multiple lab tests

Autoimmune & Inflammation

Offered as part of multiple lab tests

Autoimmune & Inflammation

Offered as part of multiple lab tests

Heavy Metals & Toxins

Exposure monitoring/investigation.

Autoimmune & Inflammation

Offered as part of multiple lab tests

Autoimmune & Inflammation

Sensorineural hearing loss, commonly referred to as nerve deafness, may be caused by genetic or acquired factors, such as infections, or it can be immunologically mediated. In the majority of SNHL cases, no cause is apparent and such cases are referred to as idiopathic SNHL. Serum antibody tests to anti-68-kD inner ear antigen can aid in identifying these cases. Using the Western blot technique in patients with progressive SNHL found 35% to be positive for a specific anticochlear antibody in their serum. Recent studies have shown that 32% of patients with idiopathic bilateral SNHL are positive by Western blot. Anti-68-kD (hsp-70) antibodies also occur in approximately 60% of patients with bilateral and 35% of patients with unilateral Ménière's syndrome, an inner ear syndrome that affects balance and hearing.

Heart Health & Cardiovascular

Thromboxane B2 (TxB2) is the stable, inactive product of prostaglandin metabolism of thromboxane A2, which is renally cleared and, therefore, can be measured in the urine. Studies have shown that thromboxane B2 is a sensitive indicator of platelet activation. Since platelets participate in atherogenesis and contribute to acute, ischemic complications, elevated TxB2 levels may reflect ongoing cardiovascular, peripheral vascular, and cerebrovascular disease processes. TxB levels may also be of interest in conditions with increased platelet turnover, such as disseminated intravascular coagulation or immune thrombocytopenia. Studies of patients with diffuse atherosclerotic disease show that TxB2 may be a more sensitive measure of platelet activation than other platelet-specific proteins. Serum or plasma TxB2 assays are typically limited to a research setting because of the significant in vitro platelet instability.Urinary TxB2 is of interest in monitoring the anticoagulant response to aspirin therapy since aspirin inhibits the formation of TxB2 in platelets. In patients responsive to aspirin therapy and taking an adequate dose, urinary 11-dehydro TxB2 levels should be reduced below a predetermined cutoff when compared to control values.

Heart Health & Cardiovascular

Aspirin (which inhibits platelet cyclooxygenase) reduces the risk of thrombosis in cardiovascular disease by impairing platelet function. Patients who do not respond to the platelet inhibitory effects of aspirin are designated as "aspirin resistant". The measurement of 11-dhTXB2 in urine (the principal metabolite of platelet cyclooxygenase derived thromboxane B2) may be used in individuals with cardiovascular disease prior to initiation of aspirin therapy, or in individuals non-responsive to aspirin therapy.

Nutrition & Vitamins

Offered as part of multiple lab tests

Autoimmune & Inflammation, General Health & Wellness

The indirect immunofluorescent test has three elements to consider in the result:1. Positive or negative fluorescence. A negative test is strong evidence against a diagnosis of SLE but not conclusive.2. The titer (dilution) to which fluorescence remains positive (provides a reflection of the concentration or avidity of the antibody). Many individuals, particularly the elderly, may have low titer ANA without significant disease substantiated after work-up.3. The pattern of nuclear fluorescence (reflecting specificity for various diseases).Cytoplasmic (non-nuclear) staining patterns may also be noted with the IFA methodology.Multiplex ANA detects up to 11 specific antibodies of the 100+ antibodies that may be found in the ANA IFA.

Genetic Testing, Nutrition & Vitamins

Offered as part of multiple lab tests

Blood Disorders, Heart Health & Cardiovascular

Aids in characterization of Antithrombin deficiency (AT, previously referred to as Antithrombin III) which is associated with increased thrombotic risk. Type I deficiency is characterized by reduction in activity and antigen levels simultaneously. With type II deficiency, activity levels are lower in comparison to the antigen levels (dysfunctional protein). Acquired deficiency, more common than inherited defects, can occur due to: liver disease, nephrotic syndrome, heparin therapy, disseminated intravascular coagulation (DIC), sepsis, and L-asparaginase chemotherapy.Anticoagulant interference: heparin therapy may lower AT levels. Other anticoagulants do not impact testing (warfarin, target specific anticoagulants such as Dabigatran, Argatroban, Rivaroxaban, Apixaban, Edoxaban).

