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• W2053449311 abstract "Preanalytical conditions, be they due to the individual's physiologic state or to exogenous factors, can affect coagulation factors, in either a transient or a persistent manner, and need to be considered in laboratory testing. These conditions include physical and mental stress, diurnal variation, hormone levels and posture at the time of blood drawing. While testing of these factors has not been exhaustive and some results are conflicting, guidelines for testing conditions can be given. Preanalytical conditions, be they due to the individual's physiologic state or to exogenous factors, can affect coagulation factors, in either a transient or a persistent manner, and need to be considered in laboratory testing. These conditions include physical and mental stress, diurnal variation, hormone levels and posture at the time of blood drawing. While testing of these factors has not been exhaustive and some results are conflicting, guidelines for testing conditions can be given. Exercise alters measures of coagulation and fibrinolysis to a variable extent depending on the intensity of the exercise. The effect depends in part on the age and physical condition of the subject [1Van den Burg P.J.H. Hospers J.E.H. Van Vliet M. Mosterd W.L. Bouma B.N. Huisveld IA. Changes in haemostatic factors and activation products after exercise in healthy subjects with different ages.Thromb Haemost. 1995; 74: 1457-64Crossref PubMed Scopus (68) Google Scholar, 2DeSouza C.A. Jones P.P. Seals DR. Physical activity status and adverse age‐related differences in coagulation and fibrinolytic factors in women.Arterioscler Thromb Vasc Biol. 1998; 18: 362-8Crossref PubMed Google Scholar]. Platelet aggregation in response to adenosine diphosphate and epinephrine is enhanced during, and within 1 h after, moderate exercise. Plasma levels of serotonin and β‐thromboglobulin are increased after moderate exercise, suggesting platelet activation [3Naesh O. Hindberg I. Trap‐Jensen J. Lund JO. Post‐exercise platelet activation‐aggregation and release in relation to dynamic exercise.Clin Physiol. 1990; 10: 221-30Crossref PubMed Google Scholar]. Concentrations of factor (F) VIII, von Willebrand factor antigen (VWF:Ag) and VWF ristocetin cofactor activity (VWF:RCo) are increased up to 2.5‐fold, starting within 2–10 min and lasting for longer than 10 h after finishing exercise, with greater effects with more intense exercise [1Van den Burg P.J.H. Hospers J.E.H. Van Vliet M. Mosterd W.L. Bouma B.N. Huisveld IA. Changes in haemostatic factors and activation products after exercise in healthy subjects with different ages.Thromb Haemost. 1995; 74: 1457-64Crossref PubMed Scopus (68) Google Scholar, 4Andrew M. Carter C. O'Brodovich H. Heigenhauser G. Increases in factor VIII complex and fibrinolytic activity are dependent on exercise intensity.J Appl Physiol. 1986; 60: 1917-22Crossref PubMed Scopus (71) Google Scholar]. No changes were observed in concentrations of FXII, FV, FVII, FII or fibrinogen after corrections for hemoconcentration [4Andrew M. Carter C. O'Brodovich H. Heigenhauser G. Increases in factor VIII complex and fibrinolytic activity are dependent on exercise intensity.J Appl Physiol. 1986; 60: 1917-22Crossref PubMed Scopus (71) Google Scholar]. Activation of coagulation is reflected by an increase in markers such as thrombin–antithrombin complexes (TAT), prothrombin fragment 1 + 2 (F1 + 2) and fibrinopeptide A (FPA). Increased thrombin generation starts within 30 min of moderate exercise. However, these increases do not exceed reference intervals even during intense exercise [1Van den Burg P.J.H. Hospers J.E.H. Van Vliet M. Mosterd W.L. Bouma B.N. Huisveld IA. Changes in haemostatic factors and activation products after exercise in healthy subjects with different ages.Thromb Haemost. 