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Biomedical subjects

M Zecca

Publications and source records attributed to M Zecca.

81 records · Page 5Linked to original sources
PubMed1989

[Fluoroprophylaxis of dental caries. Current status in the provinces of Genoa and Savona].

A total of 60 pediatricians from the districts of Genova and Savona, randomly selected, responded to a survey designed to determine several aspects of their attitude toward the prevention of dental caries and particularly the use of fluoride supplement (table II). The survey demonstrated (table III) that 80% of the physicians prescribe fluoride without knowing the fluoride content in the water supply of their region. Therefore, the dosage schedule used by 56% of the physicians is higher than the optimal, 27.5% is lower and only 16.5% use the optimal dosage as recommended by the American Academy of Pediatric, Committee on Nutrition.

Adolescent↗
PubMed1987

Kinetic analysis of the interaction of mifentidine with gastric H2-receptors in the conscious dog.

The H2-receptor antagonists mifentidine and cimetidine were compared for their ability to antagonize the activation of H2-receptors in the conscious dog. Dose-response curves to dimaprit in stimulating gastric secretion were displaced to the right in a dose-related fashion by both drugs. Schild and Eadie-Hofstee analysis of these data indicated that mifentidine and cimetidine inhibited in vivo activation of H2-receptors in a manner compatible with competitive surmountable antagonism. Mifentidine displayed a 24fold greater potency than cimetidine as H2 antagonist in the conscious dog.

Animals↗
PubMedDate not supplied

Management of graft-versus-host disease in paediatric bone marrow transplant recipients.

We discuss clinical strategies for the prophylaxis and treatment of both acute and chronic graft-versus-host disease (GVHD) with particular attention to children. Grades II to IV acute GVHD occur in 10 to 50% of patients given an allogeneic transplantation of haemopoietic stem cells (HSCT) from a genotypically HLA-identical donor. A significantly higher incidence and severity of the disease is reported in patients receiving transplants from partially matched family donors or unrelated volunteers. Younger individuals or patients receiving HSCT from younger donors develop GVHD less frequently than do older recipients. Severe acute GVHD is characterised by a significant decrease in survival probability, even though the graft-versus-leukaemia activity associated with both acute and chronic GVHD may reduce the risk of leukaemia relapse. Prophylaxis of acute GVHD usually consists of in vivo post-grafting immunosuppression with cyclosporin alone or in combination with methotrexate; methotrexate alone can be considered in leukaemia patients with a high risk of relapse. In recent years, tacrolimus is increasingly being used instead of cyclosporin, alone or in combination with methotrexate. In vitro T cell depletion in paediatric patients is usually reserved for those with transplants from partially matched family donors or unrelated volunteers. The treatment of patients with grades II to IV acute GVHD should be immediate and aggressive, as the quality and duration of the response directly correlates with survival. The overall response rate to treatment is often unsatisfactory, ranging from 40 to 50% of cases. First-line treatment usually consists of corticosteroids. In patients not responding to corticosteroids, antilymphocyte globulin and monoclonal antibodies directed towards lymphocytes and/or cytokines produced during GVHD are employed, but with variable success. Patients experiencing acute GVHD are also prone to develop chronic GVHD. whose classical treatment is based on the use of cyclosporin and corticosteroids. More recently, encouraging results in the treatment of patients with chronic GVHD have been reported with the use of extracorporeal photochemotherapy. Other drugs, such as ursodeoxycholic acid, etretinate and clofazimine, are under evaluation.

Acute Disease↗
PubMedDate not supplied

Rhabdomyosarcoma with primary osteolytic lesions simulating non-Hodgkin's lymphoma.

We report the case of an 8-year-old child presenting with the pathological fracture of two vertebral bodies due to bone lytic lesions. Physical and instrumental examinations did not show any further evidence of disease. However, bone marrow aspirate showed an infiltrate of poorly differentiated cells. When the child was transferred to the Department of Pediatrics, lymphoblastic leukemia was suspected. Although the morphology of the bone marrow biopsy could have suggested a lymphoblastic lymphoma, further immunochemical and immunological studies together with the study of tissue surface antigens resulted in a diagnosis of embryonal rhabdomyosarcoma with an unusual presentation.

Antigens, Differentiation↗
PubMedDate not supplied

Recombinant human granulocyte-macrophage colony stimulating factor (rHuGM-CSF) in cyclic neutropenia.

We describe the case of a 12-year-old boy affected by cyclic neutropenia, at high risk of developing life-threatening infections, treated with recombinant human granulocyte-macrophage colony stimulating factor (rHuGM-CSF). The drug was effective in reducing the severity of neutropenia and infectious complications in our patient. It was administered for brief periods of time, in contrast to the daily continuous administration reported for rHuG-CSF. Therefore, more extensive studies must be performed to identify the most effective time schedule for the drug. In vitro studies of hemopoietic progenitor cells were useful, in this case, to predict treatment response.

