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Giorgio Bellomo

Publications and source records attributed to Giorgio Bellomo.

8 recordsLinked to original sources
PubMed2006

Heterozygous beta-globin gene mutations as a risk factor for iron accumulation and liver fibrosis in chronic hepatitis C.

BACKGROUND: Iron accumulation is a well-known risk factor for the progression of chronic hepatitis C (CHC) to fibrosis. However, the profibrogenic role of the genes controlling iron homeostasis is still controversial. AIM: To evaluate the relative role of haemachromatosis (HFE), ferroportin and beta-globin gene mutations in promoting iron accumulation and fibrosis in patients with CHC. METHODS: Genetic analysis was performed together with the assessment of hepatic iron content and histology in 100 consecutive HIV-antibody and hepatitis B surface antigen-negative patients with biopsy-proven CHC. RESULTS: Among the patients investigated, 12 were heterozygous for various beta-globin gene mutations (39[C-->T], IVS1.1[G-->A], 22 7 bp deletion and IVS1.6[T-->C]) and 29 carried HFE (C282Y, H63D and S65C) gene mutations. One further patient was heterozygous for both HFE (H63D) and beta-globin (39[C-->T]) variants, whereas 58 had the wild-type alleles of both the genes. Hepatic iron concentration (HIC) and hepatic stainable iron were significantly higher (p<0.05) in patients with CHC carrying beta-globin mutations than in those with HFE mutations or the wild-type alleles. Multivariate analysis confirmed that the presence of beta-globin mutations was independently associated with both HIC (p = 0.008) and hepatic-stainable iron (odds ratio (OR) 6.11; 95% CI 1.56 to 23.92; p = 0.009). Moderate/severe fibrosis or cirrhosis (Ishak's score >2) was observed in 48 of 100 patients. Logistic regression demonstrated that age (OR 1.05; 95% CI 1.02 to 1.09; p<0.005) and beta-globin mutations (OR 4.99; 95% CI 1.22 to 20.3; p = 0.025) were independent predictors of the severity of fibrosis. CONCLUSIONS: Heterozygosis for beta-globin mutations is a novel risk factor for both hepatic iron accumulation and the progression to fibrosis in patients with CHC.

Adult↗
PubMed2005

Regulation of Ca2+ movements by cyclovirobuxine D in ECV304 endothelial cells.

In Fura-2/loaded ECV304 endothelial cells cyclovirobuxine D promoted a transient increase in cytosolic free Ca2+ originating from both an intracellular pool sensitive to the endoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin and the extracellular space. The intracellular pool was apparently different from that mobilized by other agents acting through IP3 generation. The integrity of the plasma membrane was an absolute requirement. In cells treated with digitonin, cyclovirobuxine D did not promote any Ca2+ release from the intracellular stores even at high concentrations and in the absence or presence of thapsigargin or sodium azide, the inhibitors of the endoplasmic reticular or mitochondrial Ca2+ uptake. Furthermore, cyclovirobuxine D was effective in halting the persistent increase in cytosolic Ca2+ caused by thapsigargin, inhibiting the operation of the "capacitative" Ca2+ membrane channels as demonstrated by the decrease in the extent of both Ca2+-overshoot and Mn2+ influx. Additional effects of cyclovirobuxine D included a depolarization of plasma membrane apparently related to an enhanced influx of Na+ from the extracellular space. The results obtained indicate that cyclovirobuxine D markedly affects intracellular Ca2+ homeostasis in ECV304 endothelial cells by both promoting a discharge of intracellular pools and by interfering with the operation of store-dependent channels via plasma membrane depolarization.

Calcium↗
PubMed2004

[Amoxicillin in tonsillectomy: preliminary data on the evaluation of serum and tissue concentrations].

Amoxicillin was administered to 50 patients with chronic recurrent tonsillitis waiting for tonsillectomy. Group A (N=16) received 2.2 g of amoxicillin plus clavulanic acid with intravenous injection 10 minutes before tonsillectomy Group B (N=34) was treated with 3 doses of amoxicillin-clavulanic acid administered orally the day before surgery, plus one oral administration 2 hours before tonsillectomy. Antibiotic doses were established on patient's weight using maximum suggested. The measures were, estimated in serum and in tonsils using High Performance Liquid Chromatography, (HPLC). The data show better efficacy of intravenous administration than oral administration.

Administration, Oral↗
PubMed2002

Inflammatory predictors of mortality in the Scandinavian Simvastatin Survival Study.

BACKGROUND AND HYPOTHESIS: The predictive value of specific markers of infection and autoimmunity for coronary events, such as the effects of statins on inflammation, is still controversial. METHODS: A case-control design was used to compare C-reactive protein (CRP) levels, seropositivity for Chlamydia pneumoniae and Helicobacter pylori, and anti-oxidized low-density lipoprotein (oxLDL) antibody levels in prerandomization blood samples from 129 participants in the Scandinavian Simvastatin Survival Study who died (cases), and from 129 matched participants who were alive during 5-year follow-up (controls). RESULTS: Patients with CRP levels in the highest quartile had an increased risk of death compared with those in the first through third quartile (odds ratio [OR] = 2.51, 95% confidence interval [CI] 1.3-4.8). Seropositivity for Chlamydia pneumoniae or Helicobacter pylori and anti-oxLDL antibody levels were similar in cases and controls (p = NS). At a 4-month control, simvastatin reduced CRP levels (p = 0.009) while placebo did not (p = NS). However, the risk of death associated with high baseline CRP levels was similar in patients randomized to placebo (OR = 2.36, 95% CI 1.06-5.26) or simvastatin (OR = 3.13, 95% CI 1.06-9.21). CONCLUSIONS: Elevated CRP levels, but not seropositivity for Chlamydia pneumoniae or Helicobacter pylori, nor levels of anti-oxLDL antibodies, predict the risk of death in patients with stable ischemic heart disease. Simvastatin treatment reduces CRP levels, but without affecting the increased risk conferred by higher CRP levels at baseline.

