Investigations

1st investigations to order

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Almost all patients with classic PNH have episodes of haemoglobinuria during haemolytic episodes.

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haemoglobinuria

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Stainable iron in the urine is evidence of intravascular haemolysis.

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haemosiderinuria

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Unilineage or multilineage cytopoenias may co-exist (e.g., leukopenia, thrombocytopoenia). Evidence of dysplastic changes in bone marrow and/or peripheral blood may suggest underlying myelodysplasia.

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anaemia or cytopoenia (e.g., granulocytopoenia, thrombocytopoenia)

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Assessed to confirm intravascular haemolysis.

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increase indicates haemolysis

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Other sources of tissue destruction may give the same result; may be resolved by isozyme testing.

Liver damage is characterised by elevated alanine aminotransferase, whereas intravascular haemolysis is not.

Sample must be processed at once to avoid in vitro haemolysis.

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increase indicates intravascular haemolysis

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Assessed to confirm intravascular haemolysis.

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elevated

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Assesses the risk of thrombosis; elevated D-dimer level suggests an increased risk.

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may be elevated

Investigations to consider

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Assessed to confirm intravascular haemolysis.

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low

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Testing should be done with at least two reagents on RBCs, granulocytes and monocytes.[2]

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>1% to 3% of anchor-deficient granulocytes indicates a diagnosis of PNH

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Done on granulocytes and monocytes. Most sensitive and accurate test.[22]

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detects glycosylphosphatidylinositol anchor; >1% to 3% deficient cells indicate PNH

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Detects missing proteins on PNH cells.

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variable

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Usually negative except after treatment with complement C5 inhibitors.

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detects IgG and C3 on the RBC surface, excludes autoimmune haemolytic anaemias

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Patients with PNH have unusually large iron losses and may be iron deficient.

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low

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Both acute and chronic renal insufficiency may occur.[10]

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variable

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