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S Basili

Publications and source records attributed to S Basili.

At least 55 records · Page 3Linked to original sources
PubMed1996

Signal-averaged electrocardiography and echocardiography in the evaluation of myocardial involvement in progressive systemic sclerosis.

To assess the myocardial involvement in progressive systemic sclerosis we evaluated the presence of late potentials by signal-averaged electrocardiography (signal-averaged ECG) and the left ventricular function by M-mode, two dimensional and Doppler echocardiography. Fifteen outpatients, 7 with diffuse progressive systemic sclerosis and 8 with CREST syndrome variant, without clinical or electrocardiographic evidence of cardiac disease were studied and compared with 18 normal subjects. Late potentials occurred in 5 out of 15 progressive systemic sclerosis patients (33%) with a significant difference versus controls (P < 0.05) and were present only in the patients with diffuse progressive systemic sclerosis (P < or = 0.001 vs. controls). All progressive systemic sclerosis patients showed a normal left ventricular systolic function. Abnormal left ventricular filling was found in 9 progressive systemic sclerosis patients (5 with diffuse progressive systemic sclerosis and 4 with CREST). A more severe impairment of the mean values of diastolic function indexes was found in diffuse progressive systemic sclerosis than in CREST. In all diffuse progressive systemic sclerosis patients at least one method showed altered results, whereas half the CREST patients showed no pathological findings with both techniques. These results confirm a lower myocardial involvement in the CREST syndrome than in diffuse progressive systemic sclerosis and consequently this is probably related to a better prognosis.

Adult↗
PubMed1996

Bleeding time does not predict gastrointestinal bleeding in patients with cirrhosis. The CALC Group. Coagulation Abnormalities in Liver Cirrhosis.

BACKGROUND/AIMS: Bleeding time, a laboratory test which explores primary hemostasis, may be prolonged in cirrhosis, but whether abnormal bleeding time identifies patients with cirrhosis who are at risk of bleeding has never been investigated. The aim of this study was to analyze the relationship between bleeding time and the risk of gastrointestinal bleeding. METHODS: Eighty consecutive patients with liver cirrhosis (47 males, 33 females; age, 60 +/- 9 years; range 31 to 83 years) and esophageal varices were enrolled in the study. RESULTS: In the whole series of patients bleeding time was 11 +/- 6 min; it increased as the degree of liver deficiency increased, from low to severe (p = 0.007). During 14 +/- 9 (median (range): 12 (1-34) months of follow-up, 28 (35%) patients experienced gastrointestinal bleeding. They had a longer bleeding time, higher incidence of previous bleeding, more severe liver failure and larger variceal size than patients who did not bleed. However, multivariate analysis (Cox's model) showed that only previous bleeding, liver failure and variceal size were independently associated with bleeding. Similar data were obtained in patients with moderate-severe liver insufficiency (B and C degree according to Child-Pugh's classification). In patients who had never bled (n = 54), the severity of liver failure and variceal size were independent predictors of bleeding. CONCLUSIONS: This study shows that bleeding time is not a predictor of gastrointestinal bleeding in patients with cirrhosis.

Adult↗
PubMed1996

Association between high values of D-dimer and tissue-plasminogen activator activity and first gastrointestinal bleeding in cirrhotic patients. CALC Group.

Cirrhotic patients with decompensated state and high serum levels of fibrin(ogen) degradation products are at high risk of bleeding. The aim of this study was to further analyse the relationship between hyperfibrinolysis and bleeding in cirrhosis by measuring plasma values of D-dimer and tissue plasminogen activator (t-PA) activity. One-hundred-twelve cirrhotic patients with oesophageal varices and without previous upper-gastrointestinal bleeding entered the study and were followed-up for 3 years. Patients were considered to have hyperfibrinolysis if they concomitantly had high values of D-dimer and t-PA activity. During the follow-up 34 (30%) patients bled. They had more severe liver failure (p = 0.0001) and variceal size (p = 0.0031) and higher prevalence of ascites (p = 0.0003), varices with red signs and hyperfibrinolysis (p = 0.0001) than patients who did not bleed. Multivariate analysis disclosed hyperfibrinolysis as the only marker predictive of bleeding (Hazard Ratio = 42.5, p < 0.001). Our findings suggest that screening for hyperfibrinolysis may be useful to identify cirrhotic patients at risk of bleeding.

