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Biomedical subjects

A Girolami

Publications and source records attributed to A Girolami.

At least 307 records · Page 17Linked to original sources
PubMed1991

Portal vein thrombosis in a patient with severe haemophilia A and post-hepatitis liver cirrhosis.

The occurrence of a portal vein thrombosis in a haemophilia A patient is reported. The patient, a 53 year old male, had been followed by us for the past 20 years in our out-patient Clinic. He was hospitalized recently for a suspected hepatic cirrhosis. Severe ascites, hepato-splenomegaly together with weight loss and mild fever were present. During the hospitalization, an ultrasound and CT scan of the liver confirmed the cirrhotic pattern and showed the presence of a portal vein thrombosis. There were no changes in the underlying coagulation defect, in fact, the patient had recurrent haemarthrosis. Furthermore, with the ultrasound examination, some focal hepatic lesions--probably due to a hepatocellular carcinoma--were also observed. The patient died because of massive haematemesis due to rupture of oesophageal varices.

Carcinoma, Hepatocellular↗
PubMed1991

Thrombosis and hemorrhage in thrombocytosis: evaluation of a large cohort of patients (357 cases).

We report clinical and laboratory findings in a large cohort of patients with thrombocytosis (357 cases). At the time of study, the patients showed a platelet number greater than 500 x 10(9)/L. The follow-up of patients ranged between 3 and 16 years. 123 patients were affected by polycythemia vera (PV), 97 by essential thrombocythemia (ET), 13 by chronic myeloid leukemia (CML) and 31 by myelofibrosis (MF). In 93 subjects, the thrombocytosis was reactive (ST). We found the highest incidence of thrombosis in PV patients, especially concerning the cerebro-vascular system; thrombosis, but in a lower percentage, was recognized in MF patients. Also, ET patients showed a number of thrombosis in peripheral arteries. Thrombosis of the coronary arteries were quite rare while 25% of MPD subjects showed peripheral vein thrombosis. We take into account that many patients showed thrombocytosis associated to one or more atherosclerotic risk factors. Hemorrhages were present especially in CML and in ET, but were not as frequent as thrombosis. The most common bleeding manifestations affected skin and mucosa. Hemorrhages after surgical procedures were also frequent. Gastro-intestinal bleeding was not strictly related to anti-aggregating therapy and occurred not only in PV but also in ET patients.

Adult↗
PubMed1991

Decreased platelet mitogenic activity in patients with diabetes mellitus.

Platelet-Derived Growth Factor is involved in the atherogenesis and in the genesis of vascular alterations in diabetes mellitus. Its evaluation in platelet extract, by means of the mitogenic stimulation of BALB/c 3T3 fibroblasts, showed significantly reduced values in ten diabetics compared with ten normal controls. Platelet poor plasma mitogenic activity was also evaluated but showed no significant difference. The release of platelet mitogens into the circulation and a resulting acquired platelet defect are suggested. A hypothetical growth inhibitory activity can be surmised, that could both contribute to angiopathy and wound healing defect typical of diabetes mellitus.

3T3 Cells↗
PubMed1991

Decrease of fibrinogen in patients with peripheral atherosclerotic disease by ticlopidine.

Ticlopidine (Ticlodone: CAS 55142-85-3) is able to develop a positive effect on claudication in patients affected by peripheral atherosclerotic disease (PAD). It is also known that ticlopidine decreases fibrinogen levels in plasma. 15 PAD patients treated with ticlopidine for 3 months were studied, evaluating the drug's effect both on maximum walking distance and on fibrinogen. Plasma fibrinogen as coagulable protein, fibrinogen antigen (Partigen method), 125I-fibrinogen survival, euglobulin lysis time and plasminogen were determined with the aim of clarifying if the decrease of plasma fibrinogen induced by ticlopidine is due to an increased destruction of a decreased production of the molecule. The normal levels of all tests before and after therapy both in ticlopidine treated patients and in the control group (acetylsalicylic acid + dipyridamol) indicate that the two hypotheses are not true. It is proposed that ticlopidine developing the known effect in decreasing the binding of fibrinogen to platelets induces a decrease only of activated fibrinogen.

