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Biomedical subjects

M Pirisi

Publications and source records attributed to M Pirisi.

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

Serum soluble vascular-cell adhesion molecule-1 (VCAM-1) in patients with acute and chronic liver diseases.

Our aim was to ascertain the degree of variation of serum soluble vascular cell adhesion molecule-1 (VCAM-1) concentrations according to the nature and the severity of an underlying liver disease. One-hundred forty sera collected from 123 patients (83 male, 40 female) with acute hepatitis (n = 14), mild chronic liver disease (n = 52) or cirrhosis (n = 57) of different etiologies as well as from 17 healthy blood donors (8 male, 9 female) were studied. Soluble VCAM-1 concentration was measured immunoenzymatically. One-way analysis of variance revealed a significant variability of the mean values of soluble VCAM-1 among groups (F = 80.02, p < 0.0001). All groups of patients had higher soluble VCAM-1 than controls; moreover, patients with acute hepatitis and patients with cirrhosis had higher soluble VCAM-1 levels than patients with mild chronic liver disease (Bonferroni's test, p < 0.01). These results did not change after stratification of patients according to the etiology (viral or toxic) of liver disease (two-way analysis of variance: grouping factor diagnosis, F = 60.39, p < 0.0001; grouping factor etiology, F = 1.73, p NS). Cholinesterase, total bilirubin, circulating thrombocytes and blood area nitrogen were the independent predictors of the concentration of soluble VCAM-1. In conclusion, patients with liver disease have high serum soluble VCAM-1, which seems to reflect more the severity of impairment of liver function rather than the etiologic nature of the disease.

Acute Disease↗
PubMed1996

Diagnostic usefulness of acute-phase protein measurement in hepatocellular carcinoma.

To compare the diagnostic usefulness as markers of hepatocellular carcinoma (HCC) of alpha1-antitrypsin, C-reactive protein, and alpha1-acid glycoprotein (all determined by nephelometric methods), we studied 132 subjects (74 male, 58 female): 43 had mild chronic liver disease, 32 cirrhosis, 24 HCC; 33 were controls. A total of 29.2% of the patients with HCC had alpha1-acid glycoprotein > 100 mg/dl, 75.0% had alpha1-antitrypsin > 220 mg/dl, 70.8% had C-reactive protein > 5 mg/L. In cirrhotics, frequencies were 3.1, 50.0 and 59.4%, respectively; in patients with mild chronic liver disease, 14.0, 11.6, and 32.6% (chi2 12.3, p < 0.01; chi2 47.3, p < 0.0001; chi2 38.0, p < 0.0001, respectively). alpha1-fetoprotein performed better than all acute-phase proteins. We conclude that, due to their low specificity and/or sensitivity, none of the three acute-phase reactants tested can be recommended for diagnostic use as biological markers of HCC in Western patients.

Acute-Phase Proteins↗
PubMed1996

Immunosuppressive treatment of the nephrotic syndrome due to mesangial lesions.

To assess the effectiveness of an intensive immunosuppressive regimen on the nephrotic syndrome due to mixed membranous and mesangial lesions, we studied 18 patients with nephrotic syndrome and miscellaneous histologic features characterized by mesangial proliferation and sclerosis, non-specific basement membrane changes such as thickening, fraying and scalloping, in the absence of extensive immune complex deposition by immunofluorescence. The patients were treated with an immunosuppressive regimen that combined prednisone and cyclophosphamide for at least 6 months with the following schedule: 1) induction with prednisone daily 250 to 750 mg i.v. for 3 to 8 days, plus cyclophosphamide 100 to 200 mg p.o. daily; 2) maintenance with prednisone 100 to 200 mg p.o. in alternate days for 30 to 75 days, and cyclophosphamide as before; 3) tapering, with prednisone in alternate day regimen, reduced on average by 25 mg every month, plus cyclophosphamide as before; 4) discontinuation of cyclophosphamide and slow withdrawal of prednisone. Treatment lasted on average 9 months, with an average cumulative dose of prednisone of 9.2 g and of cyclophosphamide of 26.7 g. At the end of treatment, 14 patients had a complete remission and 4 remained stable. On longer follow-up, one out of these 4 patients, who had renal failure before treatment, subsequently progressed to end-stage renal disease. Nine patients relapsed after an average remission of 6 years. Eight of them remitted completely on a repeat cycle. One patient refused the retreatment and progressed to end-stage renal disease within one year. After an average follow-up of 7.3 +/- 1.1 years, plasma creatinine for the whole group had fallen from 138 +/- 26 to 103 +/- 20 mumol/l and proteinuria from 6.7 +/- 0.7 to 0.4 +/- 0.2 g/d (p < 0.001). In conclusion, in patients with these forms of nephrotic syndrome this immunosuppressive regimen is highly effective in inducing remission, in preventing progression to end-stage renal disease and in treating relapses.

