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PROSPECTIVE STUDY OF DYSPLASTIC NODULES IN CIRRHOSIS: CORRELATION WITH CT VASCULAR PATTERN, HISTOLOGY AND DEVELOPMENT OF HEPATOCELLULAR CARCINOMA
Abstracts / Digestive and Liver Disease 41S (2009), S1–S167
S15
Results: PPAR-gamma*2 isoform was found in 24 cases. Twentyfour out of 52 patients had H. pylori infection. Gastric atrophy and intestinal metaplasia were detected in 14 (26%). COX-2 and NF-κB were overexpressed in 30/520 cases (24 carrier of PPAR-gamma*2 isoform; p<0.0007). COX-2 and NF-κB expression were related to PPAR-gamma polimorphisms and to atrophy and intestinal metaplasia. Conclusions: PPAR-gamma polimorphisms influence the expression of COX-2 and NF-κB in inflamed gastric mucosa. These data suggest a possible role of PPAR-gamma in gastric carcinogenesis. # B. Gastric diseases 5. Pre-cancerous lesions
OC.03.1
OC.02.6
Background and aim: Dysplastic nodules (DNs) detected in cirrhotic liver are at risk of transformation into hepatocellular carcinoma (HCC) but there is not a contrast imaging pattern diagnostic for DNs. We assess the risk of malignant transformation, the vascular pattern of contrast CT diagnostic for DNs and its correlation with HCC development. Material and methods: Between 1998 and 2002, all cirrhotic patients attending our Liver Unit with a de-novo liver node detected during surveillance with ultrasound (US) and an histological diagnosis of either low grade or high grade dysplasia, were enrolled in the study and underwent a contrast enhanced CT scan. These patients were followed with US and serum alfa-fetoprotein every 3 months, abdominal CT scan every 6 months and biopsy was repeated in case of increasing in size or changes in vascular pattern. Diagnosis of dysplasia and HCC was made according to the International Working Party criteria. Results: 36 patients were enrolled with mean age of 61 (40-74) yrs, 83% males, 39% HCV-positive, 92% Child-Pugh A, the mean node diameter was 19 (10-26) mm. 21 nodules had an histological diagnosis of low grade dysplasia while 15 high grade dysplasia. Seventeen DNs (47%) had hypervascularity at the arterial phase without wash-out in the venous phase, 15 (42%) had only the wash-out in the venous phase and 4 were negative on CT scan. During a mean follow-up of 39 months (6-121), the yearly incidence of HCC development within the DNs was 9.2%, with 8.4% further of HCC out-side the target lesion, with an over-all yearly incidence of 17.6%. Older age and high-grade dysplasia were the only risk factors associated to HCC development, being the mean yearly incidence of HCC in high grade dysplastic nodules significantly higher compared to the low grade dysplasia (33.5 vs 9.9, p=0.004). The baseline CT scan vascular pattern was unable to characterize the DNs according to histological diagnosis, nor was associated to HCC development. Conclusions: Cirrhotic patients with a DN are at high risk of developing HCC either within or outside the nodule. Enhanced follow-up should be considered for patients with DNs, as suggested by the EASL/AASLD guidelines for unsolved nodules. # F. Cirrhosis & its complications 1. Natural history
AUTOIMMUNITY SUSCEPTIBILITY GENOTYPE HLA-DRB1 OCCURS IN PATIENTS WITH ATROPHIC BODY GASTRITIS IRRESPECTIVE OF HELICOBACTER PYLORI INFECTION E. Lahner ∗ ,1 , M.L. Spoletini 2 , R. Buzzetti 2 , A. Petrone 2 , L. Vannella 1 , V.D. Corleto 1 , G. Delle Fave 1 , B. Annibale 1 1 Digestive and Liver Disease, University Sapienza, Ospedale Sant’Andrea, Roma; 2 Department of Clinical Sciences, University Sapienza, Roma
Background and aim: Atrophic body gastritis (ABG) may manifest clinically as pernicious anemia (PA) and be associated with autoimmune thyroid disease. ABG has a complex pathogenesis involving genetic and environmental factors. Hp infection is considered involved in the induction of gastric atrophy and as trigger of gastric autoimmunity. A genetic predisposition to PA and an association between PA and HLA class II alleles have been reported. Data on HLA association with ABG are scanty and its relationship to Hp is not known. The aim was to assess the association of HLA-DRB1 with ABG with respect to Hp infection. Material and methods: 110 ABG patients (69.1% female, age 53.5 years) were included. ABG diagnosis was based on hypergastrinemia and histological confirmation of body atrophy. H pylori infection was diagnosed by histology and serology. 