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 your blood panel, pharmacogenomics results across 21 genes and 101 drugs, and whole exome 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 · Intermediate metaboliser | Avoid — use prasugrel or ticagrelor instead |
| Hydralazine (Apresoline) | NAT2 · Poor metaboliser | Start low 40–75 mg/day; avoid ≥200 mg |
| Thiopurines — azathioprine, mercaptopurine, thioguanine | NUDT15 · Intermediate metaboliser | Reduce dose 30–80%; monitor blood counts closely |
| Irinotecan | UGT1A1 · Intermediate metaboliser | Increased neutropenia risk; consider dose reduction |
| Interferon — PEG-IFN-α + ribavirin (Hep C) | IFNL3 · CT genotype — unfavourable | ~30% lower response; discuss direct-acting antivirals |
| SSRIs — citalopram, escitalopram, sertraline | CYP2C19 · Intermediate metaboliser | Start at recommended dose; titrate slowly |
| Tricyclic antidepressants — amitriptyline, clomipramine | CYP2C19 · Intermediate metaboliser | Reduced clearance; monitor for accumulation |
| Proton pump inhibitors — omeprazole, lansoprazole, pantoprazole | CYP2C19 · Intermediate metaboliser | For chronic use >12 weeks, consider 50% dose reduction |
| Tacrolimus (Prograf) | CYP3A5 · Poor metaboliser | Standard dose sufficient — use TDM monitoring |
| Efavirenz | CYP2B6 · Intermediate metaboliser | Start at 400 mg/day rather than 600 mg |
| All other drugs tested — warfarin, NSAIDs, metoprolol, statins, codeine, carbamazepine, phenytoin, others | 21 genes screened | No flags — standard doses apply |
Your haemoglobin is 11.7 g/dL — below both the male reference (13.2) and the WHO anaemia threshold (13.0). Your red cell count, packed cell volume, and red cell indices all point in the same direction: fewer red cells, of normal size and colour. That last detail is the diagnostic clue — this is not classic iron-deficiency anaemia, which produces small, pale cells.
Your iron stores (ferritin 163 ng/mL, serum iron 89 µg/dL) are adequate, which further supports the kidney-EPO explanation over iron deficiency. Elevated creatinine was first noticed approximately two years ago — the kidney signal is real and it is not new.
Normocytic normochromic anaemia (normal MCV 93.3, MCH 30.7, MCHC 32.9) rules out iron deficiency (microcytic hypochromic), B12/folate deficiency (macrocytic), and acute blood loss as primary causes. Ferritin at 163 ng/mL confirms iron stores are adequate. The combination with Stage G2 CKD is the leading explanation, but the diagnosis requires: (1) urine albumin-to-creatinine ratio to quantify kidney leakage, (2) full iron studies with transferrin saturation, (3) serum EPO level, and (4) a nephrology opinion.
Stage G2 CKD (eGFR 60–89) is defined as mildly reduced kidney function. At this stage, hypertension remains the most modifiable driver — well-controlled BP directly slows the rate of progression. Annual eGFR monitoring is standard. If the urine ACR shows microalbuminuria, that changes the urgency significantly.
You are already on a statin, which is why your LDL of 90 mg/dL looks manageable on the report sheet. But under the Lipid Association of India 2023 framework — which classifies you as High Risk based on age, hypertension, and low HDL — the targets are stricter: LDL <70, Non-HDL <100, ApoB <80. All three are currently above target.
The good news: your statin muscle genes (SLCO1B1, ABCG2) are both clear — meaning a stronger statin or higher dose can be discussed without muscle side effects as a limiting factor.
Atherogenic dyslipidaemia — the combination of high triglycerides, very low HDL, and elevated small dense LDL particles (reflected by raised ApoB) — is the dominant cardiovascular pattern in insulin resistance. It is distinct from familial hypercholesterolaemia and responds poorly to statin monotherapy. The evidence-based additions are: (1) intensifying the statin to reach LDL <70, (2) adding a fibrate (fenofibrate) or high-dose omega-3 (icosapent ethyl) for the triglycerides, and (3) addressing the metabolic root through diet and exercise.
HDL of 15 mg/dL is extremely low and is the single most significant entry point for cardiovascular risk in this panel. Exercise (particularly aerobic exercise) is the most evidence-based HDL-raising intervention — even a 10–15% HDL increase from 15 would be meaningful. Weight loss in the abdominal region directly raises HDL and lowers triglycerides through the same mechanism.
Your fasting glucose (95 mg/dL) and HbA1c (5.4%) are both normal. So why is this in the prioritise list? Because to keep your sugar normal, your pancreas is producing 16.20 µU/mL of insulin at rest — that's high. The HOMA-IR score (combining fasting insulin and fasting glucose) is 3.80, against an elevated cutoff of 2.5 and a high-risk cutoff of 3.5. You are in the high-risk band.
