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Secondary Raynaud's phenomenon ( RP ) is often the sentinel clinical finding in systemic sclerosis and may precede systemic disease by several years. Altered nitric oxide metabolism plays a critical role in both fibrosis and severe secondary  RP  phenotypes in these patients. Increased flux through inducible nitric oxide synthase ( iNOS ) drives cutaneous fibrosis. Failure of flux through endothelial nitric oxide synthase ( eNOS ) contributes to increased vasoconstriction and decreased vasorelaxation. The underproduction of nitric oxide by  eNOS  is in part due to increased levels of asymmetric dimethylarginine ( ADMA ), an endogenous competitive inhibitor of nitric oxide synthase. The inhibitory effects of increased  ADMA  levels may be counteracted increasing serum  l _arginine, which is often an effective treatment strategy in these patients. As such,  l _arginine_based therapies should be considered in managing secondary  RP , particularly given their favourable safety and tolerability profile. While there is no established dosing regimen, studies of oral  l _arginine in secondary  RP  suggest that divided dosing may begin at 1_2 g/day and may be titrated up to 10 g/day. Conversely, primary  RP  is not associated with increased  ADMA  production which likely accounts for the failure of  l _arginine trials to show benefit in primary RP.

The clinical effects of l _arginine and asymmetric dimethylarginine: implications for treatment in secondary Raynaud's phenomenon