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Biomedical subjects

L Virgolini

Publications and source records attributed to L Virgolini.

At least 19 recordsLinked to original sources
PubMed1995

Incidence and diagnosis of EDTA-dependent pseudothrombocytopenia in a consecutive outpatient population referred for isolated thrombocytopenia.

Among 111 patients referred to our outpatient clinic for isolated thrombocytopenia during a 24-month period, 17 (15.3%) cases of EDTA-dependent pseudothrombocytopenia (EDTA-PTCP) were identified. EDTA-PTCP represented the second most frequent cause of thrombocytopenia in this population. The diagnosis was confirmed by the following findings: (a) normal platelet numbers immediately after blood withdrawal; (b) progressive fall of platelet counts and evident platelet clumping over time, only in EDTA-anticoagulated blood. A simple, inexpensive and quick diagnostic method was devised, that consists in evaluating the platelet number in a blood sample anticoagulated with EDTA immediately after blood withdrawal and 4 h later.

Adult↗
PubMed1995

Granulocyte colony-stimulating factor (G-CSF) allows the delivery of effective doses of CHOP and CVP regimens in non-Hodgkin lymphomas.

The aim of this study was to evaluate the role and potential benefit of G-CSF administered following standard regimen chemotherapy (CHT) in non-Hodgkin lymphomas. Twenty patients with NHL were given CHOP or CHOP/CVP CHT every 21 days. None was given G-CSF after the first cycle. After each cycle, G-CSF was administered only for: 1) ANC < 1 x 10(9)/L between cycles; or 2) delay in cycle schedule due to ANC < 1 x 10(9)/L on the planned day of treatment; or 3) development of a febrile syndrome or a documented infection, regardless the ANC. Once administered, G-CSF was maintained in the following cycles. Nineteen patients required administration of G-CSF (5 micrograms/Kg B.W.), but for different reasons only 16 were treated (a mean of 10 +/- 3 doses/cycle). Comparing 48 cycles where G-CSF was not administered, with 50 where it was, in this last group we observed: 1) a ANC significantly higher at day 7 (p < 0.0001), day 14 (p < 0.0001) and day 21 (p = 0.0030); 2) a significantly lower (p = 0.0001) incidence of neutropenias (6 vs 29); 3) a trend (p = 0.1040) in favour of lower incidence of febrile neutropenias of infections (1 vs 6); 4) a significantly lower (p < 0.0001) incidence of cycle delays (1 vs 22) with a median of 8 days (1 to 20); and 5) a significantly higher (p < 0.0001) dose intensity (99.5% vs 87.8%).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

The role of granulocyte colony-stimulating factor (filgrastim) in maintaining dose intensity during conventional-dose chemotherapy with ABVD in Hodgkin's disease.

BACKGROUND: The aim of the study was to evaluate the role and potential benefit of granulocyte colony-stimulating factor (G-CSF, Filgrastim), administered following cytotoxic chemotherapy with the ABVD regimen in Hodgkin's disease, in maintaining cycle schedule and dose intensity and in decreasing neutropenia and number of infections. PATIENTS AND METHODS: Twenty-two patients affected by high-risk Hodgkin's disease (14 localized and 8 diffuse), aged 15 to 69 years (median, 34), were given ABVD chemotherapy for a total of 6 courses (for the purpose of this study, each single course of chemotherapy was considered as two 15-day periods). No patient was given G-CSF after the first cycle. After each cycle, G-CSF was administered only for: 1)absolute neutrophil count < 1 x 10(9)/L between cycles; 2) delay in cycle schedule due to an absolute neutrophil count < 1 x 10(9)/L on the planned day of treatment; or 3) fever or a documented infection, regardless the absolute neutrophil count. Once administered, G-CSF was maintained in the subsequent cycles. RESULTS: Seventeen of 22 patients (77%) required the administration of G-CSF (5 micrograms/kg b.w.; a median of 5 doses/cycle); most of them (13/17) before the 5th dose of chemotherapy. The main reason for introducing G-CSF into therapy was neutropenia during the interval between courses (n = 4) or on the planned day of treatment (n = 11). Comparing 112 courses where G-CSF was not administered with 124 where it was, in the latter group we observed: 1) a significantly lower (P = 0.0002) incidence of cycle delays (0 vs 13), with a median delay of 7 days (5 to 11). The main reason for cycle delay was neutropenia (n = 13); 2) a greater dose intensity delivered to the patients while on G-CSF (100% vs 95.2 +/- 8.8%; P = 0.0001); 3) an absolute neutrophil count significantly higher at day 8 (P < 0.0001) and day 15 (P < 0.0001); 4) a significantly lower (P = 0.0003) incidence of neutropenia (2 vs. 17). No difference in the incidence of infections was observed between the two groups of cycles (P = 0.5889), but the duration and severity of the same were greater during chemotherapy without G-CSF, requiring antibiotic therapy and causing cycle delay. CONCLUSIONS: In conclusion, our data suggest the use of Filgrastim in Hodgkin's disease also during conventional-dose chemotherapy with ABVD. It is not required from the first dose of therapy, but as soon as neutropenia appears between cycles or on the planned day of treatment. Then, its use allows maintenance of the chemotherapy schedule and dose intensity. It also decreases frequency, duration and severity of neutropenia and its sequelae.