Insulin resistance is also the mechanism behind your lipid pattern. The same dysfunction that pushes insulin up also pushes your liver to make more triglyceride-rich VLDL (57 mg/dL, target <30) and suppresses HDL production. A 5–7 kg weight reduction can normalise fasting insulin in many people — and would address your lipids, your weight gain since 2023, and your future diabetes risk simultaneously.
HOMA-IR = (fasting insulin × fasting glucose) ÷ 405. Your calculation: (16.20 × 95) ÷ 405 = 3.80. A HOMA-IR above 2.5 is considered elevated; above 3.5 is high risk for metabolic syndrome and type 2 diabetes progression. Your value of 3.80 sits in the high-risk zone despite completely normal glucose measurements — a clear illustration of why fasting insulin is a more sensitive early marker than HbA1c or fasting glucose alone.
The most evidence-based interventions for insulin resistance, in order of effect size: (1) caloric deficit with low-glycaemic, low-refined-carbohydrate pattern — reduces hepatic glucose output directly; (2) resistance training 2–3× weekly — increases GLUT4 glucose transporters in muscle; (3) aerobic exercise 150 min/week — improves peripheral insulin sensitivity; (4) sleep ≥7 hours — one night of poor sleep raises HOMA-IR by 20–30% acutely. There is no medication currently first-line for HOMA-IR in the pre-diabetes range — lifestyle is the treatment.
Clopidogrel (Plavix) is the standard blood thinner given after a heart attack, after stenting, and during many cardiac procedures. It is a prodrug — it has to be activated in your liver by an enzyme called CYP2C19 before it actually thins the blood. Your CYP2C19 genetics (*2/*38) make you an intermediate metaboliser: you activate roughly half as much of the dose as a normal metaboliser. The published data shows a measurable increase in repeat heart attacks, stent clotting, and cerebrovascular events in patients with your genotype.
Carry this report. If you ever turn up in an emergency room with chest pain, this single page changes the prescription you walk out with.
CYP2C19 *2/*38 intermediate metaboliser status reduces clopidogrel active metabolite levels by approximately 40–50% compared to normal metabolisers (*1/*1). CPIC Grade A evidence supports using alternative antiplatelet agents (prasugrel or ticagrelor) for patients with ACS or undergoing PCI. Both prasugrel and ticagrelor are direct-acting — they do not require CYP2C19 activation — and are unaffected by this genotype at standard doses.
The same CYP2C19 genotype also affects your metabolism of proton pump inhibitors (omeprazole, lansoprazole, pantoprazole), SSRIs (citalopram, escitalopram, sertraline), and tricyclic antidepressants. Drug levels run higher on standard doses. For your long-standing acidity: if restarted on a long-term PPI, a 50% dose reduction after 12 weeks of effective control is appropriate.
Homocysteine is an amino acid your body produces and clears using vitamins B12 and folate. Yours is 13.25 µmol/L — below the LAI 2023 risk-modifier threshold of 15 (so it is not formally adding to your CV risk tier), but above the cardiovascular-optimal level of 10. Both relevant vitamins are in the lower part of their reference ranges: B12 at 410 pg/mL (range 187–883) and folate at 10.4 ng/mL (range 3.1–20.5).
Homocysteine above 10 µmol/L is associated with increased risk of cardiovascular events, stroke, and cognitive decline in population studies. The LAI 2023 uses 15 µmol/L as the formal risk-modifier threshold. Your value at 13.25 sits in the intermediate zone — not an emergency, but not optimal. Elevated homocysteine damages the endothelium (artery lining) and promotes platelet aggregation, both of which compound the cardiovascular risk profile already present from your lipid pattern.
Supplementation with methylated forms (methylcobalamin rather than cyanocobalamin, methylfolate rather than folic acid) bypasses potential MTHFR-related conversion inefficiencies and is generally preferred for homocysteine lowering. Dietary sources of B12: meat, fish, eggs, dairy. Dietary sources of folate: dark leafy greens (spinach, methi), lentils, chickpeas, asparagus.
Your potassium came back at 5.50 mmol/L, above the upper reference of 5.10. Before reading this as hyperkalaemia, the standard rule applies: a single mildly elevated potassium reading from a home blood draw, in someone with a working kidney (eGFR 72), almost always reflects mild haemolysis — red cells breaking during the draw and leaking potassium into the serum. This is not something to act on yet; it is something to repeat.
Do not change any antihypertensive medications based on this single number.
Pseudohyperkalaemia from haemolysis is common in home-draw samples, particularly if the tourniquet is left on too long, the patient clenches their fist, or the sample is delayed before centrifugation. A mild elevation (5.1–5.5) in the context of normal renal function and no symptoms almost always resolves on a repeat clean draw.
