Platelet serotonin in systemic sclerosis

Article Abstract:

Systemic sclerosis is the hardening or thickening of tissues throughout the body and is often associated with abnormalities in the small blood vessels. A more serious form of the disease, the CREST variant of systemic sclerosis, is associated with the development of Raynaud's disease, which is characterized by abnormal constriction of the blood vessels in the hands and feet upon exposure to cold or under conditions of emotional stress. The blood vessel complications of systemic sclerosis are probably related to blood vessel constriction and changes in the structure of the vessel wall. Serotonin, a natural substance released by blood platelets during their aggregation (accumulation), is a powerful blood vessel constrictor and may be involved in causing blood vessel disease. The levels of serotonin were measured in the platelets of 43 patients with systemic sclerosis, in 11 patients with Raynaud's disease, and in 38 normal subjects. Patients with Raynaud's disease or the CREST variant of systemic sclerosis had lower platelet serotonin levels than normal subjects; patients with systemic sclerosis had normal platelet serotonin levels. Ketanserin, a drug that blocks serotonin action, improved platelet serotonin levels in CREST patients. These findings suggest that in patients with systemic sclerosis, particularly those with the CREST variant, platelets are activated to release serotonin which results in decreased platelet serotonin levels and serotonin activated constriction of blood vessels. (Consumer Summary produced by Reliance Medical Information, Inc.)

Serotonin, Sclerosis

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In vitro platelet aggregability studies: lack of evidence for platelet hyperactivity in systemic sclerosis

Article Abstract:

Damage of the vascular endothelium (cellular lining of the inner blood vessel wall) is a major feature of progressive systemic sclerosis (scleroderma). As a result of endothelial damage, the subendothelium is exposed, and platelets (blood cells important in clotting) may then adhere and release agents that stimulate inflammation. Laboratory studies of platelets from patients with systemic sclerosis suggest that the cells are hyperactive, causing more extensive clot formation and greater platelet aggregation, or clumping. To better characterize these changes, platelets from 12 female patients with systemic sclerosis were compared with those from 12 healthy female subjects. The scleroderma patients had the CREST group of symptoms: calcium deposition, Raynaud's phenomenon, esophageal problems, skin hardening, and telangiectasia, or dilatation of superficial blood vessels. Responses of platelets to increasing doses of platelet activating factor, a fatty hormone that causes platelet aggregation, were similar in the two groups. Responses of the two groups to an inhibitor of platelet activating factor, BN52063, were also similar. Responses of platelets to two other natural stimulators of platelet aggregation, ADP and collagen, were also similar for the two groups. Unlike other studies, this report suggests that platelets from patients with systemic sclerosis are not hyperactive, and this may explain poor responses of patients with systemic sclerosis to antiplatelet drugs. (Consumer Summary produced by Reliance Medical Information, Inc.)

Evaluation, Systemic scleroderma, Scleroderma (Disease), Blood platelets, Cell aggregation, Platelet activating factor

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Von Willebrand factor, thrombomodulin, thromboxane, beta-thromboglobulin and markers of fibrinolysis in primary Raynaud's phenomenon and systemic sclerosis

Article Abstract:

Evidence suggests that increases in blood levels of von Willebrand factor (VWF), a substance important to blood coagulation, may correspond to increases in disease severity in patients with Raynaud's phenomenon. Researchers analyzed blood levels of VWF from patients with primary Raynaud's phenomenon (PRP, 10), diffuse systemic sclerosis (dSSc, 9), limited cutaneous systemic sclerosis (lcSSc, 17), and 19 healthy volunteers. They also measured markers of tissue and vessel injury including thrombomodulin, thromboxane, and tissue plasminogen activator antigen. Blood levels of VWF were significantly higher in patients with more advanced disease (lcSSc and dSSc) than in patients with PRP or in the controls. VWF and thromboxane levels used together as benchmarks of disease accurately identified only 62.5% of the patients with Ssc and 72.2% of the controls. The activity of tissue plasminogen activator antigen was not significantly different among the groups.

Measurement, Development and progression, Von Willebrand factor

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