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Biomedical subjects

C Alessandri

Publications and source records attributed to C Alessandri.

At least 73 records · Page 4Linked to original sources
PubMed1991

[Hypercholesterolemia: therapeutic approach].

Epidemiological observations, experimental and clinical researches have laid special stress on the importance of hypercholesterolemia in the natural development of the atherosclerotic disease and its cardiovascular complications. Primary and secondary trials have demonstrated the benefits of cholesterol-lowering therapy to modify the evolution of atherosclerotic disease. In particular, it was observed a significant reduction of incidence and mortality due to coronary heart disease, that is the most common complication of atherosclerosis. At the present time, we have a new class of cholesterol-lowering drugs which is able to inhibit the 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase, the enzyme limiting the endogenous pathway of cholesterol synthesis. The HMGCoA reductase inhibitors, according to the chemical structure, can be divided into two groups. The first includes inactive lactone prodrugs, as Lovastatin and Simvastatin, that are enzymatically hydrolyzed to the corresponding ring-opened active forms in the liver, where the HMGCoA reductase inhibitors must chiefly reduce cholesterol synthesis. To the other group belongs the Pravastatin, a drug that is administered in its active open hydroxyacid form. Several clinical studies seem to demonstrate a greater cholesterol-lowering effect of the active form of Simvastatin, probably because of its more affinity for the HMGCoA reductase enzyme. Up to now, no inhibitor of HMGCoA reductase has showed serious toxic effects in man. The remarkable therapeutic efficacy showed by Simvastatin to reduce the serum concentrations of total and LDL-cholesterol, associated with moderate side-effects, ascribes to this molecule an important role in the therapeutic approach of familial and polygenic hypercholesterolemia.

Adult↗
PubMed1991

Plasma thiobarbituric acid reactive substances a predictive marker of cerebral ischemia in patients at high risk?

The clinical meaning of high values of blood lipid peroxides, assessed as thiobarbituric acid reactive substances (TBA-RS), was investigated in 19 selected high risk patients with transient ischemic attacks (TIA). Patients were checked every 3-6 months and followed-up for 3 years. 8 patients experienced further vascular episodes, 4 having minor stroke and 4 TIA; one of the latter died from myocardial infarction. Unlike blood cholesterol and glucose. TBA-RS values discriminated patients with vascular episodes: they, indeed, showed significant higher values of TBA-RS. Discriminant analysis further indicated that TBA-RS levels differentiate patients with and without vascular accidents, suggesting that high blood values of lipid peroxides could represent a predictive sign of vascular ischemia.

Aged↗
PubMed1991

Hydrogen peroxide as trigger of platelet aggregation.

In order to verify if H2O2 affects platelet function, platelet-rich plasma and human washed platelets were incubated with subthreshold concentrations (STC) of collagen or arachidonic acid or ADP and/or with 75-150 microM H2O2. While H2O2 alone did not affect platelet aggregation, it amplified platelet aggregation response in samples stimulated with STC of arachidonic acid and collagen but not in samples stimulated with STC of ADP. When platelets were preventively treated with aspirin, a cyclooxygenase inhibitor, the platelet activation by H2O2 was not observed. Thromboxane A2 (TxA2) was not produced by human washed platelets stimulated with STC of arachidonic acid, collagen or by H2O2 alone. On the contrary, when STC of agonists were tested on platelets supplemented with H2O2 an evident TxA2 production was seen. This effect was prevented by aspirin pretreatment or by the addition of catalase, an enzyme which destroys H2O2. This study suggests that H2O2 triggers the activation of platelets exposed to STC of collagen and arachidonic acid, via the cyclooxygenase pathway.

Adult↗
PubMed1991

[Primary results of laser recanalization in the endovascular treatment of arterial stenosis and occlusion of the lower limbs. Apropos of 45 treated cases].

Forty-five lower limb arterial lesions were treated by Nd Yag laser angioplasty using 1.4 and 2 mm hybrid catheters in 31 patients. This population comprised 28 men and 3 women (average age 63.8 +/- 3 years) 20 were in Stage II, 5 in Stage III and 6 in Stage IV of Fontaine's classification. The arteriographic lesions were 22 occlusions with an average length of 12.3 cm and 23 stenoses averaging 87% luminal reduction a few millimeters long to a maximum of a string of stenoses. Seventeen of these lesions were very calcified. The stenoses were situated on the iliac artery (7 cases), superficial femoral artery (28 cases), popliteal artery (9 cases) and the tibio-peroneal artery (1 case). There were no fatalities or recourse to emergency surgery. All patients underwent complementary balloon dilatation. The immediate patency rate was 91% in stenotic and 72% in occlusive lesions. At one week, the patency rate for stenotic lesions was unchanged but it had fallen to 59% for occlusive lesions (arteriographic evaluation). Angioscopy was used 22 times: it was indissociable to laser angioplasty as it enabled diagnosis and controlled the result. The use of thermal laser with hybrid catheters (metallic window tip) in endovascular procedures is a safe and effective method of treating stenosis and occlusion of lower limb arteries.

