The natural course of non-alcoholic fatty liver disease.

Background and Aim: The present study aims to describe the characteristics and long-term clinical outcomes of patients with non-alcoholic fatty liver disease (NAFLD). Material and Methods: A total of 1308 individuals with NAFLD were seen in the Liver Diseases Outpatient Clinic. Diagnosis of NAFLD in each case was based on biochemical, radiological and histological criteria, when available. After diagnosis, all NAFLD patients were administered a conventional diet and exercise program. The median follow-up period was 55.3 months. Results: At the time of the diagnosis, the mean age was 50.8±11.3 years, and female gender was slightly predominant (51.4%). The median body mass index was 29.2±4.7 kg/m2: 39% were obese. Seventeen percent of the patients had diabetes mellitus, 53% insulin resistance, 60% hyperlipidemia, and 32% hypertension. Median serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and gamma-glutamyl transpeptidase levels were 31 U/L (range: 10-248 U/L), 45 U/L (range: 10-285 U/L) and 41 (range: 8-1200 U/L), respectively. Liver biopsy was performed in 293 individuals. The median NAFLD activity score was 5.0, median hepatic steatosis 2, ballooning 1, lobular inflammation 1, portal inflammation 0, and fibrosis 0. Of note, 41.3% of the samples (121/293) revealed the presence of fibrosis and 31% of the samples (37/121) showed significant fibrosis. With multivariate analysis, diabetes and obesity were associated with the presence of significant fibrosis. Among them, 765 patients (M/F: 353/412, mean age: 51.0±10.9) had at least six months of follow-up. In this group, from baseline to the end of the follow-up period, a significant improvement in the serum AST and ALT levels was observed. Conclusion: NAFLD is a potentially progressive disease. Diabetes and obesity were associated with the presence of advanced fibrosis.

Diagnostic and Prognostic Role of Serum Interleukin-6 in Malignant Transformation of Liver Cirrhosis.

AIM: Alpha-fetoprotein (AFP) is still the most commonly used and the single most recommended marker in the diagnosis of hepatocellular carcinoma (HCC). Interleukin (IL)-6 is a circular cytokine and its role on carcinogenesis in various hematological and solid tumors is clearly documented. A combination of serum IL-6 and AFP may provide beneficial information regarding early diagnosis of HCC. In this study, the effect of plasma IL-6 level in the diagnosis of HCC was investigated. MATERIALS AND METHODS: A total of 130 patients with liver cirrhosis, together with 30 control cases were enrolled in the trial. A diagnosis of HCC was present in 75 patients (57.6%) in the liver cirrhosis group. Blood samples were obtained from the enrolled study and control cases. Alpha-fetoprotein was quantified by chemiluminescent method. Plasma IL-6 levels of samples obtained at -80°C were quantified by human IL-6 BMS213/2 BMS213/2TEN kit. RESULTS: The HCC patients were older than the patients in the cirrhosis group (p = 0.016). On comparison of the HCC patients with the control group, AFP (p < 0.001) and IL-6 (p < 0.001) were significantly higher among the HCC patients. Comparison of HCC patients with liver cirrhosis cases with no diagnosis of HCC revealed significantly high AFP (p < 0.001) and IL-6 levels (p < 0.001) in HCC group. Cutoff value for IL-6 was calculated as 5.73 (pg/mL). No difference was detected in AFP (p = 0.600) and IL-6 (0.344) in all three subgroups. A total of 17 patients died during a mean follow-up period of 32.9 months. No correlation was found between mean AFP values and IL-6 values and survival rates. CONCLUSION: Plasma IL-6 level was found to be significant in the diagnosis of HCC. Alpha-fetoprotein and IL-6 provided no advantage in terms of early diagnosis of HCC and no correlation was observed between these markers and survival.How to cite this article: Yakut M, Özkan H, Karakaya MF, Erdal H. Diagnostic and Prognostic Role of Serum Interleukin-6 in Malignant Transformation of Liver Cirrhosis. Euroasian J Hepato-Gastroenterol 2018;8(1):23-30.

