5465 Legacy Dr. Suite 550 - Plano, TX 75024
(214) 919-4982

FAQ

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  • Hereditary Cancer
  • Blood Chemistry & Wellness
  • PHARMACY
  • Toxicology
  • Pharmacogenetics

There are three categories of cancer:  Sporadic, Familial/Multifactorial, and Hereditary.

  • Sporadic cancer is generally thought to be due a combination of environmental factors and natural aging process.
  • Familial/Multifactorial cancer generally refers to a history of cancer in families that cannot be attributed to a single gene mutation. Development of cancer in these families is likely due to a combination of mutations in multiple low risk or moderate risk cancer genes as well as environmental factors.
  • Hereditary cancer refers to cancer that is due to a single gene mutation that significantly increases an individual’s risk of certain cancers over their lifetime. Individuals are born with these singe gene mutations, and in most cases, they have been passed down from family members (inherited )for a number of generations.

Testing for inherited risk of cancer helps you and your doctor understand your risk so you can make the best choices for preventive medical care. Knowing your family history is an important first step, but testing can give you a more accurate picture of your inherited risk.

While testing is the most accurate way to determine your inherited risk of cancer, only people who have cancer in their family or personal history need to be tested. If cancer runs in your family, let your doctor know.

No. Genetic testing does not tell you if you currently have cancer. Your test results tell you about your inherited risk of developing cancer.

No. Genetic testing does not tell you whether you will develop cancer. A positive test result tells you that you have an increased risk of cancer.

The Glucose (in the CMP) and Hemoglobin A1c tests check for diabetes. The Lipid Panel measures your standard lipid and cholesterol markers. An abnormal Lipid Panel suggests you are at an increased risk of heart disease and stroke.

The CBC and CMP tests include a variety of markers that check your immune system, red blood cells, clotting system, electrolytes, kidney and liver function. Calcium is important for bone health, muscle function, and blood clotting.

An 8-12 hour fast is recommended before testing.

It typically takes 4-7 business days or less.

A serious medical condition such as heart disease, prostate cancer or diabetes can exist without noticeable symptoms for up to two years. Early detection is your best defense. A simple blood test can increase your chances of reversing potential problems, and establish a baseline of your normal ranges from which future tests can be monitored.

Questions regarding abnormal results should be discussed with your healthcare provider. For general questions, you may call once of our customer service team members.

Compounding is a process in which a pharmacist prepares customized medications that are made especially for you.

Our pharmacy has highly-trained pharmacists and the proper facility, quality control procedures and equipment to prepare custom-made medications accurately and safely

Commercially available drugs are manufactured by drug companies in mass quantities for the general population with no specific patient in mind. Compounded medications are ordered by a physician, individually prepared by a compounding pharmacy and made specifically for your unique medical needs

For the most part the answer is yes. Most of our prescriptions come from Medical Doctors (M.D.), Doctors of Osteopathic Medicine (D.O.) and Naturopathic Doctors (N.D.). Some doctors have limitations on what may be prescribed and these limitations may vary from state to state.

Yes. Our compounding pharmacy must comply with the regulations set forth by the State Board of Pharmacy. The State Board of Pharmacy sets and enforces regulations for compounding, just as it does for traditional pharmacy.
The ingredients used by our pharmacy to make compounds come from FDA-registered and inspected facilities.
Our compounding laboratory is a state-of-the-art facility equipped with today’s most modern technology. This ensures that each compound we prepare meets the stringent guidelines set forth by the United States Pharmacopeia (USP).

We have a patient-friendly billing policy. For a detailed explanation of our billing policy please contact us at 1-844-205-6782.

With testing, you know what is already in your patient’s body and whether it is safe to prescribe a medication. Medication Monitoring prevents dangerous drug interactions and also determines if a patient is taking their medication as prescribed. Testing allows physicians to make swift and informed decisions regarding pain management. When patients are taking their medication as prescribed, payers control and reduce costs. This also improves the overall quality of chronic pain management for patients.

No. Patients “self-collect” urine in an ordinary bathroom

We will provide you with specimen-collection kits that come pre-addressed and ready to ship back to us.

Once our lab receives the sample, results will be available within 48 hours.

We provide your clinic with a secure login and password to our online portal where you can order, track, and download patient results. If preferred, we also can send patient results via a secure fax or email directly
to your clinic.