1995; 74: 1457-64Crossref PubMed Scopus (68) Google Scholar, 5Weiss C. Seitel G. Bärtsch P. Coagulation and fibrinolysis after moderate and very heavy exercise in healthy male subjects.Med Sci Sports Exerc. 1998; 30: 246-51Crossref PubMed Scopus (92) Google Scholar]. An increase in global fibrinolysis is observed during exercise and immediately afterwards but soon returns to normal [4Andrew M. Carter C. O'Brodovich H. Heigenhauser G. Increases in factor VIII complex and fibrinolytic activity are dependent on exercise intensity.J Appl Physiol. 1986; 60: 1917-22Crossref PubMed Scopus (71) Google Scholar, 6Rosing D.R. Brakman P. Redwood D.R. Goldstein R.E. Beiser G.D. Astrup T. Epstein SE. Blood fibrinolytic activity in man. Diurnal variation and the response to varying intensities of exercise.Circ Res. 1970; 27: 171-84Crossref PubMed Scopus (192) Google Scholar]. An increase in tissue plasminogen activator (t‐PA) occurs early and disappears within 2 h, while plasmin‐α2‐antiplasmin complexes (PAP) are formed within 30 min and last for more than 2 h. Concentrations of D‐dimer rise quickly and the increase persists for more than 1 h [1Van den Burg P.J.H. Hospers J.E.H. Van Vliet M. Mosterd W.L. Bouma B.N. Huisveld IA. Changes in haemostatic factors and activation products after exercise in healthy subjects with different ages.Thromb Haemost. 1995; 74: 1457-64Crossref PubMed Scopus (68) Google Scholar, 5Weiss C. Seitel G. Bärtsch P. Coagulation and fibrinolysis after moderate and very heavy exercise in healthy male subjects.Med Sci Sports Exerc. 1998; 30: 246-51Crossref PubMed Scopus (92) Google Scholar]. Mental stress can affect coagulation, although studies have found conflicting results. With acute mental stress, FVIII, VWF:Ag and VWF:RCo, fibrinogen, and t‐PA increase [7Brozovic M. Physiological mechanisms in coagulation and fibrinolysis.Br Med Bull. 1977; 33: 231-8Crossref PubMed Google Scholar, 8Jern C. Eriksson E. Tengborn L. Risberg B. Wadenvik H. Jern S. Changes of plasma coagulation and fibrinolysis in response to mental stress.Thromb Haemost. 1989; 62: 767-71Crossref PubMed Scopus (195) Google Scholar, 9Jern C. Manhem K. Eriksson E. Tengborn L. Risberg B. Jern S. Hemostatic responses to mental stress during the menstrual cycle.Thromb Haemost. 1991; 66: 614-8Crossref PubMed Scopus (44) Google Scholar]. Changes in menstruating women were greatest in the luteal phase [9Jern C. Manhem K. Eriksson E. Tengborn L. Risberg B. Jern S. Hemostatic responses to mental stress during the menstrual cycle.Thromb Haemost. 1991; 66: 614-8Crossref PubMed Scopus (44) Google Scholar]. FVII was found to increase in men, but not in women [8Jern C. Eriksson E. Tengborn L. Risberg B. Wadenvik H. Jern S. Changes of plasma coagulation and fibrinolysis in response to mental stress.Thromb Haemost. 1989; 62: 767-71Crossref PubMed Scopus (195) Google Scholar]. Another study found a decrease in VWF and fibrinogen, but this may have been due to a change in plasma volume [10Snieder H. Huizink A.C. Boomsma D.Y. Van Doornen LJP. Influence of mental stress on fibrinogen, von Willebrand factor and tissue‐type plasminogen activator antigen.Fibrinolysis. 1996; 10: 137-9Crossref Scopus (4) Google Scholar]. Prolonged mental stress (continuously for 77 h) led to decreases in FV, FVIII and FIX. Only FIX had recovered 5 days after the end of the stress. No increase was observed in fibrinolysis [11Palmblad J. Blombäck M. Egberg N. Fröberg J. Karlsson C.G. Levi L. Experimentally induced stress in man: effects on blood coagulation and fibrinolysis.J Psychosom Res. 1977; 21: 87-92Crossref PubMed Google Scholar]. Concentrations of most hemostatic proteins change to effect an overall prothrombotic state during pregnancy [12Bremme K. Östlund E. Almqvist I. Heinonen K. Blombäck M. Enhanced thrombin generation and fibrinolytic activity in normal pregnancy and the puerperium.Obstet. Gynecol. 