Adolescent↗
PubMed1993

Infections in patients with acute non-lymphocytic leukemia nursed with central or peripheral venous access.

AIMS AND BACKGROUND: Infections are a major problem in patients undergoing induction chemotherapy for acute leukemia. Granulocytopenia is the single most important risk factor, but the pattern of infecting organisms can change according to nursing facilities or bacterial and fungal prophylaxis. METHODS: We reviewed the patterns and types of infections in 30 patients with acute non-lymphocytic leukemia. Eighty-nine periods of neutropenia following chemotherapy were evaluated: in 60 courses patients had central and in 29 had peripheral venous access. RESULTS: Almost all patients (97%) became febrile after the 1st course of therapy, but one-third remained apyretic after the fourth course (P = 0.002). In this series, the incidence of gram-positive, gram-negative and mycotic isolations were respectively 76%, 18% and 6%. The need for antimicrobic treatment varied in relation to the course of chemotherapy. CONCLUSIONS: We conclude that in acute non-lymphocytic leukemia the first neutropenic period following the onset of disease is the most critical regarding infectious problems. Both quinolonic prophylaxis and central venous access could be responsible for the microbiologic findings.

Adolescent↗
PubMed1993

[Gaucher's disease: study of a family from Friuli].

Gaucher's disease is the most frequent of lysosomal storage diseases. In a family study two affected sisters of a type I patient were identified. Two of them underwent splenectomy, so reaching hematological normalization.

Female↗
PubMed1993

[Update on Gaucher's disease].

Gaucher's disease is a lipidosis caused by deficiency of the enzyme glucocerebrosidase (glucosylceramidase) with secondary accumulation of glucocerebrosides in macrophage lysosomes. Three clinical forms of the disease have been described with autosomal recessive genetic basis. They are caused by many different mutations in glucocerebrosidase gene which have been recently identified. The infantile (type III) and juvenile (type II) forms involve the central nervous system and are very rare. Type I is a non neuronopathic form and is the most common lysosomal storage disease, reaching an incidence of 1 in 2500 births among Ashkenazi jews. Clinical manifestations include splenomegaly and hypersplenism, while bone and lung involvement are less common. Most patients have a mild course and a normal life expectancy, but some others suffer for heavy bone pain that greatly inhabilitate them. A distinctive storage cell is present in bone marrow, but diagnostic confirmation is based upon leucocytes or fibroblasts enzyme assay. Total or partial splenectomy is the treatment of choice for correcting hematological abnormalities. Allogeneic bone marrow transplantation was successfully employed in some cases, while studies on retroviral-mediated gene transfer are undergoing. Promising clinical results were obtained in last two years by chronic infusion of purified macrophage-targeted glucocerebrosidase enzyme. New experience is required in selecting patients for this expensive regimen and establishing duration of therapy.

Gaucher Disease↗
PubMed1990

Late presentation of metastatic pheochromocytoma: a problem case solved by I-131 MIBG scintigraphy.

A patient presented with recurrent pheochromocytoma 10 years following the apparently successful surgical cure of a right adrenal pheochromocytoma. Conventional medical imaging techniques, (chest radiograph, abdominal ultrasound, and abdominal CT) suggested local recurrence for which surgery was planned. I-131 MIBG scintigraphy revealed disseminated metastatic disease that rendered attempts at surgical cure futile. The patient was treated with three therapeutic doses of I-131 MIBG with good symptomatic palliation and improvement of some biochemical parameters.

3-Iodobenzylguanidine↗
PubMed1990

[Hypercalcemia and neoplasms: recent advances in pathogenesis].

The mechanisms of paraneoplastic hypercalcemic syndromes are heterogeneous. Neoplastic hypercalcemia without bone metastatic disease is caused by parathyroid hormone related protein, whose action is comparable to parathyroid hormone. Growth transforming factors, platelet derived growth factor, tumor necrosis factors and interleukin 1 are also involved in humoral hypercalcemia of malignancy. In addition to these substances, hypercalcemia in bone metastatic disease may be related to PGE. Tumor necrosis factors and interleukin 1 play a major role in multiple myeloma as well as in Adult T cell Leukemia/Lymphoma where overproduction of vit D3 by lymphomatous cells can also be significant.

Bone Neoplasms↗
PubMed1985

[Neutrophil leukemia. Review of the literature].

Chronic neutrophilic leukemia is a rare form of myeloproliferative disorders, with only sixteen reports in literature. Neutrophilic leukocytosis, bone marrow myeloid hyperplasia, elevated leukocytic alkaline phosphatase and the absence of Ph1 are the most import features. In this paper all the cases previously described are reviewed and diagnostic criteria and therapeutic results are outlined.

Adult↗
PubMed1984

[Acute promyelocytic leukemia. Review of the literature].

