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Biomedical subjects

S Bellucci

Publications and source records attributed to S Bellucci.

90 records · Page 5Linked to original sources
PubMed1986

Thrombocytopenia with thrombocytopathy possibly related to abnormalities of intracellular Ca++ fluxes and followed by the development of leukaemia.

A patient is described who presented a thrombocytopenia with thrombocytopathy followed by the development of a leukaemia. The disorder was characterized by decreased aggregation in the presence of ADP, and a lack of aggregation in the presence of arachidonic acid, natural endoperoxide or collagen. In parallel, 14C-serotonin release was severely decreased or nil in response to these inducers. Thrombin induced a slightly decreased aggregation and a normal 14C-serotonin release. Thromboxane B2 (T X B2) synthesis was normal after stimulation by arachidonic acid, natural endoperoxide or thrombin showing a normal arachidonate metabolism. In addition, the mepacrine test showed no significant decrease of the number of dense bodies with an average of 4.6 per platelet (versus 5.4 +/- 0.8 sd in controls). Stimulation by ionophore A 23187 failed to induce aggregation, 14C-serotonin release, or T X B2 synthesis. Furthermore, in the presence of EDTA, A 23187 did not provoke activation as reflected by 14C-serotonin release or T X B2 synthesis. Thus, in this case of thrombocytopathy, the hypothesis of abnormal intracellular Ca++ fluxes responsible for the defective platelet release phenomenon, was suggested.

Adenosine Diphosphate↗
PubMed1986

Prolonged remission in Raynaud's phenomenon after prostacyclin infusion.

We infused prostacyclin (PGI2) (7.5 ng/kg/min) during 5 h, three times at weekly intervals in 8 patients with Raynaud's phenomenon (RP). In 4 patients, improvement was long-term, more than 90 days after the last infusion (good responders); in 3 patients, improvement was mild, less than 15 days, and in one patient no improvement was observed (poor responders). Clinical response was always accompanied by improvement, although less prolonged, of capillary appearance and/or function, as judged by microscopy and/or hemodynamic tests (pulse volume index; radial artery blood flow). Lastly, increased catabolism of PGI2 seemed to be excluded in poor responders, since no statistical difference in PGI2 metabolism could be observed between the two groups.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Human platelet-tumor cell interactions vary with the tumor cell lines.

Platelets may promote the development of metastasis, and tumor cells that aggregate platelets are believed to be more malignant. We studied three different human mammary carcinoma cell lines, which had different interactions with human platelet-rich plasma (PRP). The MCF-7 and the T47-D cell lines induced an adenosine diphosphate (ADP)-mediated platelet aggregation. The third cell line, MDA-MB 231 did not induce any platelet aggregation. On the contrary, this cell line inhibited ADP- and arachidonic acid-induced platelet aggregation. This inhibiting activity is mainly adenosine-mediated. The mechanism by which platelets may contribute to the dissemination of cancer could be related to platelet growth factors. MCF-7 and T47-D cell lines induced a release of platelet-derived growth factor (PDGF). On the contrary, the MDA-MB 231 cell line did not induce any platelet release. The role of these platelet growth factors in tumor cell growth is discussed.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

[Role of prostaglandins and thromboxanes in cardiovascular physiopathology].

Prostaglandins and thromboxanes originate from lipid metabolism. Their precise role remains obscure despite our better understanding of their potent pharmacological properties reflected in their potent biological activities. Prostaglandins are most probably involved in various cardiovascular diseases, although few satisfactory methods are available to evaluate such a role in vivo. The fact that most antithrombotic drugs interfere with the arachidonic acid cascade provides a rationale to their mode of action and their use. The development of drugs acting more selectively on arachidonic acid metabolism should constitute a therapeutic improvement in cardiovascular diseases.

Arachidonic Acids↗
PubMed1985

Complete correction of Glanzmann's thrombasthenia by allogeneic bone-marrow transplantation.

Allogeneic bone marrow transplantation (BMT) successfully corrected type I thrombasthenia in a 4-year-old boy. The donor was his HLA-A, B and D identical 14-year-old brother who was heterozygous for thrombasthenia. A first transplant after conditioning with cyclophosphamide and thoracoabdominal irradiation was rejected, but a second transplant using CCNU, cyclophosphamide, procarbazine and horse antihuman thymocyte globulin in the preparative regimen was successful. Engraftment was proven by studies of platelet membrane antigens, PLA1 and glycoprotein IIb/IIIa complex and by platelet function studies. Haemorrhagic manifestations completely disappeared; platelet membrane markers and clot retraction returned promptly to normal values, and platelet aggregation tests more slowly. Twenty-four months after bone-marrow transplant, the patient was well with mild chronic hepatic graft versus host disease. BMT therefore appears to be a possible treatment for severe inherited platelet disorders.

Blood Platelet Disorders↗
PubMed1985

Detection of abnormal platelet functions with an in vitro model of primary haemostasis.

A new technique, which simulates primary haemostasis in vitro was tested using blood from control persons and from patients with a defined abnormality of primary haemostasis. The device allows the reproducible measurement of in vitro bleeding time and volume in small samples of whole blood. Inhibition of platelet adhesion and aggregation can very sensitively be detected with the new technique, which allows its possible use in clinical or pharmacological applications.

Blood Platelet Disorders↗
PubMed1984

Interactions of platelets with standard heparin and low molecular weight fractions.