Adult↗
PubMed1991

[Effects of simvastatin on atherogenic blood lipid pattern].

The effect of a 6-month treatment with simvastatin, an HMG CoA-reductase inhibitor, on serum lipoprotein pattern was investigated in patients affected by primary hypercholesterolemia. After 4-6 weeks of lipid lowering diet, 46 patients showing serum cholesterol greater than 250 mg/dl and triglycerides less than 200 mg/dl were included in the study and treated with simvastatin (10-30 mg/day) plus diet. Serum total cholesterol, LDL-cholesterol, apolipoprotein B and triglycerides levels significantly decreased at the end of the follow-up (-27%, -33%, -22%, -26% respectively). Apolipoprotein A1 showed a significant increase as well as HDL-cholesterol, HDL3-cholesterol and apolipoprotein A1/B ratio. This study provides further findings on the simvastatin efficacy to normalize the lipoprotein pattern in primary hypercholesterolemia.

Adult↗
PubMed1990

Dilute aPTT prolongation by antiphospholipid antibodies in patients with liver cirrhosis.

The behaviour of aPTT, as assessed by standard or diluted phospholipid mixture, was investigated in 20 patients suffering from liver cirrhosis. Standard aPTT was prolonged in 13 but it was corrected by 1:1 mixture with normal plasma. Dilute aPTT performed in samples mixed 1:1 with normal plasma and calculated by the difference in time between 1:80 and 1:5 phospholipid mixture was prolonged in 9 patients, who had also significantly higher titre of anticardiolipin antibodies (p less than 0.005). Unlike patients' plasma with normal dilute aPTT, the addition of 0.05 M PC/PS liposomes to patient's plasma with prolonged dilute aPTT significantly shortened dilute aPTT (p less than 0.001). This study shows the presence of antiphospholipid antibodies in some patients with liver cirrhosis; this seems to be responsible for the prolongation of dilute aPTT.

Aged↗
PubMed1990

Inhibition of cyclooxygenase-independent platelet aggregation by low vitamin E concentration.

Platelet aggregation induced by threshold concentrations of agonists such as collagen, PAF or epinephrine was inhibited in vitro by 100 microM aspirin but was restored by stimulating platelets with high concentrations of collagen, PAF or by a combination of epinephrine and PAF. Incubating aspirin-treated platelets with 50-100 microM vitamin E or vitamin E acetate inhibited platelet aggregation by high concentrations of collagen and PAF and by the combination of epinephrine and PAF; platelet thromboxane A2 formation was less than 10% in samples incubated with 100 microM aspirin. Apyrase, added to aspirin-treated platelet, did not influence platelet aggregation induced by epinephrine and PAF. The present study suggests that concentrations of vitamin E as low as 50-100 microM inhibit cyclooxygenase-independent platelet aggregation when combined with an inhibitor of the arachidonate pathway.

Apyrase↗
PubMed1989

Inhibition of cyclooxygenase-independent platelet aggregation by sodium salicylate.

The effect of acetylsalicylic acid (ASA) on platelet aggregation (PA) and thromboxane A2 (TxA2) formation was investigated in vitro and ex vivo after 1 g or 300 mg ASA administration to healthy subjects. 50-100 microM ASA inhibited PA by single aggregating agent such as platelet aggregating factor (PAF) or epinephrine and reduced to less than or equal to 5% of control platelet TxB2 formation, but did not influence PA by epinephrine plus PAF. The latter was inhibited by increasing ASA concentration. In samples incubated with 100 microM ASA and stimulated with epinephrine plus PAF, PA could be inhibited by the addition of 100-300 microM sodium salicylate. After 300 mg-1 g ASA administration to healthy subjects, the inhibition of PA by epinephrine plus PAF was more marked by highest doses of ASA. This study suggests that aspirin inhibits PA with a cyclooxygenase-independent mechanism; this effect is mediated, at least in vitro, by salicylic acid.

Adult↗
PubMed1989

Inhibition of tissue plasminogen activator inhibitor by defibrotide in atherosclerotic patients.