1992; 80: 132-7PubMed Google Scholar], presumably to protect women from bleeding at parturition. Modest increases are found for FVII and FX. Fibrinogen and FVIII increase approximately 2‐fold, and VWF 3‐fold, and remain elevated for some period post partum; limited data suggest individual variability in the length of time before the levels return to baseline. The free protein S level decreases by about 30% and may remain decreased for at least up to 2 months post partum [13Kjellberg U. Andersson N.E. Rosen S. Tengborn L. Hellgren M. APC resistance and other haemostatic variables during pregnancy and puerperium.Thromb Haemost. 1999; 81: 527-31Crossref PubMed Scopus (146) Google Scholar, 14Bremme KA. Haemostatic changes in pregnancy.Best Pract Res Clin Haematol. 2003; 16: 153-68Crossref PubMed Scopus (344) Google Scholar, 15Clark P. Brennand J. Conkie J.A. McCall F. Greer I.A. Walker ID. Activated protein C sensitivity, protein C, protein S and coagulation in normal pregnancy.Thromb Haemost. 1998; 79: 1166-70Crossref PubMed Google Scholar]. Protein C remains within the reference normal limits [12Bremme K. Östlund E. Almqvist I. Heinonen K. Blombäck M. Enhanced thrombin generation and fibrinolytic activity in normal pregnancy and the puerperium.Obstet. Gynecol. 1992; 80: 132-7PubMed Google Scholar, 13Kjellberg U. Andersson N.E. Rosen S. Tengborn L. Hellgren M. APC resistance and other haemostatic variables during pregnancy and puerperium.Thromb Haemost. 1999; 81: 527-31Crossref PubMed Scopus (146) Google Scholar]. Classic and modified (using FV‐deficient plasma) activated protein C (APC) ratios decrease; the most pronounced changes are found with the classic method [13Kjellberg U. Andersson N.E. Rosen S. Tengborn L. Hellgren M. APC resistance and other haemostatic variables during pregnancy and puerperium.Thromb Haemost. 1999; 81: 527-31Crossref PubMed Scopus (146) Google Scholar, 15Clark P. Brennand J. Conkie J.A. McCall F. Greer I.A. Walker ID. Activated protein C sensitivity, protein C, protein S and coagulation in normal pregnancy.Thromb Haemost. 1998; 79: 1166-70Crossref PubMed Google Scholar]. The increased coagulation is reflected by increased F1+2, TAT and soluble fibrin [12Bremme K. Östlund E. Almqvist I. Heinonen K. Blombäck M. Enhanced thrombin generation and fibrinolytic activity in normal pregnancy and the puerperium.Obstet. Gynecol. 1992; 80: 132-7PubMed Google Scholar, 13Kjellberg U. Andersson N.E. Rosen S. Tengborn L. Hellgren M. APC resistance and other haemostatic variables during pregnancy and puerperium.Thromb Haemost. 1999; 81: 527-31Crossref PubMed Scopus (146) Google Scholar]. With regard to the fibrinolytic system, both plasminogen activator inhibitor‐1 (PAI‐1) and the placenta‐produced PAI‐2, as well as D‐dimer increase [12Bremme K. Östlund E. Almqvist I. Heinonen K. Blombäck M. Enhanced thrombin generation and fibrinolytic activity in normal pregnancy and the puerperium.Obstet. Gynecol. 1992; 80: 132-7PubMed Google Scholar, 13Kjellberg U. Andersson N.E. Rosen S. Tengborn L. Hellgren M. APC resistance and other haemostatic variables during pregnancy and puerperium.Thromb Haemost. 