We have a very easy to read laboratory report for each patient. We also have a team of specialists on hand that can help to interpret the results if requested and answer any questions you may have.

All results are completely confidential. Many safeguards are in place to assure donors that only authorized individuals from the requesting party receive a result. Without specific authorization, no other individual can have access to a donor’s result. This policy is designed to prevent an unauthorized telephone request for a result. Results are sent by secure printers, fax, computer download, voice mail or phone contact.

Once you receive all necessary forms from the Mercury Team, work together with the provider or appropriate clinic/office staff to complete all new client paperwork.

Fax or email completed account set up forms to our support team.

Call or email with questions regarding supplies. Completed supply request forms should be sent via fax or email to our support team

Call Client Services at (714) 966-1221

Pharmacogenetics is the study of how variations in a patient’s genetics may uniquely influence their response to medicines.

The enzymes that are affected by genes belong to a large family called CYP450. The human body metabolizes medicines so it can be eliminated from the body.

Through an analysis of certain genes that metabolize certain medicine, health care professionals can have key information to determine the most appropriate dose to the most appropriate medicines for each individual patient.

Pharmacogenetics is a subset of pharmacogenomics and is defined as: The study of variations in DNA sequence as related to drug response.

Drug response includes the processes of drug absorption and disposition (e.g., pharmacokinetics (PK)), and drug effects (e.g., pharmacodynamics (PD), drug efficacy, and adverse effects of drugs).

Pharmacogenetic testing allows us to understand the genetic traits that influence the effectiveness of often-routine pharmaceutical therapies. Our one-time test provides key information that you can use for the rest of your life to identify the right medicine, for you. Physicians, health systems, and now healthcare consumers themselves use this test to avoid serious drug side effects and achieve more accurate prescribing.

A DNA characteristic that is an indicator of normal biologic processes, pathogenic processes, and/or response to therapeutic or other interventions. A genomic biomarker could, for example, be a measurement of:

  • The expression of a gene
  • The function of a gene
  • The regulation of a gene

PGx test specimens are collected at a physician’s office using a pain-less, cotton-tipped cheek swab (buccal cells). Tests are performed in a high-complexity, CLIA-certified laboratory

Genes involved in the CYPP450 metabolic system are responsible for much of the variability in drug response.  Understanding this information can help mitigate the risk of ADRs. By understanding the risks of inappropriate drug-gene interaction we may avoid the costly and dangerous risks of drug-drug interactions.

The results of pharmacogenetic test allow a healthcare professional to make a more informed therapeutic decision. They may change the current medication or class of medication prescribed, adjust dosing based on the metabolic status, or find more appropriate alternative medications based on the results

An Adverse Drug Reaction (ADR) occurs when there is appreciably harmful, costly, or unpleasant reaction, resulting from an intervention related to the use of a medicinal product, which predicts hazard from future administration and warrants prevention or specific treatment, or alteration of the dosage regimen, or withdrawal of the product. Sometime ADRs occur as a result of individual’s genetic differences in how they process a medicine or a combination of medicines.

  • ADRs are the 4th leading cause of death ahead of pulmonary disease, diabetes, AIDs, pneumonia, accidents and automobile deaths
1
  • 82% of American adults take at least one medication and 29% take five or more2
  • 42% of pts 65 and older took five or more prescription drugs in 20123
  • 32 million Americans use three or more medications daily4
  • 700,000 emergency department visits and 120,000 hospitalizations are due to Adverse Drug Events (ADE) annually5;
  • $3.5 billion is spent on extra medical costs of Adverse Drug Events (ADE) annually6
  • Polypharmacy is generally defined as the administration of more medications than are clinically indicated, usually taken concurrently to treat the same condition or disease.In a recent pilot study of 363 polypharmacy patients, pharmacogenetic testing provided a more complete understanding of patients’ conditions and treatment options.
    • The averagepatient was on a dozen medications, four of which had a genetic link.
    • 43% of the meds prescribed had a genetic conflict, including 30% with either a major conflict or outright contraindication.
    • 38% of opioid patients had a CYP conflict.
    • Among those taking SSRIs, 39% had a single gene conflict, and 44% had conflicts with both CYP and SLC6A4.

