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Abdominal ultrasonography (US) represents the first-line imaging examination in chronic liver diseases; in most cases, US, laboratory findings and the clinical context are generally sufficient to guide the diagnosis. Thanks to the considerable diffusion of US, we have seen an increased diagnosis of NAFLD in recent years, although this condition is generally silent from a clinical point of view. We have to identify the metabolic syndrome in the general population and to promptly recognize NAFLD to prevent its development into non-alcoholic steatohepatitis, cirrhosis and hepatocellular carcinoma. Among the non-invasive diagnostic techniques for NAFLD and for early vascular damage, ultrasonography represents the method of choice. In fact, besides the traditional semiotics of fundamental US of the liver, new US techniques have recently been proposed (contrast enhancement US, acoustic structure characterization), with respect to serum biomarkers and Fibroscan, for the study of liver fibrosis. Similarly, also as concerns the US measurement of carotid intima-media thickness, new automated methods with sophisticated software and radio-frequency signal have recently been introduced. Finally, we report the preliminary results of a personal experience on liver and carotid US in the epidemiology of the metabolic syndrome.

Aim: To ascertain whether carotid lesions are more prevalent in outpatients with incidental findings of nonalcoholic fatty liver disease (NAFLD) at abdominal ultrasound (US)., Methods: One hundred and fifty-four consecutive outpatients (age range 24-90 years, both sexes) referred by general practitioners for abdominal US, and drinking less than 20 g alcohol/day, underwent carotid US for an assessment of carotid intima-media thickness (c-IMT) and carotid plaque prevalence. Hepatic steatosis, visceral fat thickness and subcutaneous fat thickness were also assessed at ultrasonography., Results: Higher c-IMT values were found in the presence of NAFLD (90 patients), even after adjustment for indices of general and abdominal obesity and for the principal cardiovascular risk factors (0.84 +/- 0.10 mm vs 0.71 +/- 0.10 mm, P < 0.001). The prevalence of carotid plaques was 57.8% in the patients with NAFLD vs 37.5% in the patients without this condition (P = 0.02). The adjusted relative risk of having carotid plaques for patients with NAFLD was 1.85 (95% CI: 1.33-2.57, P < 0.001)., Conclusion: An incidental finding of hepatic steatosis may suggest the presence of silent carotid atherosclerotic lesions.

Purpose: To retrospectively and prospectively determine the rate and type of complications and their association with clinical or technical factors after percutaneous laser ablation (LA) for hepatocellular carcinoma (HCC)., Materials and Methods: The institutional research board of each center approved the study and all patients provided informed consent. By using an Internet liver tumor database of nine Italian centers, 520 patients were included with HCC nodules of any size (small, 0-3 cm; intermediate, >3-5 cm; large, >5 cm). Postprocedural complications were related to clinical or percutaneous LA factors by using the Student t and chi(2) tests. Follow-up was carried out with computed tomography (CT) at 1, 3, 6, 9, and 12 months, and primary effectiveness rate was defined as the percentage of HCCs completely ablated after percutaneous LA., Results: A total of 353 men and 147 women (age range, 24-86 years; Child-Pugh score A = 63.4%, B = 30.8%, C = 5.9%) with 647 nodules (mean diameter, 3.2 cm +/- 1.7) were treated by 1004 percutaneous LA sessions. There were four (0.8%) deaths in 520 patients; 15 (1.5%) of 1004 sessions presented major complications without any seeding. Major complications were associated with excess energy (10 520 J +/- 7073 vs 7474 J +/- 3803; P = .001) and high-risk location (P = .05). Sixty-two (6.2%) sessions resulted in minor complications associated with excess energy (P = .001), high bilirubin level (1.74 mg/dL +/- 1.10), and low prothrombin time (P = .01). Primary effectiveness rates were 60% in all HCCs and 81% in HCCs smaller than 3 cm., Conclusion: Percutaneous LA may be considered a safe treatment for small HCCs., ((c) RSNA, 2008.)

