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Biomedical subjects

T Tison

Publications and source records attributed to T Tison.

At least 19 recordsLinked to original sources
PubMed2003

Association of monoclonal gammopathy and polycythemia vera or essential thrombocythemia: study of a large cohort of patients.

Concomitant cases of monoclonal gammopathies with polycythemia vera (PV) and essential thrombocythemia (ET) have been described. We report our experience in a large cohort of patients with ET and PV and the occurrence of M protein in such a population. Retrospective evaluation of clinical and laboratory records of 164 patients with PV and 218 with ET was performed, and 500 subjects matched for sex and age were used as controls. The patients were divided into group A (younger than 55 years), group B (55-70 years), and group C (over 70 years), and the presence of M protein was sought at the time of diagnosis and later during follow-up. M protein was found in 14 patients with myeloproliferative disorders (MPDs), representing 3.6% of patients both with ET and PV, and in 10 subjects of the control group (2%). M protein was detected in 2.1% of MPD patients of group A, in 4.8% of group B, and in 5.7% of group C and in 1.6% of controls of group A, 2.7% of group B, and 2% of group C. No significant statistical difference was observed. The occurrence of M protein in PV and ET does not seem to differ from that observed in the control group. A more relevant increase in the incidence of M protein in MPDs than in the controls was observed by dividing patients and controls by age. However, no statistical significant difference was documented.

Adolescent↗
PubMed1999

Serological markers of autoimmunity in patients with hemophilia A: the role of hepatitis C virus infection, alpha-interferon and factor VIII treatment in skewing the immune system toward autoreactivity.

The aim of this study was to investigate whether the immune system of patients with hemophilia A is skewed toward an aspecific activation and to identify the causative factors. It is well known that an immune derangement does exist in patients with hemophilia A. At least three factors potentially play a role: hepatitis C virus (HCV) infection, alpha-interferon therapy and the administration of factor VIII (FVIII). Sixty human immunodeficiency virus (HIV)-negative patients with severe or moderate hemophilia A were studied retrospectively. The serological markers of autoimmunity were evaluated and the results correlated with anti-HCV antibodies, FVIII treatment and alpha-interferon therapy. The role of these factors in the development of the anti-FVIII antibody was estimated concomitantly. The prevalence of autoantibodies and anti-FVIII antibodies was higher in HCV-positive than in HCV-negative patients before any treatment, although the difference was not statistically significant. The administration of FVIII further influenced the development of autoantibodies both in HCV-negative and HCV-positive patients, with no difference being observed between the two groups. As expected, fewer HCV-negative than HCV-positive patients developed anti-FVIII antibodies after administration of FVIII (31.8% versus 38%, respectively). Therapy with alpha-interferon did not seem to enhance significantly the risk of developing autoantibodies nor anti-FVIII antibodies. We observed a high prevalence of humoral signs of autoimmunity among patients with hemophilia A. Treatment with FVIII concentrate is probably the most important triggering factor. Monitoring these patients for autoimmune manifestations is recommended.

Adolescent↗
PubMed1998

Myasthenic syndrome and oligoclonal lymphocytosis: evolution into chronic lymphocytic leukemia.

We report a patient with myasthenic syndrome who, 2 years after diagnosis, developed an oligoclonal lymphocytosis. This disorder was sustained by both kappa+ and lambda+ CD5+ B-cell clones; over the following year, the white blood cell count increased and phenotypic characterization revealed a clear imbalance in the immunoglobulin light chain ratio (84% kappa+). Accordingly, persistence of a kappa+ B-cell clone was disclosed by molecular analysis of immunoglobulin heavy chain gene rearrangements. Our results may suggest that prolonged immune system stimulation due to an autoimmune disease can drive a benign lymphoproliferation into a B-cell neoplastic process.

B-Lymphocytes↗
PubMed1998

Detection of B-cell monoclonality in fine needle aspiration by PCR analysis.

Cytologic examination of fine-needle aspiration (FNA) sometimes fails to diagnose the malignant nature of B-cell proliferations. In this study we analyzed the Ig gene rearrangement of 49 FNA samples by polymerase chain reaction (PCR) in order to evaluate whether molecular analyses can improve the accuracy of FNA. Twenty-six patients had non-Hodgkin's lymphoma, 11 had reactive lymphoid diseases, 5 had chronic inflammation and 7 had carcinoma. A semi-nested PCR was performed using an oligoprimer specific for consensus sequences of the V regions (FR3A) and two oligoprimers derived from conserved sequences of the J regions (LJH and VLJH). Histologic examination always followed the molecular and cytologic analysis. The sensitivity of PCR and FNA morphological examination in detecting a neoplastic pattern was 92% and 78%, respectively. When samples were considered inadequate for cytologic examination, PCR always reached a diagnosis consistent with the histologic features. Our results demonstrate that PCR analysis of FNA specimens is a reliable and sensitive method capable of enhancing the diagnostic accuracy of cytologic examination.

B-Lymphocytes↗
PubMed1997

Prevalence of anti-FVIII antibodies in severe haemophilia A patients with inversion of intron 22.

