Polycythemia vera classification: Difference between revisions

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Polycythemia vera is a subtype of [[myeloproliferative neoplasm]]. [[Myeloproliferative neoplasm]] may be classified according to the World Health Organization into eight subtypes:<ref name="pmid19357394">{{cite journal| author=Vardiman JW, Thiele J, Arber DA, Brunning RD, Borowitz MJ, Porwit A et al.| title=The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes. | journal=Blood | year= 2009 | volume= 114 | issue= 5 | pages= 937-51 | pmid=19357394 | doi=10.1182/blood-2009-03-209262 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19357394  }} </ref><ref name="pmid11377686">{{cite journal| author=Valent P, Horny HP, Escribano L, Longley BJ, Li CY, Schwartz LB et al.| title=Diagnostic criteria and classification of mastocytosis: a consensus proposal. | journal=Leuk Res | year= 2001 | volume= 25 | issue= 7 | pages= 603-25 | pmid=11377686 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11377686  }} </ref><ref name="pmid26137205">{{cite journal| author=Birgegård G| title=Advances and challenges in the management of essential thrombocythemia. | journal=Ther Adv Hematol | year= 2015 | volume= 6 | issue= 3 | pages= 142-56 | pmid=26137205 | doi=10.1177/2040620715580068 | pmc=4480522 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26137205  }} </ref><ref name="pmid24106449">{{cite journal |vauthors=Beatrice JM, Garanito MP |title=Essential thrombocythemia: a rare disease in childhood |journal=Rev Bras Hematol Hemoter |volume=35 |issue=4 |pages=287–9 |date=2013 |pmid=24106449 |pmc=3789436 |doi=10.5581/1516-8484.20130059 |url=}}</ref><ref name="pmid22948537">{{cite journal| author=Hayashi Y, Hirai H, Kamio N, Yao H, Yoshioka S, Miura Y et al.| title=C/EBPβ promotes BCR-ABL-mediated myeloid expansion and leukemic stem cell exhaustion. | journal=Leukemia | year= 2013 | volume= 27 | issue= 3 | pages= 619-28 | pmid=22948537 | doi=10.1038/leu.2012.258 | pmc=4506742 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22948537  }} </ref><ref name="pmid27899359">{{cite journal| author=Gotlib J| title=How I treat atypical chronic myeloid leukemia. | journal=Blood | year= 2017 | volume= 129 | issue= 7 | pages= 838-845 | pmid=27899359 | doi=10.1182/blood-2016-08-693630 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27899359  }} </ref><ref name="pmid28028025">{{cite journal |vauthors=Maxson JE, Tyner JW |title=Genomics of chronic neutrophilic leukemia |journal=Blood |volume=129 |issue=6 |pages=715–722 |date=February 2017 |pmid=28028025 |pmc=5301820 |doi=10.1182/blood-2016-10-695981 |url=}}</ref><ref name="pmid26640324">{{cite journal| author=Desterke C, Martinaud C, Ruzehaji N, Le Bousse-Kerdilès MC| title=Inflammation as a Keystone of Bone Marrow Stroma Alterations in Primary Myelofibrosis. | journal=Mediators Inflamm | year= 2015 | volume= 2015 | issue=  | pages= 415024 | pmid=26640324 | doi=10.1155/2015/415024 | pmc=4660030 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26640324  }} </ref><ref name="pmid27512192">{{cite journal |vauthors=Vidyadharan S, Joseph B, Nair SP |title=Chronic Eosinophilic Leukemia Presenting Predominantly with Cutaneous Manifestations |journal=Indian J Dermatol |volume=61 |issue=4 |pages=437–9 |date=2016 |pmid=27512192 |pmc=4966405 |doi=10.4103/0019-5154.185716 |url=}}</ref><ref name="pmid28254862">{{cite journal| author=Valent P, Akin C, Hartmann K, Nilsson G, Reiter A, Hermine O et al.| title=Advances in the Classification and Treatment of Mastocytosis: Current Status and Outlook toward the Future. | journal=Cancer Res | year= 2017 | volume= 77 | issue= 6 | pages= 1261-1270 | pmid=28254862 | doi=10.1158/0008-5472.CAN-16-2234 | pmc=5354959 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28254862  }} </ref>
