Pediatric Clinics of North America - CIPERJ

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VENOUS THROMBOEMBOLISM IN CHILDREN 311 Table 2 Thrombophilic conditions and markers tested during comprehensive diagnostic laboratory evaluation of acute venous thromboembolism in children Condition/marker Testing methods Genetic Factor V Leiden polymorphism PCR Prothrombin G20210A polymorphism PCR Elevated plasma lipoprotein(a) ELISA concentration a Acquired or genetic Antithrombin deficiency Chromogenic (functional) assay Protein C deficiency Chromogenic (functional) assay Protein S deficiency ELISA for free (ie, functionally active) protein S antigen Elevated plasma factor VIII activity b One-stage clotting assay (aPTT-based) Hyperhomocysteinemia Mass spectroscopy APAs ELISA for anticardiolipin and anti-b2-glycoprotein I IgG and IgM; clotting assay (dilute Russell viper venom time or aPTT-based phospholipid neutralization method) for LA DIC Includes platelet count, fibrinogen by clotting method (Clauss), and D-dimer by semiquantitative or quantitative immunoassay (eg, latex agglutination) Activated protein C resistance Clotting assay (aPTT based) a Although desginated here as genetic, lipoprotein(a) also may be elevated as part of the acute phase response. b Noted as worthy of consideration in original International Society on Thrombosis and Haemostasis recommendations [13]; this since has been shown a prognostic marker in pediatric thrombosis [6]. Additional testing involving the fibrinolytic system and systemic inflammatory response also is noted as worthy of consideration. [14], is provided in Table 3 for initial (ie, acute phase) and extended (ie, subacute phase) treatment. Conventional anticoagulants attenuate hypercoagulability, decreasing the risk for thrombus progression and embolism, and rely on intrinsic fibrinolytic mechanisms to dissolve the thrombus over time. The conventional anticoagulants used most commonly in children include heparins and warfarin. Heparins, including unfractionated heparin (UFH) and low molecular weight heparin (LMWH), enhance the activity of antithrombin, an intrinsic anticoagulant protein that serves as a key inhibitor of thrombin. Warfarin acts through antagonism of vitamin K, thereby interfering with g-carboxylation of the vitamin K–dependent procoagulant factors II, VII, IX, and X and intrinsic anticoagulant proteins C and S. Initial anticoagulant therapy (ie, acute phase) for VTE in children uses UFH or LMWH. LMWH increasingly is used as a first-line agent for initial anticoagulant therapy in children given the relative ease of subcutaneous over intravenous administration, the decreased need for blood monitoring
312 GOLDENBERG & BERNARD Table 3 Recommended intensities and durations of conventional antithrombotic therapies in children, by etiology and treatment agent Agents and target anticoagulant activities Duration of therapy, by Episode Initial treatment Extended treatment etiology First UFH 0.3–0.7 anti-Xa U/mL Warfarin INR 2.0–3.0 Resolved risk factor: 3–6 months LMWH 0.5–1.0 anti-Xa U/mL LMWH 0.5–1.0 anti-Xa U/mL No known clinical risk factor: 6–12 months Chronic clinical risk factor: 12 months Potent congenital thrombophilia: indefinite Recurrent UFH 0.3–0.7 anti-Xa U/mL Warfarin INR 2.0–3.0 Resolved risk factor: 6–12 months LMWH 0.5–1.0 anti-Xa U/mL LMWH 0.5–1.0 anti-Xa U/mL No known clinical risk factor: 12 months Chronic clinical risk factor: indefinite Potent congenital thrombophilia: indefinite of anticoagulant efficacy, and a decreased risk for the development of heparin-induced thrombocytopenia (HIT). UFH (which has a shorter half-life than LMWH) typically is preferred in circumstances of heightened bleeding risk or labile acute clinical status, given the rapid extinction of anticoagulant effect after cessation of the drug. In addition, UFH often is used for acute VTE therapy in the setting of significant impairment or lability in renal function because of the relatively greater renal elimination of LMWH. Common initial maintenance dosing for UFH in non-neonatal children begins with an intravenous loading dose (50 to 75 U/kg) followed by a continuous intravenous infusion (15 to 25 U/kg per hour). In full-term neonates, a maintenance dose (up to 50 U/kg per hour) may be required, especially if the clinical condition is complicated by antithrombin consumption. The starting dose for the LMWH enoxaparin in non-neonatal children commonly ranges between 1.0 and 1.25 mg/kg subcutaneously on an every-12-hour schedule; no bolus dose is given. In full-term neonates, a higher dose of enoxaparin (1.5 mg/kg) typically is necessary [15]. Some recent research has investigated whether once-daily enoxaparin dosing may be suitable for acute VTE therapy in children. For the LMWH dalteparin, initial maintenance dosing of 100–150 antifactor Xa (anti-Xa) U/kg seems appropriate based on available pediatric data [16]; however, further studies are warranted (with more robust representation of all age groups within the pediatric age range) to determine the optimal intensity and frequency of dosing of dalteparin. Heparin therapy, UFH or LMWH, is monitored most accurately by anti- Xa activity. Anti-Xa level is obtained 6 to 8 hours after initiation of UFH
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Table 1 (continued ) Factor VIII (o
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366 RODRIGUEZ & HOOTS Antifibrinoly
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368 RODRIGUEZ & HOOTS infections an