Manometric assessment of esophageal motor function in patients with primary biliary cirrhosis.

INTRODUCTION/AIM: Primary biliary cirrhosis is associated with other autoimmune diseases including Sjögren's syndrome, and scleroderma. Esophageal dysmotility is well known in scleroderma, and Sjögren's syndrome. The aim of this study is to investigate whether any esophageal motor dysfunction exists in patients with primary biliary cirrhosis. METHOD: The study was performed in 37 patients (36 women, mean age: 56.29 ± 10.01 years) who met diagnostic criteria for primary biliary cirrhosis. Thirty-seven functional dyspepsia patients, were also included as a control group. Patients entering the study were asked to complete a symptom questionnaire. Distal esophageal contraction amplitude, and lower esophageal sphincter resting pressure were assessed. RESULTS: Manometric findings in primary biliary cirrhosis patients vs. controls were as follows: Median lower esophageal sphincter resting pressure (mmHg): (24 vs 20, p=0.033); median esophageal contraction amplitude (mmHg): (71 vs 56, p=0.050); mean lower esophageal sphincter relaxation duration (sc, x ± SD): (6.10 ± 1.18 vs 8.29 ± 1.92, p<0.001); and median lower esophageal sphincter relaxation (%) (96 vs 98, p=0.019); respectively. No significant differences were evident in median peak velocity (sc) (3.20 vs 3.02, p=0.778) between patients with primary biliary cirrhosis and the functional dyspepsia patients. Esophageal dysmotility was found in 17 (45.9%) primary biliary cirrhosis patients (non-specific esophageal motor disorder in ten patients, hypomotility of esophagus in five patients, nutcracker esophagus in one patient and hypertensive lower esophageal sphincter in one patient). CONCLUSION: Esophageal dysmotility was detected in 45.9% of patients. The study suggests that subclinic esophageal dysmotility is frequent in patients with primary biliary cirrhosis.

The predictive value of mean platelet volume, plateletcrit and red cell distribution width in the differentiation of autoimmune gastritis patients with and without type I gastric carcinoid tumors.

Autoimmune gastritis is an autoimmune and inflammatory condition that may predispose to gastric carcinoid tumors or adenocarcinomas. The early diagnosis of these tumors is important in order to decrease morbidity and mortality. Platelet indices such as mean platelet volume and plateletcrit levels increase in inflammatory, infectious and malign conditions. The primary aim of this study was to explore wheter platelet indices and red cell distribution width have any predictive role in the discrimination of autoimmune gastritis patients with and without gastric carcinoid tumors. Also secondary aim of this study was to investigate whether any changes exist betwenn autoimmune gastritis and functional dyspepsia patients by means of platelet indices. Plateletcrit (0.22 ± 0.06 vs. 0.20 ± 0.03%, p < 0.001) and red cell distribution width (16.11 ± 3.04 vs. 13.41 ± 0.95%, p < 0.001) were significantly higher in autoimmune gastritis patients compared to control group. Receiver operating curve analysis suggested that optimum plateletcrit cut-off point was 0.20% (AUC: 0.646), and 13.95% as the cut off value for red cell distribution width (AUC: 0.860). Although plateletcrit (0.22 ± 0.06 vs. 0.21 ± 0.04%, p = 0.220) and mean platelet volume (8.94 ± 1.44 vs. 8.68 ± 0.89 fl, p = 0.265) were higher in autoimmune gastritis patients without carcinoid tumor compared to patients with carcinoid tumors, these parameters were not statistically significant. Changes in plateletcrit and red cell distribution width values may be used as a marker in the discrimination of autoimmune gastritis and fucntional dyspepsia patients but not useful in patients with gastric carcinoid tumor type I.

Clonal analysis of the quasispecies of antiviral-resistant HBV genomes in patients with entecavir resistance during rescue treatment and successful treatment of entecavir resistance with tenofovir.