Polycythemia vera is a subtype of [[myeloproliferative neoplasm]]. [[Myeloproliferative neoplasm]] may be classified according to the World Health Organization into eight subtypes:<ref name="pmid19357394">{{cite journal| author=Vardiman JW, Thiele J, Arber DA, Brunning RD, Borowitz MJ, Porwit A et al.| title=The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes. | journal=Blood | year= 2009 | volume= 114 | issue= 5 | pages= 937-51 | pmid=19357394 | doi=10.1182/blood-2009-03-209262 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19357394  }} </ref><ref name="pmid11377686">{{cite journal| author=Valent P, Horny HP, Escribano L, Longley BJ, Li CY, Schwartz LB et al.| title=Diagnostic criteria and classification of mastocytosis: a consensus proposal. | journal=Leuk Res | year= 2001 | volume= 25 | issue= 7 | pages= 603-25 | pmid=11377686 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11377686  }} </ref><ref name="pmid26137205">{{cite journal| author=Birgegård G| title=Advances and challenges in the management of essential thrombocythemia. | journal=Ther Adv Hematol | year= 2015 | volume= 6 | issue= 3 | pages= 142-56 | pmid=26137205 | doi=10.1177/2040620715580068 | pmc=4480522 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26137205  }} </ref><ref name="pmid24106449">{{cite journal |vauthors=Beatrice JM, Garanito MP |title=Essential thrombocythemia: a rare disease in childhood |journal=Rev Bras Hematol Hemoter |volume=35 |issue=4 |pages=287–9 |date=2013 |pmid=24106449 |pmc=3789436 |doi=10.5581/1516-8484.20130059 |url=}}</ref><ref name="pmid22948537">{{cite journal| author=Hayashi Y, Hirai H, Kamio N, Yao H, Yoshioka S, Miura Y et al.| title=C/EBPβ promotes BCR-ABL-mediated myeloid expansion and leukemic stem cell exhaustion. | journal=Leukemia | year= 2013 | volume= 27 | issue= 3 | pages= 619-28 | pmid=22948537 | doi=10.1038/leu.2012.258 | pmc=4506742 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22948537  }} </ref><ref name="pmid27899359">{{cite journal| author=Gotlib J| title=How I treat atypical chronic myeloid leukemia. | journal=Blood | year= 2017 | volume= 129 | issue= 7 | pages= 838-845 | pmid=27899359 | doi=10.1182/blood-2016-08-693630 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27899359  }} </ref><ref name="pmid28028025">{{cite journal |vauthors=Maxson JE, Tyner JW |title=Genomics of chronic neutrophilic leukemia |journal=Blood |volume=129 |issue=6 |pages=715–722 |date=February 2017 |pmid=28028025 |pmc=5301820 |doi=10.1182/blood-2016-10-695981 |url=}}</ref><ref name="pmid26640324">{{cite journal| author=Desterke C, Martinaud C, Ruzehaji N, Le Bousse-Kerdilès MC| title=Inflammation as a Keystone of Bone Marrow Stroma Alterations in Primary Myelofibrosis. | journal=Mediators Inflamm | year= 2015 | volume= 2015 | issue=  | pages= 415024 | pmid=26640324 | doi=10.1155/2015/415024 | pmc=4660030 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26640324  }} </ref><ref name="pmid27512192">{{cite journal |vauthors=Vidyadharan S, Joseph B, Nair SP |title=Chronic Eosinophilic Leukemia Presenting Predominantly with Cutaneous Manifestations |journal=Indian J Dermatol |volume=61 |issue=4 |pages=437–9 |date=2016 |pmid=27512192 |pmc=4966405 |doi=10.4103/0019-5154.185716 |url=}}</ref><ref name="pmid28254862">{{cite journal| author=Valent P, Akin C, Hartmann K, Nilsson G, Reiter A, Hermine O et al.| title=Advances in the Classification and Treatment of Mastocytosis: Current Status and Outlook toward the Future. | journal=Cancer Res | year= 2017 | volume= 77 | issue= 6 | pages= 1261-1270 | pmid=28254862 | doi=10.1158/0008-5472.CAN-16-2234 | pmc=5354959 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28254862  }} </ref>
* '''[[Polycythemia vera]]''': This is a condition of elevated [[hemoglobin]] and [[red blood cell]] mass caused by the [[Janus kinase|JAK2]] mutation.
* '''[[Polycythemia vera]]''': This is a condition of elevated [[hemoglobin]] and [[red blood cell]] mass caused by the [[Janus kinase|JAK2]] mutation.
* '''[[Essential thrombocythemia]]''': This is a condition characterized by persistent elevation in [[Platelet|platelets]] which increases the risk for [[thrombosis]] and [[hemorrhage]]. It is associated with a variety of mutations, such as [[Janus kinase|JAK2]], CALR, or MPL. These mutations are mutually exclusive. This condition can progress to [[myelofibrosis]], which carries a poor prognosis.
* '''[[Essential thrombocythemia]]''': This is a condition characterized by persistent elevation in [[Platelet|platelets]] which increases the risk for [[thrombosis]] and [[hemorrhage]]. It is associated with a variety of mutations, such as [[Janus kinase|JAK2]], CALR, or MPL. These [[mutations]] are mutually exclusive. This condition can progress to [[myelofibrosis]], which carries a poor [[prognosis]].
* '''[[Chronic myelogenous leukemia]]''', ''[[BCR]]-[[ABL1]]''–positive: This condition is a common cause of chronic [[leukemia]]. The peripheral blood of patients with chronic [[Myeloid leukemia|myelogenous leukemia]] commonly shows elevation of [[white blood cell]] precursors at all stages of maturation, including [[Metamyelocyte|metamyelocytes]], and band cells. Treatment involves oral [[tyrosine kinase]] inhibitors such as [[imatinib]], [[dasatinib]], [[bosutinib]], [[nilotinib]], or [[ponatinib]].
