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Claude Bachmeyer, MD; Pierre Toulon, MD; Robin Dhôte, MD; Boyan Christoforov, MD
Cochin Hospital

Mathieu Zuber, MD; Jean-Louis Mas, MD
Sainte-Anne Hospital Paris, France

JAMA. 1995;274(16):1266.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—A poor anticoagulant response to activated protein C (APC) has been reported to be the most common identified coagulation defect in patients with thrombophilia.^1-3 The molecular basis of APC resistance was identified in most patients as a single G-to-A substitution at position 1691 in the factor V gene, described as factor V Leiden.⁴ The resulting Arg-to-Gln mutation at position 506, the APC cleavage site in factor Va, leads to an unregulated activation of coagulation.

The cause of ischemic stroke often remains unknown, despite extensive investigations. The association with hypercoagulable states has rarely been reported.⁵ We report two cases of ischemic stroke associated with APC resistance.

Report of Cases.—CASE 1.

—A 64-year-old nonsmoking woman developed sudden onset of right complete hemiplegia and aphasia. A computed tomographic scan and magnetic resonance imaging of the head disclosed a large cerebral infarction in the left middle . . . [Full Text PDF of this Article]

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