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Biomedical subjects

F Gavosto

Publications and source records attributed to F Gavosto.

At least 55 records · Page 3Linked to original sources
PubMed1981

Idiopathic myelofibrosis: a possible role for immune-complexes in the pathogenesis of bone marrow fibrosis.

Sixteen patients with idiopathic myelofibrosis (IM) have been investigated with respect to the possibility that immune mechanisms may be of importance in the pathogenesis of bone marrow fibrosis. The following points appear relevant: (1) immune-complexes (IC) are detectable with different techniques in a high percentage of patients with IM. Their presence is associated with evidence of bone-marrow histological markers of immune activity. (2) IgG is the main Ig class in the composition of IM IC. The results obtained favour the hypothesis that autoimmune mechanisms are involved in IM patients.

Aged↗
PubMed1981

Immune-complexes (IC) in idiopathic neutropenia.

The presence of immune-complexes (IC) and antipolymorphonuclear neutrophil (PMN) autoantibodies was investigated in 28 patients with chronic idiopathic neutropenia and normal or hypercellular bone marrow, 19 with a metamyelocyte arrest and 9 with more dysplastic features. The in vivo interaction between IC and PMN membrane receptors was evaluated by means of the PMN immunohistological technique. Circulating IC was evaluated with the C1q and rheumatoid factor agglutination inhibition techniques. An anti-PM autoantibody activity was investigated by challenging Fab obtained from the sera of 22 patients with PMN from normal donors. IC were detected in a high percentage of patients; in no case could an anti-PM autoantibody activity be seen. Most patients with a metamyelocyte arrest, but only 1 with more dysplastic features, were IC+. During a follow-up period of l2-52 months, none of the patients with a metamyelocyte arrest (IC+) developed anaemia, thrombocytopenia or leukaemia, while anaemia and thrombocytopenia were almost the rule in the clinical course of dysplastic bone marrow IC- patients: 2 of them developed acute myeloblastic leukaemia.

Adult↗
PubMed1980

Different kinetic pattern of chronic myeloid leukemia: lymphoblastic and myeloblastic blastic crisis.

Cell kinetic studies were performed in 8 case of lymphoid blastic crisis (BC) of chronic myeloid leukemia at the onset of BC and during subsequent relapses. The results were compared with those found in 7 myeloblastic BC. While in the myeloblastic transformation the labeling index (LI) was always higher in bone marrow than in peripheral blood blasts, suggesting a predominant bone marrow proliferation of the leukemic cells, in the lymphoid transformation a higher LI was often found in peripheral blasts. Moreover, the lymphoblastic transformations were frequently characterized by lymphadenopathy. These findings point to the similarities between lymphoid BC and acute lymphoblastic leukemia, suggesting the possibility that a blastic event may originate in an extramedullary site and that an extramedullary BC is more likely to be lymphoid in nature.

Adult↗
PubMed1980

Immune complexes in aplastic anaemia.

Immune complexes (IC) have been detected in nine out of 15 patients presenting with idiopathic aplastic anaemia using the polymorphonuclear neutrophil immunohistochemical technique. Immunosuppressive treatment undertaken in one patient produced a gradual recovery, the bone marrow repopulation being paralleled by the disappearance of IC. The significance of IC in aplastic anaemia and the relationship with possible pathogenesis and therapy of the disease are discussed.

Adult↗
PubMed1980

Insensitivity of chronic myeloid leukemia cells to inhibition of growth by prostaglandin E1.

The influence of E prostaglandins on the in vitro growth of chronic myeloid leukemia (CML)-committed granulopoietic precursors [colony-forming unit-culture (CFU-C)] has been investigated in a double-layer agar system in which CFU-C growth was stimulated by adherent monocytes. Addition of the prostaglandin synthesis inhibitor indomethacin to the feeder layer significantly increased the number of normal CFU-C, whereas CML CFU-C were unaffected. Exogenous prostaglandin E1 inhibited CML CFU-C growth at concentrations 1000-fold higher than those necessary to produce a similar effect on normal CFU-C. These data point to a lower than normal sensitivity of CML-committed granulopoietic precursors. It is suggested that derangement of the responsiveness of CML cells to prostaglandin regulation may play a role in the pathogenesis of uncontrolled leukemic proliferation.