Adult↗
PubMed1996

[The usefulness of plasmapheresis in a case of nephrotic syndrome in Berger's disease].

Berger's disease, or IgA mesangial nephropathy, is a frequent form of focal and/or segmental proliferative glomerulonephritis that occasionally may present as nephrotic syndrome. The authors reports a clinical case of a young woman come to their observation with a severe clinical picture characterized by asthenia, anasarca, serious no selective proteinuria, microscopic hematuria, blood hypotension from mesangial proliferative glomerulonephritis IgA. Because of the null response to traditional therapy the patient was submitted to plasmapheresis "cascade model", or double filtration, a certainly experimental treatment for this disease, and a remission of the nephrotic syndrome was obtained as confirmed by follow-up at three, six months and one year. Since at present times the therapy is supportive only and no therapeutic maneuvers have been found to be consistently effective in the Berger's disease, plasma exchange plus immunodepressive therapy seems to be useful particularly in the rare patients with rapidly progressive glomerulonephritis. Further and more extensive studies and a fair follow-up are necessary to prove our results.

Adult↗
PubMed1995

Association between low-grade disseminated intravascular coagulation and endotoxemia in patients with liver cirrhosis.

BACKGROUND & AIMS: Hyperfibrinolysis may complicate the clinical course of liver cirrhosis. The aim of this study was to evaluate if, in cirrhosis, hyperfibrinolysis is primary or secondary to intravascular clotting activation and if endotoxemia is associated with activation of clotting and/or the fibrinolytic system. METHODS: Clotting, fibrinolytic indexes, and endotoxemia were studied in 41 cirrhotic patients and 20 healthy subjects. RESULTS: Twenty-seven cirrhotic patients (66%) had high plasma levels of prothrombin fragment F1 + 2, a marker of thrombin generation. Nineteen patients had elevated values of D-dimer, a marker of fibrinolysis in vivo. All patients with high values of D-dimer also had high values of prothrombin fragment F1 + 2. Endotoxemia was elevated in patients with severe liver failure and significantly correlated to prothrombin fragment F1 + 2. Thirty patients were treated for 7 days either with standard therapy (n = 15) or with standard therapy plus nonabsorbable antibiotics (n = 15). Although standard therapy did not significantly change laboratory indexes, a significant reduction of endotoxemia, prothrombin fragment F1 + 2, and D-dimer was found in those patients who received the combined treatment. CONCLUSIONS: This study shows that, in cirrhotic patients, hyperfibrinolysis is not a primary phenomenon but occurs as a consequence of clotting activation and that endotoxemia might play a pathophysiological role.

Adult↗
PubMed1995

Prognostic value of clotting and fibrinolytic systems in a follow-up of 165 liver cirrhotic patients. CALC Group.

One hundred sixty-five patients with cirrhosis diagnosed by needle liver biopsy were followed for 2 years to evaluate the relation between clotting factors and survival. Patients with spontaneous bacterial peritonitis, hepatic carcinoma, and cholestatic liver diseases were excluded. Patients were classified as A (n = 34), B (n = 75), or C (n = 56) according to Child-Pugh criteria. During the follow-up 45 patients died of liver failure or gastrointestinal hemorrhage. Nonsurvivor patients had significantly higher values of bilirubin and D-dimer, a marker of fibrinolysis in vivo, lower values of albumin, prothrombin activity, fibrinogen, prekallikrein, factor VII, and a more prolonged activated partial thromboplastin time than survivors. All these variables and Child-Pugh classification were significantly associated with survival in a univariate analysis. Multivariate analysis (Cox's model) showed that only prekallikrein and factor VII were independently predictors of survival. Ninety-three percent of patients with prekallikrein values < 32% died within 32 months of follow-up, whereas factor VII < 34% identified 93% of patients who died within 10 months of follow-up. This study suggests that factor VII is an early predictor of survival and may be a useful test to better identify cirrhotic patients who should be candidates for liver transplantation.

