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Semin Thromb Hemost 2011; 37(1): 003-006
DOI: 10.1055/s-0030-1270064
PREFACE

© Thieme Medical Publishers

Hormones, Endocrine Disorders, and Hemostasis

Massimo Franchini1 , Pier Paolo Vescovi2 , Franco Manzato3 , Emmanuel J. Favaloro4
  • 1Servizio di Immuno-ematologia e Medicina Trasfusionale, Dipartimento di Patologia e Medicina di Laboratorio, Azienda Ospedaliero-Universitaria di Parma, Parma, Italy
  • 2Divisione di Medicina, Ospedale “Carlo Poma,” Mantova; Italy
  • 3Laboratorio di Analisi Chimico-Cliniche, Ospedale “Carlo Poma,” Mantova; Italy
  • 4Department of Haematology, Institute of Clinical Pathology and Medical Research (ICPMR), Westmead Hospital, Westmead, Australia
Further Information

Publication History

Publication Date:
19 January 2011 (online)

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Welcome to another issue of Seminars in Thrombosis and Hemostasis. This issue focuses on the influence of endocrine and metabolic disorders on coagulation and fibrinolysis. Indeed, because hemostatic balance is a complex system whereby a delicate equilibrium is regulated by several factors that include hormones, it is not surprising that abnormal coagulation test results are sometimes observed in patients with abnormal hormone levels. Moreover, many endocrine and metabolic disorders may accordingly alter the hemostatic equilibrium to predispose patients to either a thrombotic or bleeding tendency.[1] [2]

The first five articles of this issue are dedicated to hemostatic changes that occur in thyroid disorders. In the first one, Vescovi and colleagues[3] summarize the current knowledge regarding the main abnormalities of the coagulation and fibrinolytic systems associated with thyroid dysfunctions. Modifications may range from subclinical laboratory abnormalities to clinically relevant hemorrhagic or thrombotic events.[4] [5] [6] The authors conclude that the overall literature data, although mostly based on uncontrolled studies, suggest that patients with hyperthyroidism or subclinical hypothyroidism may have a hypercoagulative state, whereas patients with overt hypothyroidism may have a bleeding tendency.[3] [4] [5] [6] [7]

The second article, by Marongiu and colleagues,[8] discusses the relationship between thyroid disorders and hypocoagulability. The authors observe that, even if the bleeding tendency is generally mild and may be reversed after restoration of an euthyroid state, severe hemorrhagic disorders, such as thrombocytopenia, acquired von Willebrand syndrome (aVWS), and acquired hemophilia, may complicate the course of both hyper- and hypothyroidism.[8] [9] Finally, they highlight that physicians and endocrinologists should pay particular attention both to an eventual hemorrhagic complication and to laboratory abnormalities in blood coagulation tests from their patients.

In the third article, Erem[10] updates the various coagulation changes leading to a hypercoagulable state that have been documented in both hypo- and hyperthyroidism[10] [11] and concludes that abnormal coagulation and fibrinolytic activity may be responsible for the pathogenesis of atherosclerosis and thrombosis in thyroid disorders. This latter issue is further addressed by Duntas and Biondi,[12] who summarize the most recent developments regarding the association between subclinical hypothyroidism and the increased risk of cardiovascular disease (CVD). The authors analyze the role of traditional CVD risk factors (e.g., hyperlipidemia, hypertension) and newly identified ones (C-reactive protein and retinol-binding proteins), as well as the importance of timely treatment with levothyroxine for the underlying thyroid disorder.[12] [13] [14]

The last article on the link between thyroid and hemostatic abnormalities, by Federici,[15] reports on the current knowledge of the association between hypothyroidism and aVWS, which not surprisingly complicates the clinical scenario.[15] [16] [17] Practical management of mucocutaneous bleeding in hypothyroid patients with this associated hemorrhagic condition is also presented.

The next article, by Squizzato and colleagues,[18] updates the available evidence on the influence of pituitary, adrenal, and parathyroid hormones on the coagulation and the fibrinolytic system, as well as their possible clinical implications.[18] [19] The literature supports a possible relevant clinical effect of the imbalance between coagulation and fibrinolysis on thrombotic events in endogenous Cushing's syndrome. Although the clinical relevance is still unproven, a possible hypercoagulable effect has been shown also for hyperprolactinemia, growth hormone excess or deficiency, exogenous hypercortisolism, pheochromocytoma, primary hyperaldosteronism, and hyperparathyroidism.

The endocrine manifestations associated with antiphospholipid syndrome (APS) are assessed in the next chapter by Mehdi et al.[20] Adrenal insufficiency is found to be the most common endocrine disorder associated with APS,[21] and hypopituitarism is increasingly being reported as an APS-related endocrine disorder.

Targher and colleagues[22] then summarize the current knowledge of the adverse effects of type 1 diabetes mellitus on coagulation and fibrinolysis. Although no definitive information is available, the literature data suggest overall that patients with type 1 diabetes exhibit a proinflammatory/procoagulant condition deriving from increased platelet adhesiveness, activation of the coagulation system, and decreased plasma fibrinolytic potential.[22] [23] The authors also focus on recent data from large prospective studies suggesting a strong association between procoagulant imbalance and development of chronic vascular complications in people with type 1 diabetes.[2]

Lippi et al[24] present the more recent advances on the coagulation abnormalities in patients with chronic liver disease (CLD). Although a bleeding tendency represents the most frequent and clinically severe hemostatic complication observed in patients with CLD, growing evidence now suggests that a procoagulant state may be also associated with such conditions, so that CLD patients may experience venous thrombotic complications.[25] [26] [27]

The final two articles assess some endocrine/hemostasis relationships and gender. Trigg and colleagues[28] first review recent and past evidence on the influence on hemostasis by changes in hormone status associated with the menstrual cycle, pregnancy, and hormone-based contraceptives and hormone replacement therapy.[28] [29] [30] [31] Overall, these hormonal influences may lead to an increase in the risk of venous thromboembolism (VTE) due to altered levels of clotting factors and an acquired resistance to the actions of activated protein C. The article by Brodin et al[32] deals with the still controversial relationship between testosterone and hemostasis. Indeed, although aging men with subnormal testosterone levels are at increased risk of atherosclerosis and CVD, there is presently no evidence that androgen administration to elderly men has an impact on the coagulation system or prevents the occurrence or improves the outcome of CVD.[32] [33] [34]

In conclusion, the take-home message is that hemostatic abnormalities are not infrequently observed in endocrine disorders. On the one hand, then, endocrinologists should be aware of the possibility that their patients may experience hemorrhagic or thrombotic complications either at diagnosis or during the natural history of their illness. On the other hand, some presentations of hemorrhagic or thrombotic complications to hematologists and physicians will over time be found to be associated to some endocrine disorder. We therefore hope that this new issue of Seminar in Thrombosis and Hemostasis will be of interest to a wide audience, and we sincerely thank all the authors for their valuable contributions.

REFERENCES