Genetic Testing, Nutrition & Vitamins

Offered as part of multiple lab tests

Autoimmune & Inflammation

Offered as part of multiple lab tests

Nutrition & Vitamins

Amino Acid analysis is necessary for the diagnosis of a variety of inborn errors of metabolism. These include, but are not limited to, phenylketonuria, tyrosinemia, citrullinemia, non-ketotic hyperglycinemia, maple syrup urine disease, and homocystinuria. The assay is also key for the continued monitoring of treatment plans for these disorders and useful for assessing nutritional status of patients. Our methodology is highly accurate at very low levels as well as at elevated levels.

Autoimmune & Inflammation

Offered as part of multiple lab tests

Autoimmune & Inflammation, General Health & Wellness

Offered as part of multiple lab tests

Genetic Testing, Heart Health & Cardiovascular

Type III hyperlipoproteinemia (broad β disease) is a familial dyslipidemia characterized by the combination of elevated serum cholesterol and triglycerides and the presence of the apolipoprotein E (Apo E) genotype E2/E2. Type III hyperlipoproteinemia has an incidence of 1/2,000−1/10,000. This lipid disorder is associated with a high risk of coronary heart disease and peripheral vascular disease. Onset of type III hyperlipoproteinemia is generally in adulthood but varies from late teens to old age. Before vascular disease develops there are usually no symptoms, and most patients with type III hyperlipoproteinemia are identified only from elevated serum cholesterol and triglycerides discovered during a routine screen. Symptoms include angina, heart attack, claudication, and leg pain. In untreated patients, xanthomas (fat deposits) are occasionally seen (flat in palmar creases or tuberous in joints).The E2 variant of apolipoprotein E is defective in binding to receptors that normally clear harmful lipid particles called B-VLDL from the circulation. One percent of the general population has the E2/E2 genotype, and development of the frank lipid disorder occurs in 1% to 5% of these predisposed individuals, triggered by secondary genetic, hormonal or environmental factors. Ninety-five percent of patients with type III hyperlipoproteinemia are homozygous for E2. Demonstration of the E2/E2 genotype is essential for diagnosis of type III hyperlipoproteinemia.Distinguishing this disorder from other causes of elevated cholesterol is important because effective treatment of type III hyperlipoproteinemia to prevent atherosclerosis often requires a different approach than treatment of other dyslipidemias.

Genetic Testing, Heart Health & Cardiovascular

Type III hyperlipoproteinemia (broad β disease) is a familial dyslipidemia characterized by the combination of elevated serum cholesterol and triglycerides and the presence of the apolipoprotein E (Apo E) genotype E2/E2. Type III hyperlipoproteinemia has an incidence of 1/2,000−1/10,000. This lipid disorder is associated with a high risk of coronary heart disease and peripheral vascular disease. Onset of type III hyperlipoproteinemia is generally in adulthood but varies from late teens to old age. Before vascular disease develops there are usually no symptoms, and most patients with type III hyperlipoproteinemia are identified only from elevated serum cholesterol and triglycerides discovered during a routine screen. Symptoms include angina, heart attack, claudication, and leg pain. In untreated patients, xanthomas (fat deposits) are occasionally seen (flat in palmar creases or tuberous in joints).The E2 variant of apolipoprotein E is defective in binding to receptors that normally clear harmful lipid particles called B-VLDL from the circulation. One percent of the general population has the E2/E2 genotype, and development of the frank lipid disorder occurs in 1% to 5% of these predisposed individuals, triggered by secondary genetic, hormonal or environmental factors. Ninety-five percent of patients with type III hyperlipoproteinemia are homozygous for E2. Demonstration of the E2/E2 genotype is essential for diagnosis of type III hyperlipoproteinemia.Distinguishing this disorder from other causes of elevated cholesterol is important because effective treatment of type III hyperlipoproteinemia to prevent atherosclerosis often requires a different approach than treatment of other dyslipidemias.