The chloride at 108 mmol/L (upper limit 107) is similarly a minor borderline value that should be reassessed with the repeat electrolyte panel rather than acted on independently.
Hydralazine is a vasodilator sometimes used when standard antihypertensives are not enough. Your NAT2 genetics make you a slow acetylator, meaning you clear hydralazine more slowly than average — drug levels build up higher on standard doses, increasing both efficacy and the risk of drug-induced lupus.
Tacrolimus is the cornerstone immunosuppressant after solid-organ transplantation. Your CYP3A5 genotype (*3/*3) means you clear tacrolimus slowly — the standard starting dose is appropriate for you, and a higher dose would over-suppress your immune system. Given your early kidney signal and your sister's single-kidney status, this result belongs on your file now rather than later.
The IFNL3 gene predicts clearance of hepatitis C virus on interferon-based therapy. Your CT genotype achieves sustained viral clearance roughly 30% of the time on PEG-interferon plus ribavirin, compared with about 70% for the favourable CC genotype.
Thiopurines (azathioprine, mercaptopurine, thioguanine) are used for inflammatory bowel disease, autoimmune conditions, and some cancers. Your NUDT15 genetics flag a real risk: at standard doses, intermediate metabolisers are at higher risk of bone-marrow suppression — drops in white cells and platelets that can be dangerous. The dose must be reduced to 30–80% of standard, with regular blood-count monitoring.
Efavirenz: as an intermediate metaboliser, you would run higher drug levels and an increased risk of CNS side effects (vivid dreams, dizziness, cognitive fog). Recommended starting dose: 400 mg/day rather than 600 mg.
Atazanavir: your UGT1A1 genotype gives a small chance (under 5%) of stopping the drug due to jaundice — much less than for the high-risk *28/*28 genotype. Atazanavir is not contraindicated, but your doctor should be informed.
The same CYP2C19 genotype that affects clopidogrel also slows your metabolism of citalopram, escitalopram, sertraline, amitriptyline, and proton pump inhibitors (omeprazole, pantoprazole, lansoprazole). Drug levels run higher on standard doses, increasing both efficacy and side effects.
For your long-standing acidity and history of H. pylori: if you are restarted on a long-term PPI, after 12 weeks of effective symptom control your dose can typically be reduced by 50% and still maintain the result. Share this with your gastroenterologist.
Irinotecan is a chemotherapy used for colorectal and some other cancers. Your UGT1A1 variant increases the chance of two serious dose-limiting toxicities at standard doses — severe neutropenia (low white cells) and severe diarrhoea. An oncologist would typically reduce the starting dose.
Your Vitamin D (34 ng/mL) is comfortably in the optimum range (20–50) and well clear of any deficiency or toxicity zones. For someone managing insulin resistance and a cardiometabolic profile, levels in the upper half of optimum (40–50 ng/mL) are associated with slightly better metabolic outcomes.
| # | What to do | Why it matters | When |
|---|---|---|---|
| Now — begin this week | |||
| 1 | Start a structured low-carb, high-protein eating pattern. Cut refined carbs and sugar; aim for 1.6 g/kg protein daily. | Fasting insulin 16.20 µU/mL and HOMA-IR 3.80 signal insulin resistance — the root driver of weight gain, lipid pattern, and future diabetes risk. | Begin this week |
| 2 | Add 150 minutes of zone-2 cardio plus two resistance sessions weekly. Brisk walking, cycling, or swimming counts. | Muscle is your largest glucose sink — direct treatment for insulin resistance and critically low HDL (15 mg/dL) simultaneously. | Start within 2 weeks |
| Soon — within 4–6 weeks | |||
| 3 | Book a nephrology consult to investigate the kidney signal. Bring full lipid panel, insulin results, and BP log. | Long-standing hypertension plus Stage G2 kidney signal (eGFR 72) needs specialist eyes before it progresses silently. | Within 4–6 weeks |
| 4 | Review statin dose and discuss adding a fibrate or omega-3 with your cardiologist. Target TG <150 and HDL >40. | Atherogenic dyslipidaemia (TG 283, HDL 15) is your dominant cardiovascular driver — the statin alone cannot fix it. | Within 6 weeks |
| Monitor — ongoing over next 4 weeks | |||
| 5 | Begin home BP monitoring twice daily and log for four weeks. Share readings with your physician for dose titration. | Clinic readings miss masked and nocturnal hypertension — the patterns that quietly damage kidneys and heart over time. | Next 4 weeks |
| Recheck — 6 months | |||
| 6 | Repeat fasting insulin, HbA1c, lipids, and kidney panel in six months. Same lab, same fasting protocol. | These are the markers that will show whether the lifestyle work is reversing the insulin resistance trajectory. | 6-month recheck |
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