Adult↗
PubMed1991

Fibrinolytic effects of defibrotide in atherosclerotic patients.

Defibrotide is a polydeoxyribonucleotide salt that shows antithrombotic activity through a suggested profibrinolytic mechanism. To study the effectiveness of defibrotide in atherosclerosis, we evaluated the fibrinolytic and coagulation behavior in normal subjects and patients with atherosclerotic disease, before and after single or repeated intravenous defibrotide infusion. A significant shortening of the ELT was found in all subjects. However, since neither t-PA increase nor PAI decrease was observed, we suggest that the profibrinolytic response to defibrotide may be due to mechanisms other than t-PA stimulation. Our results provide further evidence for the usefulness of defibrotide antithrombotic prophylaxis in atherosclerosis.

Arteriosclerosis↗
PubMed1990

1-Desamino-8-D-arginine vasopressin (DDAVP) infusion in type IIB von Willebrand's disease: shortening of bleeding time and induction of a variable pseudothrombocytopenia.

We have investigated the effects of 1-desamino-8-D-arginine vasopressin (DDAVP) infusion on platelet count and bleeding time in 4 patients with type IIB von Willebrand's disease (vWd). Three of four patients showed a normalization of the bleeding time within 1 h after the infusion, while bleeding time was not modified in the fourth. In accordance with the literature, thrombocytopenia was observed after DDAVP infusion, but this thrombocytopenia was due to the anticoagulants used for blood collection. In two patients (F.I., G.F.) no thrombocytopenia was observed when platelets were counted by fingerstick method but there was a 20% platelet decrease in blood samples collected in sodium citrate and a 50% decrease in samples collected in EDTA. Dramatic falls in platelet counts (70-95%) were observed in the additional two patients (C.A., D.Z.) after DDAVP infusion, when both sodium citrate or EDTA were used as anticoagulants. In the latter two patients there was also a 50% decrease in platelet count when the fingerstick method was used. The decrease in the patient's platelet count in EDTA samples after DDAVP infusion could be prevented, in part, by the previous additions of an anti GPIb monoclonal antibody and an anti GPIIb-IIIa monoclonal antibody. Thus, the thrombocytopenia observed in the four IIB vWd patients studied after DDAVP infusion seems to be, at least partially, a pseudothrombocytopenia depending on the calcium concentration in the blood samples and the availability of GPIb and GPIIb-IIIa receptors. These findings and the normalization of the bleeding time observed in three of the four patients has led us to reconsider the possible use of DDAVP in the treatment of our IIB vwd patients.

Anticoagulants↗
PubMed1990

Immunohistochemical localization of factor X-like antigen in pancreatic islets and their tumours.

The authors have investigated by immunohistochemistry the distribution of factor X-like antigen in normal pancreatic islets and in a series of 46 pancreatic endocrine tumours. It was found that both glucagon-producing (A) cells and pancreatic polypeptide-producing (PP) cells are immunoreactive for the antigen. Benign glucagonomas and PP-omas presented the highest concentrations of immunoreactive material whose intracellular distribution was consistent with localization within cell secretory granules. Some benign insulinomas also presented factor X immunostaining in spite of the absence of the antigen in normal insulin-producing B cells. Although malignant tumours usually exhibited very low or no immunostaining, two of three malignant glucagonomas showed scattered, intensely immunoreactive cells. The factor X-like antigen identified in this study was found to differ from chromogranin A and B. The possible implications of the present findings for coagulative disorders associated with glucagonomas or diabetes are discussed.

Adenoma, Islet Cell↗
PubMed1990

Thrombocytosis in young people: evaluation of 57 cases diagnosed before the age of 40.

