Lab result explainedBlood count (CBC)Last updated November 11, 2026

Hemoglobin electrophoresis: what your HbA, HbA2, HbF and HbS results mean

Hemoglobin electrophoresis (Hb electrophoresis) · Hemoglobinopathy evaluation (electrophoresis, HPLC or capillary electrophoresis) · reported in Percent of total hemoglobin for each fraction (HbA, HbA2, HbF and any variant)

Hemoglobin electrophoresis is a blood test that separates the different types of hemoglobin in your red cells and reports what percentage each one makes up. In a healthy adult, almost all of it is hemoglobin A (HbA, about 95 to 98 percent), with a small amount of hemoglobin A2 (HbA2, about 1.5 to 3.5 percent) and a trace of fetal hemoglobin (HbF, under about 2 percent). The test is how sickle cell trait and sickle cell disease, beta thalassemia trait and the other inherited hemoglobin variants (HbC, HbE, HbD and many rarer ones) are identified, and it is the standard follow-up when a blood count shows small red cells that iron deficiency does not explain.

The name has stuck even though most US laboratories now use high-performance liquid chromatography (HPLC) or capillary electrophoresis rather than the original gel method; the report looks the same whichever technique is used. Each hemoglobin type is a different combination of globin protein chains, and the inherited disorders fall into two groups: the thalassemias, where one chain is made in reduced amounts (shifting the proportions of HbA2 and HbF), and the structural variants such as sickle hemoglobin (HbS), where a chain is built with an altered shape and appears as a separate band or peak.

The commonest reasons to have the test are a microcytic blood count with a normal ferritin, a family history of sickle cell or thalassemia, a positive newborn screen, planning a pregnancy or being pregnant (the American College of Obstetricians and Gynecologists now recommends testing for everyone who is pregnant or planning to be, regardless of ancestry), and unexplained anemia or hemolysis. Results need to be read with the CBC, the ferritin and your age, because iron deficiency lowers HbA2 and can hide beta thalassemia trait, infants normally have a high HbF, and a transfusion in the previous three months adds donor hemoglobin to the mix.

Hb electrophoresis at a glance

What it measures: the percentage of each hemoglobin type in your blood, mainly HbA, HbA2 and HbF, plus any variant such as HbS, HbC or HbE.
Normal adult: HbA 95–98%, HbA2 about 1.5–3.5% (labs differ; some use 2.0–3.3%), HbF under about 2%, no variant hemoglobin.
Beta thalassemia trait: HbA2 raised to 3.5–7% (usually 4–6%), HbF often 1–5%, with small red cells and a high red cell count.
Sickle cell trait: HbA about 55–60% and HbS about 35–45%; sickle cell disease (HbSS): HbS 80–95%, no HbA, HbF 2–20%.
Alpha thalassemia trait usually gives a normal result; iron deficiency lowers HbA2 and should be corrected before the test is interpreted.
Next step: a normal result with persistent small cells points to alpha thalassemia (DNA test); any carrier result in pregnancy or before conception means offering the partner a test.

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What Hb electrophoresis measures

Hemoglobin is built from four globin chains around four heme groups. Adult hemoglobin A has two alpha and two beta chains; HbA2 has two alpha and two delta chains; fetal hemoglobin has two alpha and two gamma chains. Babies are born with 60 to 80 percent HbF, which is replaced by HbA over the first 6 to 12 months of life as gamma-chain production switches off and beta-chain production switches on. The test exploits the fact that each type carries a slightly different electrical charge: in classic electrophoresis, a hemolyzed sample is placed on a gel in an electric field and the types migrate different distances; in HPLC and capillary electrophoresis the same separation is done in a column or a thin capillary and quantified automatically.