* '''[[Chronic myelogenous leukemia]]''', ''[[BCR]]-[[ABL1]]''–positive: This condition is a common cause of chronic [[leukemia]]. The peripheral blood of patients with chronic [[Myeloid leukemia|myelogenous leukemia]] commonly shows elevation of [[white blood cell]] precursors at all stages of maturation, including [[Metamyelocyte|metamyelocytes]], and [[band cells]]. Treatment involves oral [[tyrosine kinase]] inhibitors such as [[imatinib]], [[dasatinib]], [[bosutinib]], [[nilotinib]], or [[ponatinib]].
* '''[[Chronic myelogenous leukemia]]''', ''[[BCR]]-[[ABL1]]''–negative (atypical [[CML]]): This a condition that carries a high risk for transformation into [[acute myeloid leukemia]]. It is frequently underdiagnosed since the BCR-Abl translocation is not found. Treatment considerations include [[allogeneic stem cell transplantation]].
* '''[[Chronic myelogenous leukemia]]''', ''[[BCR]]-[[ABL1]]''–negative (atypical [[CML]]): This a condition that carries a high risk for transformation into [[acute myeloid leukemia]]. It is frequently underdiagnosed since the BCR-Abl translocation is not found. Treatment considerations include [[allogeneic stem cell transplantation]].
* '''[[Chronic neutrophilic leukemia]]''': This is a condition characterized by elevation of [[neutrophil]] count and is commonly caused by a mutation in the colony-stimulating factor 3R (CSF3R) gene.
* '''[[Chronic neutrophilic leukemia]]''': This is a condition characterized by elevation of [[neutrophil]] count and is commonly caused by a mutation in the colony-stimulating factor 3R (CSF3R) gene.
* '''[[Primary myelofibrosis]]''': This is a highly lethal condition in which the bone marrow is replaced by reticulin [[fibrosis]], resulting in ineffective [[erythropoiesis]]. The etiology of this disease is abnormal [[Megakaryocytes|megakaryocyte]] proliferation and excess production of [[Transforming growth factor-β|transforming growth factor-beta (TGF-beta)]], which stimulates collagen deposition and fibrosis.
* '''[[Primary myelofibrosis]]''': This is a highly lethal condition in which the [[bone marrow]] is replaced by reticulin [[fibrosis]], resulting in ineffective [[erythropoiesis]]. The etiology of this disease is abnormal [[Megakaryocytes|megakaryocyte]] [[proliferation]] and excess production of [[Transforming growth factor-β|transforming growth factor-beta (TGF-beta)]], which stimulates collagen deposition and [[fibrosis]].
* '''[[Chronic eosinophilic leukemia]]''', not otherwise specified: This condition is of unknown etiology. There is clonal proliferation of erythropoetic precursors which results in elevated [[eosinophils]] in the blood, bone marrow or peripheral tissues.  
* '''[[Chronic eosinophilic leukemia]]''', not otherwise specified: This condition is of unknown etiology. There is clonal [[proliferation]] of erythropoetic precursors which results in elevated [[eosinophils]] in the blood, [[bone marrow]] or peripheral tissues.  
* '''[[Mastocytosis]]''': This condition is caused by mast cell proliferation and results in symptoms of coughing, wheezing, gastrointestinal upset, [[anaphylaxis]], and [[diarrhea]]. Patients typically have high levels of histamine (a peptide released by mast cells). Treatment usually involves [[imatinib]]. In 2016, it was discovered that the [[Protein kinase inhibitor|tyrosine kinase inhibitor]] [[midostaurin]] could effectively treat [[mastocytosis]], including patients who harbor the D816V mutation for which [[imatinib]] is ineffective.
* '''[[Mastocytosis]]''': This condition is caused by [[mast cell]] [[proliferation]] and results in symptoms of [[coughing]], [[wheezing]], gastrointestinal upset, [[anaphylaxis]], and [[diarrhea]]. Patients typically have high levels of [[histamine]] (a peptide released by mast cells). Treatment usually involves [[imatinib]]. In 2016, it was discovered that the [[Protein kinase inhibitor|tyrosine kinase inhibitor]] [[midostaurin]] could effectively treat [[mastocytosis]], including patients who harbor the D816V mutation for which [[imatinib]] is ineffective.
:* '''[[Cutaneous mastocytosis]]'''
:* '''[[Cutaneous mastocytosis]]'''
:* '''[[Systemic mastocytosis]]'''
:* '''[[Systemic mastocytosis]]'''
Line 26: Line 26:


===Classification of polycythemia===
===Classification of polycythemia===
Polycythemia vera is a subcategory of polycythemia in general. Classification of polycythemia in general includes primary polycythemia and secondary polycythemia. Secondary polycythemia is due to chronic [[hypoxia]] which results in compensatory increase in [[erythrocyte]] production. Secondary polycythemia is therefore characterized by a reactive increase in erythrocyte production, rather than clonal proliferation of erythrocytes.
Polycythemia vera is a subcategory of polycythemia in general. Classification of polycythemia in general includes primary polycythemia and secondary polycythemia. Secondary polycythemia is due to chronic [[hypoxia]] which results in compensatory increase in [[erythrocyte]] production. Secondary polycythemia is therefore characterized by a reactive increase in erythrocyte production, rather than clonal [[proliferation]] of erythrocytes.


* '''[[Primary polycythemia]]''' (polycythemia vera)
* '''[[Primary polycythemia]]''' (polycythemia vera)
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:* '''High altitude residence''': Elevated heights carry low oxygen content.
:* '''High altitude residence''': Elevated heights carry low oxygen content.
:* '''[[Erythropoietin]]-secreting tumors:'''
:* '''[[Erythropoietin]]-secreting tumors:'''
::* '''[[Renal cell carcinoma]]''': This is a [[malignancy]] of the kidney epithelial cells that sometimes produces the hormone [[erythropoietin]].
::* '''[[Renal cell carcinoma]]''': This is a [[malignancy]] of the kidney [[epithelial cells]] that sometimes produces the hormone [[erythropoietin]].
::* '''[[Hepatocellular carcinoma]]''': This is a [[malignancy]] of the liver epithelial cells that sometimes produces the hormone [[erythropoietin]].
::* '''[[Hepatocellular carcinoma]]''': This is a [[malignancy]] of the liver [[epithelial cells]] that sometimes produces the hormone [[erythropoietin]].


