The bleeding time in women

Berge, Lillian Nordbø; Lyngmo, V.; Svensson, B.; Nordøy, Arne

doi:10.3109/00016349309021128

Cited by 10 publications

(2 citation statements)

References 32 publications

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“…12 Bleeding times, measured by template methods, is unchanged during normal pregnancy. 13,14 PLATELET FUNCTION The number of platelets is comparable to that in nonpregnant individuals. [15][16][17][18][19] The volume of platelets is reportedly unchanged during normal pregnancy.…”

Section: Global Testsmentioning

confidence: 99%

Hemostasis during Normal Pregnancy and Puerperium

Hellgren¹

2003

Semin Thromb Hemost

409

285

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During normal pregnancy the hemostatic balance changes in the direction of hypercoagulability, thus decreasing bleeding complications in connection with delivery. The most important initial factor for acute hemostasis at delivery is, however, uterine muscle contractions, which interrupt blood flow. Global tests such as Sonoclot signature, the Thromboelastogram, and a new method analyzing overall plasma hemostasis, all show changes representative of hypercoagulability during pregnancy. Increased endogenous thrombin generation, acquired activated protein C resistance, slightly decreased activated partial thromboplastin time (aPTT) and increased prothrombin complex level (PT) measured as international normalized ratio (INR) of less than 0.9 have been reported as well. In normal pregnancy, the platelet count is within normal range except during the third trimester when benign gestational thrombocytopenia, 80 to 150 x 10 9/L, can be observed. Platelet turnover is usually normal. Activation of platelets and release of beta-thromboglobulin and platelet factor 4 are reported. The bleeding time is unchanged during normal pregnancy. Most blood coagulation factors and fibrinogen increase during pregnancy. Factor (F) XI is the only blood coagulation factor that decreases. Blood coagulation inhibitors are mainly unchanged but the level of free protein S decreases markedly and the level of tissue factor pathway inhibitor increases. Thrombomodulin levels increase during pregnancy. Fibrinolytic capacity is diminished during pregnancy, mainly because of markedly increased levels of plasminogen activator inhibitor-1 (PAI-1) from endothelial cells and plasminogen activator inhibitor-2 (PAI-2) from the placenta. Thrombin-activated fibrinolysis inhibitor is reported to be unaffected. The total hemostatic balance has been studied by analyses of prothrombin fragment 1+2, thrombin-antithrombin complex, fibrinopeptide A, soluble fibrin, D-dimer, and plasmin-antiplasmin complex. There is activation of blood coagulation and a simultaneous increase in fibrinolysis without signs of organ dysfunction during normal pregnancy. These changes increase as pregnancy progresses. During delivery, there is consumption of platelets and blood coagulation factors, including fibrinogen. Fibrinolysis improves and increases fast following childbirth and expulsion of the placenta, resulting in increased D-dimer levels. These changes are self-limiting at normal delivery. The hemostatic changes, noted during pregnancy, normalize after delivery within 4 to 6 weeks. Platelet count and free protein S, however, can be abnormal longer. Hemostasis should not be tested earlier than 3 months following delivery and after terminating lactation to rule out influences of pregnancy. PAI-1 and PAI-2 levels decrease fast postpartum, but PAI 2 has been detected up to 8 weeks postpartum. alpha 2 -antiplasmin, urokinase, and kallikrein inhibitor levels have been reported to be increased 6 weeks postpartum.

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Section: Global Testsmentioning

confidence: 99%

Hemostasis during Normal Pregnancy and Puerperium

Hellgren¹

2003

Semin Thromb Hemost

409

285

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“…9 In the original study 50 women in late pregnancy were also included for comparison with premenopausal women aged younger than 40 years (n=55), and postmenopausal women were compared with premenopausal women aged older than 40 years (n=58); the age limits were arbitrarily chosen to reduce the age differences between the groups compared. In the present study all premenopausal women (n=113) were included to achieve a larger sample.…”

Section: Methodsmentioning

confidence: 99%

Serum ferritin, sex hormones, and cardiovascular risk factors in healthy women.

