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Panminerva Medica 2002 June;44(2):107-13

language: English

Thrombosis: new culprits in an old disorder

Federman D. G., Moriarty J. P., Kravetz J. D., Kirsner R. S. *

From the VA Connecticut Health Care System West Haven, CT, USA and Department of Medicine Yale University School of Medicine, New Haven, CT, USA
*Department of Dermatology and Cutaneous Surgery Department of Epidemiology and Public Health University of Miami School of Medicine, Miami, FL, USA


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Venous throm­bo­sis is a ­cause of con­sid­er­able mor­bid­ity and mor­tal­ity. Over the ­past sev­er­al ­years, sev­er­al new caus­es of throm­bo­phil­ia ­have ­been iden­ti­fied and ­have dra­mat­i­cal­ly ­altered the ­approach to ­patients pre­sent­ing ­with throm­bo­sis. Newly ­described abnor­mal­ities asso­ciat­ed ­with throm­bo­phil­ia ­include the syn­drome of acti­vat­ed Protein C resis­tance (APCR), the pro­throm­bin 20210A muta­tion, hyper­hom­o­cys­tei­ne­mia, and ele­vat­ed lev­els of coag­u­la­tion fac­tors ­VIII and XI. Clinicians can now fre­quent­ly deter­mine caus­es of throm­bos­es ­that ­have pre­vi­ous­ly ­been ­deemed idiopath­ic. Though the ­risk fac­tors for VTE are becom­ing bet­ter ­defined, the ­cost-effec­tive ­approach to diag­no­sis and ther­a­peu­tic impli­ca­tions are not entire­ly ­clear at ­this ­point.

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