Diabetes & Blood Sugar

Offered as part of multiple lab tests

Autoimmune & Inflammation

The antiphospholipid syndrome (APS) is a unique form of acquired autoimmune thrombophilia characterized by recurrent arterial and/or venous thrombosis, pregnancy-related complications (including miscarriages, fetal deaths, premature births, and preeclampsia), and the persistent presence of antiphospholipid antibodies (aPL).2The original APS classification criteria required positivity for any one of 1) anticardiolipin (aCL) IgG or IgM antibodies or 2) lupus anticoagulant (LA) as diagnostic laboratory criteria.3In 2006, the sensitivity of the classification criteria was improved by the including positivity for 3) β2-glycoprotein 1 (β2GPI) IgG or IgM antibodies as additional laboratory criteria for APS and the specificity of diagnosis was improved by extending the requirement of persistent presence of aPL to 12 weeks.4At least one clinical (vascular thrombosis or pregnancy morbidity) and one lab-based (positive test result for LA, aCL IgG/IgM or β2GPI IgG/IgM) criterion have to be met for a patient to be classified as having APS.The antibodies associated with APS are known to react with phospholipids and/or with their binding proteins, either independently or in phospholipid–protein complexes. Early assays for antibodies to the lipid anticardiolipin were quite non-specific and were eventually replaced with assays employing complexes of cardiolipin with the protein β2GPI.2,5Assays for antibodies to β2GPI have been shown to be more specific for APS albeit with somewhat lower sensitivity. Antibodies to prothrombin (aPT), have also been shown to occur in patients with APS.6-12A large amount of data obtained mainly from retrospective studies provides contrasting evidence concerning the clinical significance of aPT antibodies.13-16It has been shown that aPT associated with LA activity or APS clinical manifestations can be detected only using assays employing purified PT antigen immobilized on irradiated plates or as a complex with the lipid phosphatidylserine (aPS/PT).10,11,14,17,18A systematic review and meta-analysis of 10 studies performed before 2014 found that aPS/PT antibody positivity is a strong risk factor for thrombosis and venous events independent from sites and type of thrombosis.6A more recent meta-analysis, published in 2020,19reviewing 15 studies published since the 2014 analysis20-34further confirmed the association between aPS/PT antibodies and thrombosis. Pooled analysis revealed a significant association between aPS/PT-IgG/IgM21-23,31,32,34and thrombotic events with mean Odds Ratio (mOR = 6.8) relative to controls. Pooled analysis further found an association between thrombotic events and aPS/PT-IgG6,20,22-29,31-34positivity (mOR = 6.7) and aPS/PT-IgM20-23,25,28-32,34positivity (mOR = 4.35). A subset of studies,21,24,26,27,31-33including 1,388 patients, evaluated the association between aPS/PT antibodies and pregnancy morbidity (PM) as defined by the 2006 criteria for the definition of APS.4Pooled analysis of the results from these studies found a statistically significant association between any PM and aPS/PT IgG/IgM positivity (mOR = 10.6) and, specifically, aPS/PT IgG positivity (mOR = 6.7).19While the tests currently included in the classification criteria for APS are able to detect the great majority of the cases, some patients present clinical manifestations highly suggestive of APS while being persistently negative for the aPL tests included in the guidelines.1,35-39These patients have been termed to have seronegative APS (SNAPS).36,37,40Testing for aPS/PT antibodies has been proposed as an additional tool to be considered when investigating a patient suspected of having APS, particularly in the absence of guideline aPL positivity9,26,28,32,36,37,40-48or as a part of risk assessment strategies.49A number of studies have found that approximately 50 percent of patients with SNAPS were positive for IgG and/or IgM aPS/PT.33,35,37,39,50,51The addition of aPS/PT to current criteria aPL assays has been reported to contribute to the identification of patients with a history of thrombosis and/or pregnancy-related morbidity that would go undiagnosed using current criteria aPL assays.21,23,32,36,37,42,45,52-56In a number of studies, aPS/PT positivity was reported to be an independent risk factor for LA activity and to occur in LA-negative SLE or APS patients with thrombosis and pregnancy loss.23,54,56Other investigators comparing different aPL combinations in patients with systemic lupus erythematosus observed that aPS/PT antibodies were significantly associated with both LA and pregnancy-related morbidity, while the combination of LA, anti-β2GPI and aPS/PT had superior diagnostic accuracy for thrombosis and pregnancy loss in APS.57,58These studies suggest that aPS/PT and LA are, at least in part, independent risk factors for clinical manifestations of APS. A recent study demonstrated that determination of aPS/PT antibodies in concert with β2GPI antibodies in patients positive for LA might be useful for identifying patients at different risk of thromboembolic events.59In addition, patients with triple positivity for LA, β2GPI and aPS/PT have been shown to be at a higher risk of developing thromboembolic events, risk even higher than that seen for the “classical” aCL, β2GPI and LA triple positivity.52,58aPS/PT have been shown to be associated with recurrent early or late abortions and with premature delivery irrespective of other aPL.51aPS/PT positivity also has been found to be predicative of non-criteria clinical symptoms4including thrombocytopenia or hemolytic anemia.34In addition to diagnosis, use of biomarkers to help predict risk of thrombosis has been addressed by the development of the anti-PhosphoLipid-Score (aPL-S) and the Global APS Score (GAPSS), Both these scoring systems include levels of aPS/PT antibodies (and not PS or PT) as components of the scoring system.19,48,49,60,61