Adult↗
PubMed1995

Non-specific increase of serum carbohydrate antigen 19-9 in patients with liver disease associated with increased circulating levels of adhesion molecules.

Sialyl-Lewisa antigen (SLe(a)), the immune determinant of carbohydrate antigen 19-9 (CA 19-9), is the ligand of E-selectin. To verify the possibility of an association between nonspecific elevation of CA 19-9 and adhesion molecules, sera from 12 patients with acute hepatitis, 55 with non-cirrhotic chronic liver disease, 33 with cirrhosis and 25 with hepatocellular carcinoma, were tested for common liver function tests. Besides, CA 19-9 and soluble forms of E-selectin, VCAM-1 and ICAM-1 were measured immunoenzymatically. One-way analysis of variance demonstrated that mean CA 19-9 concentration differed among groups (F 15.27, P < 0.0001) with the highest values found in patients with acute hepatitis. By univariate analysis, the strongest correlation of CA 19-9 was with soluble ICAM-1, which by stepwise multiple regression analysis was the only independent predictor of elevated CA 19-9 (multiple R 0.560). The association between ICAM-1 and CA 19-9 might originate in the biliary cells where they might be simultaneously overexpressed during inflammatory processes.

Acute Disease↗
PubMed1995

Reactivity to B cell epitopes within hepatitis C virus core protein and hepatocellular carcinoma.

Our aim was to investigate the existence of an association between B cell responsiveness to hepatitis C virus (HCV) core protein and progression of liver disease. In fact, the persistence of HCV infection is permitted by avoidance of viral clearance, despite chronic inflammation in the liver; this process ends with the development of hepatocellular carcinoma in many patients. On the basis of computerized prediction of antigenicity of the genomic sequence of HCV core protein, three 15-mer peptides (named Q15V, R15P, and G15V) were synthesized to be used as antigens in an enzyme immunoassay. Sera from 97 patients (65 males and 32 females) were tested: 43 patients had mild chronic liver disease (steatofibrosis, chronic persistent, or chronic active hepatitis) and 54 had cirrhosis, which was complicated by hepatocellular carcinoma (HCC) in 19. Seventy-six patients were positive to anti-HCV testing by second generation ELISA and 21 were negative. Rates of positivity for synthetic peptides in anti-HCV-positive versus anti-HCV negative patients were as follows: 53 of 76 and 0 of 21 for anti-Q15V; 41 of 76 and 0 of 21 for R15P; and 67 of 76 and 2 of 21 for G15V. Rates of positivity to anti-Q15V and anti-G15V were similar among diagnostic groups (Pearson's chi 2, 1.97, P > 0.10 and 0.45, P > 0.10), whereas anti-R15P antibodies were detected at a significantly lower rate in patients with HCC (2/13) in comparison to mild chronic liver disease (22/35) and cirrhosis (17/28) (Pearson's chi 2, 9.42, P < 0.01). We conclude that anti-R15P antibodies are uncommon in anti-HCV-positive patients with HCC. During the course of chronic HCV infection, anti-R15P testing might help to identify a subgroup at higher risk to develop HCC.

Adult↗
PubMed1995

Changes in blood lipid composition and response to interferon treatment in chronic hepatitis C.

