Review
The skin and hypercoagulable states

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Hypercoagulable states (HS) are inherited or acquired conditions that predispose an individual to venous and/or arterial thrombosis. The dermatologist can play a vital role in diagnosing a patient's HS by recognizing the associated cutaneous manifestations, such as purpura, purpura fulminans, livedo reticularis, livedo vasculopathy (atrophie blanche), anetoderma, chronic venous ulcers, and superficial venous thrombosis. The cutaneous manifestations of HS are generally nonspecific, but identification of an abnormal finding can warrant a further workup for an underlying thrombophilic disorder. This review will focus on the basic science of hemostasis, the evaluation of HS, the skin manifestations associated with hypercoagulability, and the use of antiplatelet and anticoagulant therapy in dermatology.

Section snippets

Hemostasis

Hemostasis is the physiologic response that minimizes blood loss while maintaining blood flow after an injury to a vessel. Endothelial injury triggers immediate vasoconstriction and exposes tissue factor (TF) and collagen in the subendothelial matrix, providing a surface for platelet adherence and plug formation. Traditionally, coagulation has been described as a cascade of enzyme reactions, consisting of the extrinsic and intrinsic pathways converging on the common pathway to produce an

Hypercoagulable states

Venous and arterial thromboses are major causes of morbidity and mortality. Venous thromboembolism (VTE) includes deep venous thrombosis (DVT) and pulmonary embolism (PE). Hypercoagulability, in addition to stasis (slow flow) and endothelial injury, compose the Virchow triad of risk factors for venous thrombosis.6 Several components can contribute to a thrombophilic state, including genetic and acquired risk factors (Table I), triggering factors, and/or a lack of appropriate pharmacologic or

Purpura

Purpura consists of 5- to 20-mm nonblanching erythematous to violaceous macules, often located on the lower extremities. Many HS produce noninflammatory purpura with microvascular occlusion (Fig 2, A) and the associated conditions include: PF, thrombotic thrombocytopenic purpura (TTP), warfarin (Coumadin) necrosis, heparin-induced thrombotic thrombocytopenia, calciphylaxis, and catastrophic APLA syndrome (APLS).

Purpura fulminans

PF (Fig 2) is a dermatologic emergency and presents as multiple violaceous,

The use of antiplatelet and anticoagulant therapy in dermatology

The pharmacologic treatments available for VTE include antiplatelet and anticoagulant medications (Table IV) and thrombolytic agents. Embolectomy may be performed to remove large thromboses and inferior vena cava filters can be placed to help prevent additional pulmonary emboli.

In dermatology, the most frequently reported use of antiplatelet and anticoagulant medication is for the treatment of LV. There have been reports of the use of unfractionated heparin or LMWH, such as enoxaparin92, 108,

Conclusion

Primary and secondary HS are associated with cutaneous manifestations, including purpura, PF, LR, LV (atrophie blanche), anetoderma, SVT, and chronic venous ulcers. The dermatologist can identify these abnormal findings and pursue a workup for an underlying HS. The successful use of numerous antiplatelet and anticoagulant medications have been reported in patients with HS and skin manifestations, however, prospective studies are still needed to determine the optimal treatment for many of these

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    Conflicts of interest: None declared.

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