Acute promyelocytic leukemia is characterized by bone marrow infiltration with hypergranular promyelocytes, often with Auer bodies. Clinically it is characterized by a hemorrhagic syndrome caused by a disseminated intravascular coagulation. Karyotypic studies have shown a frequent translocation t(15;17). Improved prognosis resulted from chemotherapy with DAT and treatment with heparin.

Acute Disease↗
PubMed1984

[Snake bite disease. Review of the literature].

The aetiology, the epidemiology and the pathogenesis of poisoning by viper bites in Italy are outlined. The symptomatology and therapy are also described, and it is noted that antivenom must be reserved for some selected cases.

Adolescent↗
PubMed1976

Combined hereditary deficiency of factors VII and VIII: a distinct coagulation disorder due to the 'lack' of an autosomal gene controlling factor VII and VIII activation?

A patient with a combined hereditary deficiency of factors VII and VIII is presented together with a family study. The main bleeding manifestations were easy bruising and bleeding after tooth extractions. No hemarthrosis was ever observed. The main laboratory features consisted in a mild prolongation of prothrombin time and of partial thromboplastin time. TG test was abnormal and was corrected by the addition of adsorbed normal plasma. Specific assays revealed a moderate defect of factors VII and VIII. All other clotting factors were within normal limits. The factor VII antigen in the propositus was normal or nearly normal. The factor-VIII-associated antigen was also normal. Five additional family members presented the same coagulation pattern and were variably symptomatic. The hereditary transmission pattern seems to be autosomal dominant. The defect appears to be due to a structural abnormality of a gene controlling factors VII and VIII activation.

Adult↗
PubMed1975

The effect of heparin on platelet aggregation by common inductors and by ristocetin in congenital bleeding disorders due to factor VIII or fibrinogen defects.

Platelet aggregation by various inductors was studied in citrated and heparinized plasma of the following groups of subjects: Normal, hemophilia A, combined factor V and factor VIII deficiency, v. Willeprand's disease and congenital afibrinognemia. The results may be summarized as follows: A-platelet aggregation in citrated plasm 1) platelet aggregation by common inductors ADP, adrenalin and collagen was normal in all groups of subjects but for the patients with congential afibrinogenemia in whom adrenalin induced aggregation was absent or markedly refuced whereas ADP and collagen gave slightly reduced or near normal aggregation curves. 2) platelet aggregation by ristocetin was normal in all groups of subjects but for v. Willebrand's disease in which it was absent. B-platelet aggregation in heparized plasma. 1) platelet aggregation by common inductors resulted to be normal in all groups of subjects except in congenital afibrinogenemia. In this latter case the pattern was still mildly defective but here was an increased aggregation as compared to citrated plasma. These findings have been interpretemmon inductors. 2) platelet aggregation by ristocetin resulted to be absent in all groups of subjects investigated. The possible mechanism of action of the inhibitory effect exercised py heparin with regard to restocetin is discussed.

Adenosine Diphosphate↗
PubMed1975

Failure of ellagic acid to affect platelet aggregation in normal and in factor XII deficient plasma.

Ellagic acid solutions, regardless of the concentration, failed to alter platelet aggregation induced by ADP, Adrenalin, Collagen, Thrombofax and Ristocetin in normal and in factor XII deficient plasma. A moderate inhibition was noted after addition of ADP both in normal and in factor XII deficient plasma but this was present also in the control systems and was therefore due to the buffer-dextrose solution and not to ellagic acid. These data indicate that Hageman factor plays on role in platelet aggregation.

Adenosine Diphosphate↗
PubMed1975

Platelet adhesiveness and aggregation in congenital afibrinogenemia. An investigation of three patients with post-transfusion, cross-correction studies between two of them.

Platelet adhesiveness and aggregation were studied in three patients with congenital afibrinogenemia. The results obtained may be summarized as follows: The retention of platelets to a glass-bead filter determined with the Salzman method was significantly decreased; it was normal after fibrinogen infusion. With a modification of the Hellem test the values obtained were slightly decreased. Adrenalin-induced aggregation was absent whereas ADP-and collagen-induced aggregation was near normal or slightly decreased. Thrombofax aggregation was absent in citrated plasma. The abnormalities of platelet aggregation were corrected after fibrinogen infusion or after addition in vitro of fibrinogen, hemofilia A plasma and PPP obtained from an afibrinogenemic patient after fibrinogen infusion. The abnormalities of platelet aggregation were corrected well by ADP, collagen and Thrombofax in heparinized blood, but only a slight correction of adrenalin-induced aggregation was noted. Thrombin aggregation proved to be normal with the higher concentrations, whereas it was defective with the lower ones. Ristocetin aggregation was normal in citrated plasma at the concentration of 1.5 mg per ml but it was absent at the lower concentration (1.0 mg per ml). Ristocetin aggregation was, on the other hand absent in heparinized blood regardless of the concentration. These findings are in agreement with the presence of a prolonged bleeding time in congenital afibrinogenemia and suggest that fibrinogen plays an important role in platelet aggregation and adhesiveness.

Adenosine Diphosphate↗