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Biomedical subjects

E Bartoli

Publications and source records attributed to E Bartoli.

At least 73 records · Page 4Linked to original sources
PubMed1997

Increased soluble ICAM-1 concentration and impaired delayed-type hypersensitivity skin tests in patients with chronic liver disease.

AIMS/BACKGROUND: Soluble ICAM-1 may act as an antagonist of the membrane bound form, which is essential for the adhesion of leucocytes to endothelial cells. The aim of this study was to investigate whether the presence of high concentrations of soluble ICAM-1 are related to the impairment of delayed-type hypersensitivity reactions. METHODS: The study population comprised 73 patients (53 men and 20 women) with chronic liver disease (19 with chronic hepatitis, 36 with cirrhosis and 18 with hepatocellular carcinoma), and 21 age-matched controls (11 men and 10 women). Serum soluble ICAM-1 was measured using an enzyme immunoassay. Skin tests for seven different antigens (tetanus, diphtheria, streptococcus group C, tuberculin, Candida, tricophyton, and proteus) were considered positive when diameters > or = 2 mm were recorded; the diameters of positive tests were added to calculate a cumulative score. RESULTS: Patients with chronic liver disease had fewer positive skin tests (median 2) and a lower cumulative score (median 7) than controls (median 3 and 12, respectively). Multivariate analysis suggested the existence of an independent association between alkaline phosphatase and anergy to skin tests and between soluble ICAM-1 concentrations and the cumulative score. CONCLUSIONS: The strong association observed between increased soluble ICAM-1 concentrations and impairment of delayed-type hypersensitivity skin tests suggests that soluble ICAM-1 may be implicated in the immune depression seen in patients with chronic liver disease.

Adult↗
PubMed1997

Microinjection studies on the effect of furosemide on the rat nephron.

The tubular site of furosemide (F) action was studied by the technique of diuretic microinjection (MIJ) into proximal tubules of the rat nephron. F was injected into the last proximal superficial loop of 51 proximal tubules, at the concentration of 3 x 10(-4) mol/l in an infusate that contained 14C-inulin. Collections were performed at the early distal tubule before and after MIJ. Single nephron filtration rate (SNGFR) remained unchanged, while the percent of filtered volume reabsorbed up to the site of collection was 85+/-2 before, 79+/-2% after MIJ, p < 0.005. The calculated concentration of F in the collected distal tubular fluid during the post-MIJ measurements averaged 3 x 10(-5) mol/l. This experiment was repeated by injecting F into the early proximal convolutions of 43 nephrons, while the collections were performed at the last proximal segments. In these studies of proximal volume absorption, SNGFR was 34+/-3 before, 35+/-4 nl/min after F (p > 0.6). The respective percent reabsorptions were 70+/-3 and 73+/-3% (p +/- 0.3). In order to determine whether the technique per se was suitable to detect changes in reabsorption, the proximal MIJ study was repeated by using the carbonic anhydrase inhibitor dichlorphenamide 3 x 10(-5) mol/l in the microinjectate: while SNGFR remained unchanged, percent reabsorption fell from 63+/-5 to 45+/-7% during injection of the diuretic, p < 0.03. We conclude that the technique is adequate to examine the effects of drugs, and that F does not reduce proximal volume absorption at concentrations of 3 x 10(-5) mol/l. The loop diuretic decreases distal volume absorption by abolishing the osmotic gradient between blood and tubular fluid along the early distal convoluted tubule.

Animals↗
PubMed1997

Long-term effects of erythropoietin therapy on fistula stenosis and plasma concentrations of PDGF and MCP-1 in hemodialysis patients.

