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The hemostatic system is responsible for limiting blood loss upon vascular injury and is designed to rapidly react to breaches in the endothelial cell lining. Components of this system are subject to powerful regulatory mechanisms including various antihemostatic actions of the endothelium, antihemostatic actions from proteins in plasma, and blood flow that removes activated hemostatic proteins from the growing thrombus. Awell-orchestrated balance between proand antihemostatic forces ensures hemostatic balance and avoids spontaneous bleeding or thrombotic episodes. It is evident that hemostatic balance is crucial to avoid these complications, as evidenced by the pathology associated with a deficiency of proor anticoagulant proteins (e.g., severe and spontaneous bleeding in hemophilia and substantially elevated thrombotic risk in patients with deficiencies in some of the natural anticoagulants). While congenital or acquired disorders may alter multiple components of the hemostatic system simultaneously, such complex changes in the hemostatic system may not necessarily lead to severe pathology. For example, the complex hemostatic changes in patients with liver disease lead to a hemostatic rebalance without a clinical phenotype in many patients, which demonstrates the resilience of the hemostatic system.1 Likewise, hemostatic challenges resulting from surgery or trauma are not necessarily related to a dismal hemostatic outcome.2,3 In this issue of Seminars of Thrombosis and Hemostasis, we explored consequences of remarkable physiological or pathological conditions on the hemostatic system. As we will see, some “extreme” conditions may be without clinical consequences, whereas others are related to a substantial risk of bleeding or thrombosis. Moreover, there is a remarkable set of challenges to the hemostatic system, that is, hemostatic activators or inhibitors in a variety of venoms, which are potentially useful as therapeutic agents. We will start this issue by discussing effects of physiological extremes. First, Kenet et al4 discuss the hemostatic system in the very young. It is well known that the hemostatic system in newborns and very young children has a remarkably different composition than that in adults, with decreased plasma levels of most of the activators and inhibitors. Despite these differences, most children fortunately dowell and are in excellent hemostatic balance. The paper by Kenet et al discusses those rare cases inwhichyoung children suffer from bleeding or thrombotic complications in the context of the concept of developmental hemostasis. Next, Tzoran et al5 discuss the hemostatic changes that occur as a consequence of aging. As in the very young, the hemostatic system in the oldest old is substantially different from younger adults. However, in this population, the risk of thrombotic disease increases tremendously, and interactions with chronic illnesses are associated with important thrombotic issues. The subsequent “extreme condition” is discussed by Hunt,6 who addresses hemostatic changes in extremes of bodyweight. Very low bodyweight is associated with incompletely characterized hemostatic changes, which include decreased blood cell counts and platelet hyperaggregability. Among the many clinical consequences of severe obesity is a hypercoagulable state that is related to an increased risk of venous and arterial thrombosis. The author also discusses mechanisms and clinical consequences of the hemostatic changes associated with (severe) obesity. The next paper by Kicken et al7 deals with extreme exertion. The authors propose that a hypercoagulable state induced by strenuous exercise is balanced by a concomitant

Hemostasis and Thrombosis in Extreme Physiological and Pathological Conditions