1999; 81: 527-31Crossref PubMed Scopus (146) Google Scholar]. The need to consider the phase of the menstrual cycle depends upon what is being investigated. Estradiol concentrations are lowest on cycle days (cd) 1–3 and highest on cd 13–15, followed by a decrease. Progesterone concentrations are lowest on cd 1–8 and highest on cd 21–25. Most hemostatic variables, such as FII, FX, FVII, antithrombin, APC resistance, F1+2, plasminogen, α2‐antiplasmin, PAP, and D‐dimer, show small or negligible changes with the menstrual cycle [16Blombäck M. Eneroth P. Landgren B.M. Lagerström M. Anderson O. On the intraindividual and gender variability of haemostatic components.Thromb Haemost. 1992; 67: 70-5Crossref PubMed Scopus (0) Google Scholar, 17Siegbahn A. Odlind V. Hedner U. Venge P. Coagulation and fibrinolysis during the menstrual cycle.Ups J Med Sci. 1989; 94: 137-52Crossref PubMed Google Scholar, 18Wramsby M.L. Bokarewa M.I. Blombäck M. Bremme AK. Response to activated protein C during normal menstrual cycle and ovarian stimulation.Hum Reprod. 2000; 15: 795-7Crossref PubMed Google Scholar]. Fibrinogen concentrations are lowest during menstruation and highest during the luteal phase. The concentrations of FVII and FVIIa increase up to cd 14, while protein S decreases between cd 1 and 14 [19Carr Jr, M.E. Steingold K.A. Zekert SL. Protein S during the normal menstrual cycle and during estrogen therapy for premature ovarian failure.Am J Med Sci. 1993; 306: 212-7Crossref PubMed Google Scholar, 20Kapiotis S. Jilma B. Pernerstorfer T. Stohlawetz P. Eichler H.G. Speiser W. Plasma levels of activated factor VII decrease during the menstrual cycle.Thromb Haemost. 1998; 80: 588-91PubMed Google Scholar]. The bleeding time is longest during menstruation in most reports [21Jacobs H.G. Selle G. The question of bleeding tendency after dental surgery during menstruation.Dtsch Zahnarztl Z. 1974; 29: 1074-7PubMed Google Scholar]. A number of reports on changes in FVIII, VWF:Ag and VWF:RCo [16Blombäck M. Eneroth P. Landgren B.M. Lagerström M. Anderson O. On the intraindividual and gender variability of haemostatic components.Thromb Haemost. 1992; 67: 70-5Crossref PubMed Scopus (0) Google Scholar, 22Kadir RA, Economides DL, Sabin CA, Owens D, Lee CA. Variations in coagulation factors in women: effects of age, ethnicity, menstrual cycle and combined oral contraceptive. 1999; 82: 1456–61.Google Scholar, 23Miller C.H. Dilley A.B. Drews C. Richardson L. Evatt B. Changes in von Willebrand factor and factor VIII levels during the menstrual cycle.Thromb Haemost. 2002; 87: 1082-3Crossref PubMed Scopus (58) Google Scholar, 24Feuring M. Christ M. Roell A. Schueller P. Losel R. Dempfle C.E. Schultz A. Wehling M. Alterations in platelet function during the ovarian cycle.Blood Coagul Fibrinolysis. 2002; 13: 443-7Crossref PubMed Scopus (41) Google Scholar] suggest that the concentrations are highest during the luteal phase and lowest during the follicular phase, while one study found no change [25Onundarson P.T. Gudmundsdottir B.R. Amfinnsdottir A.V. Kjeld M. Olafsson O. Von Willebrand factor does not vary during the menstrual cycle.Thromb Haemost. 2001; 85: 183-4Crossref PubMed Scopus (0) Google Scholar]. However, preanalytical conditions and cycle days for sampling differed between these studies. VWF levels appear to be lowest on cd 1–4 [23Miller C.H. Dilley A.B. Drews C. Richardson L. Evatt B. Changes in von Willebrand factor and factor VIII levels during the menstrual cycle.Thromb Haemost. 2002; 87: 1082-3Crossref PubMed Scopus (58) Google Scholar]. In terms of hormonal therapy, influences on coagulation depend in particular on estrogen content [26Lindberg U.B. Crona N. Stigendal L. Teger‐Nilsson A.C. Silfverstolpe G. A comparison between effects of estradiol valerate and low dose ethinyl estradiol on haemostasis parameters.Thromb Haemost. 