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Dabigatran for Heparin-Induced Thrombocytopenia
MAYO CLINIC PROCEEDINGS
with time-limited and time-unlimited certification, respectively, thought a grandfathered physician in a fictitious vignette should enroll in the MOC program.2 As Dr Hayes suggests, there are other ways in which the quality of our physician workforce might be measured. The National Practitioner Data Bank is not a sensitive or comprehensive measure of quality because it is based on a limited set of reportable adverse events, such as liability settlements and credentialing denials; there is little evidence that it has improved quality of care. A growing international body of research supports the use of multisource feedback for quality monitoring that incorporates both physician peer and patient feedback.8 However, physician organizations in the United States have been hesitant to incorporate such tools into qualityassurance mechanisms. Regardless, it is critical that we ensure that physicians provide high-quality care throughout their careers via a cost-effective process in which both physicians and patients place their trust and confidence. Gregory W. Ruhnke, MD, MS, MPH University of Chicago Chicago, IL
David J. Doukas, MD University of Louisville Louisville, KY 1. Levinson W, King TE Jr, Goldman L, Goroll AH, Kessler B. Clinical decisions: American Board of Internal Medicine maintenance of certification program. N Engl J Med. 2010;362(10):948-952. 2. Kritek PA, Drazen JM. Clinical decisions: American Board of Internal Medicine maintenance of certification programdpolling results [letter]. N Engl J Med. 2010;362(15):e54. 3. Iglehart JK, Baron RB. Maintenance of certification [letter]. N Engl J Med. 2012;368(13):1262-1263. 4. Ruhnke GW, Doukas DJ. Trust in residents and board examinations: when sharing crosses the boundary. Mayo Clin Proc. 2013;88(5):438-441. 5. Brennan TA, Horwitz RI, Duffy FD, Cassel CK, Goode LD, Lipner RS. The role of physician specialty board certification status in the quality movement. JAMA. 2004;292(9):1038-1043. 6. Sharp LK, Bashook PG, Lipsky MS, Horowitz SD, Miller SH. Specialty board certification and clinical outcomes: the missing link. Acad Med. 2002;77(6): 534-542.
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7. Lipner RS, Bylsma WH, Arnold GK, Fortna GS, Tooker J, Cassel CK. Who is maintaining certification in internal medicinedand why? a national survey 10 years after initial certification. Ann Intern Med. 2006;144(1):29-36. 8. Wright C, Richards SH, Hill JJ, et al. Multisource feedback in evaluating the performance of doctors: the example of the UK General Medical Council patient and colleague questionnaires. Acad Med. 2012; 87(12):1668-1678.
2. Anniccherico FJ, Alonso JL, Urbieta M, Pérez Ricarte S. Dabigatran as a therapeutic possibility in heparin-induced thrombocytopenia type II [in Spanish]. An Sist Sanit Navar. 2012;35(3):521-524. 3. Lo GK, Juhl D, Warkentin TE, Sigouin CS, Eichler P, Greinacher A. Evaluation of pretest clinical score (4 T’s) for the diagnosis of heparin-induced thrombocytopenia in two clinical settings. J Thromb Haemost. 2006;4(4):759-765. http://dx.doi.org/10.1016/j.mayocp.2013.06.013
http://dx.doi.org/10.1016/j.mayocp.2013.07.006
Dabigatran for Heparin-Induced Thrombocytopenia To the Editor: In the May 2013 issue of Mayo Clinic Proceedings, Gonsalves et al1 reviewed the new oral anticoagulants in clinical practice and were unable to identify case reports referencing the use of these agents in the treatment of heparin-induced thrombocytopenia (HIT). Recently, we reported the first case of HIT treated with dabigatran in a patient who had portal vein thrombosis secondary to essential thrombocythemia and who had previously received heparin.2 Seven days after the initiation of heparin, thrombocytopenia developed, with platelet counts decreasing from 1000 to 120 103/mL. The patient had a pulmonary embolism, a pretest clinical score (4 T’s test3) of 8 (maximum score, 8), and heparin/PF4 antibodies. Dabigatran treatment was started, and the platelet count doubled in 24 hours, with resolution of preexisting pulmonary emboli. We believe that dabigatran should be considered in the treatment of HIT because of its rapid onset of action, ease of use, and oral administration. However, this hypothesis will need to be confirmed by prospective studies. Francisco Javier Anniccherico, MD Jose Luis Alonso, PhD Hospital Complex of Pamplona Internal Medicine Navarra, Spain 1. Gonsalves WI, Pruthi RK, Patnaik MM. The new oral anticoagulants in clinical practice. Mayo Clin Proc. 2013;88(5):495-511.