BACKGROUND: Clonal analysis of quasispecies of resistant HBV genomes in patients with entecavir (ETV) resistance receiving lamivudine (3TC) plus adefovir (ADV) rescue therapy has never been performed. METHODS: A sample of 10 patients with ETV resistance who were switched to 3TC+ADV treatment were analysed for changes in viral quasispecies. Serum samples at baseline, and at months 3 and 6 of 3TC+ADV treatment could be clonally analysed in 7 of 10 patients; 3-82 clones per sample (total 1,068 clones, mean 63) were sequenced. RESULTS: 3TC+ADV therapy led to a modest decline in HBV DNA. Almost all clones had L180M and M204V 3TC resistance mutations before and during combination therapy. All clones had ≥1 of the S202G, T184F, T184A, T184L, T184I and M250V ETV resistance mutations. The percentages of detected clones bearing 3TC (rtL180M and rtM204V) and ETV mutations did not change with rescue 3TC+ADV therapy. In 7 of 8 patients with detectable HBV DNA (median 5.17 log(10) copies/ml) after a median 24 months of ADV therapy, HBV DNA became undetectable with 3TC plus tenofovir after 6 months of treatment. CONCLUSIONS: In patients with ETV resistance tenofovir is effective. Clonal analysis data indicate no selection of specific HBV mutants during rescue 3TC+ADV.

The association between precancerous gastric lesions and serum pepsinogens, serum gastrin, vascular endothelial growth factor, serum interleukin-1 Beta, serum toll-like receptor-4 levels and Helicobacter pylori Cag A status.

BACKGROUND AND OBJECTIVE: The aim of this study was to investigate the association between serum pepsinogens, serum gastrin, serum vascular endothelial growth factor, serum interleukin-1 Beta, serum toll-like receptor-4 levels and Helicobacter pylori Cag A status in patients with various gastric precancerous lesions. METHODS: One hundred and sixty two consecutive patients with various gastric lesions [38 (23.5%) H. pylori positive chronic non-atrophic gastritis, 45 (27.8%) autoimmune gastritis, 42 intestinal metaplasia and 37 dysplasia] were enrolled into the study. Serum pepsinogen I and II, gastrin 17, vascular endothelial growth factor, interleukin-1 Beta, toll-like receptor-4 levels, H. pylori Cag A status were evaluated. RESULTS: H. pylori was positive in 98 (60.5%) patients and 38 of these patients were Cag A positive. Serum pepsinogen level was significantly lower in patients with autoimmune atrophic gastritis compared to the patients with non-atrophic chronic gastritis (p<0.001), intestinal metaplasia (P<0.001) and dysplasia (P=0.002). Mean serum gastrin was 1209.6±268.48 pg/mL in patients with autoimmune atrophic gastritis and 234.95±184.018 pg/mL in patients with chronic non-atrophic gastritis. Mean toll-like receptor-4 level was 0.56±0.098 ng/mL in patient with dysplasia, and this value was higher compared to patients with chronic non-atrophic gastritis (P=0.007), autoimmune atrophic gastritis (P=0.003) and intestinal metaplasia (P=0.006). Interleukin-1 Beta level was significantly lower in patients with dysplasia compared to patients with chronic non-atrophic gastritis (P=0.034). CONCLUSIONS: Serum pepsinogens, serum gastrin and H. pylori Cag A status are important tests in detecting gastric precancerous lesions. However, toll-like receptor-4 may be a sensitive test to differentiate the patients with dysplasia from the other precancerous gastric lesions. Non-invasive tests are sensitive in the diagnosis of gastric precancerous lesions.

Effect of endogenous hypergastrinemia on gallbladder volume and ejection fraction in patients with autoimmune gastritis.