Among the adverse effects possibly associated with the use of erythropoietin (EPO) in hemodialysis patients is an increased incidence of thrombosis of the vascular access. However, little is known about the effect of EPO on the stenotic lesion in the venous outflow system, which is the leading cause of fistula thrombosis. This study was designed to explore the long-term effects of EPO treatment on progressive fistula stenosis and the plasma concentrations of some potential mediators of neointimal hyperplasia. A cross-sectional and 3-yr prospective, placebo-controlled, pilot study was performed in 30 hemodialysis patients with native arteriovenous fistula. Sixteen patients received EPO and 14 received a placebo. Venous dialysis pressure, urea recirculation, color Doppler sonography, and angiography were used to monitor vascular access patency. Compared with 60 healthy subjects, the hemodialysis patients had elevated plasma levels of platelet-derived growth factor, monocyte chemoattractant protein-1, and interleukin 6, three proteins that might be involved in the neointima formation regulating the proliferation of vascular smooth muscle cells. In addition, these patients had numerous endothelial and hemostatic abnormalities that indicated a thrombophilic state. Eleven patients, six (37.5%) receiving EPO and five (35.7%) taking placebo, developed a progressive stenosis in the venous circuit of the fistula. There was no significant difference in the vascular access, event-free survival over 36 mo between patients receiving EPO therapy and placebo. EPO induced a significant decrease in the plasma values of platelet-derived growth factor and vascular cell adhesion molecule-1 and an increase of monocyte chemoattractant protein-1 concentration. After EPO withdrawal, these parameters returned to pretreatment levels. In conclusion, long-term EPO therapy does not increase the risk of progressive stenosis of native arteriovenous fistula. The use of erythropoietin does not induce any prothrombotic change in hemostatic parameters, and further studies are required to elucidate the theoretically beneficial effects on the plasma concentration of some potential mediators of neointimal formation.

Adult↗
PubMed1997

Total radical-trapping antioxidant parameter in NIDDM patients.

OBJECTIVE: The existence of an oxidative stress in diabetes is still debated. This is largely due to the lack of good tools to assay the level of oxidative stress. The use of total radical-trapping antioxidant parameter (TRAP) has recently been proposed to explore the antioxidant property of a plasma sample. TRAP may be either directly measured by a fluorescence-based method (TRAPm) or calculated (TRAPc) by a mathematical formula, taking into account the serum levels of four natural antioxidants: protein-bound SH (thiol) groups, uric acid, vitamin E, and vitamin C. The difference between TRAPm and TRAPc is due to antioxidants, which are still unidentified, and to the possible synergism among the antioxidants. RESEARCH DESIGN AND METHODS: In this study, we evaluated malondialdehyde (MDA), TRAPm, TRAPc, protein-bound SH groups, uric acid, vitamin E, and vitamin C in 40 NIDDM patients and 40 matched normal control subjects. RESULTS: TRAPm and TRAPc were significantly lower in diabetic patients. A good correlation between TRAPm and TRAPc was found in both NIDDM patients (r = 0.68, P < 0.0001) and control subjects (r = 0.74, P < 0.0001). Protein-bound SH groups and uric acid were significantly lower in diabetic subjects, while MDA and vitamin E level were significantly higher. After correction for serum triglycerides (MDA) and cholesterol (vitamin E), MDA lost significance, while vitamin E did not. Vitamin C was not different in the two groups. CONCLUSIONS: These data show decreased TRAP levels in NIDDM patients, suggesting the existence of lower antioxidant defenses in diabetes. The decrease appears to be due to various antioxidants, some of them not yet clearly defined. TRAP may represent a more reliable estimation of serum antioxidant capacity than the measurement of each known antioxidants. The correlation found between TRAPm and TRAPc values suggests that TRAPc, easier to measure than TRAPm, might be adequately reliable for routine assessment of oxidative stress in diabetic patients.

Antioxidants↗
PubMed1997

Gastric B-cell clonal expansion and Helicobacter pylori infection in patients with autoimmune diseases and with dyspepsia. A follow-up study.

BACKGROUND: It is not clear whether gastric B-cell clonal expansion, a possible precursor of mucosa-associated lymphatic tissue (MALT) lymphoma, is exclusively linked to Helicobacter pylori infection and virulence. METHODS: In this study we followed up, for up to 33 months, 16 VDJ polymerase chain reaction-positive patients (4 with dyspepsia, 9 with Sjögren's syndrome, and 3 with other autoimmune diseases). Of these, 12 were H. pylori-positive. In addition, in H. pylori-positive patients we tested whether the serum anti-cag-A (a potential marker of virulence) was preferentially associated with B-cell clonality. RESULTS: In all but one patient clonality appeared temporally unrelated to H. pylori infection. The prevalence of anti-cagA was not higher in H. pylori/VDJ-positive patients than in controls. CONCLUSIONS: These data indicate that, in addition to H. pylori, gastric B-cell clonality may be sustained by other agents/mechanisms. Anti-cag-A does not appear to be involved in the pathogenesis of clonality.