Two methods are often combined to be sure of an identification. Alkaline electrophoresis separates HbA, HbF, HbS and HbC, but several variants travel with HbS (HbD, HbG, HbLepore) or with HbC (HbE, HbO-Arab), so a second run under acid conditions, or HPLC with its characteristic retention times, is used to tell them apart. A sickle solubility test (which only shows whether HbS is present, not how much) is sometimes added. Rare or ambiguous variants are confirmed by DNA sequencing. Alpha thalassemia is the important blind spot: because all three normal hemoglobins share the alpha chain, a shortage of alpha chains lowers all of them equally and the percentages stay normal, so alpha thalassemia trait is diagnosed by DNA testing or by exclusion.

Several things shift the percentages without any inherited disorder. Iron deficiency lowers HbA2 by around 0.5 percentage points, enough to pull a borderline beta thalassemia trait result into the normal range, so ferritin is checked first and the test repeated after iron repletion if needed. Vitamin B12 or folate deficiency, hyperthyroidism and some HIV medicines raise HbA2 slightly. HbF rises in pregnancy (usually to no more than 3 to 5 percent), with hydroxyurea treatment, during recovery of the bone marrow and in some blood cancers. A transfusion within the previous three to four months adds the donor's normal HbA and can make a person with sickle cell disease look like they have sickle cell trait, so testing is deferred where possible.

Normal range for Hb electrophoresis

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (Percent of total hemoglobin for each fraction (HbA, HbA2, HbF and any variant))	Notes
Hemoglobin A (HbA), adults	About 95–98%	Absent in sickle cell disease (HbSS) and beta-zero thalassemia major; reduced in sickle/beta-plus thalassemia and after transfusion in those conditions.
Hemoglobin A2 (HbA2), adults	About 1.5–3.5% (some labs 2.0–3.3%)	Above 3.5% suggests beta thalassemia trait; 3.3–3.5% is borderline and repeated after iron repletion. Lowered by iron deficiency and alpha thalassemia.
Fetal hemoglobin (HbF), adults	Under about 2% (often under 1%)	Mildly raised (2–5%) in some beta thalassemia carriers and in pregnancy; 5–20% in sickle cell disease; 15–30% in hereditary persistence of fetal hemoglobin; 70–98% in beta thalassemia major.
Newborns and infants	HbF 60–80% at birth, falling to adult levels by 6–12 months	Newborn screens report the pattern in order of amount: FA is normal, FAS sickle cell trait, FS sickle cell disease, FSC hemoglobin SC disease. HbA2 cannot be interpreted until about 12 months of age.
Beta thalassemia trait	HbA2 3.5–7% (usually 4–6%), HbF 1–5%, HbA the rest	With MCV under about 75 fL, RBC above 5.0 million/µL, Mentzer index under 13 and a normal ferritin.
Sickle cell trait (HbAS)	HbA about 55–60%, HbS about 35–45%, HbA2 and HbF normal	HbA is always greater than HbS in trait. A lower HbS (25–35%) suggests coexisting alpha thalassemia. Affects about 1 in 13 Black or African American newborns in the US.
Sickle cell disease (HbSS)	HbS 80–95%, HbF 2–20%, HbA2 under 3.5%, HbA 0%	HbS greater than HbA with some HbA present and a raised HbA2 indicates sickle/beta-plus thalassemia, a related disease.
Other common variants	HbSC: HbS about 50% and HbC about 50%; HbC trait: HbC 30–40%; HbE trait: HbE 25–30%	HbC and HbE traits are harmless. HbSC is a form of sickle cell disease; HbE with a beta thalassemia gene can be as severe as thalassemia major.
Alpha thalassemia trait	Normal pattern (HbA2 may be low-normal, 1.5–2.5%)	Diagnosed by DNA testing when small red cells persist with normal iron studies and a normal electrophoresis. Hemoglobin H disease (three genes affected) shows 5–30% HbH.

Abnormal pattern: raised HbA2, raised HbF or a variant hemoglobin

An abnormal electrophoresis almost always means an inherited difference in hemoglobin, and the specific pattern tells you which. A raised HbA2 (above 3.5 percent) with small red cells and a normal ferritin is beta thalassemia trait: one of your two beta-globin genes makes less beta chain, the marrow makes more HbA2 to compensate, and the red cells are small and numerous. It is a carrier state, not a disease; it causes at most a mild, stable anemia, needs no treatment and never progresses, but it matters for family planning because two carriers have a one in four chance per pregnancy of a child with beta thalassemia major.