Background: H. pylori and age are two known risk factors for atrophic gastritis and high epithelial cell turnover may be an indicator for preneoplastic changes in the stomach. We searched for an association between H. pylori, age and gastritis in the general population together with the proliferative state into the antral mucosa., Methods: We examined gastric biopsies from antrum and corpus of 117 consecutive volunteers which were endoscoped during a population study in San Marino. H. pylori status was determined by serum IgG antibodies, rapid urease test on biopsies and histology. Presence of gastritis and grading of inflammation, activity, intestinal metaplasia and atrophy were ascertained using Sydney System. On a subsample of 36 subjects without endoscopic lesions we performed an immunohistochemical study on gastric cell proliferation using PCNA. A computer-aided count was made on stained epithelial cells to evaluate labeling index. Statistical analysis was performed using chi 2 test and linear regression., Results: Inflammatory infiltrate (both activity and mononuclear cells), (p < 0.0001) and intestinal metaplasia (p < 0.004) were significantly higher in H. pylori positive subjects. Atrophic gastritis was present in 82% H. pylori positive subjects vs 17.6% (p < 0.0001). Labeling Index was significantly higher in H. pylori positive subjects (p < 0.005) and it was correlated with inflammation and atrophy (p = 0.001). Elderly H. pylori negative subjects have a lower cell turnover (p = 0.006) but H. pylori infected subjects do not show any decrease of Labeling Index with age., Conclusions: In the general population of an area with high gastric cancer rate, H. pylori infection is associated with atrophic gastritis and with hyperproliferative gastric cell state. These conditions are present either in young and old age and increase the neoplastic risk of gastric mucosa.

The prevalence of anti-HEV was assessed in 2,233 subjects aged 20-79 years in the Republic of San Marino in the years 1990-1991. The sera were tested by ELISA and further confirmed by Western blot (WB) analysis. The overall anti-HEV prevalence was 1.5%. A significant trend by age was observed. Anti-HEV prevalence was 0.6% in subjects <30 years and 3.3% in those older than 70 years of age. Family size larger than four persons (OR = 3.8; 95% CI = 1.8-13.2) was the sole independent predictor of anti-HEV positivity in the multivariate analysis. Anti-HAV and anti-HEV prevalences did not show a parallel trend by age. No association was found either between hepatitis E virus (HEV) or hepatitis C virus (HCV) infections. Follow-up samples 5 years apart were available for 38 out of 54 (70%) anti-HEV ELISA-positive subjects. Eight out of 22 (37%) WB-confirmed anti-HEV-positive subjects were still anti-HEV-positive after 5 years. However, anti-HEV remained positive in all but two (75%) of the subjects with WB-confirmed ELISA positivity value of S/CO > or = 2 (cutoff 1.2), but in only 2 out of the 14 subjects (14%) with a WB-confirmed ELISA positivity value of S/CO < 2 (P < 0.005). None of the 16 subjects ELISA-positive but not WB-confirmed was anti-HEV-positive 5 years apart. Therefore, only a relative proportion of subjects once infected with HEV maintain for at least 5 years anti-HEV antibodies.

The heterogeneity of the immune response to Helicobacter pylori has always been noticed but has never been evaluated by obtaining a quantitative measure. For this purpose, sera were tested by enzyme-linked immunosorbent assay, and 207 positive serum specimens were subsequently tested by immunoblotting. The presence or absence of six specific bands was noted. The homology of the different profiles of bands was measured by calculating the Dice coefficient, and a dendrogram was constructed. Thirty-four profiles were found, with each profile containing from 1 to 43 serum specimens. At a level of 72% similarity, 115 of the serum specimens studied fell into eight profiles. At a level of 48% similarity, 186 of the serum specimens studied fell into 22 profiles. The difference in immunoblot profiles was probably linked to the host immune response, but infection with strains carrying different antigens cannot be ruled out.

Background: CagA-positive Helicobacter pylori strains appear to increase the risk for atrophic gastritis., Aim: To verify the association between CagA status and atrophic gastritis in the general population by means of computerized image analysis., Subjects: Forty-five subjects were chosen out of a representative sample of a population at high gastric cancer risk., Methods: Helicobacter pylori status was assessed by IgG ELISA, rapid urease test and histology. Serum anti-CagA antibodies were detected by western blotting. Subjects were subdivided into 3 groups: 15 subjects Helicobacter pylori positive CagA-positive, 15 Helicobacter pylori positive CagA-negative and 15 controls Helicobacter pylori negative. Biopsies were studied using the Sydney System score. A computerized image analysis was used to count inflammatory cells in the lamina propria and to measure the area of the gastric glands., Results: Anti-CagA antibodies were associated with reduction of gland area (126,671 +/- 81,032 mu 2/mm2 vs 231,384 +/- 54,159; p = 0.0001), with increasing both of polymorphonuclear cells (426 +/- 238 cell/mm2 vs 136 +/- 69; p = 0.0001) and mononuclear cells (8675 +/- 1304 cell/mm2 vs 7141 +/- 1230; p = 0.003)., Conclusions: The association of anti-CagA antibodies with a high grade of gastric atrophy further supports the hypothesis that Helicobacter pylori CagA-positive strains can promote the multifactorial process of gastric carcinogenesis.

