RAYNAUD PHENOMENON

This review of the recent literature highlights the fact that little p rogress has been made in the diagnosis of Raynaud's phenomenon and in understanding its pathophysiology. It is still difficult to differenti ate primary from secondary Raynaud's phenomenon due to connective tiss ue diseases. The prevalence of Raynaud's phenomenon has been ascertain ed to be higher in colder climates. Vibration-induced white finger has been reaffirmed as very common in pneumatic grinder and chain saw wor kers, and is related to the duration of use of vibratory tools. In sys temic sclerosis, the presence of anticentromere antibodies was shown t o correlate with loss of digits. Increasing evidence has been reported for a generalized tendency to vasospasm in vascular beds other than t he digits; the correlation of Raynaud's phenomenon with pulmonary vaso spasm and with migraine headaches has been reaffirmed. Plasma levels o f endothelin-1, von Willebrand's factor, and tissue plasminogen activa tor have been found to be increased in Raynaud's phenomenon, but this increase may only reflect endothelial cell damage. Increased polymorph onuclear activity may also be present, but its significance is unknown . Thromboxane is probably not important in the pathophysiology of the phenomenon. Criteria continue to be proposed for the diagnosis of prim ary Raynaud's phenomenon, as opposed to secondary cases, but still are imprecise. Nifedipine is the prime nonspecific treatment, although ot her calcium-channel blocking agents show promise. Finally, more report s of radical sympathectomy of the hand and digital arteries for severe Raynaud's phenomenon with successful outcomes have appeared.