Sample Patient · 52 years · Male · For demonstration purposes only
Everything in this sample is illustrative only — so you can explore and become familiar with the report format, depth, and style.
This report brings together three blood draws, pharmacogenomics results across 53 genes and 101 drugs, and whole genome sequencing — written in plain English, for you and your doctor.
One important thing to keep in mind: your genes show a proclivity — a tendency — not a certainty. They shift the odds, they don't determine outcomes. Lifestyle, environment, and the choices you make every day play an equally important role.
How to use this report: Use the navigation bar below to jump to any section. "Blood Test Results" shows all your measured values at a glance. "Action List" tells you what to do and when. The finding cards below explain each result in depth. Tap "Tell me more" on any card for a fuller explanation.
| Drug / Drug class | Gene · Status | Recommendation |
|---|---|---|
| Clopidogrel (Plavix) | CYP2C19 · Poor metaboliser | Avoid — use prasugrel or ticagrelor instead |
| Voriconazole (Vfend) | CYP2C19 · Poor metaboliser | Consider alternative antifungal; drug levels will be very high |
| Citalopram / Escitalopram — Celexa / Lexapro | CYP2C19 · Poor metaboliser | Consider alternative SSRI or reduce dose by 50% |
| Sertraline (Zoloft) | CYP2C19 · Poor metaboliser | Consider alternative or reduce starting dose by 50% |
| Tricyclic antidepressants — amitriptyline, imipramine, clomipramine, others | CYP2C19 · Poor metaboliser | Consider alternative or reduce dose by 50% |
| Proton pump inhibitors — omeprazole, lansoprazole, esomeprazole, others | CYP2C19 · Poor metaboliser | Drug levels will be higher than usual — use lowest effective dose |
| Irinotecan (Camptosar) | UGT1A1 · Poor metaboliser | Reduce starting dose by at least one level; neutropenia risk elevated |
| Atazanavir (Reyataz) | UGT1A1 · Poor metaboliser | High risk of jaundice — consider an alternative antiretroviral |
| Fenofibrate (Tricor) | APOB · Decreased responder | Response to this triglyceride drug may be lower than expected |
| Ketamine / Propofol — anaesthetic agents | CYP2B6 · Intermediate metaboliser | Reduce dose — drug clears more slowly than average |
| Bupropion (Wellbutrin / Zyban) | CYP2B6 · Intermediate; CYP2C19 · Poor metaboliser | Increased side-effect risk — use with caution; consider alternative |
| Folic acid supplements | MTHFR · Partial deficiency | Standard folic acid converts poorly — use methylfolate form instead |
| Metformin (Glucophage) | ATM · Decreased responder | Response may be reduced — monitor blood sugar closely if prescribed |
| All other genes tested — 53 genes screened | No prescribing flags | Standard doses apply |
Your body processes the blood thinner clopidogrel far more slowly than average. Clopidogrel is a "prodrug" — it has to be activated by an enzyme called CYP2C19 before it can do its job of preventing clots. You are a poor metaboliser of this enzyme, which means clopidogrel would be substantially under-activated in your system and may not protect you as intended.
Clopidogrel only works once it's converted, by CYP2C19, into its active form. As a poor metaboliser, you convert substantially less of each dose than a normal metaboliser would — so even at standard dosing, the drug may not thin your blood as intended. Prasugrel and ticagrelor are not affected by CYP2C19 status, which is why they're the recommended substitutes if antiplatelet therapy is ever needed.
Carry this report, or at minimum this finding, somewhere accessible — ideally on your phone. If you ever turn up in an emergency room with chest pain, this is the single detail that changes the prescription you walk out with.
Yours were 121 mg/dL in February and 232 mg/dL in April — the April figure is in the "high" range (200–499). Your treating doctor has already acted on this: your fenofibrate dose was increased to 200 mg after this result, and your icosapent ethyl (prescription omega-3) is in place, with room to increase. The current plan is the right response. You are a six-day-a-week athlete with a BMI around 20, so "exercise more" is not the answer here — the levers that matter are dietary (refined carbohydrate and alcohol intake) and the medication adjustment already underway. One nuance: your pharmacogenomic panel suggests you may respond somewhat less to fenofibrate than average.
HDL is the "good" cholesterol that helps clear other fats from your blood. Yours was 54 mg/dL in February and 36 mg/dL in April, now just below the 40 mg/dL male threshold. The two readings sit alongside the triglyceride rise — when triglycerides go up, HDL commonly comes down, as the two move in opposite directions metabolically. As your triglycerides come back under control with the adjusted fenofibrate, your HDL should recover. Because you are an elite-level exerciser, the usual advice ("be more active to raise HDL") doesn't apply — your fitness is already doing its part.
Lp(a) is a genetically-determined form of cholesterol that adds to cardiovascular risk independently of your LDL. Under LAI 2023, a value of 20–49 mg/dL is a risk modifier — which is why you land in Moderate rather than Low risk. Your two readings, 38.80 and 49.30 mg/dL, both sit in this modifier band, just below the 50 mg/dL high-risk cutoff. Lp(a) is largely set by your genes and doesn't change much with lifestyle, so this isn't something you can exercise or diet away — it's simply a fixed factor your doctor keeps on file when weighing your overall risk.