Adult↗
PubMed1996

Circulating intercellular adhesion molecule 1 predicts non-specific elevation of alpha 1-fetoprotein.

Molecules governing cellular interactions have been suggested to be involved in the spurious elevation of alpha 1-fetoprotein (AFP) in non-neoplastic liver disease. To explore this controversial issue, we measured AFP, circulating intercellular adhesion molecule 1 (cICAM-1), and common liver function tests in 111 patients (71 male, 40 female). Eighty-four patients had non-neoplastic chronic liver disease and 27 had hepatocellular carcinoma. The concentration of cICAM-1 was determined immunoenzymatically. In patients with non-neoplastic chronic liver disease, univariate analysis demonstrated a significant correlation between AFP and cholinesterase (R = -0.397, P < 0.001), aspartate aminotransferase (R = 0.421, P < 0.001), bilirubin (R = 0.231, P < 0.05) and cICAM-1 (R = 0.430, P < 0.001). Multivariate analysis among these variables and AFP indicated cICAM-1 to be the strongest independent predictor of AFP. We conclude that cICAM-1 compares favourably with liver function tests in predicting non-specific AFP variations in non-neoplastic chronic liver disease, suggesting a link between targeting of the inflammatory damage to the hepatocyte and development of neoplasia.

Adult↗
PubMed1996

Endotoxin priming exacerbates acute reflux pancreatitis in the rat.

Recently, endotoxaemia has been reported as a prognostic marker in acute pancreatitis. However, the role of endotoxin in inducing or aggravating acute pancreatitis is not fully understood. We administered endotoxin 400 micrograms/kg i.p. to rats 24 h before performing either a closed duodenal loop (group B) or a sham operation (group D). Pancreatic damage and overall survival were compared with the results obtained in rats not exposed to endotoxin undergoing either closed duodenal loop (group A) or sham treatment (group C). In a first set of experiments, 24 h after laparotomy blood samples were collected and the animals were sacrificed; survival up to 8 days was estimated in a second set of experiments. Group B had higher lipase concentrations and more severe tissue damage than group C (P < 0.05). A larger number of abscesses was observed in both group B and group D as compared to group C (P < 0.05). Survival was significantly shorter in group B (P < 0.0001). We conclude that priming with endotoxin worsens the extent of pancreatic damage induced by the closed duodenal loop procedure in the rat, possibly favouring selective homing of neutrophils to the site of inflammation, in similarity to what happens in the Shwartzman phenomenon.

Animals↗
PubMed1996

Prognostic value of serum alpha-1-antitrypsin in hepatocellular carcinoma.

To evaluate serum alpha-1-antitrypsin (A1AT) as a prognostic factor in hepatocellular carcinoma, we studied 75 consecutive patients (60 male, 15 female, mean age +/- SD 63.0 +/- 9.3 years) in whom hepatocellular carcinoma developed with pre-existing cirrhosis. Median survival time was 245 days (range 4-1568+). 30 patients had serum A1AT concentration of < or = 2.20 g/l (Group A) while 45 (Group B) had alpha-1-antitrypsin > 2.20 g/l. Median survival was 518 days in Group A and 81 days in Group B (Mantel-Cox 20.95, P < 0.0001; hazard ratio 0.26, 95% confidence limits 0.15-0.46). By stepwise survival analysis, alpha-1-antitrypsin together with bilirubin, tumour size and blood urea nitrogen were chosen among 17 variables as the only independent predictors of survival. We conclude that measurement of serum A1AT concentration might be useful as an inexpensive, widely available prognostic marker of hepatocellular carcinoma.

Adult↗
PubMed1996

Immunosuppressive treatment of Berger's disease.

