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Biomedical subjects

S Viganò

Publications and source records attributed to S Viganò.

15 recordsLinked to original sources
PubMed1992

High-performance liquid chromatographic method with fluorescence detection for the determination of total homocyst(e)ine in plasma.

A high-performance liquid chromatographic method for the determination of total plasma homocyst(e)ine [H(e)] after reduction with sodium tetrahydroborate and precolumn derivatization with o-phthaldialdehyde is described. The analyses, carried out on a reversed-phase C18 column, were based on spectrofluorimetric detection. The sensitivity was 1 pmol per injection and the intra- and inter-assay relative standard deviations were 1.8% and 5%, respectively. The plasma H(e) concentration determined in 40 healthy volunteers (20-60 years old) was 12.4 +/- 2.9 microM (mean +/- S.D.), in good agreement with reference values.

Adult↗
PubMed1992

[Isosporiasis and sarcocystosis. The current findings].

A review on infections by Isospora belli and Sarcocystis spp. both in healthy and in AIDS patients is done on the basis of literature and personal data. In this view a special focus is made on isospora belli infection in AIDS because of its high recurrence after successful attack therapy. Consequently the most recent protocols for maintenance and attack therapy in these patients are reported. At the end, concerning ultrastructural pathology, the features of some Isospora belli developing stages are described by means of electron microscopy on duodenal biopsy specimens from a patient.

AIDS-Related Opportunistic Infections↗
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

Protein C antigen is not an acute phase reactant and is often high in ischemic heart disease and diabetes.

Protein C, an antithrombotic protein, was measured immunologically in 299 patients with clinical conditions associated with a high frequency of venous or arterial thromboembolism. The mean protein C antigen (PC:Ag) level was high for 48 patients with ischemic heart disease and, to a lesser extent, for 95 diabetics. In 28 patients with thrombotic strokes, 48 patients with proximal deep-vein thrombosis and in 80 patients with localized or metastatic tumors, mean PC:Ag was normal. Comparison of the pattern of changes of PC:Ag levels with those of fibrinogen, orosomucoid and prothrombin in 21 patients during the postoperative period and in 20 patients with active rheumatoid arthritis ruled out the possibility that high PC:Ag is non-specific, acute-phase reaction to inflammation, tissue injury or neoplastic growth. Therefore, high PC:Ag might be specifically related to the thrombotic tendency of these patients, but the mechanism of such a relationship remains to be clarified.

Adolescent↗
PubMed1984

Decrease in protein C antigen and formation of an abnormal protein soon after starting oral anticoagulant therapy.

Changes in protein C antigen (PC:Ag) have been compared with those in factor II, VII, IX and X antigens (II:Ag; VII:Ag; IX:Ag and X:Ag) in 10 patients starting on oral anticoagulant therapy with warfarin, monitored with thrombotest. Between days 0 and 3 of therapy, PC:Ag decreased at the same rate as VII:Ag, whilst IX:Ag, X:Ag and II:Ag decreased at progressively slower rates. On days 15 and 21, clotting proteins and PC:Ag did not differ significantly. Before and after warfarin, PC:Ag had the same mobility on crossed immunoelectrophoresis in Ca2+-free agarose gel; with Ca2+, a protein with faster anodal mobility appeared on day 1 and became maximal 5 d after warfarin was started. These findings indicate that the rate of PC decrease is closer to that of factor VII than those of factors IX, X and II, and that an abnormal PC with poor Ca2+-binding properties appears soon after treatment is started. The early decrease in the physiological inactivator (i.e. PC) might contribute to the poor antithrombotic efficacy of anticoagulant therapy during the first days.

Adult↗
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

Significance of plasma fibrinopeptide A and high molecular weight fibrinogen in patients with liver cirrhosis.

Plasma fibrinopeptide A (FPA) was measured in 50 patients with liver cirrhosis divided into 'moderate' or 'severe' cirrhotics according to standard clinical and laboratory criteria. FPA was significantly higher than in normal controls although no relation to the severity of disease was found. After a single intravenous administration of heparin there was a significant decrease in FPA levels in the patients. High molecular weight fibrinogen (HMWF) was also determined for some of the patients and was significantly greater than in the normal controls. However, there was no correlation between FPA and HMWF. The greater values of FPA and their responses to heparin indicate that there is increased thrombin formation in a number of patients with liver cirrhosis, with no apparent relation to the severity of the disease.

Female↗
PubMedDate not supplied

Decrease and rapid recovery of protein C after plasma exchange.

The anticoagulant protein, protein C (PC), was measured after 40 plasma exchanges (PEs) in 26 patients treated for a variety of disorders, most of which were immunological in nature. After 27 PEs involving exchange of 50 percent of the plasma volume with albumin and saline, mean PC activity and antigen decreased in parallel to about one-half normal levels, with good correlation between the two assays. Antithrombin III and prothrombin decreased to about the same levels as PC, with no significant differences between the percentage changes for either protein. After five PEs, during which exchange of larger plasma volumes was performed (86%), the percentage change of PC was greater than after the 50 percent exchange (38 +/- 22 vs. 55 +/- 24). To study postexchange recovery, PC was also measured serially for up to 24 hours after eight PEs (50% exchange). At 24 hours postexchange, PC levels did not differ significantly from pre-exchange levels. This study demonstrates that decreases in PC are in proportion to the volume of plasma exchanged during PE. However, PC levels returned to normal within 24 hours after PE, so that any hemostatic imbalance induced by low PC should be transient.

Antithrombin III↗