1989; 61: 65-9Crossref PubMed Scopus (83) Google Scholar]. The influence of progestins alone is not well‐known. The degree of classic APC resistance and other hemostatic changes induced by combined hormonal contraceptives is modified by the progestin, with levonorgestrel being the most effective in countering the estrogen effect [27Kemmeren J.M. Algra A. Meijers J.C. Bouma B.N. Grobbee DE. Effects of second and third generation oral contraceptives and their respective progestagens on the coagulation system in the absence or presence of the factor V Leiden mutation.Thromb Haemost. 2002; 87: 199-205Crossref PubMed Scopus (54) Google Scholar]. Currently prescribed hormonal contraceptives dampen the cyclic variation of VWF and fibrinogen seen in women not on hormonal contraceptives [22Kadir RA, Economides DL, Sabin CA, Owens D, Lee CA. Variations in coagulation factors in women: effects of age, ethnicity, menstrual cycle and combined oral contraceptive. 1999; 82: 1456–61.Google Scholar]. Regarding combined contraceptives, no data support differences in hemostasis by the mode of administration, be it oral, transdermal or the vaginal ring, although there may be variable absorption of hormones with a transdermal preparation. Baseline epidemiological studies in healthy women undergoing menopause have demonstrated increased levels of several coagulation factors, including FVIII and fibrinogen. These changes are due to both estrogen status and aging [28Meade T.W. Haines A.P. Imeson J.D. Stirling Y. Thompson SG. Menopausal status and haemostatic variables.Lancet. 1983; 1: 22-24Abstract PubMed Scopus (0) Google Scholar]. Several studies have shown that initiation of estrogen therapy activates the coagulation system in healthy postmenopausal women, with increases in F1+2, FPA, decreased APC resistance (classic method) and decreased free protein S noted [29Caine Y.G. Bauer K.A. Barzegar S. Ten Cate H. Sacks F.M. Walsh B.W. Schift I. Rosenberg R.D. Coagulation activation following estrogen administration to postmenopausal women.Thromb Haemost. 1992; 68: 392-5Crossref PubMed Scopus (220) Google Scholar, 30Luyer M.D. Khosla S. Owen W.G. Miller VM. Prospective randomized study of effects of unopposed estrogen replacement therapy on markers of coagulation and inflammation in postmenopausal women.J Clin Endocrinol Metab. 2001; 86: 3629-34Crossref PubMed Scopus (70) Google Scholar, 31Scarabin P.Y. Alhenc‐Gelas M. Plu‐Bureau G. Taisne P. Agher R. Aiach M. Effects of oral and transdermal estrogen/progesterone regimens on blood coagulation and fibrinolysis in postmenopausal women. A randomized controlled trial.Arterioscler Thromb Vasc Biol. 1997; 17: 3071-8Crossref PubMed Google Scholar, 32Oger E. Alhenc‐Gelas M. Lacut K. Blouch M.T. Roudaut N. Coller M. Abgrall J.F. Aiach M. Scarabin P.Y. Mottier D. SARAH InvestigatorsDifferential effects of oral and transdermal estrogen/progesterone regimens on sensitivity to activated protein C among postmenopausal women: a randomized trial.Arterioscler Thromb Vasc Biol. 2003; 23: 1671-6Crossref PubMed Scopus (160) Google Scholar]. The effect of transdermal HRT on coagulation is significantly less than that seen with oral preparations [31Scarabin P.Y. Alhenc‐Gelas M. Plu‐Bureau G. Taisne P. Agher R. Aiach M. Effects of oral and transdermal estrogen/progesterone regimens on blood coagulation and fibrinolysis in postmenopausal women. A randomized controlled trial.Arterioscler Thromb Vasc Biol. 1997; 17: 3071-8Crossref PubMed Google Scholar, 32Oger E. Alhenc‐Gelas M. Lacut K. Blouch M.T. Roudaut N. Coller M. Abgrall J.F. Aiach M. Scarabin P.Y. Mottier D. SARAH InvestigatorsDifferential effects of oral and transdermal estrogen/progesterone regimens on sensitivity to activated protein C among postmenopausal women: a randomized trial.Arterioscler Thromb Vasc Biol. 2003; 23: 1671-6Crossref PubMed Scopus (160) Google Scholar]. Platelet aggregation is most pronounced and beta‐thromboglobin concentrations are highest in the morning [33Dalby M.C. Davidson S.J. Burman J.F. Davies SW. Diurnal variation in platelet aggregation with PFA‐100 platelet function analyser.Platelets. 