BACKGROUND: Gastrin has a cholecystokinetic action on gallbladder motility, and cholecystokinin and gastrin act directly on the smooth muscle of the gallbladder. The aim of this study was to investigate the effect of endogenous hypergastrinemia on gallbladder motility in patients with autoimmune gastritis. METHODS: Forty-one patients (29 females, 12 males; mean age, 46 years) with autoimmune gastritis and 29 healthy subjects (17 females, 12 males; mean age, 44.8 years) were enrolled in the study. Fasting and postprandial gallbladder volumes were measured ultrasonographically with the ellipsoid technique and the ejection fraction of the gallbladder was calculated from fasting and postprandial volumes. All subjects were investigated after 12 hours of fasting and 30 minutes after a standard test meal. RESULTS: The gallbladder ejection fraction (%) of the patients with autoimmune gastritis was lower than that of the control group (46.06+/-18.28% vs 55.03+/-14.67%, P=0.032). There was no difference between patients with autoimmune gastritis and the control group in terms of the mean fasting gallbladder volume (30.38+/-12.85 vs 29.27+/-9.91 cm3, P=0.189) and the mean postprandial gallbladder volume (15.67+/-8.32 vs 13.44+/-7.69 cm3, P=0.258). Logistic regression analysis of baseline parameters revealed that "abdominal bloating" was a risk factor for the low gallbladder ejection fraction in autoimmune gastritis patients (P=0.045, F=4.40). In addition, logistic regression analysis of baseline parameters revealed that smoking (n=5, P=0.025, F=5.44) is a predictor of low gallbladder ejection fraction in patients with autoimmune gastritis. CONCLUSIONS: Patients with endogenous hypergastrinemia have a low gallbladder ejection fraction compared with healthy controls. This study shows that at least part of upper gastrointestinal symptoms observed in this patient population may be due to altered gallbladder motility.

Clinical profiles, endoscopic and laboratory features and associated factors in patients with autoimmune gastritis.

BACKGROUND/AIMS: Autoimmune gastritis (AIG) may predispose to gastric carcinoid tumors or adenocarcinomas and may also cause unexplained iron and/or vitamin B(12) deficiency. The aims of this study were to explore clinical manifestations, endoscopic findings and laboratory features of patients with AIG. METHODS: 109 patients with AIG were enrolled into the study. In addition to demographic and clinical data, gastric lesions, serum gastrin, vitamin B(12), antiparietal cell antibody (APA), current Helicobacter pylori status, and anti-H. pylori IgG were also investigated. RESULTS: The mean age of the patients was 53.06 ± 12.7 years (range 24-81; 72 (66.1%) women). The most common main presenting symptom was abdominal symptoms in 51 patients, consultation for iron and/or vitamin B(12) deficiency in 36, and non-specific symptoms including intermittent diarrhea in 15 patients. Endoscopic lesions were detected in 17 patients, hyperplastic polyps in 8, gastric carcinoid tumor in 4, fundic gland polyps in 3, and adenomatous polyps in 2 patients. H. pylori was negative in all patients in biopsy specimens; however, anti-H. pylori IgG was positive in 30 (27.5%) patients. 91 patients (83.4%) were positive for APA. CONCLUSION: In patients with AIG, the main symptoms prompted for clinical investigation were: abdominal symptoms, iron/B(12) deficiency and non-specific symptoms. 20% of patients with AIG had various gastric lesions including type I gastric carcinoids. None of the patients were positive for H. pylori by means of invasive tests; however, anti-H. pylori IgG was found in 27.5% of patients. Patients referring with non-specific abdominal symptoms such as bloating, diarrhea and iron/B(12) deficiency should be investigated for the presence of AIG.

Entecavir treatment of chronic hepatitis D.