Your uric acid is 7.90 mg/dL, modestly above the upper limit of 7.20. There is a clear, expected explanation: bempedoic acid, which you take for cholesterol, is documented to raise serum uric acid as a normal pharmacological effect. On top of that, you carry an ABCG2 gene variant (Q141K) that means your kidneys clear uric acid slightly less efficiently than average — a known interaction with this medication class. Your physician is aware and monitoring this, and the value is not dramatically elevated.
Eosinophils are a type of white blood cell that rises with allergies, certain infections, and parasites. In February yours were notably high at 21% (1,638 cells), which the lab flagged as moderate eosinophilia. This sits alongside your October IgE of 237 IU/mL — nearly three times the upper limit — which points toward an allergic or atopic cause rather than anything sinister. The reassuring part: by April your eosinophils had fallen to 8% (456 cells), nearly back to normal.
Your whole genome pharmacogenomic panel flagged several genes that matter only if specific drugs are ever prescribed, none of which you currently take. CYP2C19 (Poor Metaboliser) — beyond clopidogrel, if you are ever prescribed voriconazole, certain antidepressants, or proton-pump inhibitors, your doctor should know you process these more slowly. CYP2B6 (Intermediate Metaboliser) — if you are ever prescribed efavirenz or sertraline, a dose adjustment may be appropriate. NAT2 (Rapid acetylator) — if you are ever prescribed hydralazine or isoniazid, you may need a higher hydralazine dose. CYP2D6 (Indeterminate) — if drugs like tamoxifen, codeine, tramadol, or certain beta-blockers are ever considered, mention this to your prescriber.
Your whole genome polygenic risk scores — which combine many small genetic variants into a single estimate — flag two areas of higher-than-average inherited tendency. Your type 2 diabetes score sits in the high band (about 2.3× the average), and your hypercholesterolaemia score is also high (about 2.8×). These are South Asian–validated models, which is appropriate for you. Here is the important context: a high genetic score is a tendency, not a destiny. Your actual blood sugar today is excellent, and your cholesterol is well-managed on treatment.
| # | What to do | Why it matters | When |
|---|---|---|---|
| Now — next visit | |||
| 1 | Record your clopidogrel finding in your medical file. Ask your cardiologist to note that you are a CYP2C19 poor metaboliser. | If antiplatelet therapy is ever needed, prasugrel or ticagrelor should be used instead — this must be known before any cardiac event. | Next visit |
| Soon — 6–8 weeks | |||
| 2 | Recheck triglycerides and HDL. Repeat a fasting lipid panel to confirm your fenofibrate increase to 200 mg is bringing your triglycerides (232 mg/dL) and HDL (36 mg/dL) back to target. | If triglycerides remain above 200 mg/dL, discuss increasing icosapent ethyl with your cardiologist. | 6–8 weeks |
| 3 | Recheck uric acid. Include serum uric acid in your next blood draw to confirm the value (7.90 mg/dL) stays modestly elevated and does not climb further. | It's an expected effect of bempedoic acid plus your ABCG2 variant — routine monitoring is enough unless it rises significantly. | Next draw |
| Monitor | |||
| 4 | Watch your eosinophils. Recheck the full blood count to confirm eosinophils continue falling (1,638 → 456 cells/µL) toward normal. | If they persist, ask your doctor about correlating with allergy symptoms and considering stool examination plus specific IgE allergy screening. | Next draw |
| Annual | |||
| 5 | Keep your annual metabolic monitoring. Maintain yearly fasting glucose, HbA1c, and lipids given your high inherited diabetes and cholesterol risk scores. | Your numbers are excellent now; annual checks catch any genetic-tendency drift early while your healthy lifestyle keeps risk low. | Yearly |
A one-page summary of findings worth a conversation. Full report available on request.
Well-managed cardiometabolic profile. Familial dyslipidaemia under aggressive non-statin control; coronary calcium = 0. Items below are for ongoing management and prescribing reference.
| Finding | Value | Suggested Action |
|---|---|---|
| Lipoprotein(a) elevated | 49.3 mg/dL target <30 mg/dL |
Independent, largely inherited cardiovascular risk factor; not lowered by current lipid therapy. Confirm awareness; factor into lifelong CV risk planning and family screening. |
| Finding | Value | Context & Action |
|---|---|---|
| LDL — high-risk target not met | 94 mg/dL High-risk target <70 mg/dL |
High CV risk category; target is <70 mg/dL. On aggressive non-statin therapy. Continue titration; recheck at next visit. |
| Uric acid above range | 7.90 mg/dL | Expected effect of bempedoic acid; reduced renal clearance may contribute. Routine monitor. Flag if future urate-raising drugs are added. |
| TG / HDL | 232 / 36 mg/dL | TG high, HDL low at last draw; fenofibrate uptitrated and icosapent ethyl added. Recheck post-titration. |
References: 1. Richards S et al. (2015). Genetics in Medicine 17(5):405–24. · 2. Lee K et al. (2025). Genetics in Medicine 27(8):101454. · 3. Abu-El-Haija A et al. (2023). Genetics in Medicine 25(5):100803. · 4. Khera AV et al. (2018). Nature Genetics 50(9):1219–24. · 5. CPIC guidelines (cpicpgx.org).
Generated by the Mira One pipeline · Clinically reviewed by GenePath Dx · Educational summary, not a substitute for clinical judgement.
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