How should I interpret and manage a patient with normal fasting glucose, normal HbA1c, normal renal function, normal uric acid, low‑normal total cholesterol, borderline‑high triglycerides, low HDL‑cholesterol and borderline LDL‑cholesterol?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: February 21, 2026View editorial policy

Personalize

Help us tailor your experience

Which best describes you? Your choice helps us use language that's most understandable for you.

Interpretation and Management of Normal Metabolic Panel with Borderline Lipid Abnormalities

Your laboratory values indicate excellent glycemic control and normal renal function, but reveal an atherogenic dyslipidemia pattern (borderline-high triglycerides with low HDL-cholesterol) that warrants aggressive lifestyle intervention and cardiovascular risk assessment before considering pharmacotherapy.

Laboratory Value Interpretation

Glycemic Parameters (Excellent Control)

  • Fasting glucose 5.35 mmol/L (96 mg/dL) and HbA1c 5.50% both fall within normal ranges, indicating no diabetes or prediabetes. 1
  • These values require no pharmacologic intervention but should be monitored annually if you have risk factors (family history, obesity, sedentary lifestyle). 1

Renal Function (Normal)

  • Creatinine 56.10 μmol/L (0.63 mg/dL) indicates normal kidney function with an estimated GFR well above 90 mL/min/1.73m². 2, 3
  • Uric acid 279 μmol/L (4.7 mg/dL) is within normal range and poses no immediate concern. 3, 4

Lipid Profile (Atherogenic Dyslipidemia Pattern)

Total Cholesterol: 3.15 mmol/L (122 mg/dL) – Low-Normal

  • This value is well below the 5.2 mmol/L (200 mg/dL) threshold and requires no intervention. 1

LDL-Cholesterol: 1.44 mmol/L (56 mg/dL) – Optimal

  • This is significantly below all guideline targets (<2.6 mmol/L or 100 mg/dL for most patients, <1.8 mmol/L or 70 mg/dL for high-risk patients). 1, 5
  • No LDL-lowering therapy is indicated at this level. 5

HDL-Cholesterol: 0.95 mmol/L (37 mg/dL) – Low (Major Risk Factor)

  • This value falls below the 1.03 mmol/L (40 mg/dL) threshold for men and 1.29 mmol/L (50 mg/dL) threshold for women, constituting an independent cardiovascular risk factor. 1
  • Low HDL-cholesterol is strongly associated with increased cardiovascular risk even when LDL-cholesterol is optimal. 5

Triglycerides: 1.68 mmol/L (149 mg/dL) – Borderline-High

  • This level falls just below the 1.7 mmol/L (150 mg/dL) threshold for "mild hypertriglyceridemia" but is approaching the range where intervention is recommended. 1, 6
  • Triglycerides ≥1.7 mmol/L (150 mg/dL) are classified as a cardiovascular risk-enhancing factor. 6, 5

Non-HDL Cholesterol: 2.20 mmol/L (85 mg/dL) – Optimal

  • Calculated as total cholesterol minus HDL-cholesterol (3.15 - 0.95 = 2.20 mmol/L).
  • This is well below the target of <3.4 mmol/L (130 mg/dL) for patients with elevated triglycerides. 6, 5

VLDL: 0.76 mmol/L (29 mg/dL) – Normal

  • This calculated value (triglycerides ÷ 2.2) is within normal range. 5

Clinical Significance: Atherogenic Dyslipidemia Pattern

Your lipid profile demonstrates the classic "atherogenic dyslipidemia" pattern characterized by:

  • Borderline-high triglycerides (1.68 mmol/L / 149 mg/dL)
  • Low HDL-cholesterol (0.95 mmol/L / 37 mg/dL)
  • Normal-to-low LDL-cholesterol (1.44 mmol/L / 56 mg/dL)

This pattern is strongly associated with insulin resistance, metabolic syndrome, and increased cardiovascular risk through elevated atherogenic VLDL remnant particles and small-dense LDL particles, even when calculated LDL-cholesterol appears optimal. 6, 5


Cardiovascular Risk Assessment Required

Before determining whether pharmacotherapy is needed, you must undergo formal cardiovascular risk stratification:

Calculate 10-Year ASCVD Risk

  • Use the Pooled Cohort Equations (available online) incorporating your age, sex, race, total cholesterol, HDL-cholesterol, systolic blood pressure, diabetes status, and smoking status. 6, 5
  • If 10-year ASCVD risk ≥7.5%, statin therapy is recommended regardless of LDL-cholesterol level. 6, 5
  • If 10-year ASCVD risk 5-7.5%, shared decision-making regarding statin initiation is appropriate, especially given your low HDL-cholesterol as a risk-enhancing factor. 6, 5