    Source: Kristen Reynolds, PhD, PGXL Laboratories, manuscript in preparation

  • CYP2C19 (Clopidogrel, Antidepressants, PPIs)
  • CYP2C9 (Warfarin, NSAIDS, Sulfonylureas, Statins)
  • VKORC1 (Warfarin)
  • CYP2D6 (Opioids, Antidepressants, Antipsychotics, Beta Blockers)
  • CYP1A2 (Antipsychotics, Antidepressants)
  • CYP3A4 (Muscle relaxers, Benzodiazepines, Statins)
  • CYP3A5 (Muscle relaxers, Benzodiazepines, Statins)
  • 2B6 (Methadone)
  • SLC01B1 (Statins)
  • OPRM1 (Opioids)
  • COMT
  • MTHFR
  • Factor II
  • Factor IV

PGx “Cliff Notes”

CYP2D6: CYP2D6 is a liver enzyme responsible for metabolizing roughly 25% of all drugs, including opioids, many antidepressants, antipsychotics, beta-blockers, and tamoxifen. Detecting variants of the CYP2D6 gene that cause altered CYP2D6 enzymatic activity can identify patients who may be at increased risk of having adverse drug reactions or therapeutic failure to standard dosages of medications metabolized by CYP2D6. Roughly 10% of the population is 2D6 Poor Metabolizers (PMs), meaning they have no 2D6 enzymatic activity. Another 35% of the population is considered Intermediate Metabolizers (IMs) with decreased activity. Still another 1-3% of people are Ultra-Rapid Metabolizers. Both IMs and PMs exhibit decreased metabolic activity, which puts them at risk for side effects to drugs normally inactivated by 2D6 (e.g., venlafaxine, metoprolol), or lack of efficacy for drugs requiring activation by 2D6 (e.g., prodrugs such as opioids, tamoxifen). UMs are the other extreme, having higher than normal enzymatic activity. UMs are at increased risk of failure to active drugs because they clear the drugs too rapidly to benefit from a standard dose. UMs are also at risk of toxic side effects from prodrugs because they convert the drug into an active form more so than expected.

CYP2C19: CYP2C19 is a liver enzyme responsible for metabolizing 10-15% of medications, including clopidogrel, proton pump inhibitors, and many antidepressants. Detecting variants of the CYP2C19 gene that cause altered CYP2C19 enzymatic activity can identify patients who may be at increased risk of having adverse drug reactions or therapeutic failure to standard dosages of medications metabolized by CYP2C19. Roughly 2% of the population is 2C19 Poor Metabolizers (PMs), meaning they have no 2C19 enzymatic activity. Another 30% of the population are considered Intermediate Metabolizers (IMs) with decreased activity. Still another 28% of people are Ultra-Rapid Metabolizers. Both IMs and PMs exhibit decreased metabolic activity, which puts them at risk for side effects to drugs normally inactivated by 2C19 (e.g.,sertraline, diazepam), or lack of efficacy for drugs requiring activation by 2D6 (e.g., prodrugs such as clopidogrel). The FDA required clopidogrel to be labeled with a box warning indicating that PM patients taking clopidogrel are at increased risk of thrombotic events due to failure to convert clopidogrel to its activate component. CYP2C19 UMs are the other extreme, having higher than normal enzymatic activity. UMs are at increased risk of failure to active drugs because they clear the drugs too rapidly to benefit from a standard dose. UMs are also at risk of toxic side effects from prodrugs, such as bleeding on clopidogrel, because they convert the drug into an active form more so than expected.

CYP2C9: CYP2C9 is a liver enzyme that metabolizes approximately 10% of all drugs, including warfarin, phenytoin, non-steroidal anti-inflammatory drugs (NSAIDs), and antihyperglycemic sulphonylureas. Detecting variants of the CYP2C9 gene that cause altered enzymatic activity can identify patients who may be at increased risk of having adverse drug reactions while taking standard dosages of CYP2C9 substrates. Roughly 3% of the population are 2C9 Poor Metabolizers (PMs), meaning they have no 2C9 enzymatic activity. Another 36% of the population are considered Intermediate Metabolizers (IMs) with decreased activity. Both IMs and PMs exhibit decreased metabolic activity, which puts them at risk for side effects to drugs normally inactivated by 2C9. With respect to warfarin, 2C9 deficiency can lead to increased bleeding risk, decreased dose requirement, and a longer time to reach stable therapy. The combination of CYP2C9 genotyping with VKORC1 – the target of warfarin’s effect – and with patient physical characteristics can accurately estimate a patient’s warfarin sensitivity level, dose requirement, and ultimately provide practitioners with better guidance for optimal INR interpretation and management.