To assess whether the initial status of lipid metabolism in patients with chronic viral hepatitis might correlate with outcome of therapy, 52 patients (32 males and 20 female) with chronic hepatitis C were studied: 44 were treated with human recombinant interferon-alpha 2b (3 MU three times per week for up to 12 months), and 8 served as controls. At baseline, sera were tested for total and HDL cholesterol, HDL2, HDL3, apolipoprotein A-I, apolipoprotein B, interferon-alpha, tumor necrosis factor, and interleukin-6. Changes in blood lipids were evaluated after 3, 30, and 90 days of treatment. HDL cholesterol, apolipoprotein A-I, and HDL3 decreased by 9.4-11.4% within 4 weeks of starting interferon treatment, but this effect was sustained only in patients with a primary response to interferon. On multivariate analysis, a primary response to interferon correlated with higher apolipoprotein A-I and lower (< 2.23 pg/ml) interleukin-6 levels (p < 0.005 for both). In contrast, a sustained response was significantly more common in patients with low (< or = 13.3 pg/ml) serum interferon-alpha and lower interleukin-6 at baseline but did not correlate with any of the blood lipids. Thus, in chronic hepatitis C, interferon treatment induces specific changes in blood lipids. The concentration of apolipoprotein A-I at baseline is a strong predictor of primary response to treatment, and the likelihood of sustained response seems to be reflected by lower cytokine activation.

Adolescent↗
PubMed1995

Fatal human pulmonary infection caused by an Angiostrongylus-like nematode.

An immunocompetent man developed malaise, fever, progressive weight loss, eosinophilia, and transient pulmonary infiltrates that responded to steroid treatment but recurred after its discontinuation. Examinations of feces, bronchoalveolar lavage fluid, and pulmonary tissue obtained during a 50-day period of hospitalization yielded negative results. When a new bronchoalveolar lavage sample and a new pulmonary biopsy specimen showed nematode larvae and adult worms, treatment with thiabendazole was started. However, therapy with this agent and then with mebendazole had no impact on the patient's downhill course, which ended in respiratory distress and death. Autopsy documented an overwhelming pulmonary infection with a metastrongylid nematode resembling a species of Angiostrongylus. Histologic study revealed features of necrotizing angiitis closely mimicking those of Wegener's granulomatosis. To our knowledge, this is the first reported instance of patent metastrongylid parasitism of the human pulmonary arteries with necrotizing angiitis caused by a reaction to the parasite and/or its metabolic products.

Adult↗
PubMed1995

Hyperglycemia-induced thrombin formation in diabetes. The possible role of oxidative stress.

Diabetes is characterized by the existence of a thrombosis-prone condition, possibly related to hyperglycemia. However, the mechanism linking hyperglycemia to the activation of the coagulation cascade is still unclear. It has been recently suggested that diabetes is accompanied by increased oxidative stress. In this work, the possibility that oxidative stress may be involved in the hyperglycemia-induced coagulation activation has been evaluated. Prothrombin fragment 1 + 2 (F1 + 2), which represents a reliable marker of the amount of thrombin released in the circulation, has been chosen for studying thrombin formation in vivo. In nine type II diabetic patients and in seven healthy control subjects, matched for age and body mass index, three different experiments were performed: oral glucose tolerance test (OGTT), intravenous antioxidant glutathione (GSH) administration for 2 h, and OGTT plus intravenous GSH administration. Samples were drawn at -15 min and every 30 min from 0 to 180 min. During the OGTT, F1 + 2 significantly increased in both diabetic and healthy subjects. GSH administration during OGTT normalized this phenomenon. GSH administration alone significantly decreased F1 + 2 in diabetic patients, while no effect was observed in the normal subjects. These data suggest that hyperglycemia may induce thrombin activation, possibly inducing an oxidative stress, and that antioxidant GSH may counterbalance this effect.

Aged↗
PubMed1995

Hepatic release of erythropoietin induced by transarterial chemoembolization in patients with hepatocellular carcinoma.