313 (47.3% female, age 34 years) Hp-negative controls with no history of autoimmune disease and anemia were included. Genomic DNA was extracted from venous blood, PCR-coamplified for HLA-DRB1 and typed using a reverse line blot assay. Results: The HLA DR3 and DR4 alleles showed a significantly higher prevalence in ABG patients with respect to controls (30.3% and 26.9% vs 17.2% and 14.4%, respectively, p=0.01). In ABG patients carrying the HLA DR3 and/or DR4 genotype, the presence of AITD or the positivity to thyroid peroxidase autoantibodies and the presence of body atrophy associated with intestinal metaplasia were more frequently observed than in ABG patients without these genotypes. The presence of PA (45.4% vs 37.8%, p=0.60), corpus-restricted atrophy (75% vs 71.1.%, p=0.86), parietal cell (84.6% vs 88%, p=0.95) and intrinsic factor autoantibodies (32.1% vs 20%, p=0.94) as well as of active (20.4% vs 26.7%, p=0.65) and past (38.4% vs 44.4%, p=0.67) Hp infection showed a similar distribution among the two groups. Conclusions: The HLA DR3 and DR4 genotypes are associated with ABG and are harboured in about half of these patients. In ABG patients these genotypes are not significantly associated neither with the presence of Hp infection nor with gastric autoimmune features. These findings show a role of genetic susceptibility genes for autoimmunity in ABG, whose presence occur irrespectively from Hp infection, suggesting that the occurrence of autoimmune and Hp-induced gastric atrophic damage is widely overlapping. # B. Gastric diseases 5. Pre-cancerous lesions
PROSPECTIVE STUDY OF DYSPLASTIC NODULES IN CIRRHOSIS: CORRELATION WITH CT VASCULAR PATTERN, HISTOLOGY AND DEVELOPMENT OF HEPATOCELLULAR CARCINOMA M. Iavarone, A. Sangiovanni, G. Ronchi, L.V. Forzenigo, A. Aghemo, P. Lampertico, M. Colombo First Division of Gastroenterology, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena. University of Milan, Milano
OC.03.2 MULTIMODAL TREATMENT OF HCC IN CIRRHOTIC LIVER, THE ROLE OF SURGERY. THE EXPERIENCE OF THE LIVER TRANSPLANT CENTRE OF TURIN G. Carbonaro, D. Reggio ∗ , M. Palisi, S. Mirabella, G. Paraluppi, R. Romagnoli, C. Giordanino, G. Saracco, P. Carucci, M. Salizzoni Aso San Giovanni Battista, Torino Background and aim: The HCC treatment in our centre is carried out according to 4 stages, similar to the Barcelona’s criteria. Stage 0: Child A patients with a lesion less than 3 cm without portal hypertension (Ixp).Stage 1: Patients with lesion less than 3 cm and Ixp or within the Milan criteria. Stage 2: Child patients A-B outside Milan criteria but still resectables (adequate remnant liver, without major vascular infiltration).Stage 3: Patients who are not susceptible from the curative treatments. Material and methods: We retrospectively analised 380 patients sub-
S15
Results: PPAR-gamma*2 isoform was found in 24 cases. Twentyfour out of 52 patients had H. pylori infection. Gastric atrophy and intestinal metaplasia were detected in 14 (26%). COX-2 and NF-κB were overexpressed in 30/520 cases (24 carrier of PPAR-gamma*2 isoform; p<0.0007). COX-2 and NF-κB expression were related to PPAR-gamma polimorphisms and to atrophy and intestinal metaplasia. Conclusions: PPAR-gamma polimorphisms influence the expression of COX-2 and NF-κB in inflamed gastric mucosa. These data suggest a possible role of PPAR-gamma in gastric carcinogenesis. # B. Gastric diseases 5. Pre-cancerous lesions
OC.03.1
OC.02.6
Background and aim: Dysplastic nodules (DNs) detected in cirrhotic liver are at risk of transformation into hepatocellular carcinoma (HCC) but there is not a contrast imaging pattern diagnostic for DNs. We assess the risk of malignant transformation, the vascular pattern of contrast CT diagnostic for DNs and its correlation with HCC development. Material and methods: Between 1998 and 2002, all cirrhotic patients attending our Liver Unit with a de-novo liver node detected during surveillance with ultrasound (US) and an histological diagnosis of either low grade or high grade dysplasia, were enrolled in the study and underwent a contrast enhanced CT scan. These patients were followed with US and serum alfa-fetoprotein every 3 months, abdominal CT scan every 6 months and biopsy was repeated in case of increasing in size or changes in vascular pattern. Diagnosis of dysplasia and HCC was made according to the International Working Party criteria. Results: 36 patients were enrolled with mean age of 61 (40-74) yrs, 83% males, 39% HCV-positive, 92% Child-Pugh A, the mean node diameter was 19 (10-26) mm. 21 nodules had an histological diagnosis of low grade dysplasia while 15 high grade dysplasia. Seventeen DNs (47%) had hypervascularity at the arterial phase without wash-out in the venous phase, 15 (42%) had only the wash-out in the venous phase and 4 were negative on CT scan. During a mean follow-up of 39 months (6-121), the yearly incidence of HCC development within the DNs was 9.2%, with 8.4% further of HCC out-side the target lesion, with an over-all yearly incidence of 17.6%. Older age and high-grade dysplasia were the only risk factors associated to HCC development, being the mean yearly incidence of HCC in high grade dysplastic nodules significantly higher compared to the low grade dysplasia (33.5 vs 9.9, p=0.004). The baseline CT scan vascular pattern was unable to characterize the DNs according to histological diagnosis, nor was associated to HCC development. Conclusions: Cirrhotic patients with a DN are at high risk of developing HCC either within or outside the nodule. Enhanced follow-up should be considered for patients with DNs, as suggested by the EASL/AASLD guidelines for unsolved nodules. # F. Cirrhosis & its complications 1. Natural history