Over the past 13 years 57 cases of primary thrombocytosis in young people have been studied. Only patients with a platelet count over 500 x 10(9)/liter and a follow-up longer than 2 years were considered. Thrombocytosis in young people represents approximately 25% of total cases referred to our department during this period. The most common causes are essential thrombocythemia (20 cases) and secondary thrombocytosis (22 cases). The highest platelet counts are found in essential thrombocythemia patients. Most of our patients were discovered by a fortuitous hematological examination. In contrast, 5 out of the polycythemic patients were recognized after a thrombosis. The same was true for 2 out of 20 essential thrombocythemia subjects. Four subjects (2 essential thrombocythemia and 2 secondary thrombocytosis) were diagnosed after hemorrhages. The overall survival was very good except for leukemic patients and thrombocytosis secondary to neoplasms. Vascular complications after diagnosis were scarce: 2 polycythemia vera patients showed bleedings during antiaggregating therapy. None of our patients developed epithelial cancer, malignant lymphoma or myelofibrosis. Vascular traumata seem more frequent in polycythemia vera regardless of age. Therefore, it seems useful to treat polycythemic patients, while no therapy seems to be indicated in other forms of thrombocytosis.

Adult↗
PubMed1990

Multiple, relapsing thrombosis in a young man with primary thrombocytosis.

We report the case of a relatively young man with multiple and fatal thrombosis associated with essential thrombocythaemia. The clinical and laboratory examinations performed before his death were in agreement with the diagnostic criteria proposed by PVSG. The autopsy revealed myocardial infarction and pulmonary embolisms. This case suggests that young patients with primary thrombocytosis should be treated with antiplatelet agents in spite of the absence of other thrombotic risks.

Humans↗
PubMed1990

Characterization of polymorphic markers in the von Willebrand factor gene and pseudogene.

Three TaqI restriction fragment length polymorphisms (RFLP) detected by the central portion of von Willebrand factor cDNA, which recognizes the true gene and in addition pseudogenic sequences, were characterized and mapped. Small cDNA fragments which hybridized with DNA from families with von Willebrand disease were used. Two of the RFLP, recognized by 1.7 and 0.45 kb cDNA fragments, are not in linkage either with von Willebrand disease or with RFLP located in the von Willebrand factor (vWF) gene, which indicates their pseudogenic location. These markers located in 22q11, near to the bcr gene, provide new tools for the study of several somatic and constitutional alterations affecting this chromosomal region. The third RFLP is recognized by a cDNA fragment corresponding to the N-terminal portion of mature vWF and is localized in the true gene. Since significant linkage disequilibrium with other informative RFLP is not present, this marker contributes to the definition of family haplotypes associated with von Willebrand disease.

Blotting, Southern↗
PubMed1990

Platelet aggregation and pseudothrombocytopenia induced by 1-desamino-8-D-arginine vasopressin (DDAVP) in type IIB von Willebrand's disease patient.

Our study shows that the thrombocytopenia described in type IIB von Willebrand's disease (vWd) after 1-desamino-8-D-arginine vasopressin (DDAVP) infusion is, at least partially, a pseudothrombocytopenia. There was a discrepancy in platelet counts in blood anticoagulated with EDTA (less than 10 x 10(3)/microliters) or citrate (55 x 10(3)/microliters) in one patient with type IIB vWd and chronic thrombocytopenia (80 x 10(3)/microliters) after DDAVP infusion. Furthermore, DDAVP induced a normalization of patient's prolonged bleeding time. Spontaneous platelet aggregation (SPA) observed in platelet-rich plasma before DDAVP infusion was inhibited completely by monoclonal antibodies which block binding of fibrinogen, vWf and fibronectin to GPIIb-IIIa. SPA was partially inhibited by a monoclonal antibody which blocks the binding of vWf to GPIb. After DDAVP, in contrast, SPA partially persisted in the presence of anti-GPIIb-IIIa monoclonal antibodies but was completely inhibited by anti-GPIb monoclonal antibody. Therefore GPIb and GPIIb-IIIa complex seem to play a different role in SPA before and after DDAVP infusion into type IIB vWd.

Adult↗