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Inherited Thrombophilic Disorders

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Inherited Thrombophilic Disorders 9 Inherited thrombophilic disorders Dorit Blickstein INTRODUCTION In contrast to the simple, reliable and inex- pensive laboratory tests used to investigate Inherited thrombophilia is thought to increase bleeding disorders such as prothrombin time the risk of pregnancy related venous thrombo- (PT) and partial thromboplastin time (PTT), embolism (VTE), including deep vein throm- no such diagnostic means exist for testing/ bosis (DVT) and pulmonary embolism (PE). screening of hypercoagulable states. Moreover, Pregnancy is a hypercoagulable state due the literature holds that thrombophilia testing/ to the increased concentration of coagulation screening is expensive. For example, Wu and factors, decreased natural anticoagulants and colleagues2 calculated the incremental cost- fibrinolytic activity1. The pregnant woman is effectiveness ratio (ICER; the lower the ICER therefore at increased risk for VTE and this the more cost-effective the strategy to avoid a predisposition is much accentuated in patients major adverse clinical outcome) for universal with thrombophilia. Thus it is important to screening prior to prescribing combined con- identify this group of patients before or early traception, for example, is as high as £202,402 in pregnancy in order to tailor appropriate pre- (UK), whereas for hormone replacement it is ventive means. far less (£6824) (UK). Stated another way, it is not cost-effective to perform routine thrombo- philia screening before prescribing hormonal THE APPROACH TO VENOUS therapy. Several authorities have maintained THROMBOEMBOLISM that screening the general population is not justified mainly because of the above men- The clinical approach to acute VTE is the tioned financial considerations3–5. Therefore, same in patients with or without inherited in order to avoid indiscriminate thrombophilia thrombophilia. However, most patients with screening and waste of health resources, one a confirmed episode of VTE will eventually must consider the indication, advantages and undergo thrombophilia screening if acquired pitfalls of such an investigation. Injudicious causes are excluded. Obviously, the clinical thrombophilia screening should therefore be utility of testing is the a priori assumption that discouraged. the test results are likely to improve health Every testing/screening should be based on outcome. In this context, one should remem- the prevalence of each inherited thrombophilic ber that screening is performed in the absence condition and the association of each with the of disease, whereas testing is performed in the risk of VTE. Several inherited thrombophilic presence of symptoms or signs. It follows that conditions predispose to venous thrombosis. in the case of thrombophilia the actual workup The most important are factor V Leiden muta- is for testing rather than for screening. tion, prothrombin gene mutation, protein C, 111 PRECONCEPTIONAL MEDICINE protein S and antithrombin deficiency, elevated purpura fulminans without sepsis. Because this factor VIIIc and hyperhomocysteinemia6. The circumstance is suspected to manifest a homo- frequency of the natural anticoagulant protein zygous state of protein C and S deficiencies, S, protein C and antithrombin deficiencies is first degree relatives should also be screened. low in the general population (<1% in total) Warfarin decreases the level of the natu- as well as in patients with VTE (5% in total), ral anticoagulant protein C and S, as well as but the frequency of gain of functional muta- vitamin K-dependent coagulation factors. In tions – factor V Leiden and prothrombin gene some patients receiving warfarin, the decrease mutation – is common in the general popula- in anticoagulants is faster than the decrease tion (3–7% and 3%, respectively) as well as in coagulation factors, and they develop skin in patients with VTE (25% and 10%, respec- necrosis. Accordingly, patients who sustained tively). The prevalence of factor V Leiden and warfarin skin necrosis are suspected to be het- prothrombin gene mutation is 10–15% in the erozygous for protein C and S deficiency and Caucasian population but increases to about should therefore be investigated. 