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Blood, 15 January 2008, Vol. 111, No. 2, pp. 474.
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INSIDE BLOOD
Comment on Ruggeri et al, page 666
Steel to heal? MPD surgical conundrums
Ruben A. Mesa
MAYO CLINIC
In this issue of Blood, Ruggeri and colleagues highlight the high risk of vascular events in patients with essential thrombocythemia and polycythemia vera undergoing operative procedures even with current "optimal" surgical prophylaxis.
Surgical interventions in the BCR-ABL–negative chronic myeloproliferative disorders (MPDs) of essential thrombocythemia (ET) and polycythemia vera (PV) are inherently challenging based on the intrinsic risk of both disorders for thrombotic and/or hemorrhagic events. Baseline risks for arterial and/or venous thrombotic events have classically been associated with 2 main features: increasing age in MPD patients (> 60 years of age) and prior vascular events, with potential contributions from cardiovascular risk factors and extreme thrombocytosis (> 1000-1500 x 109/L).1 Newly identified vascular risk factors, leukocytosis2 and high JAK2V617F allele burden,3 also appear to have predictive value. Current short-term management strategies for PV and ET patients have been directed at (1) control of erythrocytosis, (2) near universal antiplatelet therapy, and (3) the addition of myelosuppressive therapy to normalize thrombocytosis in intermediate and high-risk patients. Optimal perioperative management of MPD patients has largely been based on clinical experience and anecdotal evidence, with published reports of the high risk of vascular complications (24%) in patients undergoing therapeutic splenectomy4 urging caution when operating on this group.
Ruggeri and colleagues have assembled a retrospective analysis of 311 operative interventions in 255 MPD patients, with a risk of vascular events in 16.8% of cases, despite perioperative heparin (54.3%), antiplatelet therapy (15.4%), and/or cytoreduction (74%). These sobering results were found despite the fact that the vast majority of these surgical interventions were elective (91.9%) and conducted when a maximal amount of surgical prophylaxis was employed. There are limits in the interpretation of this data: given the multicenter, retrospective nature of this report, the preoperative prophylaxis employed was heterogeneous, making it difficult to ascertain which aspects of prophylaxis (heparin, antiplatelet therapy, cytoreduction, or a combination thereof) were most effective. The complexity of predicting which patient will have an event was further corroborated by the lack of an observed correlation between known risk factors (such as age, white cell or platelet count, hematocrit, type of MPD, sex, or prior vascular event) and developing a thrombosis. These results highlight our incomplete understanding about the origin of vascular events in MPD patients, weaknesses in the ability of our current management strategies to identify patients at risk, and the incomplete ability of currently available agents for MPDs to prevent vascular complications.
Management of MPD patients undergoing elective or emergent surgery is challenging, and the data from Ruggeri and colleagues suggest that despite optimal efforts, there will be a greater risk of vascular events. Defining the optimal perioperative prophylaxis (antiplatelet therapy, perioperative heparin, cytoreduction to a normal platelet count, and/or control of erythrocytosis) will require prospective comparison with defined regimens. In addition, the development of more efficacious targeted therapy for MPDs (ie, JAK2 inhibitors5) may have a greater impact on preventing vascular events than do current modalities.
Footnotes
Conflict-of-interest disclosure: The author declares no competing financial interests. 
REFERENCES
- Finazzi G and Barbui T. Risk-adapted therapy in essential thrombocythemia and polycythemia vera. Blood Rev 2005; 19:243–252.[CrossRef][Medline]
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- Landolfi R, Di Gennaro L, Barbui T, et al. Leukocytosis as a major thrombotic risk factor in patients with polycythemia vera. Blood 2007; 109:2446–2452.[Abstract/Free Full Text]
- Vannucchi AM, Antonioli E, Guglielmelli P, et al. Clinical profile of homozygous JAK2 617V>F mutation in patients with polycythemia vera or essential thrombocythemia. Blood 2007; 110:840–846.[Abstract/Free Full Text]
- Mesa RA, Nagorney DS, Schwager S, Allred J, Tefferi A. Palliative goals, patient selection, and perioperative platelet management: outcomes and lessons from 3 decades of splenectomy for myelofibrosis with myeloid metaplasia at the Mayo Clinic. Cancer 2006; 107:361–370.[Medline]
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- Pardanani A, Hood J, Lasho T, et al. TG101209, a small molecule JAK2-selective kinase inhibitor potently inhibits myeloproliferative disorder-associated JAK2V617F and MPLW515L/K mutations. Leukemia 2007; 21:1658–1668.[CrossRef][Medline]
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Related Article in Blood Online:
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Postsurgery outcomes in patients with polycythemia vera and essential thrombocythemia: a retrospective survey
- Marco Ruggeri, Francesco Rodeghiero, Alberto Tosetto, Giancarlo Castaman, Francesca Scognamiglio, Guido Finazzi, Federica Delaini, Caterina Micò, Alessandro M. Vannucchi, Elisabetta Antonioli, Valerio De Stefano, Tommaso Za, Luigi Gugliotta, Alessia Tieghi, Maria Gabriella Mazzucconi, Cristina Santoro, and Tiziano Barbui, for the Gruppo Italiano Malattie Ematologiche dell'Adulto (GIMEMA) Chronic Myeloproliferative Diseases Working Party
Blood 2008 111: 666-671.
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