Current medical and surgical management of Raynaud's syndrome
ABSTRACT Raynaud's syndrome (RS) is characterized by episodic digital ischemia induced by cold or emotional stress. Pathophysiologic mechanisms include temporary vasospasm and fixed digital artery obstruction. A number of pharmacologic and invasive therapies have been studied to treat RS symptoms; however, there are no specific treatments that are currently approved by the U.S. Food and Drug Administration specifically for RS. Of the available pharmacologic agents, calcium-channel blockers remain the preferred initial treatment for vasospastic RS, although many vasodilators have been studied and found to be efficacious. Vasodilators are less effective in treating digital artery obstruction, and no treatments have been found to be universally beneficial, although the phosphodiesterase V inhibitors have been gaining in popularity. Invasive therapies may have a role in selective cases. In this review, the current evidence of treatment for RS is summarized.
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ABSTRACT: Raynaud's phenomenon (RP) is characterised by transient ischaemia in the extremities in response to cold or emotions. It can be primary (idiopathic) or secondary to an underlying disease. The pathophysiology of RP is multifactorial and complex. Microvascular impairment is a hallmark of the disease. The objective of this work is to review the different pharmacological treatments currently used in the management of RP, from their mechanism of action to the available evidence regarding their efficacy. We also propose to discuss potential pharmacological targets such as the potentiation of the nitric oxide pathway, or the inhibition of the RhoA-Rho kinase pathway. The last part of this review deals with drug-induced RP. Among various medications, beta-blockers, interferons, tyrosine-kinase inhibitors or cytotoxic agents such as bleomycin are involved.Thérapie 03/2014; 69(2):115-128. DOI:10.2515/therapie/2013068 · 0.51 Impact Factor
- Nursing 04/2014; 44(4):57-9. DOI:10.1097/01.NURSE.0000444727.60395.f8
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