BACKGROUND: Hepatitis D virus (HDV) requires hepatitis B surface antigen (HBsAg) to propagate infection and cause disease. Entecavir is a nucleoside analog with potent antiviral efficacy, and in the woodchuck animal model it also decreased hepatitis B virus (HBV) cccDNA and woodchuck surface antigen. The aim of this study was to investigate the efficacy of entecavir in chronic hepatitis D (CHD). METHODS: This single-center study was conducted in patients with compensated liver disease. All patients had to have detectable hepatitis HDV RNA and elevated levels of alanine aminotransferase (ALT). Entecavir was given at a dosage of 1 mg/d for 1 year. The primary end point was achievement of undetectable HDV RNA at the end of treatment. RESULTS: Thirteen consecutive patients were assessed. All patients had detectable HDV RNA, and 8 had detectable HBV DNA at baseline. At the end of treatment, HBV DNA became undetectable in all patients (P = .001). No significant decline in HDV RNA, ALT, or quantitative HBsAg levels was observed. The primary end point of undetectable HDV RNA at the end of treatment was achieved in 3 patients who had significantly lower baseline HDV RNA levels than nonresponders (2.99 log(10) copies/mL ± .70 vs 4.68 ± .97; P = .0185). In all 3 patients, ALT levels were also normal at the end of treatment. CONCLUSIONS: One year of entecavir treatment is ineffective in CHD. Any generalized beneficial effect of nucleoside/nucleotide analog treatment may necessitate prolonged treatment. Patients with CHD with HBV dominance, which is likely to occur in the later phases of CHD, may be a reasonable patient cohort in which to target nucleoside/nucleotide analog therapy.

The effect of endogenous hypergastrinemia on lower esophageal sphincter pressure and esophageal motility.

BACKGROUND/AIMS: The effect of exogenous hypergastrinemia on esophageal motor function has been well documented. However, it is not known whether chronic endogenous hypergastrinemia influences esophageal motility and lower esophageal sphincter pressure. The purpose of this study was to investigate the effect of chronic hypergastrinemia on lower esophageal sphincter pressure and esophageal motility in patients with significantly elevated serum gastrin levels. METHODOLOGY: 37 patients (28 women; mean age, 53.7 years) with autoimmune gastritis and 35 functional dyspepsia patients participated in this study. Esophageal motility testing was performed by using an eight-lumen water-perfused catheter. Ten wet swallows were given and each contraction was analysed for lower esophageal sphincter pressure, lower esophageal sphincter relaxation, contraction amplitude and peak velocity. RESULTS: Mean serum fasting gastrin level was 1382.8±731.9pg/mL in patients with autoimmune gastritis and 107±83.9pg/mL in the control group (p=0.000). Mean lower esophageal sphincter pressure (31.6±14.42mmHg vs. 20.5±8.05mmHg, p=0.000) and mean contraction amplitude (82.48±35.0mmHg vs. 58.11±21.75mmHg, p=0.001), in hypergastrinemic patients were significantly higher than in the control group. CONCLUSIONS: These results suggest that in patients with autoimmune gastritis, prolonged and significant elevation of serum gastrin levels, increases lower esophageal sphincter pressure and esophageal body contraction amplitude. However, this increase in lower esophageal sphincter pressure does not cause upper gastrointestinal symptoms in patients with autoimmune gastritis.

Diagnostic and prognostic role of serum glypican 3 in patients with hepatocellular carcinoma.

