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A Santarossa

Publications and source records attributed to A Santarossa.

5 recordsLinked to original sources

The use of antiproteolytic mixture fails to modify the abnormal von Willebrand factor pattern in myeloproliferative disease.

Abnormalities of von Willebrand factor, with reduction of higher molecular weight multimers, was described in patients with increased platelet number. We have studied twelve patients with myeloproliferative disease (9 patients with Essential Thrombocytosis and 3 patients with Polycythemia Vera). Blood samples were collected either with citrate and antiproteolytic mixture (EDTA 6 mM, Aprotinin 200 U/ml, N-ethylmaleimide 5 mM in sodium citrate 3.8%). VIIIR: RCoF was found decreased in all patients studied, using both anticoagulants, while VIIIR: Ag was within normal range. Higher molecular weight multimers were found decreased or absent both in samples collected with citrate and in those collected using the antiproteolytic mixture. These data suggested that von Willebrand factor abnormalities observed in myeloproliferative disease are not due to a proteolytic degradation that's supposed to happen in vitro during blood samples collection and manipulation.

Anticoagulants↗

Fibrinolytic behavior in long-standing branch retinal vein occlusion.

The aim of our study was to evaluate the fibrinolytic system in patients with retinal branch vein occlusion (RVO). The following tests were carried out: prothrombin time, partial thromboplastin time (PTT), fibrinogen degradation products, euglobulin lysis time, fibrinogen, pasminogen, antithrombin III, alpha 2-antiplasmin and alpha 2-macroglobulin. Comparing the results of patients with those of normal controls, only the fibrinogen increase and PTT shortening were significantly different. All other tests taken into account were within normal limits. Only the patients without other associated diseases (diabetes or hypertension) showed a significant activation of fibrinolysis (either with respect to normal or to other RVO patient groups). In conclusion, no important fibrinolytic impairment was seen in our longstanding RVO patients. Fibrinolytic activation seen in patients without verified associated diseases may be related to the presence of a sound endothelium, still able to release plasminogen activators in response to RVO. The fibrinogen and PTT changes in RVO were probably due to other associated diseases.

Aged↗

Study on a new chromogenic substrate for the prothrombin time determination.

The aim of our study was to evaluate the possibility of using a chromogenic substrate for the prothrombin time determination. The reagent used by us (Chromoquick) is composed of a human placenta thromboplastin and chromogenic substrate (Tos-Gly-Pro-Arg-5-amino-2-nitrobenzoic acid-isopropylamide), calcium chloride and a buffer. Normal subjects, patients with liver disease, patients on oral anticoagulant therapy, patients on heparin therapy, heterozygous and homozygous patients for prothrombin complex defects and other miscellaneous conditions have been investigated. The results of chromoquick have been related with standard prothrombin time obtained using a human placenta thromboplastin (Thromborel) and rabbit brain and lung thromboplastin (Simplastin). The normal range was 18-23 s for chromoquick and 13.5-15.5 s for the standard prothrombin times using Thromborel and Simplastin. In all groups of patients examined we noticed a significant correlation between the chromogenic and the classic prothrombin times with r values varying between +0.505 and +0.947. The statistical significance resulted from p values varying between less than 0.05 and less than 0.001. Only in the case of some heterozygotes for prothrombin complex factor defects the values obtained have not been unequivocal in the sense that in a few instances the heterozygotes seemed to escape detection. Therefore, it seems that the introduction of chromogenic substrates in laboratory practice for the prothrombin time determination is possible and can offer considerable advantages like standardization and automation. The only disadvantage may be caused by costs involved.

Acenocoumarol↗

Clotting changes in borderline hypertension.

Coagulation factors evaluated in a group of patients with borderline hypertension. The following tests were carried out: prothrombin time (PT) and partial thromboplastin time (PTT), Factor VIII coagulant activity, Factor VIII antigen and Factor VIII ristocetin cofactor, Factor XII and Factor XI activities. These tests were selected for their relationship to the contact coagulative activation near the vascular wall. Comparing the results with those of normal controls, Factor VIII coagulant activity, Factor XII and PTT levels were significantly higher. Other tests were all within normal limits in both groups. High Factor VIII and Factor XII levels associated with PTT shortening suggest that an increased synthesis and/or release of these coagulation factors was present in our patients. Activated coagulation seems to be present in borderline hypertension before the appearance of clinical signs of vascular lesions.

Adult↗