Aged↗
PubMed1995

Increased rate of thrombin generation in hepatitis C virus cirrhotic patients. Relationship to venous thrombosis.

BACKGROUND: Venous thrombosis may complicate the clinical course of liver cirrhosis (LC), but the pathogenesis is still uncertain. We have previously demonstrated that antiphospholipid (aPL) antibodies were a risk factor for thrombosis. In the same study it was also evident that there was a higher prevalence of hepatitis C virus (HCV) infection in patients with thrombosis, and an association between anti-HCV positivity and aPL. METHODS: In a case-control study, 18 consecutive patients with LC, who had suffered from splanchnic venous thrombosis (n = 12), or thrombophlebitis (n = 6), were matched for age, sex, and degree of liver failure with 36 LC patients without thrombosis. RESULTS: In comparison to patients without thrombosis, patients with thrombosis had higher prevalence of HCV infection (p = 0.0027), positivity for aPL antibodies (p = 0.0003), and higher values of fragment F1+2, a marker of thrombin generation (p = 0.0083). While F1+2 values were similar in aPL (+) and aPL (-) patients, HCV patients had significantly higher values of F1+2 than patients with hepatitis B virus (HBV) infection and/or alcoholism (2.6 +/- 0.94 vs 1.5 +/- 0.66, p = 0.0001). CONCLUSIONS: These data suggest that in LC, HCV infection may contribute to clotting system activation, thus predisposing patients to venous thrombosis.

Adult↗
PubMed1994

Relationship between lipoprotein(a) levels in serum and some indices of protein synthesis in liver cirrhosis.

Recent research has demonstrated that the major site of apolipoprotein(a) synthesis, the characteristic protein of lipoprotein(a) (Lp(a)), is the liver and that patients affected by liver cirrhosis have low serum concentrations of Lp(a). Nevertheless, it is still not clear whether Lp(a) behaviour in these patients is related to reduced hepatic protein synthesis, or to decreased serum lipid levels or to both these conditions. In order to investigate further the behaviour of Lp(a) and, in particular, its relationship with some indices of blood lipids and coagulation, 30 patients affected by liver cirrhosis have been studied. Significantly low serum values of Lp(a) were observed in patients with more severe hepatic injury included in classes B and C according to the Child-Pugh score. Lipoprotein(a) was directly correlated with prothrombin plasma activity and with apolipoprotein B-100 and albumin concentrations in serum. This study confirms low serum levels of Lp(a) in cirrhotic patients and suggests that its decrease could be partly due to impaired liver protein synthesis.

Apolipoprotein B-100↗
PubMed1994

Bleeding time in patients with cirrhosis: relation with degree of liver failure and clotting abnormalities. C.A.L.C. Group. Coagulation Abnormalities in Cirrhosis Study Group.

Patients with cirrhosis suffer from a complex haemostatic disturbance, due to abnormalities in clotting and fibrinolytic system activation and in primary haemostasis. The latter is indicated by a prolongation of bleeding time, which is a reliable indicator of platelet function in vivo. To further assess the relationship between bleeding time, degree of liver failure and clotting abnormalities in patients with cirrhosis, bleeding time was investigated in a prospective study of 70 consecutive patients with cirrhosis diagnosed by liver-needle biopsy, of whom 19 belonged to Child-Pugh class A, 29 to B and 22 to C. Among patients with cirrhosis, 40% had an abnormal bleeding time (> 10 min), and 42% had a platelet count < 100,000/microliters. Patients with severe liver failure (class C) had a lower platelet count and a more prolonged bleeding time than patients in classes A and B. Bleeding time was significantly inversely correlated to platelet count, fibrinogen, prothrombin activity and packed cell volume, and directly correlated to serum bilirubin and D-dimer. However, in class C patients, only a significant inverse correlation between bleeding time and fibrinogen was observed. These findings indicate that in cirrhosis worsening of platelet function is closely related to the degree of liver failure. The inverse correlation between bleeding time and fibrinogen indicates that a low value of this clotting parameter may account in part for platelet dysfunction.

