Investigations

1st investigations to order

haemoglobin (Hb)

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Hb will be normal in alpha-thalassaemia silent carrier and may be slightly low in alpha-thalassaemia trait.

The Hb level is variable in Hb H disease: approximately 70-110 g/L (7-11 g/dL) in deletional disease and 40-90 g/L (4-9 g/dL) in non-deletional disease.[16]

Result

normal to low

mean corpuscular volume (MCV)

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The MCV correlates with phenotypic and genotypic worsening of the disease. Patients with alpha-thalassaemia silent carrier have a normal to slightly low MCV, whereas those with deletional alpha-thalassaemia trait usually have an MCV of approximately 54 femtolitres (range 46-76 femtolitres).[16]​​​ Those with non-deletional Hb H disease will have an MCV of approximately 65 femtolitres (range 48.7 to 80.7 femtolitres).[16] Patients with Hb H/Constant Spring will have an MCV that is normal to mildly low, and those homozygous for Hb Constant Spring will often have a normal MCV.

Result

low

mean corpuscular haemoglobin (MCH)

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MCH will be normal to low (24-29 picograms/cell) in those with 1 alpha-thalassaemia silent carrier, and it will be low (<27 picograms/cell) in those with >1 alpha-globin deletion or in those with non-deletional mutations.

Mean MCH is approximately 17 picograms for deletional Hb H disease and 19 picograms for non-deletional Hb H disease.[16]

Result

low

red blood cell count

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Should be performed in all patients.

Result

increased; variable, corresponding to severity

peripheral smear

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Carefully review for findings consistent with alpha-thalassaemia, including microcytosis, hypochromia, increased polychromasia, target cells, and anisopoikilocytosis.[16]

Misshapen and even fragmented red cells may be found in patients with Hb H disease, and characteristic inclusion bodies may be seen on staining with a supravital dye such as brilliant cresyl blue.[16]

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In homozygous Hb Constant Spring, the cells will be normal or slightly small in size, and basophilic stippling may be prominent.[6]

Result

abnormal shape and size of cells

reticulocyte percentage

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In Hb H disease, the reticulocyte percentage is elevated (2.5% to 4.0% for deletional Hb H; 5.5% to 6.5% for non-deletional Hb H) and may be further increased during acute infections or haemolytic crises.​​[16]

Result

increased

serum iron

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If microcytosis (MCV <78 femtolitres) or hypochromia (MCH <27 picograms) is present, iron status should be assessed to differentiate between anaemia due to thalassaemia and iron-deficiency anaemia.

Result

normal or elevated

serum ferritin

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If microcytosis (MCV <78 femtolitres) or hypochromia (MCH <27 picograms) is present, iron status should be assessed to differentiate between anaemia due to thalassaemia and iron-deficiency anaemia.

If serum ferritin levels suggest elevated iron status, liver iron overload should be assessed. Serum ferritin levels may underestimate liver iron concentration.[56]

Guidelines suggest MRI evaluation of liver iron if serum ferritin is >674.1 picomol/L (>300 nanograms/mL) in patients with Hb H disease.[16]

Result

normal or elevated

Investigations to consider

brilliant cresyl blue staining of red blood cells

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Numerous inclusion bodies are typically seen in Hb H disease.[16] Believed by some experts to be more reliable than Hb electrophoresis for diagnosis of Hb H disease. 

May be reduced or absent in the presence of heterozygous beta-thalassaemia such as Hb S, Hb C, Hb E, or beta-thalassaemia.​​[46][57]​​​

Result

demonstrates Hb H inclusions in peripheral blood red cells

Hb electrophoresis

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Hb H and Hb Bart can be detected as fast-moving haemoglobins. Will not pick up alpha-thalassaemia silent carrier or alpha-thalassaemia trait outside of the newborn period (Hb Barts), and will not differentiate deletional from non-deletional forms of Hb H (except for Hb Constant Spring). Patients with Hb H disease and concomitant heterozygous beta-haemoglobinopathies such as Hb S, Hb C, Hb E, or beta-thalassaemia have low or absent Hb H, which may confound the diagnosis of Hb H disease.

Result

presence of Hb H, Hb Bart, and concomitant haemoglobinopathies (Hb E, Hb S, Hb C, Hb D)

Hb fractionation by high-performance liquid chromatography (HPLC)

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Hb fractionation by HPLC provides fast separation and precise estimation of haemoglobin variants.

Will not pick up alpha-thalassaemia silent carrier or alpha-thalassaemia trait outside of the newborn period (Hb Barts), and will not differentiate deletional from non-deletional forms of Hb H (except for Hb Constant Spring). Patients with Hb H disease and concomitant heterozygous beta-haemoglobinopathies such as Hb S, Hb C, Hb E, or beta-thalassaemia have low or absent Hb H, which may confound the diagnosis of Hb H disease.

Result

presence of Hb H, Hb Bart, and concomitant haemoglobinopathies (Hb E, Hb S, Hb C, Hb D)

gap-polymerase chain reaction (gap-PCR)

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Seven of the most common alpha-thalassaemia deletions (-alpha(3.7), -alpha(4.2), --(FIL), --(THAI), --(MED), -(alpha)(20.5) , --(SEA)) can be diagnosed by gap-PCR.[16]

Result

detects specific deletions

multiplex ligation-dependent probe amplification

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Used to detect deletions and duplications in the alpha-globin gene cluster causing alpha-thalassaemia.[16]

Result

detects deletion alleles

direct sequencing/reverse dot blot

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Used to detect non-deletional alpha-thalassaemia mutations.[16]​​[51][53]

Result

detect non-deletional alpha-thalassaemia mutations

MRI (hepatic or cardiac)

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Liver iron overload can be assessed by R2 or R2* MRI.[16][55]

Guidelines suggest MRI evaluation of liver iron concentration if serum ferritin is >674.1 picomol/L (>300 nanograms/mL) in patients with Hb H disease.[16]

​Cardiac iron loading is assessed by T2* cardiac MRI.[16] Cardiac iron loading is uncommon in non-transfused patients.

Result

liver or cardiac iron in patients with iron overload is demonstrated by difference in organ-to-muscle signal intensity

superconducting quantum interference devices (SQUID)

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Liver iron overload can be assessed by superconducting quantum interference devices (SQUID).[54][55]

Guidelines suggest evaluation of liver iron concentration if serum ferritin is >674.1 picomol/L (>300 nanograms/mL) in patients with Hb H disease.[16]

Result

liver iron in iron overload

liver biopsy

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MRI is preferred to liver biopsy for assessment of iron overload where possible as it has better accuracy and fewer procedural risks. Liver biopsy may be used where assessment of histology is needed.[21]

Guidelines suggest evaluation of liver iron concentration if serum ferritin is >674.1 picomol/L (>300 nanograms/mL) in patients with Hb H disease.[16]

Result

liver iron ≥5 mg Fe/g dry weight on liver biopsy indicates need for iron chelation therapy

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