It has been shown previously that erythropoietin expression in vitro by hepatoma cells increases in response to hypoxia. To verify whether hypoxia of the tumor might result in hepatic release of erythropoietin in vivo, serum erythropoietin concentrations were measured immunoenzymatically in 12 patients (5 women, 7 men) who underwent transarterial chemoembolization for hepatocellular carcinoma. Peripheral blood samples were collected at baseline, and after 6 hours and 1, 2, 3, and 7 days after the procedure. In a second set of experiments, performed in three male patients also undergoing chemoembolization for hepatocellular carcinoma, paired blood samples were collected after catheterization of the hepatic veins and of the right antecubital vein. None of the patients had erythrocytosis. In comparison with a baseline mean value +/- SEM of 100.6 +/- 12.6 micrograms/L, serum erythropoietin concentrations were the following; +6 hours, 55.4 +/- 18.0 (P < .001); +1 day, 102.4 +/- 24.7 (P = NS), +2 days, 183.0 +/- 31.1 (P < .05); +3 days, 155.0 +/- 26.0 (P < .05); +7 days, 153.3 +/- 27.4 (P < .05) (matched Student's t-test). The ratio of hepatic vein/antecubital vein serum erythropoietin concentrations increased from 0.85 at baseline to 1.30 at +2 days, paralleling the increase of aspartate transaminase (r = .914, P < .005). After chemoembolization, no correlation was found between serum erythropoietin and alpha-1-fetoprotein concentrations. The concentration of the latter, stable initially, decreased 7 days after the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Immunosuppressive treatment of the glomerulonephritis of systemic lupus.

To evaluate the results, the long-term prognosis and the rates of complication of an immunosuppressive regimen with corticosteroids and cyclophosphamide in the treatment of the nephritis of systemic lupus erythematosus, 21 patients with lupus glomerulonephritis were studied. Renal biopsies were performed in 17/21 of them and indicated diffuse proliferative (6 patients), diffuse mesangial (4) and membranous (7) glomerulonephritis. Treatment was structured in 4 phases: 1) induction with methylprednisolone 250 mg i.v. for 7-14 days, and cyclophosphamide 100-200 mg p.o., q.d., or 20 mg/kg i.v. every 28 days; 2) maintenance with prednisone p.o., 2 mg/kg q.o.d. for 45 days, and cyclophosphamide as before; 3) tapering, with reduction of prednisone by 15% each month for 4 months; 4) indefinite maintenance with prednisone slowly tapered to the least effective q.o.d. dose and cyclophosphamide discontinued after six months of treatment. This cycle was repeated in the event of a relapse. After a first immunosuppressive cycle, 20/21 patients achieved remission of glomerulonephritis. Plasma creatinine fell from 97 +/- 6 to 80 +/- 3 microMol/l (p < 0.01). Proteinuria fell from 2.1 +/- 0.4 to 0.2 +/- 0.4 g/d (p < 0.0001) and the nephrotic syndrome, present in 8 patients, disappeared. After an average of 20 +/- 7 months, 8 patients relapsed: all remitted again after a repeat cycle, but 1 later progressed to end-stage renal failure during pregnancy. After an average of 56 months 4 out of these 8 patients relapsed again: 1 progressed to end-stage renal disease following an abortion and 3 remitted completely after a third cycle. Thus, 18 out of 21 patients are presently in remission with an average dose of prednisone of 13.7 mg/day after an average follow-up of 52 +/- 38 months (range 2 to 156). Three patients are presently off treatment. In 16 patients with extended follow-up of 2 to 13 years, anti-nuclear antibodies, anti-DNA antibodies, albuminuria and cylindruria fell below post-cycle levels (p < 0.001 for all). We conclude that intensive immunosuppression with steroids and cyclophosphamide can achieve excellent long-term results in the treatment of systemic lupus with glomerulonephritis.

Adrenal Cortex Hormones↗
PubMed1994

Value of serum C-reactive protein measurement in the detection of hepatocellular carcinoma superimposed on liver cirrhosis.

We investigated whether, in Italian patients, C-reactive protein (CRP) determination could be considered a useful adjunct, complementary to alpha 1-fetoprotein, in the detection of liver cancer. CRP was determined by particle-enhanced nephelometry in 171 subjects (102 male, 69 female). Fifty-five patients had mild chronic liver disease (CLD), 45 cirrhosis (CIR), 38 hepatocellular carcinoma (HCC); 33 subjects were healthy controls. Patients with HCC and CIR had higher CRP levels (P < 0.05) than those found in patients with CLD and controls. CRP higher than 5 mg/l was found in 30/38 (78.9%) patients with HCC, 28/45 (62.2%) patients with CIR, 16/55 (29.1%) patients with CLD (chi 2 56.0, P < 0.0001). Sensitivity, specificity and diagnostic accuracy of CRP in diagnosing HCC with respect to CLD+CIR were: 78.9%, 56.0% and 34.9%. However, when considered only in the subgroup of patients with alpha 1-fetoprotein below or equalling 30 ng/ml, they were 50.0%, 54.3% and 4.3% respectively. In conclusion, CRP concentration is frequently elevated in patients with HCC, however, it does not seem to improve the ability of alpha 1-fetoprotein to discriminate HCC from CIR.