VKORC1: VKOR is a liver enzyme responsible for activating blood clotting factors. The VKORC1 gene that makes the VKOR enzyme is subject to genetic variability that causes increased warfarin sensitivity and decreased warfarin dose requirement. Nearly 75% of the population possesses this variant. VKORC1 genotyping in combination with CYP2C9 testing and a patient’s physical characteristics can accurately estimate the patient’s warfarin sensitivity level, dose requirement and provide practitioners with better guidance for optimal INR interpretation and management.

CYP3A4: CYP3A4 is a liver enzyme that, in concert with CYP3A5, metabolizes approximately 50% of medications, including many of the statins, benzodiazepines, antibiotics, and antipsychotics. Detecting variants of the CYP3A4 gene that cause altered enzymatic activity can identify patients who may be at increased risk of having adverse drug reactions while taking standard dosages of 3A4 substrates. Roughly 4-10% of the general population possesses inherited differences in 3A4 that cause decreased metabolism. These Decreased Metabolizers may be at increased risk for dose-dependent side effects to drugs normally inactivated by 3A4.

CYP3A5: CYP3A5 is a liver enzyme that, in concert with CYP3A4, metabolizes approximately 50% of medications, including many of the statins, benzodiazepines, antibiotics, and antipsychotics. Detecting variants of the CYP3A5 gene that cause altered enzymatic activity can identify patients who may be at increased risk of having adverse drug reactions while taking standard dosages of 3A5 substrates. More than half of the general population (60-80%) possesses inherited differences in 3A5 that cause decreased metabolism. These Decreased Metabolizers may be at increased risk for dose-dependent side effects to drugs normally inactivated by 3A5.

CYP1A2: CYP1A2 is a liver enzyme that metabolizes many medications, including theophylline, diazepam, caffeine, many antidepressants, and antipsychotics. CYP1A2 enzymatic activity can be induced by several medications, substrates, and constituents of tobacco smoke. CYP1A2 can also be inhibited by several medications. Detecting inherited variants of the CYP1A2 gene that cause altered enzymatic activity, particularly in the presence of an inducer, can identify patients who may be at increased risk of having adverse drug reactions or therapeutic failure to standard dosages of CYP1A2 medications.

SLC6A4: SLC6A4 is the gene that makes the serotonin transporter in the brain. The role of the serotonin transporter is to shuttle the potent brain chemical serotonin from one neuron to another. Inhibiting serotonin transport is associated with improved mood; thus the effectiveness of many antidepressant drugs (namely selective serotonin reuptake inhibitors, SSRIs) is thought to be due to their inhibition of the serotonin transporter. Nearly 75% of people have an inherited form of the SLC6A4 gene that can lead to decreased response to SSRI therapy. The Short (S) form of the transporter is associated with delayed response to SSRI antidepressants and increased risk of adverse drug reactions (ADRs) during antidepressant therapy. Patients who possess two copies of the Short (S) form may be more likely to benefit from non-SSRI therapies.

SLCO1B1: SLCO1B1 is the gene that makes a liver enzyme called OATP1B1, which helps transport statins medications into the liver more effectively. Roughly 15% of the population possesses the *5 variant, an inherited form of SLOC1B1 which increases risk of statin-induced muscle damage, or myopathy, by 3 to 5 fold. Risk of myopathy with the *5 variant is most closely associated with simvastatin and to a lesser extent, atorvastatin. Patients with the *5 variant may need the lowest doses of simvastatin or an alternative statin to reduce risk of myopathy.

COMT: In the brain, catechol-O-methyltransferase helps break down certain chemical messengers called neurotransmitters. These chemicals conduct signals from one nerve cell to another. Catechol-O-methyltransferase is particularly important in an area at the front of the brain called the prefrontal cortex, which organizes and coordinates information from other parts of the brain. This region is involved with personality, planning, inhibition of behaviors, abstract thinking, emotion, and working (short-term) memory. To function efficiently, the prefrontal cortex requires signalling by neurotransmitters such as dopamine and norepinephrine. Catechol-O-methyltransferase helps maintain appropriate levels of these neurotransmitters in this part of the brain.