BACKGROUND: The aim of our study was to determine whether immunosuppressive treatment is effective in preventing and reversing the evolution of Berger's disease toward chronic renal failure. METHODS: We studied 20 unselected, consecutive patients with biopsy-proven Berger's disease who met the criteria for disease progression. They had proteinuria, significant histologic changes, persistent hematuria, and red cell casts. The treatment consisted of prednisone in an alternate-day regimen and cyclophosphamide, either in a daily oral administration or in a monthly intravenous pulse injection, both given for a 6-month cycle. Five patients had chronic renal failure (as disclosed by plasma creatinine of 230 +/- 71 mumol/L), hypertension, and proteinuria (2.7 +/- 0.8 gm/day), whereas the remaining 15 patients had normal renal function (plasma creatinine, 97 +/- 18 mumol/L) and less severe proteinuria (1.9 +/- 1.1 gm/day). However, even these 15 patients had a significant number of risk factors heralding progression to chronic renal failure. RESULTS: Over an average follow-up of 8.7 +/- 3.7 years (range, 5 to 15 years), all patients but one had complete disease remission, including five patients with incipient chronic renal failure. Relapse occurred in two patients who were healed after a repeat treatment cycle. Over the entire follow-up period, no patient progressed to chronic renal failure and plasma creatinine concentration remained stable, even in subjects in whom it was high before treatment (257 +/- 79 versus 230 +/- 71 mumol/L; p > 0.05). CONCLUSION: The immunosuppressive treatment of patients with Berger's disease with high probability of progression appears to be effective in the prevention of end-stage renal disease.

Adolescent↗
PubMed1996

Regression of Henoch-Schönlein disease with intensive immunosuppressive treatment.

OBJECTIVE: To assess the results of a new immunosuppressive cycle, which had given favorable results in other immune-mediated glomerulonephritides, in the treatment of Henoch-Schönlein disease. METHODS: Eight patients (seven male and one female; age range, 13 to 61 years) with biopsy-proved Henoch-Schönlein were treated with the following protocol: (1) induction with 250 to 750 mg intravenous methylprednisolone every day for 3 to 7 days plus 100 to 200 mg oral cyclophosphamide every day, (2) maintenance with 100 to 200 mg oral prednisone on alternate days plus cyclophosphamide, as before, for 30 to 75 days; (3) tapering, with prednisone reduced on average by 25 mg every month while the cyclophosphamide dose remained the same, and (4) discontinuation, after at least 6 months, with abrupt interruption of cyclophosphamide and slow tapering of prednisone. The results were assessed in terms of remission, improvement, progression of disease, kidney failure, and death, unambiguously defined. The follow-up extended up to 12 years. RESULTS: Seven of eight patients had a complete remission that was maintained indefinitely thereafter. Plasma creatinine levels decreased on average from 211 +/- 81 to 92 +/- 27 mumol/L (p < 0.01) and urine protein excretion decreased from 1.9 +/- 0.8 to 0.3 +/- 0.1 gm/day (p < 0.01). One patient died of intestinal infarction caused by atherosclerotic mesenteric artery thrombosis. CONCLUSIONS: Our data suggest that an intensive immunosuppressive regimen that combines prednisone and cyclophosphamide at high doses can be effective in healing Henoch-Schönlein disease.

Administration, Oral↗
PubMed1996

Increased circulating intercellular adhesion molecule-1 levels in type II diabetic patients: the possible role of metabolic control and oxidative stress.

Blood levels of the circulating form of the integrin intercellular adhesion molecule-1 (ICAM-1), malondialdehyde (MDA), and hemoglobin A1c (HbA1c) were studied at baseline and 3 months after improved metabolic control in 25 type II diabetic patients without signs of macroangiopathy, and were compared with those in 15 matched healthy normal controls. Circulating ICAM-1 and MDA levels were increased in diabetic patients, both at baseline and 3 months later. However, with improving metabolic control HbA1c, circulating ICAM-1, and MDA significantly decreased. A significant correlation between circulating ICAM-1, HbA1c, and MDA was found in diabetic patients at each time. Multiple regression analysis considering circulating ICAM-1 as the dependent variable and HbA1c and MDA as independent variables, showed a significant correlation between the three variable at each time. Similar correlations were found in control subjects. These data show increased levels of circulating ICAM-1 in type II diabetic patients, independent of the presence of macroangiopathy. Moreover, these results suggest that oxidative stress and metabolic control might participate in determining increased circulating ICAM-1 levels in both type II diabetic patients and normal subjects.

