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Biomedical subjects

L Gugliotta

Publications and source records attributed to L Gugliotta.

At least 73 records · Page 4Linked to original sources
PubMed1985

Release of platelet-activating factor in human leukemia.

Cellular release of platelet-activating factor (PAF) was assessed in a series of human acute and chronic lymphoid and myeloid leukemias at presentation or in an active phase of the disease. PAF-like material, showing physicochemical properties similar to those of synthetic PAF and of PAF released from IgE-sensitized rabbit basophils, was found in cultures of cells from 5 of 6 acute lymphoblastic leukemias (ALL) (2 of 2 T-ALL and 3 of 4 common ALL) and from 13 of 24 B-cell chronic lymphocytic leukemias after stimulation with ionophore A23187 with or without phytohemagglutinin in the presence of acetyl coenzyme A. On the other hand, PAF was released only from 2 of 10 acute myeloblastic leukemias; both of them were of the more mature monoblastic subtype or M5 according to the French-American-British classification. Cells from all three cases of chronic myeloid leukemia studied were also capable of producing PAF. In eight cases of acute lymphoid and myeloid leukemia, the in vivo release of PAF was assessed by testing the plasma levels of this mediator. Only in two cases (one ALL and one acute myeloblastic leukemia) could detectable levels of circulating PAF be demonstrated; it is of interest that both of these cases showed clinical and hematological features of disseminated intravascular coagulation. No PAF was documented in the plasma of the five chronic leukemias tested (four B-cell chronic lymphocytic leukemias and one chronic myeloid leukemia). These findings indicate that lymphoid and myeloid leukemic cells have a different capacity of releasing PAF, possibly related to the level of cell differentiation rather than to an intrinsic property of the neoplastic cells. Furthermore, in some cases, an intravascular release of PAF may occur.

Animals↗
PubMed1984

High fibrinopeptide A (FPA) levels in acute non-lymphocytic leukemia are reduced by heparin administration.

Plasma levels of fibrinopeptide A (FPA) in 30 untreated patients with acute non-lymphocytic leukemia (ANLL) were significantly higher than in 30 healthy controls (p less than 0.001). Patients without laboratory signs of disseminated intravascular coagulation (DIC) had levels of FPA higher than controls (p less than 0.02) but markedly lower than patients with DIC (p less than 0.001). Five patients with M3 leukemia had a higher mean FPA level (p less than 0.02) and a lower peripheral blast cell count (p less than 0.05) than patients with other cytological subtypes of ANLL. When patients with M3 were excluded, a significant correlation was observed between the peripheral blast cell counts and the FPA levels (r = 0.66, p less than 0.001). FPA levels were similar with body temperature either above or below 38 degrees C. After intravenous bolus of heparin FPA dropped to normal levels in 14 out of 17 patients who had high baseline values. These findings indicate that intravascular thrombin formation, which probably result from the expression of procoagulant activities of blast cells, is the main cause of high FPA in the majority of patients with acute non-lymphocytic leukemia.

Acute Disease↗
PubMed1984

Liver dysfunction rather than intravascular coagulation as the main cause of low protein C and antithrombin III in acute leukemia.

Protein C, a newly identified inhibitor of blood coagulation, was measured immunologically in 58 patients with untreated acute leukemias and compared with that of normal subjects. On the average, slightly lower values were found. However, the 17 patients with overt laboratory pictures of decompensated disseminated intravascular coagulation (DIC), including 11 cases with acute promyelocytic leukemia, had protein C concentrations no lower than those of the remaining 41 patients without DIC. Antithrombin III activity and antigen were normal and, like protein C, not lowered in DIC. The concentrations of both proteins were closely correlated with changes in the indexes for liver synthetic function. A subgroup of 13 patients with hyperleukocytic leukemias had lower protein C and antithrombin III, in line with the more compromised synthetic function of their livers. Our findings indicate that liver impairment rather than DIC is the main cause of the changes in the two naturally occurring inhibitors of blood coagulation.

Adult↗
PubMed1982

Biochemical and metabolic aspects of platelet dysfunction in chronic myeloproliferative disorders.

Fifty-two patients with chronic myeloproliferative disorders (13 with polycythemia vera; 23 with primary thrombocythemia; 6 with myelofibrosis and 10 with chronic granulocytic leukemia) had low platelet levels of adenine nucleotides and serotonin and abnormal uptake and storage of the amine. The storage pool deficiency was confined to the substances contained in the platelet dense bodies, because alpha-granule and lysosome markers were present in normal amounts. In chronic granulocytic leukemia the storage defect was usually less marked but was accompanied by a decreased formation of thromboxane B2 and normal platelet aggregation in response to arachidonic acid. There was no clearcut relationship of these biochemical abnormalities to prolongation of bleeding time or to thrombotic and hemorrhagic symptoms. The defect was still present in 15 patients after treatment had returned the cell counts to the normal range. Normal levels of 5HT and adenine nucleotides were observed in 8 patients whose platelet counts were high after splenectomy for non-hematological reasons. These findings suggest that biochemical abnormalities are related to the presence in the bone marrow of abnormal clones, resulting in the production of defective platelets.