Bone Marrow↗
PubMed1980

The role of immune complexes in blood disorders.

The aim of this review is to prevent the role of immune complexes (IC) in blood disorders. Fundamental to this role are the multiple interactions among IC and humoral and cellular receptors which give origin to several biologically active compounds and to profound metabolic, functional, and morphological changes in the involved cells. The end product of all these interactions may be both a phlogistic process and an alteration of blood cells. On this basis, clinical and experimental evidence is provided to demonstrate that IC may be produced as a consequence or a side effect of blood disorders (explaining some peculiar disturbances or proving to be of prognostic importance) or may even be the primary pathogenetic event.

Agranulocytosis↗
PubMed1979

Idiopathic neutropenia with normocellular bone marrow: an immune-complex disease.

The presence of circulating immune-complexes (IC) and their in vivo interaction with polymorphonuclear neutrophils (PMN) have been detected in two cases of idiopathic neutropenia with normocellular bone marrow. The injection of patients' sera into New Zealand White rabbits caused a striking neutropenia due to sequestration of PMN in the vascular bed of kidneys and lungs. The kinetics of PMN disappearance from peripheral blood and the pattern of sequestration overlapped that induced by the injection of pre-formed soluble IC. Treatment with plasmapheresis caused an early and lasting increase of PMN; rabbit PMN were almost unaffected by the injection of patient serum after the course of plasmapheresis. These data are consistent with the possibility that idiopathic neutropenia with normocellular bone marrow may be caused by persistent in vivo interaction between IC and circulating PMN.

Adult↗
PubMed1978

Kinetically oriented manipulation of drug management in acute leukaemia.

The evaluation of the kinetic characteristics of the blast population in AL, at the outset of the disease, establishes its growth rhythm and hence the degree of invasivity. Cases with a higher 3H-Tdr labelling index also display a higher growth fraction, birth and growth rates and a shorter generation time, in other words, greater cell growth potential and invasivity. The labelling index could thus represent an immediate guide to prognosis. Particularly when combined with other prognosis factors, it can be employed to divide AL into high and low growth and invasivity forms. A distinction of this kind can thus be made the basis of differentiated therapeutic programming, whereby more or less aggressive cytocidal drug associations and doses can be administered to improve the therapeutic index and the quality of life.

Acute Disease↗
PubMed1976

Persisting production of out-of-cycle blasts during methotrexate therapy in acute leukaemia.

Kinetics of the blast populations in two cases of acute lymphoblastic leukaemia during treatment with methotrexate have been studied in vivo. Beside a striking cytocidal effect on blasts arrested in the S phase and a synchronization and a slowing of those in the G2 phase, the most important finding was the persistence of a flux of drug-affected cells from the proliferation of the non-proliferating compartment. Some of these non-proliferating cells were able to re-enter subsequently the mitotic cycle. This fact can explain why a cell-cycle-specific drug fails to eradicate completely acute leukaemic cells in man.

Adult↗
PubMed1975

L-1210 and human acute leukemia kinetics as related to therapy.

Comparative considerations are made between human acute leukemia (AL) and mouse transplantable L-1210 leukemia. The main kinetic parameters, such as the growth fraction (GF), growth rate, and cell cycle times, of both human and mouse diseases, are compared. The striking differences in cell kinetics and in response to treatment may be viewed as depending on different leukemogenesis mechanisms. Therefore, some improvement in human AL chemotherapy is considered possible both by researching a more rational employment of cytostatic drugs, and studying other animal models quite similar to the human disease, such as AKR leukemia.

Acute Disease↗