Abstract
Sneddon’s syndrome is a rare but severe progressive chronic disease, characterized by multiple discoloration skin patches called Livedo racemosa and recurrent cerebrovascular events. It mainly affects women aged around 40. Considering the two main forms, antiphospholipid (APS) positive and negative, the available treatments are directed at either one of them. The idiopathic form (APS negative) is associated with a more severe prognosis as chronic oral anticoagulant therapy (COA) is more difficult to manage. One therapeutic perspective in controlling disease progression in these patients is by understanding the protein Z deficiency in these patients as a deciding factor in the success of the COA therapy.