Drug & Alcohol Testing

Offered as part of multiple lab tests

Hormone Testing, Anti-Aging

Offered as part of multiple lab tests

Hormone Testing, Anti-Aging

Offered as part of multiple lab tests

Nutrition & Vitamins

Amino acid analysis is necessary for the diagnosis of a variety of inborn errors of metabolism. These include, but are not limited to, phenylketonuria, tyrosimemia, citrullinemia, non-ketotic hyperglycinemia, maple syrup urine disease, and homocystinuria. The assay is also key for the continued monitoring of treatment plans for these disorders and useful for assessing nutritional status of patients. Our methodology is highly accurate at very low levels as well as at elevated levels.

Nutrition & Vitamins

Acylglycines are an important class of metabolites that are used in the diagnosis of several organic acidurias and mitochondrial fatty acid oxidation disorders.This test is intended for the diagnosis and monitoring of several organic acidemias and fatty acid disorders affecting multiple metabolic pathways.Disorders diagnosed by Acylglycines assay:Isovaleric acidemia3-Methylcrotonyl-Co-A-carboxylase deficiencyShort-chain acyl-CoA dehydrogenase(SCAD) deficiencyEthylmalonic EncephalopathyPropionic acidemiaGlutaric aciduria type-1, 2 and 3Medium-chain acyl-CoA dehydrogenase(MCAD)Beta-ketothiolase deficiency17-Beta-hydroxysteroid dehydrogenase deficiencyIsobutyryl-CoA dehydrogenase deficiencyShort/branched-chain acyl-CoA dehydrogenase deficiency (SBCADD)The test will also allow physicians to determine dietary compliance or the effectiveness of dietary/cofactor therapy for their patients. It can also be used, alone or in conjunction with other tests, to confirm the findings of a positive expanded newborn screen.

Drug & Alcohol Testing

Offered as part of multiple lab tests

Autoimmune & Inflammation, Drug & Alcohol Testing

In the absence of antiadalimumab antibodies, the adalimumab drug level typically reflects the total adalimumab concentration in serum. In the presence of antiadalimumab antibodies, the adalimumab level typically reflects the antibody-unbound fraction of adalimumab concentration in serum.This assay provides clinically valid antibody results at drug levels well above treatment targets (>30 μg/mL). Failure of adalimumab therapy may not always be due to the presence of antiadalimumab antibodies. In addition, the absence of antiadalimumab antibodies does not guarantee positive response to treatment.

Autoimmune & Inflammation, Drug & Alcohol Testing

In the absence of antiadalimumab antibodies, the adalimumab drug level typically reflects the total adalimumab concentration in serum. In the presence of antiadalimumab antibodies, the adalimumab level typically reflects the antibody-unbound fraction of adalimumab concentration in serum.This assay provides clinically valid antibody results at drug levels well above treatment targets (>30 μg/mL). Failure of adalimumab therapy may not always be due to the presence of antiadalimumab antibodies. In addition, the absence of antiadalimumab antibodies does not guarantee positive response to treatment.

Autoimmune & Inflammation

Offered as part of multiple lab tests

Autoimmune & Inflammation

Offered as part of multiple lab tests

Mental Health & Neurological, Autoimmune & Inflammation

Offered as part of multiple lab tests

Mental Health & Neurological, Autoimmune & Inflammation

Offered as part of multiple lab tests