Diabetes Mellitus, Type 2↗
PubMed1996

Hepatocellular sulfobromophthalein uptake at physiologic albumin concentrations: kinetic evidence for a high affinity/low capacity sinusoidal membrane system.

BACKGROUND/AIMS: Controversy exists regarding the nature of the hepatocyte membrane transport system for sulfobromophthalein and other organic anions and its driving forces. Most studies have been performed in the absence of albumin, the plasma sulfobromophthalein binding protein, or using very low albumin concentrations. We have shown that in the latter case uptake kinetics reflect dissociation/diffusion events and not membrane transport. In contrast, without albumin very high sulfobromophthalein concentrations reach the cell surface and may overwhelm a high affinity/low capacity system operating in vivo. The aim of this study was to test the latter hypothesis. METHODS: Sulfobromophthalein uptake was measured by rapid filtration in isolated hepatocytes without albumin (up to 13 microM sulfobromophthalein) and with 600 microM albumin (sulfobromophthalein:albumin from 0.03:1 to 1:1), a physiologic setting which greatly reduces the unbound BSP concentration. Unbound sulfobromophthalein concentration was estimated according to a three binding site model. RESULTS: In the absence of albumin, kinetic parameters for sulfobromophthalein uptake were similar to those reported in the literature (K(m):7.1 +/- 1.2 microM; V(max): 452 +/- 37 pmol/min/5 x 10(4) cells). In the presence of albumin, sulfobromophthalein uptake displayed much greater affinity and much lower capacity (K(m): 80 +/- 11 nM; V(max): 60 +/- 9 pmol/min/5 x 10(4) cells). CONCLUSIONS: These findings suggest that in the absence of albumin, resulting high sulfobromophthalein concentrations overload (and make undetectable) a high affinity/low capacity system operating at physiologic albumin concentrations (i.e. at low unbound sulfobromophthalein concentrations). Previously characterized transport systems may be operating only under defined conditions. These findings could explain the apparent controversy regarding the nature of the sulfobromophthalein transport system and its driving forces.

Animals↗
PubMed1996

Widespread clonal B-cell disorder in Sjögren's syndrome predisposing to Helicobacter pylori-related gastric lymphoma.

Helicobacter pylori has been identified as a critical antigenic stimulus to the development of gastric lymphoma, but additional factors should be required for such evolution. This topic is now of major importance to clarify the pathobiology of gastric lymphomagenesis. Peculiar autoimmune diseases, such as Sjögren's syndrome, are well known to predispose to B-cell lymphomas. We report on a patient with Sjögren's syndrome and a widespread B-cell lymphoproliferative disorder. A pathological picture of low-grade lymphoma was observed in the stomach, concomitantly with H. pylori infection. However, the B-cell disorder was definitely nonmalignant in the other tissues involved, i.e., the parotid gland and lymph nodes, which are the characteristic targets of Sjögren's syndrome-associated lymphoproliferation. After H. pylori eradication, a dramatic regression of gastric lymphoma into chronic gastritis was observed, but no amelioration occurred in the parotid and nodal involvement. Multiple molecular analyses showed the expansion of the same B-cell clone in synchronous and metachronous lymph node, parotid, and gastric lesions before and after H. pylori eradication. Thus, H. pylori played a crucial role in the local boosting of B-cell lymphoproliferation, but the underlying B-cell disorder was that associated with the autoimmune disease and was nonmalignant. The comprehensive clinical, pathological, and molecular approach allowed us to then distinguish the role of peculiar individual predisposing factors and of local infection in the pathobiology of mucosa-associated lymphoid tissue-associated lymphoproliferation.

Aged↗