2000; 11: 320-4Crossref PubMed Google Scholar, 34Haus E. Cusulos M. Sackett‐Lundeen L. Swoyer J. Circadian variations in blood coagulation parameters, alpha‐antitrypsin antigen and platelet aggregation and retention in clinically healthy subjects.Chronobiol Int. 1990; 7: 203-16Crossref PubMed Google Scholar, 35Kapiotis S. Jilma B. Quehenberger P. Ruzicka K. Handler S. Speiser W. Morning hypercoagulability and hypofibrinolysis. Diurnal variations in circulating activated factor VII, prothrombin fragment F1+2, and plasmin‐plasmin inhibitor complex.Circulation. 1997; 96: 19-21Crossref PubMed Google Scholar, 36Undar L. Ertugrul C. Altunbas H. Akca S. Circadian variations in natural coagulation inhibitors protein C, protein S and antithrombin in healthy men: a possible association with interleukin‐6.Thromb Haemost. 1999; 81: 571-5Crossref PubMed Google Scholar]. FV activity, VWF:Ag and FVII antigen are unchanged, while FVIII activity, FVIIa and F1+2 are highest in the morning, as are protein C and S concentrations. Antithrombin is either unchanged or peaks in the afternoon [34Haus E. Cusulos M. Sackett‐Lundeen L. Swoyer J. Circadian variations in blood coagulation parameters, alpha‐antitrypsin antigen and platelet aggregation and retention in clinically healthy subjects.Chronobiol Int. 1990; 7: 203-16Crossref PubMed Google Scholar, 35Kapiotis S. Jilma B. Quehenberger P. Ruzicka K. Handler S. Speiser W. Morning hypercoagulability and hypofibrinolysis. Diurnal variations in circulating activated factor VII, prothrombin fragment F1+2, and plasmin‐plasmin inhibitor complex.Circulation. 1997; 96: 19-21Crossref PubMed Google Scholar, 36Undar L. Ertugrul C. Altunbas H. Akca S. Circadian variations in natural coagulation inhibitors protein C, protein S and antithrombin in healthy men: a possible association with interleukin‐6.Thromb Haemost. 1999; 81: 571-5Crossref PubMed Google Scholar]. Global fibrinolysis is lowest [6Rosing D.R. Brakman P. Redwood D.R. Goldstein R.E. Beiser G.D. Astrup T. Epstein SE. Blood fibrinolytic activity in man. Diurnal variation and the response to varying intensities of exercise.Circ Res. 1970; 27: 171-84Crossref PubMed Scopus (192) Google Scholar, 37Fearnly G. Balmforth G. Fearnley E. Evidence of a diurnal fibrinolytic rhythm; with a simple method of measuring natural fibrinolysis.Clin Sci. 1957; 16: 645-50PubMed Google Scholar, 38Andreotti F. Kluft C. Circadian variation of fibrinolytic activity in blood.Chronobiol Int. 1991; 8: 336-51Crossref PubMed Google Scholar] in the early morning, as is t‐PA activity, while PAI‐1 activity and antigen are highest at that time. PAP is low in the morning and plasminogen is unchanged [35Kapiotis S. Jilma B. Quehenberger P. Ruzicka K. Handler S. Speiser W. Morning hypercoagulability and hypofibrinolysis. Diurnal variations in circulating activated factor VII, prothrombin fragment F1+2, and plasmin‐plasmin inhibitor complex.Circulation. 1997; 96: 19-21Crossref PubMed Google Scholar, 38Andreotti F. Kluft C. Circadian variation of fibrinolytic activity in blood.Chronobiol Int. 1991; 8: 336-51Crossref PubMed Google Scholar]. Circadian variations in fibrinolytic components are not affected by lifestyle, dietary habits or ethnic differences. Posture during blood drawing is of importance, as the hematocrit increases by up to 15% between lying down and assuming a sitting position [39Guder W.G. Narayanan S. Wisser H. Zawta B. Samples: From the patient to the laboratory. GIT Verlag GMBH, 2001: 18Google Scholar]. The influences of fasting (totally