Child↗
PubMedDate not supplied

[Bone marrow transplantation in the treatment of severe aplastic anemia].

Bone marrow transplantation (BMT) in patient affected by severe aplastic anemia (SAA), is successful in 70-80% of cases, when performed with HLA identical brother or syngeneic twin as donors, and in 11-45% of cases when performed from aploidentical-identical related or HLA identical unrelated donor. The different conditioning regimens (Cy alone or in combination with TBI) have shown similar results in the long term outcomes. Cyclosporin-A is very effective in avoiding rejection and controlling GVHD.

Anemia, Aplastic↗
PubMedDate not supplied

Myelodysplastic syndromes: the pediatric point of view.

Myelodysplastic syndromes (MDS) are clonal disorders of the multipotent hematopoietic stem cell characterized by ineffective hematopoiesis and associated with marrow hypercellularity, increased intramedullary cell death and peripheral cytopenias of varying severity. Patients with myelodysplasia have a propensity (20% to 30% of cases) to undergo transformation into acute myeloid leukemia (AML), and a large body of evidence indicates that MDS represent steps in the multiphasic evolution of AML. Progression of the disease is characterized by expansion of the abnormal clone and inhibition of normal hematopoiesis leading to deterioration of the blood cell count and/or development of AML. MDS are relatively unusual in childhood, representing only 3% of pediatric hematological malignancies, although it has been reported that up to 17% of pediatric AML cases may have a previous myelodysplastic phase. The first systematic attempt at morphological classification of MDS was provided by the French-American-British (FAB) group. However, the FAB classification of MDS is only partially applicable in children. Some variants are extremely rare or absent (refractory anemia with ring sideroblasts and chronic myelomonocytic leukemia), and other peculiar pediatric disorders, represented by juvenile chronic myelogenous leukemia (JCML) and the monosomy 7 syndrome, are not included. Moreover, since there is a partial overlap between pediatric MDS and myeloproliferative disorders and the variants occurring in young children have rather specific features, some confusion still surrounds the nosographical definition of childhood MDS, so that none of the proposed classifications are widely accepted and used. Characteristically, some genetic conditions such as Fanconi's anemia, Shwachman's and Down's syndromes predispose to the development of MDS in childhood. The most common variants of childhood MDS are represented by JCML and the monosomy 7 syndrome, both disorders typically occurring in young children. JCML is characterized by a spontaneous growth of granulocyte-macrophage progenitors that show a striking hypersensitivity to granulocyte-macrophage colony-stimulating factor. Clinical presentation resembles that of some myeloproliferative disorders, with massive organomegaly usually not observed in the classically reported variants of MDS. Clinical features of the monosomy 7 syndrome resemble those observed in JCML and a differential diagnosis between these two entities relies upon the higher percentage of fetal hemoglobin, the more pronounced decrease in platelet count and, in some cases, the lack of the peculiar cytogenetic abnormality in the latter. With the number of children being cured of cancer constantly rising, a significant increase in secondary or chemotherapy-related myelodysplasia is being observed, and these disorders represent a formidable challenge for pediatric hematologists due to their poor response to chemotherapy.(ABSTRACT TRUNCATED AT 400 WORDS)

Child↗
PubMedDate not supplied

Itraconazole can increase systemic exposure to busulfan in patients given bone marrow transplantation. GITMO (Gruppo Italiano Trapianto di Midollo Osseo).

Busulfan (BU) is an alkylating drug frequently used to prepare patients for bone marrow transplantation (BMT). Several studies have documented that there is important interpatient variability in BU disposition and systemic exposure, and that other drugs with a common metabolic pathway are capable of influencing BU clearance. We compared the BU pharmacokinetics and pharmacodynamics of 13 patients given BMT and receiving BU and itraconazole, with those of 26 matched controls who did not receive any anti-fungal agent, and with those of 13 matched patients treated with fluconazole as prophylaxis against fungal infections. The effect of itraconazole was best reflected in BU clearance since the BU dose was modified in some patients. BU clearance was decreased by an average of 20% in patients receiving itraconazole as compared to control patients and patients receiving fluconazole (p < 0.01). Mean BU clearance was 7.653 +/- 1.871 l/hr.m2 in the itraconazole patients, 10.103 +/- 2.007 l/hr.m2 in the fluconazole group and 9.373 +/- 1.702 l/hr.m2 in the control group. In this study itraconazole, but not fluconazole, markedly affected the pharmacokinetics of BU as an increase of BU plasma concentrations was observed. The nature of this interaction has not yet been fully characterized. Itraconazole and its analogues are inhibitors of both cytochrome P450 and lipoxygenase and since itraconazole can modulate BU pharmacokinetics, oxidative catabolism is probably a determinant of BU metabolism. This hypothesis should be tested in human metabolic studies.

Adolescent↗