A separate band or peak labeled HbS means you carry the sickle gene. If HbA is present and greater than HbS (typically 55 to 60 percent HbA, 35 to 45 percent HbS), you have sickle cell trait, which is carried by about 8 to 10 percent of Black Americans and smaller numbers of people of Mediterranean, Middle Eastern, Indian and Hispanic ancestry. People with trait are healthy and do not have sickle cell disease, though rare complications (blood in the urine, exertional heat injury and rhabdomyolysis during extreme exertion, kidney concentrating defects and a small increase in blood clot and kidney cancer risk) are recognized. If HbS makes up 80 to 95 percent with no HbA, the result indicates sickle cell disease; if HbS and HbC are each about half, it indicates hemoglobin SC disease; and HbS greater than HbA with some HbA present indicates sickle/beta-plus thalassemia.

A raised HbF in an adult has several meanings. Values of 2 to 5 percent accompany some beta thalassemia carriers and are also seen in pregnancy. Values of 15 to 30 percent with an otherwise normal count are usually hereditary persistence of fetal hemoglobin, a harmless condition; the same range with small cells may be delta-beta thalassemia. Very high HbF (70 to 98 percent) with severe anemia in a child is beta thalassemia major. Acquired rises in HbF occur with hydroxyurea treatment (the intended effect in sickle cell disease), during marrow recovery after chemotherapy or in aplastic anemia, and occasionally in leukemias and other marrow disorders, which is why an unexplained HbF rise in an adult is followed up.

Common causes

Beta thalassemia trait (minor)
HbA2 3.5–7%, HbF normal to 5%, MCV 60–75 fL, RBC above 5.0 million/µL, hemoglobin normal or mildly low. The most common cause of a raised HbA2. Iron deficiency can mask it by lowering HbA2.
Beta thalassemia intermedia and major
Two affected beta genes. HbF 70–98% with little or no HbA in major, presenting in the first two years of life with severe anemia; intermedia is milder with HbF 10–50%. Both need specialist care.
Sickle cell trait (HbAS)
One sickle gene: HbS 35–45% with HbA greater than HbS. Carriers are healthy; the result matters for partner testing and for precautions during extreme exertion, dehydration and high altitude.
Sickle cell disease (HbSS, HbSC, HbS/beta thalassemia)
HbS 80–95% with no HbA (SS); HbS and HbC each about 50% (SC); or HbS greater than HbA with raised HbA2 (S/beta-plus thalassemia). All cause chronic hemolysis and vaso-occlusive crises and are managed in a sickle cell program.
Hemoglobin C, E, D and other structural variants
HbC trait (HbC 30–40%) and HbE trait (HbE 25–30%) are harmless carrier states common in West African and Southeast Asian ancestry respectively; homozygous HbC and HbE cause mild anemia with target cells. HbE combined with beta thalassemia is a serious disease common in Southeast Asia.
Hereditary persistence of fetal hemoglobin and delta-beta thalassemia
HbF 15–30% in adults with normal or slightly small red cells and no anemia. HPFH is benign and can lessen the severity of coexisting sickle cell disease; delta-beta thalassemia behaves like thalassemia trait.
Acquired rise in HbF
Pregnancy (usually under 5%), hydroxyurea and other HbF-inducing drugs, recovery from chemotherapy or aplastic anemia, juvenile myelomonocytic leukemia and other myeloid disorders, and occasionally hyperthyroidism.
Acquired rise in HbA2
Vitamin B12 or folate deficiency, hyperthyroidism, HIV infection (particularly with zidovudine treatment) and some unstable hemoglobins raise HbA2 modestly, usually to no more than 3.5–4%, without small red cells.
Compound heterozygotes and rare variants
Inheriting two different abnormal genes (HbS with HbD-Punjab, HbS with HbO-Arab, HbE with beta thalassemia) produces patterns that need acid electrophoresis, HPLC retention times or DNA sequencing to identify, and some of these combinations behave as significant disease.