Bleeding Time↗
PubMed1994

Prevalence of lupus anticoagulant in patients with cirrhosis: relationship with beta-2-glycoprotein I plasma levels.

We have previously demonstrated that patients with cirrhosis may be positive for lupus anticoagulant and anticardiolipin antibodies. The prevalence and clinical value of antiphospholipid antibodies in cirrhosis have never been described. Besides, it has not yet been determined if serum levels of beta-2-glycoprotein I, which is synthesized by the liver and mediates the interaction between cardiolipin and anticardiolipin antibodies affects lupus anticoagulant detectability in cirrhosis. We evaluated the prevalence of lupus anticoagulant in 63 patients with cirrhosis and related it to beta-2-glycoprotein I serum levels. We also analyzed whether lupus anticoagulant and anticardiolipin antibodies were associated with previous thrombotic complications. Eleven patients (18%) were lupus anticoagulant positive; 14 (22%) had high values of anticardiolipin antibodies. Fourteen patients had a previous history of splanchnic venous thrombosis (n = 9) or thrombophlebitis (n = 5). A significant association between lupus anticoagulant (p = 0.0001), anticardiolipin antibodies (p = 0.0001) and venous thrombosis was found. Patients with severe liver failure had significantly lower beta-2-glycoprotein I levels than those with moderate (p < 0.01) or low (p < 0.001) hepatic insufficiency. Among 14 anticardiolipin antibodies positive patients, six with severe liver failure were lupus anticoagulant negative and had beta-2-glycoprotein I values below 100 micrograms/ml. In four of these, basal values of dilute activated partial thromboplastin time were not modified by the addition of 50 micrograms/ml of exogenous beta-2-glycoprotein I. This study shows that antiphospholipid antibodies are relatively frequent in cirrhosis and that beta-2-glycoprotein I levels are not so low as to affect lupus anticoagulant detectability.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Apolipoproteins C-II and C-III in peripheral arterial disease.

Apolipoprotein (apo) C-II and apo C-III serum concentrations were investigated in 119 normotriglyceridemic male subjects with peripheral arterial disease (PAD) or coronary heart disease (CHD) or without clinical manifestations of atherosclerotic disease. All subjects included in the study had similar blood levels of total cholesterol (< 400 mg/dL). High-density lipoproteins cholesterol (HDL-C) subfractions and apo A-I serum levels were significantly lower in CHD patients, as were apo A-I/apo B and HDL-cholesterol/total cholesterol ratios. Apo C-II and apo C-III showed similar serum concentrations in all three groups of subjects, but apo C-II/apo C-III ratio was significantly lower in PAD patients as compared with that in CHD patients and control subjects. This study confirms that PAD may be associated with a particular lipoprotein derangement that primarily involves very low-density lipoprotein catabolism.

Adult↗
PubMed1994

Hypercoagulability state in patients with chronic obstructive pulmonary disease. Chronic Obstructive Bronchitis and Haemostasis Group.