α-Feto protein (AFP) is the widely used tumor marker in the diagnosis of hepatocellular carcinoma (HCC). The aim of this study was to assess the diagnostic and prognostic validity of a novel marker, serum Glypican-3 (GPC3) and to compare AFP in patients with HCC. One hundred and twenty-eight patients (75 patients with HCC, 55 patients with cirrhosis, and 28 healthy controls) were included in this study. Cut-off value of GPC3 was 3.9 pg/ml. AFP was divided into four subgroups, according to cut-off values with 13, 20, 100, and 200 ng/ml. Sensitivity, specificity, and positive and negative predictive values of GPC3 and AFP13, AFP20, AFP100, AFP200 subgroups and also GPC3+AFP13, GPC3+AFP20 , GPC3+AFP100 , GPC3+AFP200 combinations were compared. Serum GPC3 levels were significantly higher in patients with HCC and cirrhosis compared with control subjects (P<0.05). The median serum GPC3 levels were 3.9 pg/ml in controls, 5.51 pg/ml in patients with cirrhosis, and 5.13 pg/ml in those with HCC. The median serum AFP levels were 1.37 ng/ml in controls, 2.32 ng/ml in cirrhotics, and 50.65 ng/ml in HCC patients. The sensitivity, specificity, and positive and negative predictive values of GPC3 was 61.33, 41.82, 58.97, and 44.43%, respectively. The values for AFP were 68.57, 94.55, 94.12, and 70.27%, respectively. There was no correlation between GPC3 levels and prognostic parameters. GPC3 is not a useful diagnostic and prognostic marker for HCC.

Serum connective tissue markers as predictors of advanced fibrosis in patients with chronic hepatitis B and D.

BACKGROUND/AIMS: Liver biopsy to assess fibrosis is invasive and prone to sampling error. While algorithms of serum markers to predict fibrosis stage have been described for chronic hepatitis C, these cannot be applied equally well to hepatitis B. METHODS: We therefore determined 9 serum fibrosis markers, liver biochemical tests and ultrasound parameters in 109 consecutive adult patients with chronic hepatitis B and D. All patients had compensated liver disease. Using the METAVIR score, advanced disease was defined as fibrosis stage ≥F2, and active inflammation as grade ≥A2. A gold standard was created considering splenomegaly and/or platelets <150,000 as indicators of advanced fibrosis irrespective of histology. Area under receiver operating characteristics curves was used for assessment of single markers and odds ratio for their combinations. RESULTS: Patients with advanced disease were older, had lower albumin, higher gamma glutamyl transferase and lower platelet. Levels of 6 of the 9 fibrosis markers, tissue inhibitor of metalloproteinases-1, procollagen type III aminoterminal propeptide, matrix metalloproteinase-2, laminin, hyaluronan and collagen IV correlated with advanced fibrosis. Markers useful for fibrosis prediction also predicted marked inflammation. Using the gold standard, age, prothrombin time, gamma glutamyl transferase and albumin were independent predictors of fibrosis with odds ratio's of 3.11, 4.18, 3.35 and 5.25, respectively. Their combined use predicted fibrosis with an odds ratio of 228.8. Tissue inhibitor of metalloproteinases-1 and hyaluronan were powerful predictors of fibrosis (Odds ratio's of 8.65 and 8.38). Their combined use revealed an odds ratio of 28.6, when compared with the gold standard. CONCLUSION: In conclusion, advanced liver fibrosis in chronic hepatitis B and D may be predicted with use of these two fibrosis markers.

Multiparametric assessment of vascular function and atherosclerosis in patients with autoimmune gastritis: a comparative study.

BACKGROUND/AIMS: Patients with autoimmune gastritis might have accelerated atherosclerosis due to autoimmunity and chronic inflammation. Endothelial dysfunction often precedes manifest atherosclerosis. The aim of the present study was to evaluate the risk factors of early atherosclerosis by using several different techniques. METHODS: A total of 99 patients with autoimmune gastritis were compared to 42 healthy age sex-matched subjects. Patients with a known risk factor for atherosclerosis were excluded. Intima-media thickness of the common carotid artery, pulse wave velocity and flow-mediated dilation of brachial artery were measured. Clinical data and laboratory parameters (serum gastrin, antiparietal cell antibody, anti-Hp IgG, serum vitamin B(12) and lipid profile) were also determined. RESULTS: Intima-media thickness (mm) of the carotid artery was significantly higher in autoimmune gastritis (0.062 ± 0.031 vs. 0.042 ± 0.007, P < 0.001) than in healthy individuals. Flow-mediated dilation was significantly lower in patients with autoimmune gastritis compared to control group (13.91 ± 6.68% vs. 20.37 ± 7.80%, P = 0.021) and there was a significant increase in pulse wave velocity (m/s) in autoimmune gastritis patients compared to controls (9.25 ± 3.42 vs. 6.40 ± 0.91, P = 0.001). Antiparietal cell antibody positivity (P = 0.05), low vitamin B(12) level (P = 0.05), and age (P = 0.002) were the predictors of high pulse wave velocity (>14 m/s). CONCLUSION: Patients with autoimmune gastritis may have an increased risk for the development of early atherosclerosis. As early preventive treatment for accelerated atherosclerosis is available, it is important to detect those patients with autoimmune gastritis who would benefit from such treatment.