Defibrotide, an antithrombotic drug, was previously shown to activate fibrinolysis. In order to elucidate the relationship between defibrotide treatment and fibrinolysis, ten atherosclerotic patients were given 1200 mg/day defibrotide intravenously for 7 days and then 400 mg/day intramuscularly for another 20 days. t-PA antigen assessed before and after venous occlusion was not affected by the treatment. Tissue PAI activity significantly decreased and t-PA activity, measured after venous occlusion, increased after 8 and 28 days of treatment; both these changes disappeared after defibrotide was discontinued. No particular side effects were detected throughout the investigation. The study suggests that defibrotide increases t-PA activity by reducing PAI activity.

Adult↗
PubMed1989

Blood lipid peroxides in TIA: relation to platelet function and metabolic profile.

Patients with transient ischemic attacks (TIA) were previously shown to have high plasma values of thiobarbituric acid-reactive substances (TBA-RS). To study whether these changes could be related to platelet activability, TBA-RS was investigated in 24 TIA patients before and 24 h after 1 g aspirin, an inhibitor of platelet cyclooxygenase pathway. Baseline TBA-RS values were significantly higher in TIA than in controls. Conversely, TIA patients had TBA-RS values after aspirin similar to controls, suggesting that the increase of plasma TBA-RS was not attributable to platelet hyperfunction. The evaluation of metabolic profile showed that patients with highest TBA-RS had hypercholesterolemia, hypertriglyceridemia, and/or diabetes mellitus. This study suggests that the increase of plasma TBA-RS in TIA could be an epiphenomenon of altered metabolic pathway.

Administration, Oral↗
PubMed1989

Interrelation between factor VII, prekallikrein, and hyperfibrinolysis in advanced cirrhosis.

Factor VII and prekallikrein activities were studied in 37 patients with liver cirrhosis who were in a decompensated state. Sixteen of them died 30-70 days after admission; 21 survived and were discharged after 30-80 days. Seven who died and six survivors had signs of hyperfibrinolysis: factor VII activity differentiated the two groups independently of the presence of hyperfibrinolysis. The presence of hyperfibrinolysis significantly reduced prekallikrein activity, which did not differentiate clearly survivors from non-survivors. Long term follow up of survivors showed a good correlation between factor VII and prekallikrein activities with long term survival. Hyperfibrinolysis seemed to influence the clinical course of patients: 87% of patients with hyperfibrinolysis who died had fatal haemorrhagic episodes. Low factor VII activity may be a precursor of terminal liver insufficiency.

Adult↗
PubMed1989

[Multiple synostosis syndrome].

An autosomal dominant syndrome is related to multiple fusion of joints, conductive deafness and craniofacial changes.

Abnormalities, Multiple↗
PubMed1988

Inhibition by picotamide of thromboxane production in vitro and ex vivo.

The effect of picotamide on platelet function has been studied in vitro and ex vivo. Picotamide at micromolar concentrations inhibited platelet aggregation induced by ADP, arachidonic acid and collagen, and it also inhibited the production of thromboxane A2 (TxA2). Unlike aspirin, picotamide did not affect the synthesis of prostacyclin by blood vessels. In eight healthy subjects who took picotamide 1200 mg/d platelet aggregation and TxA2 production were inhibited. Picotamide appears to be an antiplatelet drug that reduces TxA2 synthesis without affecting cyclo-oxygenase activity.

Adult↗
PubMed1988

Influence of hydroxyl radical scavengers on platelet function.

The influence of four hydroxil radical (OH.) scavengers on platelet function was investigated. OH. scavengers inhibited ADP, collagen, arachidonic acid, PAF-induced platelet aggregation, and platelet cyclooxygenase pathway activation, which was studied by evaluating platelet malondialdehyde and serum thromboxane A2 formation. The latter was not affected by superoxide dismutase, catalase, or metal ion chelants such as desferioxamine or DETAPAC. The detection of deoxyribose degradation by stimulated platelets suggested that platelets produce OH.. This study shows that activated platelets produce free radicals and that antioxidant agents such as OH. scavengers inhibit platelet function.

Adult↗
PubMed1988

Leukocyte response in patients suffering from acute stroke.

The oxidation of adrenaline to adrenochrome has been shown to reflect the activation of leukocytes in vivo. We tested the in vivo activation of leukocytes by measuring plasma oxidation of adrenaline to adrenochrome in patients suffering from cerebral ischemia, cerebral hemorrhage, and transient ischemic attacks and in healthy subjects. Patients with cerebral ischemia and cerebral hemorrhage had significantly higher values than healthy subjects, while patients with transient ischemic attacks had values similar to those of healthy subjects. In some patients with cerebral ischemia, the test was repeated 4 and 15 days after the acute event, but the follow-up data did not differ from baseline values. Our study shows that leukocyte activation occurs in cerebral ischemia and cerebral hemorrhage.

Acute Disease↗