Since there is some clinical evidence that the clinical course of patients with chronic obstructive pulmonary disease (COPD) may be complicated by thrombosis in the pulmonary vessels, we studied whether a hypercoagulability state (HS) does occur in COPD. Plasma levels of prothrombin F1 + 2 fragment, a marker of thrombin generation, D-dimer, a marker of in vivo thrombin and plasmin activation, and fibrinogen were measured in 37 COPD patients and in 30 controls matched for sex and age. COPD patients had significantly higher values of F1 + 2 (p = 0.0001) and fibrinogen (p = 0.0005) than healthy subjects. The difference persisted after excluding smoking patients. F1 + 2 was not correlated with PaO2 (r = 0.02, p > 0.05) and PaCO2 (p = 0.12, p > 0.05). In six patients with stable COPD and F1 + 2 greater than 1.65 nM (mean + 2 SD of controls) subcutaneous calcium-heparin therapy (5000 IU t.i.d. for 15 days) significantly reduced F1 + 2 (p = 0.03) and PaCO2 (p = 0.01). This study shows that COPD patients have an ongoing prothrombotic state which could potentially account for thrombosis occurring in pulmonary vessels. The effect of calcium-heparin treatment on clotting system activation and blood gas may suggest this treatment as potential candidate for prospective study in COPD patients.

Adult↗
PubMed1994

[Calcium antagonists in the therapy of arterial hypertension in the aged].

A large number of epidemiologic and interventional studies go to show that acute cerebral and cardiac events and chronic organ injury are significantly less frequent in treated compared to untreated elderly hypertensives. These observations clearly show that hypertension in the elderly must be treated. As to water-electrolyte metabolism, activity of the renin-angiotensin-aldosterone axis as well as volemia are reduced in the elderly while extravascular liquid compartment and activity of the natriuretic atrial factor are both increased. In addition, there is reduction of the baroceptor reflexes accompanied by vasoconstriction and hypertrophy of the smooth muscles associated with increased intracellular calcium ion content. These pathophysiologic conditions appear to supply the rationale for the preference accorded to calcium channel blockers compared to other drugs usually employed in the management of younger hypertensives. Moreover, second generation dihydropyridines, thanks to their liposolubility and ties with calcium channel subunits, show rapid onset and long action that allows for a single daily dose and lowers the incidence of side effects. A large number of interventional trials employing calcium channel blockers have demonstrated the efficacy of these drugs for reducing arterial hypertension. However, these trials concern young hypertensives whereas there is a lack of similar studies in elderly subjects, were clinical trials are few and involve limited numbers of subjects. Results of multicentre studies, at present in progress, will permit to assess the efficacy and incidence of side effects of second generation calcium channel blockers in hypertension of the elderly.

Age Factors↗
PubMed1994

[Relationship between blood fibrinogen and plasma lipoproteins in patients with hypercholesterolemia].

OBJECTIVE: Subjects with risk factors of atherosclerotic cardiovascular disease showed frequently high plasma levels of fibrinogen. Nevertheless, the relationship between hyperfibrinogenemia and atherosclerotic risk factors is not yet well known. In particular, some studies showed a correlation between hyperlipoproteinemia and high plasma levels of fibrinogen, even if the mechanism(s) involved in the hyperfibrinogenemia associated with hyperlipoproteinemia is not completely clear. STUDY DESIGN AND SUBJECTS: In this retrospective study on 139 out-patients, affected by hyperlipoproteinemia type II, the relationship between fibrinogen plasma levels and some lipid parameters, such as total cholesterol (CT), triglycerides, LDL-cholesterol, HDL-cholesterol (HDL-C), lipoprotein (a), apolipoproteins (Apo) A-I and B was evaluated. RESULTS: Fibrinogen plasma levels showed a significant inverse correlation with HDL-C (r = -0.25), HDL-C/CT (Rho = -0.22), Apo A-I (r = -0.33) serum concentration and a direct significant correlation with triglycerides serum levels (r = 0.22). Multiple stepwise regression analysis confirms the independence of association between Apo A-I and fibrinogen plasma levels. CONCLUSION: In patients with type II hyperlipoproteinemia, the increase of fibrinogen plasma levels seems to be related to the modification of serum concentration of specific lipoprotein, such as those rich in triglycerides and those with high density.

Adult↗
PubMed1994

[Effects of simvastatin on plasma lipoproteins].