Clinical characteristics and evaluation of patients with large hiatal hernia and Cameron lesions.

OBJECTIVES: Cameron lesions are located at the neck of large hiatal hernias, and are associated with anemia or overt gastrointestinal (GI) bleeding. The aim of this study was to investigate the clinical and endoscopic properties of patients with Cameron lesions. METHODS: Eighteen patients were diagnosed as having large hiatal hernia and Cameron lesions. Patients with Cameron lesions (n = 18) were compared to patients with large hiatal hernias without Cameron lesions (n = 26), by means of presenting symptoms and endoscopic findings. RESULTS: The mean age of patients with Cameron lesions was significantly higher than patients without Cameron lesions (71.1 ± 11.63 vs 56.7 ± 17.4 years, P = 0.005). The ratio of female patients with Cameron lesions was higher compared to patients with large hiatal hernia without Cameron lesions (14/18 [77.7%] vs 12/26 [46.1%], P = 0.00). While 12 of 18 patients with Cameron lesions had overt GI bleeding, none of the patients with large hiatal hernia without Cameron lesions had signs of GI bleeding. Fifteen of 18 patients had ulcers in the hernia sac and the others had linear erosions. There was no significant difference between patients with and without Cameron lesions by means of hemoglobin levels (11.1 ± 2.20 vs 12.2 ± 2.5 g/dL, P = 0.157). CONCLUSION: Most patients with large hiatal hernia and Cameron lesions presented with overt GI bleeding. Patients with Cameron lesions tend to be older females. In patients with anemia and GI bleeding, large hiatal hernia and Cameron erosions should also be considered.

Diagnostic and prognostic validity of Golgi protein 73 in hepatocellular carcinoma.

BACKGROUND: Golgi protein 73 (GP73) expressions have been detected in hepatocellular carcinoma (HCC) and bile duct carcinoma. AIM: Our purpose was to determine the serum levels of GP73 in patients with HCC and to compare them with α-fetoprotein (AFP) levels. MATERIALS AND METHODS: Seventy-five patients with HCC, 55 patients with cirrhosis and 28 healthy controls were included. RESULTS: The median serum GP73 levels were 0.27 ng/ml (range = 0.078-4.95) in controls, 0.32 ng/ml (range = 0.078-39.63) in cirrhotics and 0.21 ng/ml (range = 0.053-4.98) in those with HCC. The median serum AFP levels were 1.37 ng/ml (range = 0.61-6.89) in controls, 2.32 ng/ml (range = 0.61-85.24) in cirrhotics and 50.65 ng/ml (range = 0.8-37,642) in HCC patients (p < 0.0001 for HCC vs. controls and cirrhotics). The sensitivity, specificity, and positive and negative predictive values of GP73 were 82, 9, 55 and 27%, respectively. Whereas the levels were 68, 94, 94 and 70%, respectively, for AFP(13) and 60, 98, 97 and 64% for AFP(20), respectively. There was no correlation between GP73 levels and other prognostic parameters including tumor size, tumor type, Child-Pugh classification, TNM staging, Cancer of the Liver Italian Program score, portal vein thrombosis and extrahepatic metastasis. CONCLUSIONS: GP73 has a lower diagnostic and prognostic value for HCC. AFP is superior to GP73 for diagnosis of early HCC.