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Biomedical subjects

C Alessandri

Publications and source records attributed to C Alessandri.

At least 109 records · Page 6Linked to original sources
PubMed1984

Prekallikrein behaviour in chronic active hepatitis and in cirrhotic patients.

Prekallikrein (Prekk), antithrombin III (ATIII), plasminogen and alpha 2-antiplasmin were evaluated in chronic active hepatitis and in liver cirrhotic patients and correlated with Normotest. Prekk, ATII and plasminogen were significantly decreased in chronic active hepatitis as well as in liver cirrhosis. Alpha 2-antiplasmin levels in chronic active hepatitis patients did not differ from controls; liver cirrhotic patients, on the contrary, showed significantly low values of alpha 2-antiplasmin, Prekk, ATIII and plasminogen were significantly correlated with Normotest in both groups, but when cirrhotic patients were divided into the compensated and decompensated state only Prekk was correlated with Normotest in the decompensated state. The investigation seems to suggest that Prekk could be a reliable index for protein liver failure.

Adult↗
PubMed1983

[Erythrocyte deformability in chronic respiratory insufficiency].

The red blood cell deformability was evaluated in 10 patients suffering from chronic respiratory failure and in 10 normal volunteers. Patients with chronic respiratory failure showed a pH of 7.36 +/- 0.04, a pCO2 of 48.7 +/- 7.3 mmHg and a pO2 of 61.2 +/- 10.2 mmHg and had a decreased red blood cell deformability if compared with normal volunteers (p less than 0.001). The red blood cell deformability of patients suffering from chronic respiratory failure showed a weak correlation with pO2 (r = 0.50, p less than 0.05).

Aged↗
PubMed1982

Effects of ticlopidine on platelet function and blood coagulation.

A double blind study was performed on 20 atherosclerotic patients. A placebo was administered to one group of 10 patients (group A) and ticlopidine (500 mg/day) was administered to another group of 10 patients (group B) for one month. ADP and collagen-induced platelet aggregation (PA), platelet malondialdehyde (MDA) produced by thrombin stimulation and plasma beta-thromboglobulin (beta TG) levels, prothrombin time, activated partial thromboplastin time (APTT) fibrinogen, antithrombin (AT) III fibrin(ogen) degradation products, alpha 2-antiplasmin and plasminogen were evaluated in both groups before and after treatment. No changes in PA, MDA and beta TG were seen in group A. Group B showed a significant decrease of PA, beta TG and a significant increase of MDA. No changes on blood coagulation data were seen in either group. This study suggests that ticlopidine is able to inhibit platelet function in vivo.

Adult↗
PubMed1982

Influence of ascorbic acid on platelet aggregation in vitro and in vivo.

With the objective of investigating more thoroughly the relationship between ascorbic acid and platelet aggregation (PA) in particular, in vitro and in vivo studies were made whether interferences exist, Scaling amounts of ascorbic acid were added to platelet-rich plasma (PRP) samples to determine the level at which the inhibition of the PA was induce by ADP and arachidonic acid (AA), and endoplatelet malondialdehyde (MDA) concentrations decreased. Changes in PA and MDA were not observed in the PRP control samples Also, in 10 healthy volunteers, an i.v. infusion of ascorbic acid (2 g) produced PA inhibition and a reduction of MDA concentrations.

Ascorbic Acid↗
PubMed1982

Improvement of some blood coagulation factors in cirrhotic patients treated with low doses of heparin.

Effects of subcutaneous calcium-heparin and vitamin K administration were studied in 30 cirrhotic patients showing low values of prothrombin time, antithrombin III, fibrinogen, platelet count, plasminogen, alpha 2-antiplasmin, raised levels of fibrin(ogen) degradation products and prolonged activated partial thromboplastin time. A group of 10 patients was first treated with K vitamin for 15 d; after vitamin K therapy interruption, a treatment with 5000 IU (8000 IU in 1 patient) every 12 h of subcutaneous calcium-heparin was started. In another group of 20 patients a treatment with 5000 IU (8000 IU in 2 patients) every 12 h of subcutaneous calcium-heparin was started immediately. The heparin administration in both groups had been performed for at least 2 weeks. No significant changes of blood coagulation picture were observed after vitamin K administration, while calcium-heparin treatment showed an increase in prothrombin time, fibrinogen, platelet count, plasminogen, alpha 2-antiplasmin, a decrease in fibrin(ogen) degradation products and a shortened activated partial thromboplastin time. There was no significant change in antithrombin III values.

Blood Coagulation Factors↗
PubMed1982

The effects of gliclazide on platelet function in patients with diabetes mellitus.

Eighteen diabetic patients with abnormal platelet function were treated for 1 month with gliclazide (80 to 160 mg/day). Platelet aggregation, circulating beta-thromboglobulin levels and platelet malondialdehyde concentrations were significantly reduced after 30 (but not 15) days of treatment. Although fasting and post-prandial glycaemia significantly improved in these patients, similar changes in platelet function were noted in 5 other patients in whom glycaemia did not change. Gliclazide therapy, therefore, brought about an improvement in platelet function and a reduction activation in the thromboxane metabolic pathway, possibly by a direct on the platelets.

Adult↗