Berge

Bønaa

Nordøy

1994

Arterioscler Thromb

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The protective effect of endogenous sex hormones is commonly believed to explain the gender gap in the risk of coronary heart disease and the diminished protection in women when menopause occurs. Recent reports indicate that iron overload, due to cessation of menstrual bleeding, may be an important factor. We therefore investigated iron stores by serum ferritin measurements in healthy premenopausal (n=113) and postmenopausal (n=46) women. Ferritin levels were higher in postmenopausal than in premenopausal women, both in blood donors (43.4 versus 23.1 /xg/L, f<.001) and in nondonors (71.7 versus 32.8 fig/L, P<.001). Serum ferritin was positively correlated with age (r=.36, P<.001). After age adjustment, serum ferritin was positively correlated with hemoglobin, hematocrit, serum total cholesterol, and C oronary heart disease (CHD) is an uncommon disease in premenopausal women. 1 Most often, this has been attributed to the endogenous sex hormones, although the effects of age and menopause are difficult to separate.The benefits of estrogens have hitherto been related to the effects on serum lipids, as postmenopausal women experience elevation of serum low-density lipoprotein (LDL) cholesterol and trigh/ceride concentrations, 2 factors associated with an increased risk of CHD. 3It has been speculated that factors other than serum lipids are influenced by the menopause. Data from the Framingham Study suggested that removal of the uterus was as important as oophorectomy or a natural menopause in regard to the risk of CHD. 4 This led Sullivan 5 to propose regular menstrual blood loss as the protective factor and related the postmenopausal risk of CHD to an accumulating iron overload, reflected in raised levels of the iron storage protein, ferritin. The mechanisms, he suggested, might involve oxidant activity of iron-dependent enzymes. 6 Recently, Lauffer 7 reported a positive correlation between CHD mortality and the amount of iron in the liver. Similarly, Salonen et al 8 found an increased risk of myocardial infarction in men with elevated serum ferritin, and the association was even stronger in subjects with high serum LDL cholesterol levels.The aim of the present study was to investigate the cross-sectional relation between serum ferritin, sex hor- low-density lipoprotein (LDL) cholesterol. Total cholesterol was correlated with age (r=.66, / > <.001), as were LDL cholesterol (r=.6O, P<.01) and high-density lipoprotein cholesterol (r=.32, P<.01). Neither ferritin nor serum lipids were directly associated with female sex hormone levels. The mutual relation between ferritin, hemoglobin, and hematocrit probably only indicates their usefulness as measures of body iron. The parallel rise in serum ferritin, total cholesterol, and LDL cholesterol might contribute to the increased risk of coronary heart disease among postmenopausal women. {Arteriosder Thromb. 1994;14:857-861.) Key Words• women cholesterol ferritin menopause mones, and cardiovascular risk factors in healthy women. MethodsThe present investigation was p...

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Hemostatic factors and ischemic heart disease risk among postmenopausal women

Meilahn

1995

J Thromb Thrombol

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The following is a review of (largely) epidemiologic evidence on whether changes in plasma hemostatic concentrations occur with menopause and with postmenopausal hormone therapy which may have an impact on risk of ischemic heart disease. To date, only plasma fibrinogen has been positively associated with long-term risk of disease among women; however, data are sparse. Taken together, the evidence supports an impact of endogenous sex hormone levels on thrombotic potential and points to a modest increase in a number of plasma hemostatic factor levels at menopause. Results of studies of estrogen therapy are somewhat conflicting. Observational findings suggest that, except for possibly the Factor VII level, estrogen therapy may prevent the menopause-related rise in plasma hemostatic factors. In contrast, controlled experiments have found increased markers of thrombin generation with use of common formulations of estrogen therapy. The hemostatic effects found with oral preparations do not appear to occur with transdermal forms of estrogen although data are limited. Overall, the evidence shows menopause to have an impact on plasma levels of hemostatic factors which appears to be modified by use of oral estrogen. Whether these alterations in plasma levels have an impact on risk of ischemic heart disease among postmenopausal women remains to be demonstrated.

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The bleeding time in women

Cited by 10 publications

References 32 publications

Hemostasis during Normal Pregnancy and Puerperium

Hemostasis during Normal Pregnancy and Puerperium

Serum ferritin, sex hormones, and cardiovascular risk factors in healthy women.

Hemostatic factors and ischemic heart disease risk among postmenopausal women

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