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Biomedical subjects

J Zahavi

Publications and source records attributed to J Zahavi.

14 recordsLinked to original sources
PubMed1991

An abnormal pattern of multiple platelet function abnormalities and increased thromboxane generation in patients with primary thrombocytosis and thrombotic complications.

Platelet aggregation (PA) induced by ADP, collagen and epinephrine, plasma levels of beta-thromboglobulin (beta TG) and thromboxane B2 (TXB2) and serum TXB2 generation were studied in 11 patients with primary thrombocytosis (7 with essential thrombocythaemia and 4 with polycythaemia vera) and compared with 16 healthy subjects. 5 patients suffered from peripheral vascular ischaemia and another 3 had venous thrombosis, but none had bleeding complications. The patients showed an abnormal pattern of platelet function and of thromboxane generation distinct from the healthy subjects in three aspects. a) Shape change was 5-26 times greater, the lag-time of collagen PA was 2.3-2.9 times longer and the extent of epinephrine PA was nil or very low. ADP- or collagen-induced PA was also reduced (p less than 0.02). b) Plasma TXB2 generation (corrected to a normal platelet concentration) stimulated by the three PA inducers was within the range of the healthy subjects in spite of the reduced extent of PA. c) Plasma beta TG level and serum TXB2 generation (both corrected to a normal platelet concentration) were 2.9-7.1 times higher (p less than 0.001) indicating enhanced in vivo platelet activation and possibly increased thrombin generation. These abnormalities were not detected in another 4 patients with secondary thrombocytosis. The abnormal pattern of platelet function and thromboxane generation can be a useful laboratory method in the evaluation of patients with primary thrombocytosis. It might also explain the thrombotic complications which occurred in 8 of the patients in a manner such that increased or normal TXB2 generation overcomes the reduced extent of PA. In this respect, the pronounced serum TXB2 synthesis might be a marker of intravascular thrombosis.

Female↗
PubMed1979

beta-Thromboglobulin, platelet production time and pletelet function in vascular disease.

Plasma beta-thromboglobulin (beta TG) levels were measured in 103 healthy controls and 112 patients suffering from either peripheral vascular disease (PVD), or cerebrovascular disease (CVD) or deep vein thrombosis (DVT). Plasma beta TG was significantly elevated in 46 PVD patients and 24 recent DVT patients compared to controls, but did not differ significantly in 18 chronic DVT and 24 old CVD patients. In addition, heparin neutralizing activity (HNA) and platelet aggregation induced by adenosine diphosphate, 1-epinephrine and thrombin were compared in 33 out of the 46 PVD patients to 33 controls. The mean HNA was significantly shorter in the PVD patients than in controls. The rate and extent of platelet aggregation were increased in PVD patients compared to controls, but the difference was not statistically significant. Platelet production time (PPT) was measured in 20 controls, 35 PVD patients, nine chronic DVT and 12 chronic CVD patients; significantly shorter PPT was only observed in 14 patients with advanced PVD compared to controls, suggesting increased platelet consumption in these patients. All four assays (plasma beta TG, HNA, platelet aggregation and PPT) were performed in 25 patients; no correlation between the four tests was found in these patients suggesting that the tests were measuring various aspects of platelet function. These results suggest that in vivo platelet consumption as well as platelet aggregation and 'release reaction' are presumably enhanced in PVD and recent DVT patients and that plasma beta TG and PPT assays may be better and more specific indicators of in vivo platelet activation than in vitro platelet aggregation test.

Adolescent↗
PubMed1979

A modified non-radioisotope method for measurement of platelet production time.

Platelet production time (PPT), based on the measurement of malondialdehyde (MDA) production prior to and after the intake of acetylsalicylic acid (ASA), was determined in 20 healthy subjects. High MDA levels were produced by stimulating platelet lipid peroxidation with arachidonic acid, resulting in a reliable, sensitive and accurate technique. PPT correlated well with platelet survival time measured by 51Cr autologous labelled platelets when both methods were used simultaneously in the same patients. This modified non-radioisotope method might serve as a useful aid in the diagnosis of platelet disorders, thromboembolic diseases associated with increased platelet consumption and for the evaluation of drugs affecting platelet function.

Aspirin↗
PubMed1979

Subendocardial infarction and thrombocytopenia.

Two female patients who suffered from drug-induced thrombocytopenic purpura and subendocardial myocardial infarction are presented. One of them died from cerebral haemorrhage and diffuse subendocardial punctate haemorrhages were found at post-mortem. The abnormal haemostasis which is associated with thrombocytopenia might induce diffuse damage of the myocardium and might impair heart performance. This finding may be more frequent than hitherto appreciated and calls for serial electrographic tracings in thrombocytopenic patients.

Anti-Inflammatory Agents↗
PubMed1977

Quantitative venographic assessment of deep vein thrombosis in the evaluation of streptokinase and heparin therapy.

A technique of quantitative venography has been developed in which values are assigned to the deep veins of the calf, knee, thigh, and pelvis, based upon the calculated volume and degree of occlusion of these venous segments. A maximum score of 40 units reflects complete thrombosis of all segments. This technique has been applied to a randomized, single-blind study of streptokinase versus heparin treatment. Each group of 12 patients had similar mean inital venographic scores; follow-up venograms were performed 5 days after the start of therapy. Streptokinase patients with high initial scores (larger than 20) showed a mean improvement of 12.1 units, while those with low initial scores(less than 20) were essentially unchanged. Heparin patients with high scores had a minimal mean improvement of 1.1 units, but those with low scores had a significant mean extension of thrombosis of 8.6 units. Patients with symptoms for less than 7 days showed greated mean improvement (12.7 units) with streptokinase that those with a longer duration of symptoms (2.0 units); heparin patients in these subgroups showed a mean worsening of 7.5 units and no change, respectively. Extrinsic venous obstruction by tumor did not prevent an excellent response to streptokinase. No single test of coagulation of fibriolysis was a reliable indicator of the degree of venographic response to lytic therapy. Pyrexia and hemorrhagic complications occurred in over one-half of the streptokinase patients; one had an anaphylactic reaction, and one died of intracerebral hemorrhage during therapy. The data suggest that lytic therapy is best restricted to the patient with acute extensive thrombosis. Also, continuous infusions of heparin according to current guidelines may be inadequate to prevent thrombus growth in some patients.

Adolescent↗