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370 RODRIGUEZ & HOOTS Fig. 3. Schem
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372 RODRIGUEZ & HOOTS protein is no
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374 RODRIGUEZ & HOOTS [2] Berntorp
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376 RODRIGUEZ & HOOTS [42] Carcao M
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378 ROBERTSON et al von Willebrand
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380 ROBERTSON et al Fig. 2. A propo
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382 ROBERTSON et al a heterogenous
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384 ROBERTSON et al of considering
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386 ROBERTSON et al Type 2M Type 2M
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388 ROBERTSON et al Desmopressin is
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390 ROBERTSON et al References [1]
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392 ROBERTSON et al [46] Nesbitt IM
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394 BLANCHETTE & BOLTON-MAGGS A key
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396 BLANCHETTE & BOLTON-MAGGS recep
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398 BLANCHETTE & BOLTON-MAGGS and p
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400 BLANCHETTE & BOLTON-MAGGS Fig.
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404 BLANCHETTE & BOLTON-MAGGS the s
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406 BLANCHETTE & BOLTON-MAGGS findi
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408 BLANCHETTE & BOLTON-MAGGS as a
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410 BLANCHETTE & BOLTON-MAGGS splen
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412 BLANCHETTE & BOLTON-MAGGS with
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414 BLANCHETTE & BOLTON-MAGGS react
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416 BLANCHETTE & BOLTON-MAGGS [16]
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422 FASANO & LUBAN of storage and t
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424 FASANO & LUBAN Leukocyte reduct
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426 FASANO & LUBAN RBCs is decrease
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Table 1 Blood component characteris
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430 FASANO & LUBAN Alloimmunization
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432 FASANO & LUBAN of individual un
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434 FASANO & LUBAN patients have an
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436 FASANO & LUBAN adults; therefor
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438 FASANO & LUBAN [21]. Meta-analy
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440 FASANO & LUBAN Pretransfusion m
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442 FASANO & LUBAN [55,56]. This is
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444 FASANO & LUBAN [20] Roseff SD,
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Pediatr Clin N Am 55 (2008) 447-460
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THALASSEMIA UPDATE 449 hypochromia
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THALASSEMIA UPDATE 451 Fig. 1. Chan
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THALASSEMIA UPDATE 453 delivery of
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THALASSEMIA UPDATE 455 thromboses i
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THALASSEMIA UPDATE 457 On the basis
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THALASSEMIA UPDATE 459 [31] Kan YW,
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ORAL IRON CHELATORS 463 large iron-
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ORAL IRON CHELATORS 465 of 50 child
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ORAL IRON CHELATORS 467 Table 2 Com
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ORAL IRON CHELATORS 469 use in Nort
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ORAL IRON CHELATORS 471 needed to d
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ORAL IRON CHELATORS 473 in liver fi
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ORAL IRON CHELATORS 475 in the lowe
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ORAL IRON CHELATORS 477 Other oral
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ORAL IRON CHELATORS 479 [12] Borgna
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ORAL IRON CHELATORS 481 [55] Wonke
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HYDROXYUREA FOR CHILDREN WITH SICKL
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Fig. 1. Guideline for initiating, m
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504 TRACY & RICE congenital spheroc
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506 TRACY & RICE and antibodies aga
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508 TRACY & RICE limited splenic vo
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512 TRACY & RICE German experience
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514 TRACY & RICE Table 1 Effect of
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516 TRACY & RICE decreased bilirubi
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518 TRACY & RICE [13] Bader-Meunier
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