50% in patients with recurrent thromboem- bolic phenomena. Because selection for thrombophilia test- Family history ing/screening is required, a rather long list of candidates has been created over the years. To Patients with first degree relatives who have simplify this list, these candidates have been had a VTE at a young age or as a pregnancy grouped under three subheadings7–21. complication are candidates for screening. Venous thromboembolism Previous adverse pregnancy outcomes Age is the single most important factor for The association of some adverse pregnancy VTE, and hence, young patients (defined as outcomes with inherited thrombophilia is con- <50 years) who experienced previous VTE troversial. Since placenta-mediated pregnancy after an event that is no longer present, such complications are thought to result from as minor surgery or bone fracture, should placental micro/macrothrombosis in blood undergo evaluation. However, even if there is vessels, one might assume that thrombo- no identifiable risk factor for VTE,patients with philia should increase thrombotic risk. How- unprovoked VTE at any age, should be screened ever, conflicting data exist for the link between for thrombophilia. Similarly, the association pregnancy complications and thrombophilic of VTE in the absence of any other risk factor risk factors. A recent meta-analysis of 25 except the use of exogenous estrogens (oral con- studies on 11,183 women found a significant traception and hormone replacement) or preg- association between pregnancy complications nancy, should lead to screening, as is the case and thrombophilia, especially for early and for patients with recurrent VTE at any age or early late recurrent pregnancy loss associated with age of onset. In addition to the common sites of antiphospholipid antibodies (APLA), factor V DVT, it has been suggested that patients with Leiden and the prothrombin gene mutation13. superficial thrombophlebitis without malignancy Data evaluation demonstrated a strong asso- and those with DVT at unusual sites (cerebral, ciation between factor V Leiden and recurrent mesenteric, portal or hepatic) under the age pregnancy loss, as well as severity of preg- of 50 years also should be evaluated. This cat- nancy complications in the second and third egory includes the rare event of a neonate with trimesters compared to first trimester. The 112 Inherited thrombophilic disorders evaluation, however, indicates that the rela- Clot based assays like protein S and factor tionship between thrombophilia and pregnan- VIII should not be performed during the acute cy complications is confounded by ethnicity, phase of VTE, during pregnancy, or during oral severity of illness and method of testing14. contraception and warfarin treatment. Tests In contrast, other recent studies failed to should be performed at least 2–3 months after demonstrate an association between throm- pregnancy and withdrawal of oral contracep- bophilia and adverse pregnancy outcome15–25. tion, and 1 month after warfarin treatment is While thrombophilias are associated with completed. placental-mediated pregnancy complications, Antithrombin levels may be determined their causal contribution is weak. The associa- during acute VTE before unfractionated hep- tion makes biological sense (consistent with arin (UFH) or low molecular weight heparin the pathophysiological theory of the devel- (LMWH) treatments are initiated, as both opment of pregnancy complications) but the interact with antithrombin. This is because association is inconsistent, non-specific, with- antithrombin concentrate replacement may be out biological gradient and with no convincing necessary for acute VTE, together with hepa- evidence from clinical studies for causal asso- rin or LMWH treatment for severe antithrom- bin deficiency. ciation18,21. Publication bias also plays a role Screening seems to be unnecessary in in the interpretation of findings in relevant patients on prolonged anticoagulant treatment studies. (malignancy or recurrent VTE) because the It is therefore not surprising that the lat- decision for treatment has already been made. est American College of Chest Physicians Likewise, in patients with a personal or famil- (ACCP) guidelines on VTE, thrombophilia ial VTE history, there is no need for routine and antithrombotic therapy recommend that preoperative screening, as the results will not only women who have had recurrent early loss change the recommended thromboprophylax- (three or more miscarriages), unexplained late is policy in most of them7. pregnancy loss, and severe or recurrent pre- eclampsia or intrauterine growth restriction 26 (IUGR) be screened for APLA . WHY PERFORM THROMBOPHILIC TESTS? WHEN TO TEST FOR The rationale to perform thrombophilia test- THROMBOPHILIA? ing is mainly to establish the genetic basis of the VTE5,29. Once known, the etiologic factor Coagulation factors and natural anticoagula- or presence of combined defects may be com- tion levels change during acute VTE, under municated to the patients and may influence 7,27,28 specific medication and during pregnancy . the duration of treatment and establish the Biochemical evaluation can be postponed until potential risk for recurrence. This knowledge the treatment duration (3–6 months) for an also may help in providing thromboprophylax- acute VTE is over, whereas polymerase chain is
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