Acute promyelocytic leukemia differential diagnosis: Difference between revisions
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|Acute promyelocytic leukemia | |Acute promyelocytic leukemia | ||
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* Prior exposure to alkylating agents | |||
* Prior exposure to topoisomerase II inhibitors | |||
* Translocation between chromosomes 15 and 17 | * Translocation between chromosomes 15 and 17 | ||
* Creation of PML-RAR''alpha''gene product | * Creation of PML-RAR''alpha''gene product | ||
* Differentiation block in myeloid cells | |||
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* Low [[white blood cell]] count (typically) | * Low [[white blood cell]] count (typically) | ||
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* [[Mucosal bleeding]] | * [[Mucosal bleeding]] | ||
* [[Bruising]] | * [[Bruising]] | ||
* | * Evidence of infection | ||
* | * Pallor | ||
* [[Thrombosis]] | |||
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* All-''trans'' retinoic acid (ATRA) | * All-''trans'' retinoic acid (ATRA) | ||
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* Chromosomal instability | * Chromosomal instability | ||
* Sporadic mutations | * Sporadic mutations | ||
* Prior exposure to benzene | |||
* Prior exposure to alkylating agents | |||
* Prior exposure to topoisomerase II inhibitors | |||
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* [[ | * [[Anemia]] | ||
* [[Thrombocytopenia]] | * [[Thrombocytopenia]] | ||
* | * [[Neutropenia]] | ||
* Elevated LDH | |||
* Elevated uric acid | |||
* Elevated phosphorus | |||
* Elevated potassium | |||
* Low calcium | |||
* Greater than 20% myeloblasts on bone marrow aspirate | |||
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* Pyrexia | * Pyrexia | ||
* | * Evidence of infection | ||
* | * Pallor | ||
* | * Mucosal bleeding (less common than in acute promyelocytic leukemia) | ||
* Bruising (less common than in acute promyelocytic leukemia) | |||
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* | * Cytarabine | ||
* | * Anthracycline | ||
* Enasidenib | |||
* Liposomal daunorubicin plus cytarabine | |||
* Gemtuzumab ozogamycin | |||
* Midostaurin | |||
* [[Stem cell transplant]] | |||
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* | * Variable prognosis based on cytogenetic and molecular profile | ||
* | * Four new FDA-approved therapies became available in 2017 | ||
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| | |Acute lymphoblastic leukemia | ||
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* | * Chromosomal instability | ||
* Sporadic mutations | |||
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* | * [[Anemia]] | ||
* [[Thrombocytopenia]] | |||
* [[Neutropenia]] | |||
* Elevated LDH | |||
* Elevated uric acid | |||
* [[ | * Elevated phosphorus | ||
* | * Elevated potassium | ||
* Elevated | * Low calcium | ||
* Greater than 20% lymphoblasts on bone marrow aspirate | |||
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* | * Neurologic deficits | ||
* | * Pallor | ||
* Lymphadenopathy | |||
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* | * HyperCVAD (cyclophosphamide, vincristine, doxorubicin, dexamethasone) | ||
* | * R-HyperCVAD (inclusion of rituximab) | ||
* | * Peg-asparaginase | ||
* Intrathecal methotrexate | |||
* Intrathecal cytarabine | |||
* Blinatumomab (bispecific T cell engager) | |||
* Inotuzumab ozogamycin (anti-CD22 antibody) | |||
* Tisagenlecleucel (chimeric antigen receptor T (CAR-T) cell therapy) | |||
* [[Stem cell transplant]] | |||
| | | | ||
* | * Sanctuary sites include the central nervous system (CNS) and testes | ||
|- | |- | ||
| | |Chronic myeloid leukemia | ||
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* | * Translocation between chromosomes 9 and 22 | ||
* Creation of BCR-Abl gene product | |||
| | | | ||
* | * Elevated [[white blood cell]] count | ||
* Presence of [[white blood cell]] precursors at various stages of maturation | |||