MTHFR (Methylenetetrahydofolate Reductase): encodes the protein MTHFR. Its job is to convert one form of folate (5,10-Methylenetetrahydofolate) to another form of folate (5-Methyltetrahydrofolate). 5-Methyltetrahydrofolate is used to convert Homocysteine (a “bad” amino acid) to Methionine (a “good” amino acid).

Research shows that high homocysteine levels and/or those with the mutation show a higher propensity for thrombosis (blood clots), arteriosclerosis (hardening of arteries), Alzheimer’s, stroke, heart attack, Fibromyalgia, migraines (especially with “Aura” migraines), osteoporotic fractures, bone marrow disorders and for those of child bearing years, it has found to be connected to higher incidences of Down syndrome, Spina bifida, other Neural Tube Defects, Trisomy, miscarriage, stillbirth, implantation failure, placental abruption, preeclampsia, higher incidences of autism, amongst others.

Because of the mutation, absorption of Folic Acid is hindered and anyone with MTHFR will require 200% more Folic Acid then a typical person.

Factor V Leiden: is a mutation of one of the clotting factors in the blood called factor V. This mutation can increase your chance of developing abnormal blood clots (thrombophilia), usually in your veins.

Factor II: deficiency is a very rare blood clotting disorder that results in excessive or prolonged bleeding after an injury or surgery. Factor II, also known as prothrombin, is a protein made in your liver that plays an essential role in blood clotting. It is one of about 13 clotting factors involved in the proper formation of blood clots.

  • CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5 enzymes metabolize 90% percent of drugs.1,2Source: http://www.aafp.org/afp/2007/0801/p391.html
    1. Wilkinson GR. Drug metabolism and variability among patients in drug response. N Engl J Med. 2005;352:2211–21.
    2. Slaughter RL, Edwards DJ. Recent advances: the cytochrome P450 enzymes. Ann Pharmacother. 1995;29:619–24.

cyp1a2cyp3a4cyp2d6cyp2c19cyp2c9

  • Normal Metabolizer. Normal metabolizers can generally metabolizes standard doses of a drug.
  • Intermediate Metabolizer. Intermediate metabolizers are considered to have less capacity than normal, thus might not metabolize medicines at a normal rate with normal doses. A lower dose may prevent the unmetabolized medicine from building up in the body and possibly causing adverse side effects.
  • Poor Metabolizer. Poor metabolizers have very low enzymatic capacity and activity. It is possible to have side effects even with a very low drug dose, because the enzyme is very slow to break down the drug.
  • Rapid or Ultra-rapid Metabolizers. The types of patients have highly active enzymatic capacity to metabolize medicines. These patient types may require a higher dose in order for the drug to work as normal.

Yes, you will need the signature of a healthcare professional to order a test.

Pharmacogenetic (drug sensitivity) testing is reimbursed under specific diagnosis codes related to a patient’s comorbidities, for specific medical necessity. PGx testing is typically covered only for specific medications and conditions and is not used for general screening. Depending on your insurance plan, you may still be responsible for a deductible or co-payment.

A list of medical necessity questions may include:

  • Patient is taking 4 or more medications.
  • Patient may be experiencing adverse drug reaction(s) to one or more medications.
  • Seeking to choose safer dosages.
  • Test results will be clinically useful to the medical management of the patient (i.e., initiate a new course of therapy, alter an existing therapy or a level of surveillance)
  • Patient is taking certain psychiatric or neurological (anti- depressants, anti-psychotics, anticonvulsants, mood stabilizers, stimulants).
  • Patient is taking opioids.
  • Seeking explanation to abnormal Urine Drug Test
  • Patient is taking antithrombotic medications (i.e. Clopidogrel or Warfarin).
  • Patient is taking cardiovascular medications, such as beta-blockers, antiarrhythmics and/or statins.

No CLIA waiver is required. The ordering healthcare professional does not perform the genetic laboratory test in the medical office. Thus, healthcare professional’s office does not bill for any technical codes.

We bill for laboratory testing procedures and the resulting reporting.  A healthcare professional’s office bills for services related to patient care, including office visits, supplemental reports, and any other services provided outside of the PGx test.

Pharmacogenetic test results are sent directly from the lab to the healthcare professionals office. It is up to the patient and / or physician to decide if they would like to provide the report to their insurance carrier for any reason.