Interpretation
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Reading File
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Reading File
Finding Sources
This is a Bio-Rad D-10 HPLC report for hemoglobin fractionation. Here is a full interpretation:
Bio-Rad D-10 HPLC — Patient Report Interpretation
Key Results
| Fraction | Area % | Reference Range | Interpretation |
|---|---|---|---|
| HbF | 23.6% ⚠️ | <1% (adults) | Markedly elevated |
| HbA2 | 4.6% | 2.0–3.5% | Elevated |
| HbA0 | 6.2% | ~95–98% (normal) | Severely reduced |
| S-Window | 63.0% | — | Likely represents HbS or other variant |
| HbA1a | 4.1% | — | Minor fractions |
Interpretation
This pattern is most consistent with: Sickle-β⁺ Thalassemia (HbS/β⁺-thalassemia)
Evidence:
-
S-Window = 63.0% — The dominant peak eluting at ~4.20 min in the S-window strongly suggests HbS (or less likely another variant co-eluting in this window such as HbD or HbG).
-
HbF = 23.6% (markedly elevated) — Elevated HbF is a hallmark of:
- β-thalassemia (as a compensatory response to reduced/absent β-globin chain production)
- Sickle-β thalassemia
- The asterisk (*) indicates the instrument flagged this as outside its expected range.
-
HbA2 = 4.6% (elevated above 3.5%) — HbA2 >3.5% is diagnostic of β-thalassemia trait/minor. In this context combined with HbS, it confirms a β-thalassemia gene on one allele.
-
HbA0 = 6.2% (severely reduced) — In normal adults, HbA constitutes ~95–98%. Here it is only 6.2%, indicating severely impaired normal β-globin production. In HbS/β⁰ thalassemia, HbA0 would be 0%; the presence of a small HbA0 fraction (~6.2%) favors β⁺ (not β⁰) thalassemia — i.e., some residual β-globin chain production persists.
Summary Diagnosis
Sickle-β⁺ thalassemia (HbS/β⁺-thal) — compound heterozygote inheriting one HbS allele and one β⁺-thalassemia allele. This is confirmed by:
- Dominant S-window fraction (~63%)
- Small but present HbA0 (6.2%) — rules out β⁰ thalassemia
- Elevated HbA2 >3.5% (β-thalassemia marker)
- Markedly elevated HbF (compensatory)
This is a clinically significant sickling disorder, generally milder than homozygous HbSS (sickle cell disease) but can still cause vaso-occlusive crises, especially under physiologic stress.
Clinical Correlation Needed
- CBC with peripheral smear — expect microcytosis, hypochromia, sickle cells, target cells
- Family studies — parental HPLC to confirm genotype
- Molecular confirmation (β-globin gene sequencing) to precisely characterize the thalassemia mutation and distinguish from HbSS + HPFH if there is any doubt
- Iron studies — to exclude concomitant iron deficiency (which can lower HbA2 artificially)
References: Goldman-Cecil Medicine, 26th ed. — β-thalassemia diagnosis criteria (HbA2 >3.5% = β-thal minor); Robbins & Kumar Basic Pathology — β-thalassemia major Hb electrophoresis patterns