Adenine Nucleotides↗
PubMed1982

Platelets in primary thrombocythemia: electron microscopic study.

The ultrastructural analysis of platelets from patients with Primary Thrombocythemia (PT) showed some anomalous features. Platelets having structural modifications of their organelles were observed and a decrease in the number of dense bodies was seen. Freeze-fracture analysis of the plasma membrane of platelets from PT patients showed a significant increase in the number of intramembranous particles (IMP).

Adult↗
PubMed1981

T gamma cell deficiency in idiopathic thrombocytopenic purpura (ITP).

A significant reduction in the proportion and absolute number of circulating T gamma (suppressor) lymphocytes was observed in 15 adult patients with idiopathic thrombocytopenic purpura (ITP). The proportion of T gamma cells was also reduced in the spleen of four patients so investigated. This abnormality was not seen in 5 patients cured by splenectomy whilst it persisted in 3 who remained thrombocytopenic after splenectomy. The proportion of Tmu (helper) lymphocytes in ITP was normal. These findings, similar to those reported in systemic lupus erythematosus, suggest that an inbalance of the immunoregulatory T-cell subsets may be important in the pathogenesis of ITP.

Adult↗
PubMed1981

Chronic idiopathic thrombocytopenic purpura (ITP): site of platelet sequestration and results of splenectomy. A study of 197 patients.

51Cr-platelet kinetics study was performed in 197 patients with chronic ITP after corticosteroid therapy had failed to induce a long lasting remission. The incidence of splenic, spleno-hepatic, hepatic and diffuse platelet sequestration site was 58%, 17%, 6% and 19%, respectively. Splenic and spleno-hepatic sequestration sites were more frequent in patients less than 30 years old and in patients with a platelet count lower than 50 x 10(9)/1. 111 patients were splenectomized shortly after the study. Normalization of the platelet count was obtained more frequently in patients with splenic and spleno-hepatic sequestration than in the others. Labelled platelet sequestration site was the best predictor of the outcome of splenectomy. Platelet kinetics is a non-invasive investigation that should be performed early after the diagnosis of chronic ITP in all patients eligible for splenectomy.

Adolescent↗
PubMed1980

Defibrination in adult acute lymphoblastic leukaemia. Report of four cases.

Defibrination is a rare event in acute lymphoblastic leukaemia (ALL). This paper describes four cases of acute defibrination in a series of 52 adult patients with ALL. All four patients had blood clotting tests consistent with or suggesting defibrination prior to therapy, but haemorrhages and unequivocal laboratory evidence of defibrination developed only after leukaemic blast cells had been destroyed early during therapy for remission induction. All patients received supportive therapy, and three of them were also given a continuous IV heparin infusion. Haemorrhages were controlled and blood clotting tests were improved within 12--48 h.

Adolescent↗
PubMed1977

Acute promyelocytic leukemia: results of therapy and analysis of 13 cases.

Acute promyelocytic leukemia (APL) was diagnosed in 13 of 84 adult patients (15.4%) with acute myeloid leukemia (AML) first admitted between 1972 and 1976. All patients had clinical and/or laboratory evidence of defibrination syndrome. Four patients died of cerebral hemorrhage within 2 days of admission. Two patients died of generalized infection on days 7, and 16, respectively, after admission. The remaining 7 patients (54%) underwent complete remission (CR) with daunomycin, arabinosyl cytosine, and adriamycin. All patients received massive platelet transfusion, no heparin, and no granulocyte transfusion. CR was more frequent in patients with a very low blast cell count and a fibrinogen level higher than 100 mg/100 ml. Median survival of these seven CR patients with APL is similar (15 months) to that of CR patients with other types of AML treated at the same institution during the same period.

Adolescent↗
PubMedDate not supplied

Successful treatment of essential thrombocythemia in a pregnancy with recombinant interferon-alpha 2a.

Essential thrombocythemia (ET) in pregnancy is associated with adverse perinatal outcome, which is likely due to thrombosis of the uteroplacental circulation. Obstetrical management is still controversial. Different therapeutic protocols have been adopted, including the use of aspirin, plateletpheresis, and interferon. We herein report a case of ET treated with interferon-2 alpha from 13 weeks gestation until term. Therapy was well tolerated, leading to a linear reduction of platelet and white blood cell count that rapidly returned within normal limits. A healthy, 3,020-g male infant was delivered at 40 weeks gestation. Albeit further experience is required, recombinant interferon-alpha 2a may play an important role in preventing complications in pregnant patients with ET.

Adult↗
PubMedDate not supplied

Ascorbic acid for the treatment of chronic refractory idiopathic thrombocytopenic purpura (ITP).

We describe our experience with ascorbic acid in the treatment of chronic refractory ITP. Nine patients, 5 males and 4 females aged 27-74 years, 4 of whom were previously splenectomized, received the drug at a daily dose of 2 grams. After 2-12 months (median 4) of treatment, a partial response was observed in only one patient, while no response was registered in the other eight. Our data, analyzed together with those of the literature, allow us to conclude that ascorbic acid may not be considered a drug of interest in the treatment of chronic refractory ITP.

Adult↗