The availability of fibrinogen receptors on platelets after ADP stimulation, was investigated in order to analyze platelet hyperaggregability induced by heparin. Unfractionated heparin increased the binding of fibrinogen on ADP-treated platelets. The results varied according to both the donor platelets and the kind of heparin preparation used. Beef lung heparin was more active than porcine intestinal mucosa heparin (P less than 0.001). Low molecular weight (LMW) heparin fractions however did not significantly increase the binding of fibrinogen to ADP-treated platelets. The effect of standard heparin and LMW heparin on the aggregation of normal platelets induced by the addition of plasma from patients with heparin-induced immune thrombocytopenia was also studied. Concerning heparin-induced immune thrombocytopenia we have shown that the plasma cofactor present in some patient plasma may induce platelet aggregation both in the presence of standard-heparin and in the presence of LMW heparin fractions. Therefore, one has to be careful when replacing standard heparin by LMW heparin or heparinoids since each patient may react differently.

Adenosine Diphosphate↗
PubMed1983

[Molecular abnormalities in recurrent thromboembolic disease].

The diagnosis and treatment of apparently idiopathic recurrent thromboembolic disease (RTED) still raise difficult problems. However, recent data suggest that abnormalities of coagulation and fibrinolysis factors are important. Hereditary antithrombin III (AT III) deficiency or abnormal AT III, and hereditary protein C deficiency with autosomal dominant transmission have been associated with severe familiar RTED. More recently, we described a dysfibrinogenemia characterized by abnormal fibrin polymerization and abnormal plasminogen binding to the fibrin clot, responsible for familial RTED. Disorders of fibrinolytic activity in RTED are represented, in 70% of the cases, by reduced release or lack of production by endothelial cells of a vascular plasminogen activator. Hereditary plasminogen deficiency or abnormal plasminogen, although rare, are regularly responsible for RTED.

Antithrombin III Deficiency↗
PubMed1983

[Parameters of hemostasis in Behçet's disease].

Venous thrombosis occurred frequently in Behçet's disease. In 12 patients with Behçet's disease of whom 6 have had leg venous thrombosis, some parameters of hemostasis or fibrinolysis have been studied. Platelet count, fibrinogen level, factor VIII coagulant activity, factor VIII antigen, plasminogen and antithrombin III level were in the normal range. Fibrinolytic capacity in response to venous occlusion of the arms was the same in patients and in healthy subjects, in the patients, there was no difference in regard to the occurrence of venous thrombosis. These parameters seemed therefore not able to detect the thrombotic tendency in this disease. These results are discussed with the other reports of the literature.

Adult↗
PubMed1983

The defective prothrombin consumption in Bernard-Soulier syndrome. Hypotheses from 1948 to 1982.

Bernard-Soulier syndrome (BSS) was described in 1948 as a constitutional platelet disorder characterized by giant sized platelets, a prolonged bleeding time, and a defect in prothrombin consumption. The accurate mechanisms of these abnormalities remain unexplained, especially the defect in prothrombin consumption on which we focus in this paper. Several hypotheses are proposed: firstly, a defective reaction between the platelet membrane, where the phospholipid composition is abnormal, and the proteins which initiate thromboplastin generation such as collagen, factor XI; secondly, an abnormal reaction between thrombin, whose synthesis is increased, and its receptor, possibly glycoprotein V, which is defective; lastly, as factor VIII/vW binding is diminished, an abnormal dissociation of the complex VIII/vW-VIIIc at the site of the platelet membrane, which leads to an inactivation of factor VIIIc.

Binding Sites↗
PubMed1982

[Moschkowitz's syndrome, or thrombotic thrombocytopenic purpura].

Moschcowitz's syndrome is a rare condition with poor prognosis. It is characterized by a microangiopathic haemolytic anaemia associated with thrombocytopenia, neurological symptoms and renal involvement. The vascular lesions consist of hyaline microthrombi, predominantly made up of platelet aggregates, disseminated in the smaller vessels. The physiopathological mechanisms are still poorly understood and probably multiple. Recent studies have demonstrated abnormalities in the endothelial synthesis of prostacyclin, and in many cases the lack of a plasma factor has been held responsible for intravascular disseminated platelet aggregation. The latest therapeutic attempts suggest that the most effective treatment probably is fresh plasma transfusions associated or not with plasma exchanges.

Adult↗
PubMed1982

[Thrombotic thrombocytopenic purpura or Moschcowitz syndrome].

Moschcowitz syndrome or thrombotic thrombocytopenic purpura is a rare disorder with a poor prognosis. This syndrome is characterized by a microangiopathic hemolytic anemia with thrombocytopenia, neurologic symptoms and renal disease. The vascular lesion consists of disseminated hyaline thrombi in the microvasculature composed mainly of platelet aggregates. The mechanisms are still poorly understood and are probably multiple. Recent data focus on an abnormal endothelial synthesis of prostacyclin and the presence of a factor (or the reduction of its inhibitor) in plasma able to induce intravascular disseminated platelet aggregation. The most efficient therapy seems to be infusions of fresh plasma with or without plasma exchange.

Adolescent↗
PubMedDate not supplied

[Thrombosis in disseminated lupus erythematosus].

In the course of disseminated lupus erythematosus (DLE), the development of arterial or venous thrombosis is sometimes observed. They are rare in the course of hematological forms of DLE, in which the more or less constant leucopenia is accompanied to variable extent by the affection of the other blood-lines: thrombocytopenia and/or thrombocytopathy and/or hemolytic anemia. The discovery of a circulating anticoagulant seems to be correlated with the existence of thrombosis. In fact it involves antiphospholipid antibodies, responsible for the protraction of certain coagulation tests, which shows up their existence. Recent studies have shown recognition of the membrane phospholipids of the vascular endothelial cell. A functional imbalance in this would be observed to encourage the synthesis of factors favorable to thrombosis.

Abortion, Spontaneous↗