Abstract
RAYNAUD-attacks, i.e. cold induced episodes of hypoperfusion of the upper extremities are characterized by a “tricolore-phenomenon”. They are thought to occur as a consequence of vasospastic diseases (M. RAYNAUD). However, abnormal high viscosity may cause a very similar secondary phenomenon in hematological diseases, especially due to an overproportional increase in blood viscosity at low shear in hypothermia. Previously, anticonstrictive interventions (e.g. sympathectomy, vasodilator drugs) were applied, more recently plasmapheresis was recommended, albeit with variable success. Such therapy would be logical in case of a humoral cause of RAYNAUD-attacks. Simple hemorheological tests (rheoaggregometry of red cell aggregation, plasma viscosity, hematocrit determination) appears to differentiate clearly between primary M. RAYNAUD and secondary RAYNAUD-phenomena in disorders such as systemic sclerosis, rheumatoid arthritis. In the latter, there is a strongly increased tendency to red cell aggregation, demonstrable in accelerated rate of aggregate formation and in a highly abnormal shear resistance of the aggregates in flow.
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