Screen for Metabolic Syndrome

You should be evaluated for metabolic syndrome, which is diagnosed when ≥3 of the following are present: 1

  • Waist circumference >102 cm (men) or >88 cm (women)
  • Triglycerides ≥1.7 mmol/L (150 mg/dL) – you are borderline
  • HDL-cholesterol <1.03 mmol/L (40 mg/dL) men or <1.29 mmol/L (50 mg/dL) women – you meet this criterion
  • Blood pressure ≥130/85 mmHg or on antihypertensive medication
  • Fasting glucose ≥5.6 mmol/L (100 mg/dL) or known diabetes – you do not meet this criterion

Assess for Secondary Causes

Before initiating any lipid-lowering therapy, the following must be evaluated: 6, 5

  • Thyroid function (TSH) – hypothyroidism commonly causes dyslipidemia
  • Fasting insulin or HOMA-IR – to assess for insulin resistance
  • Liver function tests (AST, ALT) – to exclude hepatic steatosis
  • Detailed alcohol history – even 1 oz daily can raise triglycerides by 5-10%
  • Medication review – thiazide diuretics, beta-blockers, oral estrogens, corticosteroids, antiretrovirals, and atypical antipsychotics can worsen lipid profiles

Management Algorithm

Step 1: Intensive Lifestyle Modifications (First-Line for All Patients)

Lifestyle interventions can lower triglycerides by 20-70% and raise HDL-cholesterol by 10-20%, potentially eliminating the need for pharmacotherapy. 6, 5

Weight Management (Most Effective Intervention)

  • Target 5-10% body weight reduction if overweight/obese, which yields approximately 20% triglyceride reduction and 5-10% HDL-cholesterol increase. 6, 5
  • In some individuals, weight loss alone can reduce triglycerides by 50-70%. 6

Dietary Modifications

  • Restrict added sugars to <6% of total daily calories (≈30 g on a 2000-kcal diet) because sugar intake directly stimulates hepatic triglyceride synthesis. 6, 5
  • Limit total dietary fat to 30-35% of calories for borderline-high triglycerides. 6, 5
  • Restrict saturated fat to <7% of total energy and replace with monounsaturated fats (olive oil, nuts, avocado) or polyunsaturated fats (fatty fish, flaxseed). 6, 5
  • Eliminate trans fatty acids completely – they lower HDL-cholesterol and raise triglycerides. 6, 5
  • Increase soluble fiber to >10 g/day from oats, beans, lentils, and vegetables. 6, 5
  • Consume ≥2 servings of fatty fish per week (salmon, trout, sardines, mackerel) to provide omega-3 fatty acids. 6, 5

Physical Activity

  • Engage in ≥150 minutes/week of moderate-intensity aerobic exercise (or 75 minutes/week vigorous activity), which reduces triglycerides by approximately 11% and raises HDL-cholesterol by 5-10%. 6, 5
  • Resistance training 2-3 times per week can further improve lipid profiles. 6

Alcohol Intake

  • Limit alcohol to ≤1-2 drinks per day for men, ≤1 drink per day for women. Even modest intake (≈1 oz daily) can raise triglycerides by 5-10%. 6, 5
  • Complete abstinence is required if triglycerides exceed 2.8 mmol/L (250 mg/dL). 6

Smoking Cessation

  • If you smoke, cessation is mandatory – smoking lowers HDL-cholesterol by 10-15% and significantly increases cardiovascular risk. 5

Step 2: Reassess Lipid Panel After 6-12 Weeks of Lifestyle Optimization

  • Obtain a fasting lipid panel 6-12 weeks after implementing intensive lifestyle changes to evaluate response. 6, 5
  • If triglycerides remain ≥1.7 mmol/L (150 mg/dL) and HDL-cholesterol remains low after documented adherence to lifestyle modifications, proceed to Step 3. 6, 5

Step 3: Pharmacotherapy Decision Based on Cardiovascular Risk

If 10-Year ASCVD Risk ≥7.5% OR Diabetes (Age 40-75) OR Established ASCVD:

  • Initiate moderate-to-high intensity statin therapy immediately (e.g., atorvastatin 10-20 mg or rosuvastatin 5-10 mg daily) alongside continued lifestyle optimization. 6, 5
  • Do NOT delay statin initiation while attempting lifestyle changes alone in high-risk patients – both should occur concurrently. 6, 5
  • Statins provide a dose-dependent 10-30% triglyceride reduction and proven cardiovascular mortality benefit through LDL-cholesterol lowering. 6, 5
  • Lipid targets while on statin therapy:
    • LDL-cholesterol <2.6 mmol/L (100 mg/dL) – you already meet this
    • Non-HDL-cholesterol <3.4 mmol/L (130 mg/dL) – you already meet this
    • Triglycerides <2.3 mmol/L (200 mg/dL), ideally <1.7 mmol/L (150 mg/dL)
    • HDL-cholesterol >1.03 mmol/L (40 mg/dL) men, >1.29 mmol/L (50 mg/dL) women 6, 5

If 10-Year ASCVD Risk 5-7.5%:

  • Engage in shared decision-making regarding statin initiation, considering your low HDL-cholesterol as a risk-enhancing factor. 6, 5
  • Factors favoring statin therapy include family history of premature ASCVD, chronic kidney disease, metabolic syndrome, or persistently elevated triglycerides ≥1.7 mmol/L (150 mg/dL). 6, 5

If 10-Year ASCVD Risk <5%:

  • Continue intensive lifestyle modification for at least 3 months before considering pharmacotherapy. 6, 5
  • Re-measure fasting lipid panel in 6-12 weeks after lifestyle implementation. 6, 5
  • Consider moderate-intensity statin only after shared decision-making if risk-enhancing factors are present and lipid abnormalities persist despite documented adherence to lifestyle changes. 6, 5

Step 4: Add-On Therapy If Triglycerides Remain ≥2.3 mmol/L (200 mg/dL) After 3 Months

This step is only relevant if your triglycerides rise above 2.3 mmol/L (200 mg/dL) despite statin therapy and lifestyle optimization:

Preferred Add-On: Icosapent Ethyl (Prescription EPA)

  • Icosapent ethyl 2 g twice daily (total 4 g/day) is indicated for patients with established cardiovascular disease OR diabetes plus ≥2 additional cardiovascular risk factors (e.g., hypertension, smoking, family history, age >50 years men/>60 years women, chronic kidney disease). 6, 5
  • The REDUCE-IT trial demonstrated a 25% relative risk reduction in major adverse cardiovascular events (NNT = 21 over 4.9 years). 6, 5
  • Icosapent ethyl is the only triglyceride-lowering agent FDA-approved for cardiovascular risk reduction. 6, 5
  • Monitor for atrial fibrillation (incidence 3.1% vs 2.1% with placebo). 6, 5

Alternative Add-On: Fenofibrate

  • Fenofibrate 54-160 mg daily may be considered if triglycerides remain >2.3 mmol/L (200 mg/dL) after 3 months of optimized lifestyle and statin therapy AND you do NOT meet icosapent ethyl criteria. 6, 5
  • Fenofibrate provides 30-50% triglyceride reduction and modest HDL-cholesterol increase. 6, 5
  • When combined with statins, use fenofibrate (NOT gemfibrozil) due to a markedly better safety profile; consider lower statin doses (atorvastatin ≤20 mg or rosuvastatin ≤10 mg) in patients >65 years or with renal impairment. 6, 5
  • Important caveat: The ACCORD trial demonstrated no cardiovascular event reduction when fenofibrate was added to simvastatin in diabetics, so fenofibrate's role is primarily triglyceride lowering without proven cardiovascular benefit. 6, 5

Monitoring Strategy

  • Reassess fasting lipid panel 6-12 weeks after implementing lifestyle modifications. 6, 5
  • If statin therapy is initiated, recheck lipids 4-8 weeks after starting or adjusting dose. 6, 5
  • Calculate non-HDL-cholesterol (total cholesterol minus HDL-cholesterol) and aim for <3.4 mmol/L (130 mg/dL) as a secondary target when triglycerides are elevated. 6, 5
  • If fenofibrate is added, obtain baseline and follow-up creatine kinase levels and monitor for muscle symptoms, especially when combined with statins. 6, 5
  • Monitor renal function at baseline, 3 months, and then every 6 months while on fenofibrate. 6, 5

Treatment Goals

  • Primary goal: Maintain triglycerides <1.7 mmol/L (150 mg/dL) to minimize cardiovascular risk. 6, 5
  • Secondary goal: Raise HDL-cholesterol to >1.03 mmol/L (40 mg/dL) for men or >1.29 mmol/L (50 mg/dL) for women. 6, 5
  • Tertiary goal: Maintain non-HDL-cholesterol <3.4 mmol/L (130 mg/dL). 6, 5
  • Quaternary goal: Keep LDL-cholesterol <2.6 mmol/L (100 mg/dL) for most patients, <1.8 mmol/L (70 mg/dL) for very high-risk patients. 5