Symptoms that can go with it

Usually none for carriers: beta thalassemia trait, sickle cell trait, HbC trait and HbE trait are found on screening or in pregnancy
A mild, lifelong anemia that has not responded to iron, sometimes with slight tiredness
In sickle cell disease: episodes of severe pain in the bones, chest, abdomen or joints, fatigue, jaundice, recurrent infections and delayed growth in children
In thalassemia major and intermedia: pallor, poor growth, an enlarged spleen and liver, bone changes and jaundice from early childhood
In sickle cell trait, rarely: blood in the urine, or collapse with muscle pain and dark urine during extreme exertion in heat
Gallstones at a young age in any condition with increased red cell breakdown
A family history of anemia, thalassemia, sickle cell, early splenectomy or regular transfusions

Low HbA2 or low/absent HbA

A low HbA2 (under about 1.5 to 2 percent) is less often discussed but has two common explanations. The first is iron deficiency, which reduces HbA2 production by around 0.5 percentage points; in someone who also carries beta thalassemia trait, that is enough to pull a true value of 3.8 percent down to a falsely normal 3.3, so a low or borderline HbA2 with a low ferritin should be repeated once iron stores are rebuilt. The second is alpha thalassemia, in which the shortage of alpha chains affects HbA2 slightly more than HbA, giving a low-normal or low HbA2 with small red cells and normal iron studies; this is the pattern that leads to DNA testing. Rare delta-chain mutations (delta thalassemia) also lower HbA2 and can mask a coexisting beta thalassemia trait.

Absent or markedly reduced HbA means both beta-globin genes are affected. No HbA at all with 80 to 95 percent HbS is sickle cell disease; no HbA with very high HbF is beta-zero thalassemia major; HbA present but less than HbS is sickle/beta-plus thalassemia. A recent transfusion can add donor HbA to any of these patterns and make the disease look like a carrier state, which is why the test is ideally done before transfusion or at least three months after one. In a newborn, HbA is normally only 20 to 40 percent of the total, so an infant's report is read against age-specific expectations rather than adult ranges.

Common causes

Iron deficiency
Lowers HbA2 by about 0.5 percentage points and can hide beta thalassemia trait. Ferritin under 30 ng/mL should prompt iron repletion and a repeat electrophoresis in three months before thalassemia trait is excluded.
Alpha thalassemia trait and hemoglobin H disease
Two missing alpha genes give small red cells with HbA2 of 1.5–2.5% and a normal HbF; three missing genes give hemoglobin H disease with 5–30% HbH, a moderate hemolytic anemia and an enlarged spleen.
Delta thalassemia
A rare reduction in delta-chain production lowers HbA2 on its own and, when co-inherited with beta thalassemia trait, produces a normal HbA2 despite true carrier status; DNA testing is needed when the CBC strongly suggests thalassemia.
Sickle cell disease and beta-zero thalassemia major
HbA is absent because neither beta gene produces normal beta chain; the hemoglobin is almost entirely HbS or HbF respectively.
Sickle/beta-plus thalassemia and HbE/beta thalassemia
HbA is present but reduced, with HbS or HbE as the major component and a raised HbA2; these compound states behave as disease rather than trait.
Recent transfusion
Donor red cells contribute normal HbA for up to three to four months and can make sickle cell disease look like trait or normalize a thalassemia pattern. Testing is deferred or interpreted with the transfusion date in mind.

