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L Catani

Publications and source records attributed to L Catani.

61 records · Page 4Linked to original sources

Ticlopidine in the treatment of thrombotic thrombocytopenic purpura: report of two cases.

The observation of two clinical cases make possible an evaluation of the potential therapeutic activity of platelet function inhibitors in thrombotic thrombocytopenic purpura (TTP). In particular, the clinical and hematological effects of ticlopidine (TC), employed alone in two TTP patients, are reported. The mechanism of action of this peculiar antiplatelet drug is mainly represented by the inhibition of fibrinogen binding on the platelet surface. In the first patient, a 45-year-old female in whom plasma-exchange (PE) and corticosteroids (C) led to a partial remission (platelets 80 x 10(9)/l), treatment with TC at a dose of 750 mg/day was carried out, and after 6 weeks a normal platelet count was observed. A complete remission was maintained for 31+ months, even after reduction of the TC dose to 250 mg/day. In the second patient, an 18-year-old female affected by relapsing TTP, a complete remission obtained with PE and C was maintained for 19 months in concomitance with TC treatment, started at a dose of 750 mg/day and lowered to 250 mg/day. After 11 months of treatment at this low dosage there was a relapse (platelets 20 x 10(9)/l), but the increase of the TC dose to 750 mg/day in a few weeks induced a complete remission again. These data, in accord with a few other recent preliminary reports, suggest that TC, even alone, may play an interesting role in the management of TTP patients.

Adolescent↗

Negligible hemostatic toxicity of intermediate-dose Erwinase in adult patients with acute lymphoblastic leukemia: preliminary data.

The hemostatic toxicity of low dose L-asparaginase from Erwinia carotovora (Erwinase) has been reported to be negligible in adult patients with acute lymphoblastic leukemia (ALL); conversely, no consistent data have been obtained when Erwinase is administered at intermediate doses. We report preliminary clinical and laboratory hemostatic data from 10 adult patients with ALL treated during induction phase with intermediate doses of Erwinase (20,000 IU/m2s.c. every other day, for a total of six administrations). No thrombotic or hemorrhagic events were registered and the mean values of PT, aPTT, fibrinogen, antithrombin and D-dimer did not change during treatment. Only one patient showed a decrease of antithrombin (48% on day 8) requiring temporary suspension of Erwinase therapy. These data suggest that intermediate doses of Erwinase also have negligible hemostatic toxicity in adult patients with ALL.

Adolescent↗

Increased P-selectin plasma levels in patients with thrombotic thrombocytopenic purpura.

BACKGROUND: Thrombotic thrombocytopenic purpura (TTP) is a rare vascular disorder of unknown etiology. There is evidence to support the hypothesis that platelets and endothelium play a pivotal pathogenetic role. Immunological assays for plasma thrombomodulin and P-selectin levels have recently been made available and they allow simple evaluation of endothelial damage and endothelial/platelet activation, respectively. In this study, we measured the plasma levels of thrombomodulin, P-selectin and von Willebrand factor in 9 TTP patients during active disease and at the time of complete remission (CR). METHODS: Thrombomodulin, P-selectin and von Willebrand factor were measured by enzyme immunoassay. RESULTS: Mean thrombomodulin and von Willebrand factor plasma values were always within the normal range. P-selectin plasma levels, both in the active phase of the disease and in CR (median 312 and 185 ng/mL, respectively), were significantly higher than in normal controls (mean 96 +/- 35 ng/mL, mean 88 ng/mL; p < 0.05). However, the mean value of P-selectin in CR (median 185 ng/mL) was significantly lower than that observed at diagnosis (p < 0.05). In addition, an inverse relationship between P-selectin plasma levels and platelet count (r = -0.526; p = 0.03) was observed. CONCLUSIONS: These findings suggest that activation of platelets and/or endothelium may play a relevant role in the pathogenesis of TTP.

Adult↗