The role of low density lipoprotein (LDL) cholesterol as well as of that transported by other lipoproteins, such as high density lipoprotein (HDL), in the pathogenesis of atherosclerotic disease has been pointed out by several studies. Nevertheless, recent researchers have suggested that cholesterol transported by other lipoproteins, e.g. very low density lipoproteins (VLDL), could play a role in the atherosclerotic disease. Consequently the evaluation of non-HDL cholesterol could provide a more significant index of the atherosclerotic risk in hyperlipoproteinemic patients. Clinical investigations have shown that the competitive inhibitors of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase are very effective to decrease LDL-Cholesterol serum concentration, but their effect on the cholesterol of other lipoproteins is not well known. The effect of 6 months of treatment with simvastatin (20 mg/day) on lipoproteinemic pattern was retrospectively studied in 102 patients with primary hypercholesterolemia. A significant reduction in serum levels of non-HDL-cholesterol and VLDL-cholesterol together with the expected reduction of total cholesterol, apolipoprotein B 100, LDL-cholesterol and an increase of HDL cholesterol were observed. Triglyceride serum behaviour was inversely correlated with HDL cholesterol during the study. Our data suggest that simvastatin can reduce the cholesterol of all potentially atherogenetic lipoproteins and could improve the inverse cholesterol transport system expressed by the HDL cholesterol transport system expressed by the HDL cholesterol increment by a mechanism probably dependent on normalisation of the plasma lipoprotein pattern in atherosclerotic disease.

Adult↗
PubMed1993

Chronic obstructive pulmonary disease. A possible correlation between platelet aggregation tests and respiratory indexes. ECOB Group.

It has been suggested that thrombotic events occurring in patients with chronic obstructive pulmonary disease could be partially due to abnormalities in blood coagulation and fibrinolysis, as well as to changes in platelet function. In the present study in vitro platelet aggregation, in addition to clotting activity, has been studied in 20 patients with chronic obstructive pulmonary disease and different degrees of alteration of blood gas analysis. The results obtained suggest that the presence of a condition of platelet hypoaggregability characterizes patients with marked hypercapnia and/or hypoxemia, whereas the improvement of respiratory indexes is followed by a trend to normalization, or, more often, to an increase of platelet activity.

Aged↗
PubMed1993

Hyperfibrinolysis resulting from clotting activation in patients with different degrees of cirrhosis. The CALC Group. Coagulation Abnormalities in Liver Cirrhosis.

This study explored the relationship between clotting activation and tissue plasminogen activator and its inhibitor in cirrhotic patients with different degrees of liver failure. Sixty-seven patients (40 men, 27 women; age = 31-77 yr) with cirrhosis diagnosed by liver biopsy were divided into three subgroups (A, B and C) on the basis of Child-Pugh classification. Tissue plasminogen activator antigen and activity, plasminogen activator inhibitor antigen and activity, fibrin/fibrinogen degradation products, and D-dimer were measured in each patient. Forty-two patients with normal levels of fibrin/fibrinogen degradation products and D-dimer showed significant progressive decreases of plasminogen activator inhibitor antigen levels (p < 0.01) and activity (p < 0.0001) from class A to class C. This decrease was significantly related to prothrombin time (p < 0.003). Tissue plasminogen activator values were not different in the three Child classes. Twenty-five patients (7 class B and 18 class C) with high circulating values of fibrin/fibrinogen degradation products and D-dimer had higher values of tissue plasminogen activator antigen (20.0 +/- 10.1 ng/ml vs. 5.9 +/- 3.0 ng/ml; p < 0.0001) and activity (6.9 +/- 2.2 U/ml vs. 2.1 +/- 1.3 U/ml; p < 0.0001) and lower values of plasminogen activator inhibitor antigen (6.9 +/- 4.1 ng/ml vs. 14.8 +/- 5.6 ng/ml; p < 0.0001) and activity (4.1 +/- 2.8 U/ml vs. 9.8 +/- 3.7 U/ml; p < 0.0001) than did patients with normal values of fibrin/fibrinogen degradation products and D-dimer.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