Abstract
During aging there are significant modifications of the mechanism of hemostasis, including blood coagulation, fibrinolysis, platelets and vascular factors. A tendency toward thrombophilia is usually observed in the presenile age (45 to 60) with an increase of coagulability (reduction of antithrombin III and increase of fibrinogen turnover), a decrease of fibrinolytic activity and an increase of platelet aggregation. In the actual senile age, after 70, such a tendency may disappear and normal values or even signs of hypocoagulability may be found, in association with an increased capillary fragility and hemorrhagic diathesis. The thrombophilic tendency may be more marked in the presence of predisposing diseases such as diabetes, hypertension, obesity and atherosclerosis. Today the role of gamma-carboxy-glutamic acid has been emphasized, insofar the abnormal proteins, which are formed due to the action of antivitamin K (indirect anticoagulants) or in the absence of vitamin K (as in malabsorption syndrome, frequently observed in the aged), do not contain gamma-carboxy-glutamic acid and act through an inhibition of factor Xa,thus increasing indirectly the antithrombin III activity. Therefore indirect and direct anticoagulants may be similar in this respect, namely enhancing antithrombin III activity. Thrombophilia in the arteriosclerotic aged subjects may be interpreted today as the consequence of a latent, intravascular coagulation syndrome.
Besides the increased capillary fragility in the aged, which may be corrected by means of a number of drugs (e.g. aminaphtone, “vascular factor”, etc.), the small vessels in the aged nay exhibit some typical findings, e.g, in the conjunctiva, especially in cases of arteriosclerosis, hypertension, diabetes etc. The action of some drugs on microcirculation may be evaluated by studying the modifications of the conjunctival vessels, in addition to the other findings concerning blood viscosity and erythrocyte deformability.
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