In ReplydDabigatran for Heparin-Induced Thrombocytopenia We thank Drs Anniccherico and Alonso for bringing to our attention their recent experience with dabigatran for the treatment of portal vein thrombosis secondary to heparininduced thrombocytopenia (HIT) in a patient with essential thrombocythemia.1 Unfortunately, this case report was not included in our review of the literature2 because it was published in Spanish and we focused only on articles published in English. Nevertheless, we believe that their successful experience is noteworthy and warrants further discussion. We agree with their points that dabigatran has a rapid onset of action and that its oral route of administration makes it an attractive alternative to the currently approved, parenterally administered treatments for HIT such as argatroban, lepirudin (currently unavailable in the United States), and bivalirudin3 (approved by the US Food and Drug Administration only for patients with HIT undergoing percutaneous coronary intervention). However, until further data are available, we advise caution for the following reasons: (1) dabigatran is metabolized by the liver and excreted mainly by the kidneys and (2) most patients with HIT are diagnosed in the inpatient setting and may have coexisting renal or hepatic dysfunction, either of which can increase the systemic concentration of dabigatran to unsafe levels and thus increase the risk of bleeding. Given its Mayo Clin Proc.
n
September 2013;88(9):1035-1037 www.mayoclinicproceedings.org
with time-limited and time-unlimited certification, respectively, thought a grandfathered physician in a fictitious vignette should enroll in the MOC program.2 As Dr Hayes suggests, there are other ways in which the quality of our physician workforce might be measured. The National Practitioner Data Bank is not a sensitive or comprehensive measure of quality because it is based on a limited set of reportable adverse events, such as liability settlements and credentialing denials; there is little evidence that it has improved quality of care. A growing international body of research supports the use of multisource feedback for quality monitoring that incorporates both physician peer and patient feedback.8 However, physician organizations in the United States have been hesitant to incorporate such tools into qualityassurance mechanisms. Regardless, it is critical that we ensure that physicians provide high-quality care throughout their careers via a cost-effective process in which both physicians and patients place their trust and confidence. Gregory W. Ruhnke, MD, MS, MPH University of Chicago Chicago, IL
David J. Doukas, MD University of Louisville Louisville, KY 1. Levinson W, King TE Jr, Goldman L, Goroll AH, Kessler B. Clinical decisions: American Board of Internal Medicine maintenance of certification program. N Engl J Med. 2010;362(10):948-952. 2. Kritek PA, Drazen JM. Clinical decisions: American Board of Internal Medicine maintenance of certification programdpolling results [letter]. N Engl J Med. 2010;362(15):e54. 3. Iglehart JK, Baron RB. Maintenance of certification [letter]. N Engl J Med. 2012;368(13):1262-1263. 4. Ruhnke GW, Doukas DJ. Trust in residents and board examinations: when sharing crosses the boundary. Mayo Clin Proc. 2013;88(5):438-441. 5. Brennan TA, Horwitz RI, Duffy FD, Cassel CK, Goode LD, Lipner RS. The role of physician specialty board certification status in the quality movement. JAMA. 2004;292(9):1038-1043. 6. Sharp LK, Bashook PG, Lipsky MS, Horowitz SD, Miller SH. Specialty board certification and clinical outcomes: the missing link. Acad Med. 2002;77(6): 534-542.
