Insufficient knowledge of the pathogenic mechanisms in the Raynaud phenomenon, both primary and secondary, and also the difficulty of precise evaluation of every therapeutic used has shown that all of the treatments adopted have, for the time being, proved unsatisfactory. Nevertheless, at the present juncture it has been suggested to make distinction between various aetiopathogenic mechanisms, making it possible to divide them into: microvascular systemic reflexes and local mechanisms (local hyperreactivity of the vascular wall and increase of the viscosity of the blood). The relative preponderance of each differs from one patient to another in an individual form. On the other hand, in patients in whom such mechanisms cannot be demonstrated, the pathogeny could be related to a lowering of the basal circulation. Thus, the measures or agents suggested at the present time have as their fundamental orientation the bases previously set forth. In this sense, a special consideration is that which corresponds to the vasodilator drugs. Among these, a distinction is drawn according to the mechanism of action. These are of 2 types: on the one hand, vasodilators that relax the vascular wall directly, so increasing both the muscular and cutaneous irrigation, and, on the other hand, agents which interfere with the action of the sympathetic which primarily produces an increase of the cutaneous microcirculation. As the Raynaud phenomenon is catalogued as a pathology due to reflex vasospasm, the 2 types of vasodilator drugs have been used with variable success. The authors go on to deal with these drugs, and then turn their attention to hypotensives, fibrinolytics and plasmapheresis by which a notable diminution of the viscosity of the blood is obtained thus facilitating the passage of the blood through several vessels that were previously narrowed. It is obvious that this article cannot be condensed into an abstract, but its concluding words underline the topicality of the subject. They are as follows: '...the new therapeutic actions, based on a better knowledge of the aetiopathogenic mechanisms, have perhaps opened a door for future investigations, although for the present moment there has been no total resolution of the problem'. There are 11 references to the literature.
|Journal||Revista Espanola de Reumatologia|
|Publication status||Published - 1 Jan 1979|