Acute promyelocytic leukemia differential diagnosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2]

Differentiating Acute promyelocytic meukemia from other Diseases

Acute promyelocytic leukemia can be distinguished from other types of AML based on morphologic examination of a bone marrow biopsy or aspirate. Definitive diagnosis requires testing for the RARα fusion gene. This may be done by polymerase chain reaction (PCR), fluorescent in situ hybridization (FISH), or conventional cytogenetics of peripheral blood or bone marrow.

Characteristic	Causes	Laboratory abnormalities	Physical examination	Therapy	Other associations
Acute promyelocytic leukemia	Translocation between chromosomes 15 and 17 Creation of PML-RARalphagene product	Low white blood cell count (typically) Anemia Neutropenia Thrombocytopenia Low fibrinogen	Mucosal bleeding Bruising Infections Fatigue	All-trans retinoic acid (ATRA) Arsenic trioxide Cytarabine Anthracycline	Presence of Auer rods in promyelocytes High risk for early death from hemorrhagic complications
Acute myeloid leukemia	Chromosomal instability Sporadic mutations	Schistocytes on peripheral blood smear Low hemoglobin Thrombocytopenia Elevated creatinine	Bleeding Thrombosis Pyrexia Altered mental status Neurologic deficits Impaired urine output	Treatment of the underlying cause Plasmapheresis if thrombotic thrombocytopenia purpura is the underlying cause	Can be life-threatening pending the underlying cause TTP required immediate treatment
Paroxysmal cold hemoglobinuria	Production of Donath-Landsteiner antibody, triggered by viral or bacterial infection	Positive Donath-Landsteiner antibody Microscopic hematuria Negative Coombs' test for IgG or C3d Negative cold agglutinin titer Indirect hyperbilirubinemia Reticulocytosis Low haptoglobin Elevated LDH	Hematuria in the presence of cold weather Jaundice	Removal of offending agent Steroids Alternative immunosuppression	Associated with syphilis Maternal IgG can cross the placenta and affect the fetus
Paroxysmal nocturnal hemoglobinuria	Genetic defect in anchoring proteins for complement factors on red blood cells	Hemolysis due to loss of complement inhibition on the red blood cell surface, which in turn is due to defect in CD55 (decay accelerating factor) and CD59	Splenomegaly Abdominal tenderness Pallor	Eculizumab Immunosuppressive therapy	Associated with myelodysplastic syndrome Associated with mesenteric and portal venous thrombosis Risk for progression to acute myeloid leukemia
Hereditary spherocytosis	Mutation in ankyrin Mutation in alpha- or beta-spectrin Mutation in band 3 Mutation in protein 4.2	Positive eosin-5-maleimide binding to red blood cells Positive osmotic fragility testing Spherocytes on peripheral blood smear	Pallor Jaundice Splenomegaly	Removal of offending medication High-dose vitamin B6 (up to 200mg daily) Avoidance of splenectomy Symptomatic transfusion support with iron chelation as needed	Can be autosomal dominant or recessive
Pernicious anemia	Autoimmune gastritis Production of anti-intrinsic factor antibodies Production of anti-parietal cell antibodies	Low vitamin B12 level Presence of anti-intrinsic factor antibodies Presence of anti-parietal cell antibodies	Gastrointestinal discomfort Weakness Tingling Paresthesias	Lifelong vitamin B12 therapy (1000mcg daily)	Associated with diabetes, thyroid disease, vitiligo and other autoimmune conditions
Chronic lymphocytic leukemia	Mutations in hematopoietic stem cells and B lymphocytes	Elevated absolute lymphocyte count Anemia (Rai stage III) and thrombocytopenia (Rai stage IV)	Lymph node enlargement Splenomegaly in Rai stage II Hepatomegaly in Rai stage II Pallor Bleeding	Chemotherapy with rituximab Ibrutinib Venetoclax	Secondary autoimmune hemolytic anemia occurs in 10-25% of patients with CLL Treatment with corticosteroids or anti-leukemic therapy will correct the underlying anemia