AUTOIMMUNITY SUSCEPTIBILITY GENOTYPE HLA-DRB1 OCCURS IN PATIENTS WITH ATROPHIC BODY GASTRITIS IRRESPECTIVE OF HELICOBACTER PYLORI INFECTION E. Lahner ∗ ,1 , M.L. Spoletini 2 , R. Buzzetti 2 , A. Petrone 2 , L. Vannella 1 , V.D. Corleto 1 , G. Delle Fave 1 , B. Annibale 1 1 Digestive and Liver Disease, University Sapienza, Ospedale Sant’Andrea, Roma; 2 Department of Clinical Sciences, University Sapienza, Roma
Background and aim: Atrophic body gastritis (ABG) may manifest clinically as pernicious anemia (PA) and be associated with autoimmune thyroid disease. ABG has a complex pathogenesis involving genetic and environmental factors. Hp infection is considered involved in the induction of gastric atrophy and as trigger of gastric autoimmunity. A genetic predisposition to PA and an association between PA and HLA class II alleles have been reported. Data on HLA association with ABG are scanty and its relationship to Hp is not known. The aim was to assess the association of HLA-DRB1 with ABG with respect to Hp infection. Material and methods: 110 ABG patients (69.1% female, age 53.5 years) were included. ABG diagnosis was based on hypergastrinemia and histological confirmation of body atrophy. H pylori infection was diagnosed by histology and serology. 313 (47.3% female, age 34 years) Hp-negative controls with no history of autoimmune disease and anemia were included. Genomic DNA was extracted from venous blood, PCR-coamplified for HLA-DRB1 and typed using a reverse line blot assay. Results: The HLA DR3 and DR4 alleles showed a significantly higher prevalence in ABG patients with respect to controls (30.3% and 26.9% vs 17.2% and 14.4%, respectively, p=0.01). In ABG patients carrying the HLA DR3 and/or DR4 genotype, the presence of AITD or the positivity to thyroid peroxidase autoantibodies and the presence of body atrophy associated with intestinal metaplasia were more frequently observed than in ABG patients without these genotypes. The presence of PA (45.4% vs 37.8%, p=0.60), corpus-restricted atrophy (75% vs 71.1.%, p=0.86), parietal cell (84.6% vs 88%, p=0.95) and intrinsic factor autoantibodies (32.1% vs 20%, p=0.94) as well as of active (20.4% vs 26.7%, p=0.65) and past (38.4% vs 44.4%, p=0.67) Hp infection showed a similar distribution among the two groups. Conclusions: The HLA DR3 and DR4 genotypes are associated with ABG and are harboured in about half of these patients. In ABG patients these genotypes are not significantly associated neither with the presence of Hp infection nor with gastric autoimmune features. These findings show a role of genetic susceptibility genes for autoimmunity in ABG, whose presence occur irrespectively from Hp infection, suggesting that the occurrence of autoimmune and Hp-induced gastric atrophic damage is widely overlapping. # B. Gastric diseases 5. Pre-cancerous lesions
PROSPECTIVE STUDY OF DYSPLASTIC NODULES IN CIRRHOSIS: CORRELATION WITH CT VASCULAR PATTERN, HISTOLOGY AND DEVELOPMENT OF HEPATOCELLULAR CARCINOMA M. Iavarone, A. Sangiovanni, G. Ronchi, L.V. Forzenigo, A. Aghemo, P. Lampertico, M. Colombo First Division of Gastroenterology, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena. University of Milan, Milano
OC.03.2 MULTIMODAL TREATMENT OF HCC IN CIRRHOTIC LIVER, THE ROLE OF SURGERY. THE EXPERIENCE OF THE LIVER TRANSPLANT CENTRE OF TURIN G. Carbonaro, D. Reggio ∗ , M. Palisi, S. Mirabella, G. Paraluppi, R. Romagnoli, C. Giordanino, G. Saracco, P. Carucci, M. Salizzoni Aso San Giovanni Battista, Torino Background and aim: The HCC treatment in our centre is carried out according to 4 stages, similar to the Barcelona’s criteria. Stage 0: Child A patients with a lesion less than 3 cm without portal hypertension (Ixp).Stage 1: Patients with lesion less than 3 cm and Ixp or within the Milan criteria. Stage 2: Child patients A-B outside Milan criteria but still resectables (adequate remnant liver, without major vascular infiltration).Stage 3: Patients who are not susceptible from the curative treatments. Material and methods: We retrospectively analised 380 patients sub-