| RAYNAUD'S: MAIN MENU | ||||
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| Raynaud's Research | ||||
| This page was written by Shelley Ensz, and has not yet been medically edited. Scleroderma (SD) affects everyone differently. Just because something is listed here does not mean an individual patient will ever experience it. See Disclaimer. | ||||
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| Raynaud's Research | ||||
| Another way to grow blood vessels. PGC-1alpha, a key metabolic regulatory molecule, senses a dangerously low level of oxygen and nutrients when circulation is cut off and then triggers the formation of new blood vessels to re-supply the oxygen-starved area – a process known as angiogenesis. EurekAlert! 02/20/08. | ||||
| Researchers discover new way to reverse poor circulation and heal wounds. The study mechanism suggests new ways to treat conditions that involve poor circulation like peripheral artery disease. Furthermore, the same signals that influence circulation in some tissues drive cell growth elsewhere. EurekAlert! 02/14/08. | ||||
| Cooling-induced contraction and protein tyrosine kinase activity of isolated arterioles in secondary Raynaud's phenomenon. The results of this study support the view that the hallmark of Raynaud's phenomenon associated with scleroderma, cooling-induced vasospasm, appears to be mediated by an increase in PTK (protein tyrosine kinase) activity possibly exacerbated by impaired endothelium-dependent vasodilation. PubMed. Rheumatology (Oxford). 2005 Feb 3. | ||||
| Pathogenesis of Raynaud's phenomenon. A key point is that Raynaud's phenomenon can be either primary (idiopathic) or secondary to a number of underlying conditions, and that the pathogenesis and pathophysiology vary between these conditions. PubMed. Rheumatology (Oxford). 2005 Mar 1. | ||||
| Increased circulating levels of tissue kallikrein in systemic sclerosis correlate with microvascular involvement. T-kallikrein levels are increased in patients with SSc, particularly in lSSc, and are associated with early and active capillaroscopic patterns. T-kallikrein may play a part in SSc microvascular changes. PubMed. Ann Rheum Dis. 2005 Mar;64(3):382-7. (Also see: Causes of Scleroderma) | ||||
| The Relationship Between In Vivo Micro- and Macro-vascular Dysfunction in Raynaud’s Phenomenon. Simultaneous abnormalities of micro- and macro-vascular digital blood flow occur in UCTD and systemic sclerosis (SSc). Marina E. Anderson. 1679/502. ACR 2004. | ||||
| The myth of pulmonary Raynaud's phenomenon: the contribution of pulmonary arterial vasospasm in patients with systemic sclerosis related pulmonary arterial hypertension. Pulmonary vasospasm in response to peripheral and centrally administered cold pressor challenge is unlikely to contribute to persistence of pulmonary arterial hypertension in patients with systemic sclerosis. PubMed. Ann Rheum Dis. 2004 Dec;63(12):1627-1631. (Also see: Pulmonary Hypertension) | ||||
| Chromosome aberrations in Raynaud's phenomenon. Our results show that circulating lymphocytes of only pre-scleroderma Raynaud's phenomenon subjects undergo chromosomal damage, as detected by the micronucleus assay, at a higher rate than expected. PubMed. Eur J Dermatol. 2004 Sep-Oct;14(5):327-31. | ||||
| Increased tyrosine phosphorylation mediates the cooling-induced contraction and increased vascular reactivity of Raynaud's disease. Increased levels of protein tyrosine kinase (PTK) are mechanistically associated with increased contractile responsiveness to cooling. This study tests the hypothesis that increased PTK activity mediates the increased vascular reactivity to agonists and cooling associated with primary Raynaud's disease (RD). PubMed. Arthritis Rheum. 2004 May;50(5):1578-85. | ||||
| Coexistence of Erythromelalgia and Raynaud's phenomenon. A review of the literature indicates that causative and pathophysiologic similarities between the 2 conditions may exist in some cases. Rare reports of coexistence of the 2 disease processes further strengthen such research findings. PubMed. J Am Acad Dermatol. 2004 Mar;50(3):456-60. | ||||
| Raynaud's phenomenon and the vascular disease in scleroderma. Immune involvement in the early stages of the disease and mechanism of vascular repair in advanced cases are some of the highlights of last year's progress. PubMed. Curr Opin Rheumatol. 2004 Nov;16(6):718-22. | ||||