Critical Pitfalls to Avoid

  • Do NOT ignore low HDL-cholesterol (<1.03 mmol/L or 40 mg/dL) – it remains an independent cardiovascular risk factor even when LDL-cholesterol is optimal. 5
  • Do NOT delay cardiovascular risk assessment – formal 10-year ASCVD risk calculation is essential to determine whether pharmacotherapy is indicated. 6, 5
  • Do NOT overlook secondary causes (hypothyroidism, insulin resistance, excess alcohol, offending medications) – correcting these can improve lipid profiles by 20-50% and may eliminate the need for additional agents. 6, 5
  • Do NOT rely on over-the-counter fish oil supplements for cardiovascular benefit – only prescription icosapent ethyl has proven outcome data. 6, 5
  • Do NOT start fenofibrate at your current triglyceride level (1.68 mmol/L or 149 mg/dL) – lifestyle modification is first-line, and fenofibrate is reserved for triglycerides ≥2.3 mmol/L (200 mg/dL) after lifestyle optimization. 6, 5
  • Do NOT use bile acid sequestrants if triglycerides exceed 2.3 mmol/L (200 mg/dL) – they can worsen hypertriglyceridemia. 5

Summary Recommendation

Your laboratory values indicate excellent glycemic control and normal renal function, but reveal an atherogenic dyslipidemia pattern (borderline-high triglycerides with low HDL-cholesterol) that warrants:

  1. Immediate implementation of intensive lifestyle modifications (weight loss if overweight, dietary changes, aerobic exercise ≥150 min/week, alcohol moderation, smoking cessation if applicable). 6, 5

  2. Formal cardiovascular risk assessment (10-year ASCVD risk calculation, metabolic syndrome screening, evaluation for secondary causes). 6, 5

  3. Reassessment of fasting lipid panel in 6-12 weeks after documented adherence to lifestyle changes. 6, 5

  4. Statin therapy initiation if 10-year ASCVD risk ≥7.5%, diabetes (age 40-75), or established ASCVD – do NOT delay pharmacotherapy in high-risk patients. 6, 5

  5. Consideration of add-on therapy (icosapent ethyl or fenofibrate) only if triglycerides remain ≥2.3 mmol/L (200 mg/dL) after 3 months of optimized lifestyle and statin therapy. 6, 5

The cornerstone of your management is aggressive lifestyle intervention, which can lower triglycerides by 20-70% and raise HDL-cholesterol by 10-20%, potentially eliminating the need for pharmacotherapy if you are at low-to-moderate cardiovascular risk. 6, 5

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

[Effect of Serum Uric Acid on Renal Function of Patients with Abnormal Glucose Metabolism].

Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 2015

Guideline

Management of Mixed Dyslipidemia and ASCVD Risk‑Based Lipid Therapy

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Guideline

Hypertriglyceridemia Management

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Related Questions

What are the recommendations for a patient with slightly elevated glucose levels, low total cholesterol and LDL levels, and impaired renal function?
How often should LDL (Low-Density Lipoprotein) and HbA1c (Hemoglobin A1c) levels be monitored in a patient with type 2 diabetes?
What treatment is recommended for a patient with elevated Low-Density Lipoprotein (LDL) and impaired glucose regulation, indicated by a Hemoglobin A1c (HbA1c) of 5.9?
Interpret the lipid panel and recommend management for a 27‑year‑old male with a family history of type 2 diabetes, impaired fasting glucose (7.2 mmol/L) and HbA1c 5.9%, whose labs show total cholesterol 4.32 mmol/L, triglycerides 1.84 mmol/L, HDL‑C 0.86 mmol/L, LDL‑C 2.62 mmol/L, and non‑HDL‑C 3.46 mmol/L.
Does a patient with elevated LDL-C and HbA1c require modification in management?
How should I evaluate and manage a 32‑year‑old man with a 5‑year history of plaque psoriasis who stopped red meat and seafood, has persistent facial and neck rash for 7 months, and now has a new widespread maculopapular eruption?
In an adult patient with fibromyalgia on duloxetine, pregabalin, and cannabidiol who is hospitalized for severe refractory pain despite high‑dose morphine, should morphine be administered as hourly bolus doses or via a patient‑controlled analgesia (PCA) pump?
Is menstrual cramping primarily caused by the drop in progesterone or the drop in estrogen?
What mean arterial pressure (MAP) target should be used in adult septic shock, and should patients with chronic hypertension have a higher MAP goal?
What is the role of corticosteroids and antibiotics in the management of nasal polyposis?
Why am I experiencing uterine cramping and pressure similar to 9 days post‑ovulation while taking 200 mg oral progesterone twice daily?

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.