Symptoms that can go with it

None in iron-deficiency-related low HbA2 beyond the symptoms of iron deficiency itself (tiredness, pallor, hair shedding)
Usually none in alpha thalassemia trait; a mild, stable anemia found incidentally
Fatigue, jaundice, gallstones and an enlarged spleen in hemoglobin H disease, with episodes of worse anemia during infections or with oxidant drugs
Pain crises, fatigue, jaundice and infections in sickle cell disease when HbA is absent
Severe anemia, poor growth and bone changes from infancy in beta thalassemia major

Read it alongside

Hemoglobin, MCV and MCH — small, pale cells with a normal or near-normal hemoglobin are the setting in which the test is most informative.
RBC count and Mentzer index — a high red cell count with small cells (index under 13) predicts a thalassemia result; a low count predicts iron deficiency.
Ferritin and iron saturation — iron deficiency must be excluded or corrected before a normal or borderline HbA2 can be trusted.
RDW — normal or mildly raised in thalassemia trait and HbE or HbC trait; high in iron deficiency and in sickle cell disease.
Reticulocyte count, LDH, bilirubin and haptoglobin — raised reticulocytes, LDH and bilirubin with a low haptoglobin show active hemolysis, as in sickle cell disease and hemoglobin H disease.
Peripheral smear — target cells in thalassemia, HbC and HbE; sickle cells only in sickling disease, not in trait; Howell-Jolly bodies once the spleen has stopped working.
Sickle solubility test — a quick yes/no for HbS used in emergencies and pre-operatively; it cannot tell trait from disease and is negative in infants under about 6 months.
Partner's CBC and electrophoresis — the relevant 'next test' when a carrier state is found before or during pregnancy.

What usually happens next

If HbA2 is raised and ferritin is normal, you have beta thalassemia trait: no treatment is needed, iron should be avoided unless ferritin is low, and the result should be recorded so that future microcytosis is not mistaken for iron deficiency.
If the result is normal but your red cells remain small with a normal ferritin, the likely explanation is alpha thalassemia trait; DNA testing (alpha-globin gene deletion analysis) confirms it and is most useful before a pregnancy.
If ferritin is low, treat the iron deficiency first and repeat the electrophoresis after about three months, since iron deficiency lowers HbA2 and can hide a carrier state.
If you are a carrier of any variant (beta thalassemia, HbS, HbC, HbE, alpha thalassemia) and pregnant or planning a pregnancy, your partner should be offered a CBC and electrophoresis; if both of you carry a relevant gene, genetic counseling and the option of prenatal or preimplantation testing are discussed, ideally before 10 to 12 weeks.
If the pattern shows sickle cell disease, hemoglobin SC, HbS/beta thalassemia, hemoglobin H disease or thalassemia major or intermedia, expect referral to a hematologist or a comprehensive sickle cell or thalassemia program.
If you were transfused in the previous three to four months, ask for the test to be repeated once that window has passed.

Diet, lifestyle and natural levers with evidence

What can move Hb electrophoresis once the cause is known. Nothing here replaces finding the cause.

Correct iron deficiency before relying on the result

Strong evidence

Nothing you eat or take changes which hemoglobin genes you carry, but iron status changes what the test shows. Iron deficiency lowers HbA2 by about 0.5 percentage points and can hide beta thalassemia trait; repleting iron (oral iron raises hemoglobin about 1 g/dL every two to three weeks, with ferritin recovering over three to six months) restores HbA2 to its true level. Conversely, carriers should not take iron unless ferritin is low, as thalassemia increases iron absorption and stores can rise.

Check ferritin before and after; long-term iron in thalassemia trait or intermedia can cause iron overload.

Time the test around transfusion and pregnancy

Strong evidence

Donor cells from a transfusion contribute normal HbA for three to four months and can turn a disease pattern into an apparent trait, so the test is done before transfusion or at least three months after. Pregnancy raises HbF modestly (usually under 5 percent) and lowers the red cell count, so results in pregnancy are interpreted with those shifts in mind rather than retested later, because the information is needed early for partner testing.

Hydration and heat precautions during extreme exertion with sickle cell trait

Moderate evidence

Sickle cell trait carries a small but real risk of exertional rhabdomyolysis and collapse during very intense exercise in heat, dehydration or at altitude. In a study of nearly 48,000 US Army soldiers, those with trait had a 54 percent higher risk of exertional rhabdomyolysis but no higher risk of death once universal precautions (gradual conditioning, rest breaks, free access to fluids, stopping at the first symptoms) were in place. The same precautions are recommended by the NCAA and military for athletes and recruits with trait.

