Figure 6

Novel European Asiatic Clinical, Laboratory, Molecular and Pathobiological (2015-2020 CLMP) criteria for JAK2V617F trilinear polycythemia vera (PV), JAK2exon12 PV and JAK2V617F, CALR and MPL515 thrombocythemias: From Dameshek to Constantinescu-Vainchenker, Kralovics and Michiels

Jan Jacques Michiels*, King H Lam, Fibo Ten Kate, Dong-Wook Kim, Myungshin Kim, Vasily Shuvaev, Francisca Valster, Vincent Potters, Wilfried Schroyens, Mihaela Andreescu, Adrian Trifa, Achille Pich and Hendrik De Raeve

Published: 03 April, 2020 | Volume 3 - Issue 1 | Pages: 001-020


Figure 6:

State of the art treatment according to Dameshek [2,4] of a newly diagnosed PV patient (Ht 0.63, Hb 12.9 mmol/L, erythrocytes 7.1 x1012/L and MCV 89 fL) with repeated vene sections as confirmed by Pearson & Wetherley-Mein [48] and Messinazy, et al. [49] of the London PV Study Group [46,47]. Repeated venesections for more than 1 year (from August 2012 to September 2013) was needed to induce a complete hematological remission (CHR) reaching the desired plateau of Ht 0.45, Hb 9.0 mmol/L, and MCV of 66 fL. While on low dose aspirin neither microvascular nor major thrombosis did occur. Once the iron deficiency state is reached the erythrocytes remain microcytic and reach values of 7.0 to 7.2x1012/L without further need of phlebotomy due to the persistence of the iron deficienct state [2,30]. Correction of the Ht from 0.63 to below 0.45 is associated with reduction of major venous and arterial thrombotic events [8,9,48,51], but the microvascular thrombotic syndrome of associated thrombocythemia persisted. Low dose aspirin in ET in the Dutch Collaborative Low dose Aspirin in Thrombocythemia (Dutch CLAT) Van Genderen studies [89-91,99] and low dose aspirin on top of phlebotomy or hydroxurea in the European Collaborative Low dose Aspirin in PV (ECLAP, [50]) reduced the incidences of microvascular disturbances and major thrombosis from above 50% per 100 pt/yr to less than 3% per 100 pt/yr in both ET and PV [91,94], but does not prevent the progression of JAK2 mutated MPN disease in terms of JAK2 mutation load, MPN disease burden like progressive leukocythemia, thrombocythemia, splenomegaly and constitutional symptoms [6,7,34].

Read Full Article HTML DOI: 10.29328/journal.ijbmr.1001011 Cite this Article Read Full Article PDF

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