Adult↗
PubMed1994

Prediction of serum markers of fibrosis by levels of circulating intercellular adhesion molecule-1 in acute and chronic liver disease.

To clarify the link between cytotoxic damage to the hepatocyte and the development of fibrosis, we immunoenzymatically measured serum prolyl hydroxylase (hPH), type IV collagen (CL-IV) and circulating intercellular adhesion molecule-1 (clCAM-1). The population studied was comprised of 122 patients with liver disease (acute hepatitis; mild chronic liver disease; cirrhosis; hepatocellular carcinoma) and 33 patients with extrahepatic diseases. Similar patterns were observed for hPH, CL-IV, and clCAM-1, that were higher in patients with acute hepatitis and hepatocellular carcinoma than in those with mild chronic liver disease (Bonferroni's test for pairwise comparisons, p < 0.01). Liver function tests and markers of fibrosis showed a strict correlation, which disappeared when the linear effect of clCAM-1 was removed. The ability to predict serum hPH and CL-IV from clCAM-1 might suggest the existence of a causal relationship between fibrosis and targeting of cytotoxic damage.

Acute Disease↗
PubMed1994

Thrombocytopenia of chronic liver disease corrected by erythropoietin treatment.

To investigate the possibility of correcting thrombocytopenia of chronic liver disease, 19 patients (6 male and 13 female) with long-term chronic liver disease and platelet count < or = 85,000/microliters were studied. Either a short-term course (7-20 days) of recombinant human erythropoietin, 4000 U daily SQ (12 patients) or placebo (7 patients) was administered. Treatment was interrupted if the platelets rose to > or = 100,000/microliters or if no significant increase was noted after 14 days. After treatment, platelets increased in the recombinant human erythropoietin group (from a baseline value of 70,000 +/- 11,184 to 101,250 +/- 37,625/microliters), while no difference was noted in the placebo group (70,714 +/- 9928 vs 70,000 +/- 10,231/microliters). The increase in the platelet count in the recombinant human erythropoietin group was significant, both compared to baseline values (paired Student's t-test, t = -3.80, p < 0.005) and to the results of treatment in the placebo group (unpaired Student's t-test, t = 2.71, p < 0.02). Eight out of 12 recombinant human erythropoietin-treated patients (66%) reached > or = 100,000/microliters platelets while four (33%) did not. In comparison to responders, non-responders had a significantly lower baseline platelet count (58,500 +/- 7937 vs 75,750 +/- 7498/microliters, t = -3.69, p = 0.004) and failed more frequently than responders to improve their haematocrit in response to recombinant human erythropoietin (Pearson chi 2 = 4.687, p = 0.03). When treatment was discontinued, the platelet count reverted to baseline in a few weeks. In conclusion, recombinant human erythropoietin treatment transiently corrected mild thrombocytopenia in patients with chronic liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Circulating intercellular adhesion molecule-1 (cICAM-1) concentration in liver disease. Relationship with cholestasis and functioning hepatic mass.

The authors measured immunoenzymatically circulating intercellular adhesion molecule-1 (cICAM-1) concentration in 135 patients with liver disease of either viral or toxic etiology: 13 had acute hepatitis; 58 had mild chronic liver disease; and 64 had cirrhosis (superimposed in 30 by hepatocellular carcinoma). Forty patients with extrahepatic diseases (19 with malignancies) and 28 healthy blood donors were tested as controls. One-way analysis of variance demonstrated a significant variability of cICAM-1 concentration among groups (F = 76.67, P < .0001), the highest value being recorded in acute hepatitis (Bonferroni's test for pairwise comparisons, P < .01). Total bilirubin showed a strong correlation with cICAM-1 (R = 0.766, P < .001). By stepwise multiple regression analysis the independent predictors of cICAM-1 concentration were chosen in the following order: total bilirubin; aspartate aminotransferase; cholinesterase; alpha-1-antitrypsin; and immunoglobulins. Thus, in addition to inflammation, cholestasis and decline of functioning hepatic mass may influence cICAM-1 concentration.

Adolescent↗