L-glutamine and folate in sickle cell disease

Moderate evidence

For people whose result shows sickle cell disease, pharmaceutical-grade L-glutamine (0.3 g/kg twice daily) reduced the median number of pain crises from 4 to 3 over 48 weeks and acute chest syndrome from 23 to 9 percent in a 230-person randomized trial; it is a prescription product in the US and complements, rather than replaces, hydroxyurea, which raises HbF. Daily folic acid (usually 1 mg) is routinely recommended in sickle cell disease and thalassemia intermedia and major because rapid red cell turnover depletes folate. Neither changes the electrophoresis result in carriers.

L-glutamine causes nausea and constipation in some people and has not been studied in kidney or liver impairment; discuss it with your sickle cell team.

When to see a clinician promptly

In sickle cell disease: a temperature of 101.3°F (38.5°C) or higher, chest pain or difficulty breathing, sudden weakness, trouble speaking or vision loss, an erection lasting more than four hours, or severe pain not controlled at home: each is an emergency.
In a child with sickle cell disease: sudden pallor, lethargy and a rapidly enlarging abdomen (possible splenic sequestration) need emergency care.
Blood in the urine, or collapse with severe muscle pain and dark urine during exertion, in someone with sickle cell trait.
A result showing any carrier state when you or your partner are pregnant, ideally before 10 to 12 weeks, so that partner testing and counseling can be arranged in time.
A microcytic anemia that has not responded to three months of iron, which should prompt electrophoresis rather than more iron.
Worsening anemia, jaundice or an enlarging spleen in anyone with thalassemia intermedia or hemoglobin H disease, particularly during an infection or after a new medicine.

Frequently asked questions

What is a normal hemoglobin electrophoresis result?

In an adult: HbA about 95 to 98 percent, HbA2 about 1.5 to 3.5 percent, HbF under about 2 percent, and no variant hemoglobin such as HbS, HbC or HbE. Laboratories differ slightly in their HbA2 cut-off (3.3 to 3.7 percent). A normal result excludes beta thalassemia trait (provided you are not iron deficient) and the structural variants, but does not exclude alpha thalassemia trait, which usually gives a normal pattern.

What is the normal HbA2 range and what does a high HbA2 mean?

Normal HbA2 is about 1.5 to 3.5 percent of total hemoglobin; most people are between 2 and 3. A value above 3.5 percent (typically 4 to 6) with small red cells and a normal ferritin means beta thalassemia trait, a harmless carrier state. Values of 3.3 to 3.7 are borderline and are repeated once iron deficiency has been excluded or treated. Mild rises without small cells can come from B12 or folate deficiency, hyperthyroidism or HIV treatment.

Does hemoglobin electrophoresis show sickle cell trait?

Yes. Sickle cell trait appears as HbS making up about 35 to 45 percent of hemoglobin with HbA about 55 to 60 percent; HbA is always greater than HbS in trait. Sickle cell disease appears as HbS 80 to 95 percent with no HbA. The quick sickle solubility test used in emergencies only shows that HbS is present and cannot tell trait from disease; electrophoresis or HPLC is needed for that.

Why is hemoglobin electrophoresis done in pregnancy?

To find out whether you carry a hemoglobin variant or thalassemia gene before the baby is born. ACOG recommends a CBC with red cell indices and hemoglobin electrophoresis (or HPLC) for everyone who is pregnant or planning to be, regardless of ancestry. If you are a carrier, your partner is tested; if both of you carry a relevant gene, there is a one in four chance per pregnancy of an affected child, and counseling and prenatal or preimplantation diagnosis can be offered. The test is best done early, as pregnancy itself raises HbF slightly and iron deficiency, common in pregnancy, lowers HbA2.

Can hemoglobin electrophoresis detect alpha thalassemia?