| Nailfold videocapillaroscopic (NVC) patterns and serum autoantibodies in systemic sclerosis. NVC is an appropriate tool for differential diagnosis between primary and secondary Raynaud's (RP) through the clear recognition of the early NVC scleroderma pattern. The presence of anti-Scl70 antibodies seems be related to earlier expression of the active and late NVC patterns of SSc microvascular damage. The presence of ACA seems to be related to delayed expression of the late NVC pattern. PubMed. Rheumatology (Oxford). 2004 Mar 16. (Also see: Antibodies) | ||||
| Clinical Trials | ||||
| The Topical Application Of Nitroglicerin Cream Improves Raynaud Phenomenon (RP) At Hands In Systemic Sclerosis Patients: A Pilot, Open Label Study. Our data show that nitroglicerin cream is safe, reduces the intensity and the frequency of RP attacks. Effects are rapid and long lasting. Although the results should be confirmed on wider groups of patients, nitroglicerin cream might be considered as an alternative topical therapy for RP. G. Fiori. AB0503 EULAR 2007. | ||||
| Vascana Findings To Be Presented At International Scleroderma Conference. The Vascana presentation will focus on its phase III clinical trial results and on MediQuest's proprietary Topical Amphi-Matrix (TAM) drug delivery system. With the TAM technology, Raynaud's patients will be able to apply a non-systemic, topical formulation at the affected area to deliver relief. Medical News Today. 05/19/07. | ||||
| Effect of Clonazepam on Raynaud's Phenomenon and Fingertip Ulcers in Scleroderma. We report a case of Raynaud's phenomenon and digital ulcers responding to clonazepam. Further research is warranted to test the robustness of this preliminary finding. The Annals of Pharmacotherapy: Vol. 41, No. 9, pp. 1544-1547. 2007. (Also see: Digital Ulcers ) | ||||
| Increase in circulating endothelial precursors by atorvastatin in patients with systemic sclerosis (SSc). The results of this pilot study suggest that atorvastatin treatment can increase CEPs (circulating endothelial precursors) and may be effective in improving Raynaud's phenomenon, even in SSc patients who have CEP dysfunction intrinsically. Arthritis & Rheumatism Journal. Volume 54, Issue 6, Pages 1946 - 1951. (June 2006). (Also see: Medications) | ||||
| Therapeutic Angiogenesis of Ischemic Digits from Patients with Systemic Sclerosis and Related Disorders by Implanting their own Peripheral and Bone Marrow Mononuclear Cells. Autologous bone marrow mononuclear cell implantation might be effective for ischemic digits of the patients with systemic sclerosis and related disorders, although superiority of the bone marrow cells to peripheral mononuclear cells was small. M. Iwamoto. FRI0132 EULAR 2005. | ||||
| The Role of Nitric Oxide in Raynaud's | ||||
| Serum nitric oxide (NO)) metabolites and disease activity in patients with systemic sclerosis. Serum NO(x) in SSc patients were elevated compared to healthy controls. Serum NO(x) level was determined by multiple factors including age, prednisolone use, and elevated pulmonary arterial pressure. (PubMed) Clin Rheumatol. 2008 Mar;27(3):315-22. Epub 2007 Aug 15. (Also see: Raynaud's ) | ||||
| Understanding How Temperature Regulation Occurs. Experiments involving 11 young men and women showed that NK-1 receptors contribute to active vasodilation [the rise in skin blood flow] and that a combined NK-1 receptor desensitization and nitric oxide inhibition further diminishes active vasodilation. Medical News Today. 10/28/06. (Also see: Digital Ulcers ) | ||||
| Endothelial Dysfunction Correlates with Reduced Nitric Oxide Production in Systemic Sclerosis (SSc). The ability of the brachial arteries to dilate in response to hyperemia is reduced in SSc and seems correlated to the reduction of circulating nitric oxide (NO). Hyperemia induced low levels of FMD% and the low levels of NO and angiotensin system components suggest a widespread endothelial dysfunction in SSc patients. F. Bartoli. FRI0083 EULAR 2005. | ||||
| Hopkins Researchers Discover how Nitric Oxide Prevents Blood Vessel Inflammation. "Nitric oxide may regulate exocytosis this way in a variety of diseases," says Lowenstein, an associate professor of medicine at Hopkins. "For example, nitric oxide blocks exocytosis from lymphocytes, reducing autoimmune damage." Johns Hopkins Medicine. 10/17/03. | ||||
| Beauty and the Beast. The nitric oxide paradox in systemic sclerosis. Clearly, more work is needed to understand the mechanisms involved in patients in whom the protective function of NO is deficient. Furthermore, new strategies to block the toxic effects of NO or enhance its beneficial effects may open a new avenue in the management of endothelial injury and vascular insufficiency in SSc. Rheumatology 2002; 41: 843-847. | ||||
| Raynaud's Studies | ||||
| Digital (Finger and Toe) Ulcers. ISN. Gangrene and Amputations. ISN. Scleroderma Clinical Trials. ISN. Scleroderma Research Registries. ISN. |