Aged↗
PubMed2002

Inverse association between carotid intima-media thickness and the antioxidant lycopene in atherosclerosis.

BACKGROUND: Antioxidants may prevent atherosclerosis by interfering with endothelial activation, which involves the expression of endothelial adhesion molecules. The aim of this study was to explore the relationship between plasma levels of some lipid-soluble antioxidants (gamma-tocopherol, alpha-tocopherol, lycopene, beta-carotene, and ubiquinone), carotid maximum intima-media thickness (IMTmax), an index of atherosclerotic extension/severity, and soluble adhesion molecules (vascular cell adhesion molecule-1 [VCAM-1], intercellular adhesion molecule-1 [ICAM-1], and E-selectin), which are taken as a reflection of vascular cell expression of adhesion molecules. METHODS: We studied 11 healthy control subjects, 11 patients with uncomplicated hypertension (UH), and 11 patients with essential hypertension plus peripheral vascular disease (PVD) who were matched for age, sex, smoking habit, and body mass index. RESULTS: Patients with PVD had elevated IMTmax (2.7 [1.1-3.1] mm, median [range]) compared with both patients with UH(1.2 [0.8-2.4] mm) and control subjects (1.0 [0.6-2] mm). In patients with PVD, soluble (s)VCAM-1 and sICAM-1 were also significantly higher than in the 2 other categories. Plasma levels of lycopene had a trend toward lower values in patients with PVD compared with other groups (P =.13). A statistically significant correlation was found between lycopene and IMTmax (r = 0.42, P =.014) at univariate analysis, which persisted at multivariate analysis (P <.05) and was independent of low-density lipoprotein cholesterol, creatinine clearance, and plasma insulin. Plasma lycopene did not significantly correlate with any of the soluble adhesion molecules tested. CONCLUSIONS: We conclude that the inverse relationship of plasma lycopene with IMTmax is compatible with a protective role of this natural dietary antioxidant in atherosclerosis, although the mechanism of protection does not apparently involve a decrease in endothelial activation measured through soluble adhesion molecules.

Analysis of Variance↗
PubMed2002

Autoantibodies against oxidatively modified lipoproteins and progression of carotid restenosis after carotid endarterectomy.

BACKGROUND: The purpose of this study was to determine whether LDL oxidation could play an important pathogenic role in early restenosis after carotid endarterectomy. An immunologic and biochemical study was performed on a group of patients who underwent carotid endarterectomy, and the degree of intima-media thickness was measured 6 months after surgery. SUMMARY OF REPORT: Fifty-two consecutive patients were included in the study. The presence of antibodies against oxidized LDL in the serum at the time of surgery was evaluated and compared with echo Doppler flow imaging 6 months after the operation. A statistically significant correlation was found between the arterial wall thickness at the site of surgery and the absolute value of IgG antibodies against oxidized LDL (P<0.012) and IgM immunocomplexes (P<0.043). CONCLUSIONS: The presence of antibodies against oxidized LDL at the time of surgery seems to predict a greater intima-media wall hyperplasia at 6 months after surgery, usually recognized as early restenosis.

Aged↗
PubMedDate not supplied

Circulating antibodies recognising oxidatively-modified low-density lipoproteins in patients with IgA nephropathy, membranous glomerulonephritis and focal glomerulosclerosis.

BACKGROUND: Oxidation of low-density lipoproteins (LDL) generates molecular epitopes that play a pathologic role in experimental glomerular diseases and can also elicit an immune response and the generation of anti-oxidatively-modified LDL antibodies. METHODS: We investigated, for the first time in humans, the enhanced induction of LDL oxidation in chronic glomerulonephritis, the presence of circulating antibodies against oxidatively-modified LDL in patients with IgA glomerulonephritis (IgA GN) or with nephrotic syndrome associated with focal glomerulosclerosis (FGS) and primary membranous glomerulonephritis (MGN). The antibody levels were measured by enzyme-linked immunosorbent assay (ELISA) using native and copper-, peroxidase-, hypochlorite-, and peroxynitrite-oxidized LDL. RESULTS: Compared to control subjects, the three groups of patients, particularly the IgA GN patients, had higher serum levels of antibodies recognising LDL oxidised with the four different modalities and higher concentrations of cholesterol in circulating immune complexes. None of these were significantly correlated with any demographic, histological or biochemical laboratory finding. In patients with IgAGN, we investigated the possible confounding effects of cardiovascular risk factors (hypercholesterolemia, hypertension, diabetes and overt atherosclerosis). Although the concentration of cholesterol in circulating immune complexes was significantly higher in patients with cardiovascular risk factors, no significant differences were observed in the level of anti-oxidised-LDL antibodies. This analysis, however, was impossible in FGS and MGN patients because of the high prevalence of hypercholesterolemia in these groups. CONCLUSIONS: These results suggest that IgA GN, MGN and FGS are associated with an enhanced immune response to LDL oxidised with different stimuli mimicking the pro-oxidant environment occurring in vivo, mirrored by the increased levels of specific antibodies, very likely linked to enhanced in vivo LDL oxidation which might participate in glomerular damage and progression.

Adult↗