overnight or only fat‐fasting in the morning), caffeine‐containing beverages and smoking have not been sufficiently investigated. However, lipemic plasma interferes with many assays. Abstaining from smoking for 2 h prior to the venipuncture is recommended, because of a potential effect on platelet aggregation. For venipuncture for coagulation studies, the patient should: 1Abstain from intense physical exercise for at least 24 h and from physical activity (rushing) just prior to venipuncture.2Be provided with an environment where physical stress and mental stress are lessened.3Abstain from fatty foods and smoking on the morning of the venipuncture; the patient should be fasting for PAI‐1 and global fibrinolysis assays.4Have samples obtained early in the morning (7.00–9.00 am) after sitting in a relaxed position for 20–30 min. Specifically for women: 1For the diagnosis of von Willebrand disease (VWD) in fertile women, blood samples should be obtained on cd 1–4. This may aid in the diagnosis in women with borderline values obtained at other times.2Combined oral contraceptives and HRT should be withdrawn for at least 2 months before testing. This is especially true for testing of free protein S, protein S activity and APC resistance (classic method).3For the diagnosis of inherited disorders of hemostasis (particularly VWD, FVIII deficiency, and protein S deficiency) samples should be obtained when normal menstrual cycles have returned or at least 2 months post partum. All abnormal values obtained in connection with pregnancy, including testing for phospholipid antibodies, should be verified with repeat blood sampling. Standardized international studies of potential influences on coagulation, especially hormonal influences, should be performed using newer global hemostatic assays. Because of the significance of VWD and disorders of platelet function resulting in bleeding symptoms in women, improved understanding of hormonal effects on these factors, and improved laboratory testing for such, is needed. The authors state that they have no conflict of interest." @default.
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• W2053449311 cites W138463622 @default.
• W2053449311 cites W139639132 @default.
• W2053449311 cites W142384375 @default.
• W2053449311 cites W1833068323 @default.
• W2053449311 cites W1840835766 @default.
• W2053449311 cites W1848074731 @default.
• W2053449311 cites W1909490248 @default.
• W2053449311 cites W1972472202 @default.
• W2053449311 cites W1979650632 @default.
• W2053449311 cites W1983634929 @default.
• W2053449311 cites W1985280544 @default.
• W2053449311 cites W2011013456 @default.
• W2053449311 cites W2011784685 @default.
• W2053449311 cites W2052760576 @default.
• W2053449311 cites W2069072110 @default.
• W2053449311 cites W2070146050 @default.
• W2053449311 cites W2072157130 @default.
• W2053449311 cites W2073720156 @default.
• W2053449311 cites W2085177307 @default.
• W2053449311 cites W2090870013 @default.
• W2053449311 cites W2121971394 @default.
• W2053449311 cites W2126249243 @default.
• W2053449311 cites W2127025895 @default.
• W2053449311 cites W2128203581 @default.
• W2053449311 cites W2131703274 @default.
• W2053449311 cites W2158754705 @default.
• W2053449311 cites W2164267996 @default.
• W2053449311 cites W2394785257 @default.
• W2053449311 cites W2396772007 @default.
• W2053449311 cites W2407219552 @default.
• W2053449311 cites W2413770017 @default.
• W2053449311 cites W2415466662 @default.
• W2053449311 cites W2415726463 @default.
• W2053449311 cites W2417791203 @default.
• W2053449311 cites W2418757070 @default.
• W2053449311 cites W2462546431 @default.
• W2053449311 cites W91310628 @default.
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