The aim of our study was to investigate whether haemophilia A patients with inversion of intron 22 are at high risk for non-inhibitory anti-FVIII antibodies development detected by ELISA. It is known that patients with severe forms of haemophilia A are more likely to develop anti-FVIII antibodies. The incidence of inhibitory anti-FVIII antibodies in patients with factor VIII gene inversion has been extensively evaluated, but if this defect has to be considered a predisposing factor is still debatable. Non-inhibitory anti-FVIII antibodies are attracting interest, due to the potential influence on FVIII half-life. Our data show that FVIII gene inversion was a major predisposing factor for anti-FVIII antibodies development.

Adolescent↗
PubMed1996

High incidence of anti-FVIII antibodies against non-coagulant epitopes in haemophilia A patients: a possible role for the half-life of transfused FVIII.

The occurrence of antibodies (Abs) capable of inhibiting factor VIII (FVIII) coagulant activity is a severe complication in haemophilia A, leading to the inhibition of transfused FVIII activity. It is not known whether, or to what extent, post-transfusion antibodies may also arise against non-coagulant epitopes. Therefore we set up a system capable, in theory, to detect all the FVIII-induced antibodies by use of an enzyme-linked immunoassorbent assay (ELISA) based on coating human recombinant FVIII onto polystyrene microtitre plates. Serum samples from 23 patients affected by haemophilia A of different gravity (22 referred to our Centre and one to the Bari Centre) were analysed. Although only one patient was positive at Bethesda assay, the presence of antibodies in ELISA was detected in 39% of patients in variable degrees; transfusion with FVIII was found to induce a raise in antibody titre, arguing in favour of the specificity of the phenomenon. The clinical relevance of these non-inhibitory antibodies was evaluated in three patients; although half-life did not show any change in the patients without or with low amount of antibodies, FVIII clearance was found enhanced in the patient displaying high titre antibodies. We propose detection of anti-FVIII antibodies by ELISA when routinely assessing haemophilia A patients.

Adolescent↗
PubMed1995

CD25-negative hairy cell leukaemia: intracytoplasmic detection of Tac antigen and interferon-induced surface expression.

Hairy cell leukaemia (HCL) is a chronic lymphoproliferative disease of B-cell lineage. One of the peculiar immunophenotypic markers is the strong expression of the p55 chain of the interleukin-2 receptor (IL2R), recognized by anti-CD25 (or anti-Tac) monoclonal antibody. However, it is known that in rare cases CD25 may not be detectable, even when variant forms of HCL are excluded. The possibility has not been investigated that in these situations CD25 is present in the cytoplasm of the neoplastic cells. This paper describes a case in which the clinical, histological, and electron microscopic features were consistent with a typical HCL. Immunophenotype analysis showed the whole spectrum of markers of HCL, except for the expression of IL2R. The soluble form of the molecule was, however, increased in the patient's serum. Cytospin staining of the neoplastic B cells with anti-CD25 clearly demonstrated the presence of IL2R in the cytoplasm of hairy cells. When the cells were cultivated in vitro in the presence of interferon-alpha 2b, CD25 was detectable at the membrane level. These findings suggest that at least some cases of CD25-negative HCL may express cytoplasmic IL2R.

Aged↗
PubMed1995

Failure of B cells of chronic lymphocytic leukemia in presenting soluble and alloantigens.

B-cell-type chronic lymphocytic leukemia (B-CLL) patients have immunological abnormalities of both B and T lymphocytes. Since T cell defects might depend upon a defective accessory function of neoplastic B lymphocytes, we analyzed the ability of peripheral blood B cells of seven B-CLL patients to stimulate allogenic normal T cells in mixed lymphocyte reaction (MLR) and to present tetanus toxoid (TT) to autologous T cells. In both systems, neoplastic B lymphocytes show a defective antigen-presenting function, which is more evident with disease progression. Such a defect cannot be ascribed to a decreased MHC class II molecule expression nor to an abnormal IL-1 beta production, but it can be partially accounted for by a low B7 expression. Pretreatment of neoplastic B cells with interleukin-4 (IL-4) restores primary MLR, but has little effect on the response to TT. The effect of IL-4 is not mediated by quantitative modifications of class II and B7 molecule expression or of IL-1 beta production.

Antigen Presentation↗
PubMed1993

Prevalence of specific thrombotic accidents in patients with thrombocytosis.

The prevalence of specific thrombotic accidents recognized in 260 patients with thrombocytosis are reported. Ninety one were affected by PV, 86 by ET, 20 by MF and 63 by ST. The highest incidence of thrombosis was in the PV group. About half of ET and MF patients experienced a thrombosis. In all the patients thrombosis preferentially affected the cerebrovascular district (17.3% of the cases). Coronary artery disease occurred in PV while peripheral vascular disease was frequent in ET. Portal vein district thrombosis is not rare during the course of all MPD (7.1%). Apparently, deep vein thrombosis occurs in all patients with both primary and secondary thrombocytosis.

Adult↗
PubMed1991

Use of a radioimmunoassay for 5-hydroxytryptamine (5-HT) in thrombocytosis.

A decrease in intra-platelet 5-hydroxytryptamine (5-HT) may be a possible marker for primary thrombocytosis and there are several different methods for the measurement of platelet 5-HT content (e.g. fluorimetry, high-performance liquid chromatography and radioimmunoassay). The present study has shown that, in laboratories with radioprotected areas, radioimmunoassay of 5-HT is a simple method which correlates well with a standard fluorimetric technique and yields satisfactory results in patients with thrombocytosis.

Adult↗
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

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↗