* Presence of excess metamyelocytes, basophils, eosinophils, and band cells | |||
| | | | ||
* Splenomegaly | * Splenomegaly | ||
* Abdominal tenderness | * Abdominal tenderness | ||
* Pallor | * Pallor | ||
* Evidence of infection | |||
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* [[ | * [[Imatinib]] | ||
* Immunosuppressive therapy | * [[Nilotinib]] | ||
* [[Dasatinib]] | |||
* [[Bosutinib]] | |||
* [[Ponatinib]] | |||
* [[Omacetaxine]]* Immunosuppressive therapy | |||
| | | | ||
* | * High response rate to tyrosine kinase inhibitors | ||
* | * Risk for development of T315I kinase domain mutation | ||
* | * Typically does not require [[stem cell transplant]] | ||
|- | |- | ||
|- | |- | ||
|[[Chronic lymphocytic leukemia]]<ref name="pmid28102226">{{cite journal| author=Kipps TJ, Stevenson FK, Wu CJ, Croce CM, Packham G, Wierda WG et al.| title=Chronic lymphocytic leukaemia. | journal=Nat Rev Dis Primers | year= 2017 | volume= 3 | issue= | pages= 16096 | pmid=28102226 | doi=10.1038/nrdp.2016.96 | pmc=5336551 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28102226 }} </ref> | |[[Chronic lymphocytic leukemia]]<ref name="pmid28102226">{{cite journal| author=Kipps TJ, Stevenson FK, Wu CJ, Croce CM, Packham G, Wierda WG et al.| title=Chronic lymphocytic leukaemia. | journal=Nat Rev Dis Primers | year= 2017 | volume= 3 | issue= | pages= 16096 | pmid=28102226 | doi=10.1038/nrdp.2016.96 | pmc=5336551 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28102226 }} </ref> | ||
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* | * Chromosomal instability | ||
* Sporadic mutations | |||
* Infections | |||
| | | | ||
* Elevated absolute lymphocyte count | * Elevated absolute lymphocyte count (in all stages) | ||
* Anemia (Rai stage III) | * Presence of >5000 clonal B cells per microliter in peripheral blood | ||
* Anemia (in Rai stage III) | |||
* Thrombocytopenia (in Rai stage IV) | |||
| | | | ||
* [[Lymph node enlargement]] | * [[Lymph node enlargement]] in Rai stage I | ||
* [[Splenomegaly]] in Rai stage II | * [[Splenomegaly]] in Rai stage II | ||
* [[Hepatomegaly]] in Rai stage II | * [[Hepatomegaly]] in Rai stage II | ||
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* [[Bleeding]] | * [[Bleeding]] | ||
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* | * Fludarabine | ||
* Cyclophosphamide | |||
* Rituximab | |||
* Obinutuzumab | |||
* Ofatumumab | |||
* Ibrutinib | * Ibrutinib | ||
* Venetoclax | * Venetoclax | ||
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* | * Associated with [[autoimmune hemolytic anemia]], which occurs in 10-25% of patients with CLL | ||
* Treatment with corticosteroids or anti-leukemic therapy will correct the | * Associated with [[immune thrombocytopenia purpura]] | ||
* Associated with [[pure red cell aplasia]] | |||
* Treatment with corticosteroids or anti-leukemic therapy will correct the autoimmune complications of CLL | |||
|} | |} | ||
Revision as of 05:52, 6 May 2018
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Acute promyelocytic leukemia Microchapters |
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Differentiating Acute promyelocytic leukemia from other Diseases |
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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 |
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| Acute promyelocytic leukemia |
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| Acute myeloid leukemia |
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| Acute lymphoblastic leukemia |
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| Chronic myeloid leukemia |
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| Chronic lymphocytic leukemia[1] |
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References
- ↑ Kipps TJ, Stevenson FK, Wu CJ, Croce CM, Packham G, Wierda WG; et al. (2017). "Chronic lymphocytic leukaemia". Nat Rev Dis Primers. 3: 16096. doi:10.1038/nrdp.2016.96. PMC 5336551. PMID 28102226.