1036
7. Lipner RS, Bylsma WH, Arnold GK, Fortna GS, Tooker J, Cassel CK. Who is maintaining certification in internal medicinedand why? a national survey 10 years after initial certification. Ann Intern Med. 2006;144(1):29-36. 8. Wright C, Richards SH, Hill JJ, et al. Multisource feedback in evaluating the performance of doctors: the example of the UK General Medical Council patient and colleague questionnaires. Acad Med. 2012; 87(12):1668-1678.
2. Anniccherico FJ, Alonso JL, Urbieta M, Pérez Ricarte S. Dabigatran as a therapeutic possibility in heparin-induced thrombocytopenia type II [in Spanish]. An Sist Sanit Navar. 2012;35(3):521-524. 3. Lo GK, Juhl D, Warkentin TE, Sigouin CS, Eichler P, Greinacher A. Evaluation of pretest clinical score (4 T’s) for the diagnosis of heparin-induced thrombocytopenia in two clinical settings. J Thromb Haemost. 2006;4(4):759-765. http://dx.doi.org/10.1016/j.mayocp.2013.06.013
http://dx.doi.org/10.1016/j.mayocp.2013.07.006
Dabigatran for Heparin-Induced Thrombocytopenia To the Editor: In the May 2013 issue of Mayo Clinic Proceedings, Gonsalves et al1 reviewed the new oral anticoagulants in clinical practice and were unable to identify case reports referencing the use of these agents in the treatment of heparin-induced thrombocytopenia (HIT). Recently, we reported the first case of HIT treated with dabigatran in a patient who had portal vein thrombosis secondary to essential thrombocythemia and who had previously received heparin.2 Seven days after the initiation of heparin, thrombocytopenia developed, with platelet counts decreasing from 1000 to 120 103/mL. The patient had a pulmonary embolism, a pretest clinical score (4 T’s test3) of 8 (maximum score, 8), and heparin/PF4 antibodies. Dabigatran treatment was started, and the platelet count doubled in 24 hours, with resolution of preexisting pulmonary emboli. We believe that dabigatran should be considered in the treatment of HIT because of its rapid onset of action, ease of use, and oral administration. However, this hypothesis will need to be confirmed by prospective studies. Francisco Javier Anniccherico, MD Jose Luis Alonso, PhD Hospital Complex of Pamplona Internal Medicine Navarra, Spain 1. Gonsalves WI, Pruthi RK, Patnaik MM. The new oral anticoagulants in clinical practice. Mayo Clin Proc. 2013;88(5):495-511.
In ReplydDabigatran for Heparin-Induced Thrombocytopenia We thank Drs Anniccherico and Alonso for bringing to our attention their recent experience with dabigatran for the treatment of portal vein thrombosis secondary to heparininduced thrombocytopenia (HIT) in a patient with essential thrombocythemia.1 Unfortunately, this case report was not included in our review of the literature2 because it was published in Spanish and we focused only on articles published in English. Nevertheless, we believe that their successful experience is noteworthy and warrants further discussion. We agree with their points that dabigatran has a rapid onset of action and that its oral route of administration makes it an attractive alternative to the currently approved, parenterally administered treatments for HIT such as argatroban, lepirudin (currently unavailable in the United States), and bivalirudin3 (approved by the US Food and Drug Administration only for patients with HIT undergoing percutaneous coronary intervention). However, until further data are available, we advise caution for the following reasons: (1) dabigatran is metabolized by the liver and excreted mainly by the kidneys and (2) most patients with HIT are diagnosed in the inpatient setting and may have coexisting renal or hepatic dysfunction, either of which can increase the systemic concentration of dabigatran to unsafe levels and thus increase the risk of bleeding. Given its Mayo Clin Proc.
n
September 2013;88(9):1035-1037 www.mayoclinicproceedings.org