==References==
==References==

Revision as of 20:42, 21 January 2019

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohamad Alkateb, MBBCh [2]; Shyam Patel [3]

Overview

Polycythemia vera is a subtype of myeloproliferative neoplasm. Myeloproliferative neoplasm may be classified according to the World Health Organization into eight subtypes: chronic myelogenous leukemia, chronic neutrophilic leukemia, polycythemia vera, primary myelofibrosis, essential thrombocythemia, chronic eosinophilic leukemia, mastocytosis, and myeloproliferative neoplasms, unclassifiable. The classification of polycythemia is subdivided into primary polycythemia (which is a clonal process caused by the JAK2 mutation) and secondary polycythemia (which is a reactive process due to a state of chronic hypoxia). There are numerous causes of secondary polycythemia, and most of these causes are cardiopulmonary in origin.

Classification

Classification of myeloproliferative neoplasms

Polycythemia vera is a subtype of myeloproliferative neoplasm. Myeloproliferative neoplasm may be classified according to the World Health Organization into eight subtypes:[1][2][3][4][5][6][7][8][9][10]

There are no subcategories within polycythemia vera.

Classification of polycythemia

Polycythemia vera is a subcategory of polycythemia in general. Classification of polycythemia in general includes primary polycythemia and secondary polycythemia. Secondary polycythemia is due to chronic hypoxia which results in compensatory increase in erythrocyte production. Secondary polycythemia is therefore characterized by a reactive increase in erythrocyte production, rather than clonal proliferation of erythrocytes.

References

  1. ↑ Vardiman JW, Thiele J, Arber DA, Brunning RD, Borowitz MJ, Porwit A; et al. (2009). "The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes". Blood. 114 (5): 937–51. doi:10.1182/blood-2009-03-209262. PMID 19357394.
  2. ↑ Valent P, Horny HP, Escribano L, Longley BJ, Li CY, Schwartz LB; et al. (2001). "Diagnostic criteria and classification of mastocytosis: a consensus proposal". Leuk Res. 25 (7): 603–25. PMID 11377686.
  3. ↑ Birgegård G (2015). "Advances and challenges in the management of essential thrombocythemia". Ther Adv Hematol. 6 (3): 142–56. doi:10.1177/2040620715580068. PMC 4480522. PMID 26137205.
  4. ↑ Beatrice JM, Garanito MP (2013). "Essential thrombocythemia: a rare disease in childhood". Rev Bras Hematol Hemoter. 35 (4): 287–9. doi:10.5581/1516-8484.20130059. PMC 3789436. PMID 24106449.
  5. ↑ Hayashi Y, Hirai H, Kamio N, Yao H, Yoshioka S, Miura Y; et al. (2013). "C/EBPβ promotes BCR-ABL-mediated myeloid expansion and leukemic stem cell exhaustion". Leukemia. 27 (3): 619–28. doi:10.1038/leu.2012.258. PMC 4506742. PMID 22948537.
  6. ↑ Gotlib J (2017). "How I treat atypical chronic myeloid leukemia". Blood. 129 (7): 838–845. doi:10.1182/blood-2016-08-693630. PMID 27899359.
  7. ↑ Maxson JE, Tyner JW (February 2017). "Genomics of chronic neutrophilic leukemia". Blood. 129 (6): 715–722. doi:10.1182/blood-2016-10-695981. PMC 5301820. PMID 28028025.
  8. ↑ Desterke C, Martinaud C, Ruzehaji N, Le Bousse-Kerdilès MC (2015). "Inflammation as a Keystone of Bone Marrow Stroma Alterations in Primary Myelofibrosis". Mediators Inflamm. 2015: 415024. doi:10.1155/2015/415024. PMC 4660030. PMID 26640324.
  9. ↑ Vidyadharan S, Joseph B, Nair SP (2016). "Chronic Eosinophilic Leukemia Presenting Predominantly with Cutaneous Manifestations". Indian J Dermatol. 61 (4): 437–9. doi:10.4103/0019-5154.185716. PMC 4966405. PMID 27512192.
  10. ↑ Valent P, Akin C, Hartmann K, Nilsson G, Reiter A, Hermine O; et al. (2017). "Advances in the Classification and Treatment of Mastocytosis: Current Status and Outlook toward the Future". Cancer Res. 77 (6): 1261–1270. doi:10.1158/0008-5472.CAN-16-2234. PMC 5354959. PMID 28254862.


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