Usually not. Because HbA, HbA2 and HbF all contain alpha chains, a shortage of alpha chains lowers all three equally and the percentages stay normal; HbA2 may be at the low end of normal. Alpha thalassemia trait is suspected when red cells are small, ferritin is normal and electrophoresis is normal, and it is confirmed by DNA testing for alpha-globin gene deletions. Hemoglobin H disease, the more severe three-gene form, does show up as an HbH peak of 5 to 30 percent.

Why does iron deficiency matter for this test?

Iron deficiency reduces HbA2 by around 0.5 percentage points, which is enough to pull a beta thalassemia carrier's result from, say, 3.8 percent into the normal range, so the carrier state is missed. Ferritin should be checked alongside the electrophoresis; if it is low, iron is replaced and the electrophoresis repeated after about three months. The opposite also matters: thalassemia carriers are often given iron for years for an 'anemia' that iron cannot fix, so a confirmed result should be kept in your records.

What is HbF and why would it be high in an adult?

HbF is fetal hemoglobin, the main hemoglobin before birth, normally under 2 percent after the first year of life. Mild rises (2 to 5 percent) occur in some beta thalassemia carriers and in pregnancy. Levels of 15 to 30 percent with a normal count are usually hereditary persistence of fetal hemoglobin, a benign inherited trait. HbF is also raised by hydroxyurea (intentionally, in sickle cell disease), during bone marrow recovery and in some marrow disorders, and it is very high in beta thalassemia major. An unexplained rise in an adult is worth a hematology opinion.

Can I have the test after a blood transfusion?

It is better to wait. Transfused red cells carry the donor's normal HbA and survive for up to three to four months, so a test done soon after a transfusion can make sickle cell disease look like sickle cell trait or normalize a thalassemia pattern. If the result is needed urgently, it can still be done, but it must be interpreted with the transfusion date in mind, and DNA testing, which is unaffected by transfusion, is an alternative.

What do newborn screening results like FA, FAS and FS mean?

Every US state screens newborns for sickle cell disease. Results list the hemoglobins present in order of amount: FA (fetal then adult) is normal; FAS means sickle cell trait; FS means sickle cell disease or sickle/beta-zero thalassemia; FSC means hemoglobin SC disease; FC means HbC disease. Because babies have mostly HbF at birth, an abnormal screen is confirmed by repeat testing at a few months of age, and HbA2 cannot be assessed for beta thalassemia trait until about 12 months.

References

Hemoglobin electrophoresis. MedlinePlus, US National Library of Medicine (2023)View source
Hemoglobinopathies in pregnancy: ACOG Practice Advisory. American College of Obstetricians and Gynecologists (2022)
Data and statistics on sickle cell disease. Centers for Disease Control and Prevention (2024)View source
Sickle cell disease. Merck Manual Professional Version (2024)
Thalassemias. Merck Manual Professional Version (2024)
Muncie HL Jr, Campbell JS. Alpha and beta thalassemia. American Family Physician (2009)
Piel FB, Steinberg MH, Rees DC. Sickle cell disease. New England Journal of Medicine (2017)
Mosca A, Paleari R, Ivaldi G, Galanello R, Giordano PC. The role of haemoglobin A2 testing in the diagnosis of thalassaemias and related haemoglobinopathies. Journal of Clinical Pathology (2009)
Bain BJ. Haemoglobinopathy diagnosis: algorithms, lessons and pitfalls. Blood Reviews (2011)
Nelson DA, Deuster PA, Carter R 3rd, Hill OT, Wolcott VL, Kurina LM. Sickle cell trait, rhabdomyolysis, and mortality among U.S. Army soldiers. New England Journal of Medicine (2016)
Niihara Y, Miller ST, Kanter J, et al.. A phase 3 trial of L-glutamine in sickle cell disease. New England Journal of Medicine (2018)
Evidence-based management of sickle cell disease: expert panel report, 2014. National Heart, Lung, and Blood Institute (2014)View source

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