In 1990-1991, the prevalence of antibodies to hepatitis A virus infection (anti-HAV) was assayed by the ELISA method among 1528 apparently healthy subjects, 20-85 years old in the Republic of San Marino. Subjects were selected from the list of residents by a random stratified sampling procedure with a proportional allocation by age, sex and district of residence. The overall anti-HAV prevalence was 64.7%; it increased from 28.6% in subjects 20-30 years old to 97% in those > 60 years (p < 0.01). No gender difference was observed. At the multivariate analysis age > 40 years (OR: 39.5; 95% CI: 12.4-126) and lowest level of schooling (OR: 1.8; 95% CI: 1.1-2.9), which is a good indirect indicator of socio-economic status, resulted both independent predictors of anti-HAV seropositivity. These findings reflect the improved sanitation standards in this area and indicate that the proportion of non-immune adults is increasing with a higher risk of symptomatic infection in the near future.

Mucosa-associated lymphoid tissue (MALT) showing a follicular structure can develop in the gastric mucosa as a response to Helicobacter pylori infection. We emphasize the importance of anti-H. pylori antibiotic therapy in the elimination of acquired MALT. Of the 200 patients studied, acquired MALT was found in 70 of the 151 H. pylori-positive patients, whereas it was present in only five of the 49 H. pylori-negative patients. Thirty-eight H. pylori-positive and MALT-positive patients were treated with antibiotic therapy and reevaluated after 6 months: 21 patients were H. pylori negative/MALT negative, 12 were H. pylori positive/MALT positive, four were H. pylori negative/MALT positive, one was H. pylori positive/MALT negative. In the control group (n = 20), H. pylori and acquired MALT were still present at follow-up. One patient with histological and immunohistochemical evidence of low-grade B-cell gastric MALT lymphoma underwent antibiotic treatment and was reexamined after 8, 12, and 24 weeks: histological examination of biopsy samples showed regression of the MALT lymphoma in tandem with the disappearance of H. pylori colonization. Our data confirm the correlation between H. pylori infection and acquired MALT, as documented by the ability of antibiotic therapy to induce the disappearance of acquired MALT and regression of MALT lymphoma. Considering the potential evolution of MALT into low-grade B-cell MALT lymphoma, H. pylori eradication should play a role in the prevention of this tumor.

The close association between Campylobacter pylori (CP), gastritis and peptic ulcer is now well established. Moreover increasing evidence has been collected of a major etiological role of CP in type B chronic gastritis. For this reason, searching for CP is essential in all patients with upper gastrointestinal symptoms. Scanning electron microscopy (SEM) is a most reliable technique for studying the distribution of microorganisms and their relationship to the gastric mucosal surface. The aim of this paper is to compare SEM to other routine methods of detection for CP, such as Giemsa staining on histological sections and Urease Microtiter Test (MT) on fresh tissue and to investigate the surface morphology of gastric mucosa colonized by CP and to correlate it with the histopathological picture. Thirty-seven biopsies taken from the gastric body and the antrum of 22 patients were used for each type of determination. The different parameters were graded semiquantitatively. Histology showed a normal mucosa in 4 cases, chronic superficial gastritis in 12 and chronic atrophic gastritis in 21 cases. SEM was more sensitive than histology and Urease MT in detecting Campylobacter pylori. This is due to the patchy distribution of this bacterium on gastric mucosa. For this reason SEM should always be performed when routine tests are negative. The presence of CP correlated significantly (p less than 0.001, Spearman Rank Correlation Test) with the neutrophilic infiltrate, thus with the "activity" of the gastritis. The CP associated gastritis has no distinctive surface features other than the presence of the bacterium. SEM morphology of surface gastric mucous cells suggests that CP does not damage the lining epithelium directly. Neutrophils and inflammatory mediators could be involved in the production of the mucosal lesions.