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Biomedical subjects

G Fiandino

Publications and source records attributed to G Fiandino.

26 records · Page 2Linked to original sources
PubMedDate not supplied

[Bone marrow aplasia].

Aplastic anaemia is a haematological syndrome in which pancytopenia is due to a depletion, damage of inhibition of hemopoietic stem cells. The pathogenetic factors are still unclear: damage or inhibition of hemopoietic stem cells may be direct or indirect mediated through changes in the cellular humoral environment; evidence is accumulating that in some cases these processes are of autoimmune nature. The prognostic evaluation is based on hematological parameters at diagnosis: severe aplastic anemia (SAA) is defined by the following criteria: neutrophils less than 0.5 X 10(9)/l; reticulocytes less than 0.5 X 10(9)/l and platelets less than 20 X 10(9)/l. Survival rates in children with SAA are poor; the probability of survival at 1 year from diagnosis being 10%. In this form treatment is based on supportive therapy (transfusion and prevention of infections) and on a specific therapy: immunosuppression and/or BMT. BMT is reserved to patient with an HLA identical sibling donor and may be curative in 70-80% of cases. To date the use of antilymphocytoglobulin in SAA has also given satisfactory results with a favorable response in 50-60% of cases.

Anemia, Aplastic↗
PubMedDate not supplied

[The glucose-6-phosphate dehydrogenase/6-phosphogluconate dehydrogenase ratio in the identification of glucose-6-phosphate dehydrogenase heterozygosity].

Deficiency in human G-6PD is a widespread X-linked disorder, which is mainly characterized by susceptibility to hemolytic anaemia after the ingestion of certain drugs or toxic substances (e.g. pyrimidine derivates contained in fava beans). G-6PD deficiency in hemizygous males in easily detectable since enzymatic activity is almost absent. In heterozygous subjects the determination of enzymatic activity on red cell lysate cannot detect a partial G-6PD deficiency. Cytochemical methods as methemoglobin reduction test or tetrazolium reduction test are more sensitive than spectrophotometric quantitative test, but are not suitable for screening purposes. We measured both G-6PD activity and 6-PGD activity in G-6PD heterozygous females and we evaluated the G-6PD/6PGD ratio. We tested this ratio also in thalassemic traits and in G-6PD heterozygotes with thalassemic trait in order to detect the interference of thalassemic pathology with the phenotypic expression of the gene for G-6PD. We found that the mean G-6PD values were statistically reduced in G-6PD heterozygous females; on the contrary the measurement of true G-6PD activity alone is not a good tool for discriminating heterozygous subjects with and without thalassemic trait. Actually 100% and 79% of values observed were in the normal range +/- 2 DS respectively. The mean G-6PD/6-PGD ratio in heterozygotes for G-6PD deficiency with and without thalassemic trait was lower than normal and the individual values of G-6PD/6-PGD ratio were in the normal range +/- 2 DS only in a few subjects (8.3% and 10.7% respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

[Therapy of idiopathic thrombocytopenic purpura].

Various treatment strategies for acute and chronic idiopathic thrombocytopenic purpura (ITP) in childhood are reviewed. In acute ITP steroids induce a prompt improvement of symptoms and a rapid increase in platelet count; the use of high dose intravenous immunoglobulin is a valid alternative treatment to steroids. In chronic ITP splenectomy is still the most successful treatment, as it induces remission in 60-80% of patients. The risk for severe infections after splenectomy is still considerable in children; therefore other treatment schedules are suggested (i.v. immunoglobulin, courses of steroids, high dose methylprednisolone). In this paper we report 100 pediatric cases with acute ITP and 36 with chronic ITP.

Acute Disease↗
PubMedDate not supplied

[Acute non-lymphatic leukemia in children].

40 children (23 males, 17 females) have been diagnosed have ANLL during the period from february 1970 to september 1981. According to FAB classification, 24 cases were M1,-M2, 9 M3, 3 M4, 3 M5 and 1 M6. At diagnosis, 20 patients (50%) had leukocytes less than 10.000/mmc, 6 (15%) had leukocytes greater than 50.000mmc. Hb levels was 7 g% in 16 patients (40%); 10 children had hepatosplenomegaly (25%), 7 splenomegaly (18%) and 5 lymphoadenomegaly (13%). 4 patients had cutaneous or mucous infiltrates. None had meningeal involvement at diagnosis. According to the year of diagnosis, 3 groups can be identified. In the group I (1970-73), 11 patients have been treated with not codified combination chemotherapy as ARA-C, 6-TG, DNR, CTX, Metil-GAG. In the group II (1974-76) and in the group III (1977-81), the patients (respectively 12 and 17) have been treated according to the following protocols: LAM-5 (3), TRAP (5), COAP (1), LAM 80 (2), AIL 7402 (8), AIL 7604, AIL 7801 (6). Immunotherapy has been performed in 7 cases. CNS prophylaxis (MTX i.t. +/-ARA-C +/- RT) was given in 5 patients of group II and in 6 of group III. I patients of group I (45%), 6 of group II (50%) and 13 of group III (76%) achieved CR. Median duration of remission was 5 months in the group I and in 17 in group II and III.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