Vascular Health and Risk Management Open Access Full Text Article Advances in the treatment of Raynaud’s phenomenon Dovepress open access to scientific and medical research R e V i e w Terri L Levien Drug information Pharmacist and Clinical Associate Professor, College of Pharmacy, w ashington State University Spokane, w A, USA Correspondence:Terri L Levien Pharmacotherapy Department, wSU Spokane, PO Box 1495, Spokane, w A 99210-1495, USA Tel +1 (509) 358-7661 Fax +1 (509) 358-7744 email levient@wsu.edu submit your manuscript | www.dovepress.com Dovepress Abstract: Raynaud’s phenomenon is a common condition characterized by vasospasm of the digital arteries and resulting cyanosis and redness. It often does not require pharmacologic management, but in some cases symptoms are severe and pharmacologic management is necessary. Calcium channel blockers are often used first-line, but in some patients are ineffective. Patients with severe symptoms or intolerance to available therapies have prompted explora- tion of alternative therapies, including endothelin antagonists, phosphodiesterase-5 inhibitors, antioxidants, newer vasodilators, statins, and botulinum toxin. These newer therapies provide the focus for this review. Keywords: Raynaud, iloprost, bosentan, phosphodiesterase-5 inhibitors Raynaud’s phenomenon (RP) is the transient digital ischemia that occurs upon exposure to cold temperature or emotional distress. It most commonly affects the fingers. RP occurs as a result of vasoconstriction of the digital arteries, precapillary arterioles, and cutaneous arteriovenous shunts.1 The initial white phase is marked by demarcated pale skin caused by vasoconstriction and cessation of regional blood flow. The second phase is a cyanotic phase as the residual blood in the finger desaturates. The attack usually ends with rapid reflow of blood to the digits, which results in a red appearance of the digits. The attack is often accompanied by pain or paresthesia due to sensory nerve ischemia. The prevalence of RP in the general population is approximately 3 to 5 percent.1,2 Primary RP is characterized by symmetric attacks; the absence of tissue necrosis, ulceration, or gangrene; the absence of a secondary cause; normal nailfold capillaries; a negative test for antinuclear antibody; and a normal erythrocyte sedimentation rate. Symptoms are generally mild, and age of onset is generally younger than 30 years.1,3 In contrast with primary RP, a secondary cause is suggested by age of onset greater than 30 years; episodes that are intense, painful, asymmetric, or associated with ischemic skin lesions; concomitant symptoms suggestive of a connective tissue disease; specific autoantibodies; and evidence of microvascular disease on micros- copy of nail-fold capillaries.1,3 Up to 90% of patients with systemic sclerosis have secondary RP.4 Over 140 years since its first description, the pathophysiology of RP remains incompletely understood and is likely multifactorial. Vascular, intravascular, and neural abnormalities have all been implicated in the pathophysiology of RP. Among vascular Vascular Health and Risk Management 2010:6 167–177 © 2010 Levien, publisher and licensee Dove Medical Press Ltd.This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited. 167