A retrospective study demonstrating properties of nonvariceal upper gastrointestinal bleeding in Turkey.

BACKGROUND/AIMS: Helicobacter pylori infection, non-steroidal anti-inflammatory drugs and peptic ulcer are considered as the major factors for upper gastrointestinal system bleeding. The objective of the study was to determine the sociodemographic and etiologic factors, management and outcome of patients with non-variceal upper gastrointestinal system bleeding in Turkey. METHODS: Patients who admitted to hospitals with upper gastrointestinal system bleeding and in whom upper gastrointestinal endoscopy was performed were enrolled in this retrospective study. The detailed data of medical history, comorbid diseases, medications, admission to intensive care units, Helicobacter pylori infection, blood transfusion, upper gastrointestinal endoscopy, and treatment outcome were documented. RESULTS: The most frequent causes of bleeding (%) were duodenal ulcer (49.4), gastric ulcer (22.8), erosion (9.6), and cancer (2.2) among 1,711 lesions in endoscopic appearances of 1,339 patients from six centers. Seven hundred and four patients were evaluated for Helicobacter pylori infection and the test was positive in 45.6% of those patients. Comorbid diseases were present in 59.2% of the patients. The percentage of patients using acetylsalicylic acid and/or other non-steroidal anti-inflammatory drug was 54.3%. Bleeding was stopped with medical therapy in 66.9%. Only 3.7% of the patients underwent emergency surgery, and a 1.1% mortality rate was determined. CONCLUSIONS: Patients with upper gastrointestinal system bleeding were significantly older, more likely to be male, and more likely to use non-steroidal anti-inflammatory drugs. Though most of the patients were using gastro-protective agents, duodenal and gastric ulcers were the contributing factors in more than 70% of the upper gastrointestinal bleeding. The extensive use of non-steroidal anti-inflammatory drug is a hazardous health issue considering the use of these drugs in half of the patients.

Efficacy of insulin-sensitizing agents in nonalcoholic fatty liver disease.

AIM: To investigate the efficacy of insulin-sensitizing agents in nonalcoholic fatty liver disease (NAFLD) patients. METHODS: This is an open-label, randomized, a single-center study. Sixty-four patients, with impaired glucose metabolism and elevated alanine aminotransferase for at least 6 months before enrollment and NAFLD activity score at least 5 in liver biopsy, were randomized as group 1 and received metformin 1700 mg/day, group 2 received rosiglitazone 4 mg/day, and group 3 received a combination of metformin 1700 mg/day and rosiglitazone 4 mg/day for 12 months. RESULTS: Baseline demographic and laboratory findings were similar in all the three groups, except baseline insulin level that was significantly higher in group 1 and group 3 versus group 2 (P<0.05). Serum transaminase levels showed a significant decrease after treatment in both group 2 and group 3. Serum gamma-glutamyl transpeptidase levels decreased significantly only in the group 3. However, there was no significant change in liver tests of group 1. Postprandial glucose levels showed significant decrease in all of the three groups. Homeostasis model assessment-insulin resistance was reduced significantly in only group 2. NAFLD score was significantly decreased on follow-up biopsy of the patients in group 2 and group 3. Fibrosis did not change significantly after the treatment. CONCLUSION: Rosiglitazone therapy seems to be more effective in metabolic control and histological improvement in NAFLD patients with impaired glucose metabolism.

Macrophage migration inhibitory factor expression and MIF gene -173 G/C polymorphism in nonalcoholic fatty liver disease.

AIM: To investigate the macrophage migration inhibitory factor (MIF) expression and -173 G/C polymorphism of the MIF gene in nonalcoholic fatty liver disease (NAFLD). METHOD: Ninety-one patients with diagnosis of NAFLD and 104 healthy controls were included in the study. MIF -173 G/C polymorphism was detected using the PCR-restriction fragment length polymorphism based method. NAFLD was stratified as nonalcoholic steatohepatitis (NASH), probable NASH and steatosis, respectively in groups 1, 2 and 3, according to NAFLD Activity Score. MIF expression was detected by immunohistochemistry staining. RESULTS: Mean age of the patients was 50.1+/-9.6 years, and 54 of them were male. Serum alanine aminotransferase and aspartate aminotransferase were 50/83, 42/63 and 31/32, respectively in groups 1, 2 and 3, (P<0.05). Both the MIF expression of hepatocytes and mononuclear cells were more prominent in groups 1 and 2 than group 3. There was no correlation between MIF expression of hepatocytes and fibrosis stage. However, MIF expression of mononuclear cells significantly increased according to fibrosis stage (P<0.05, R : 0.2). There was no significant correlation between MIF genotype and MIF expression in the liver. CONCLUSION: MIF expression is significantly increased especially by mononuclear cells in liver tissue of patients with NASH secondary to inflammation. Thus, it should be considered as a consequence not a causal factor.

Common SPINK-1 mutations do not predispose to the development of non-alcoholic fatty liver disease.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is common in obese and diabetics. Serine protease inhibitor Kazal-1 (SPINK-1) protein is highly expressed in the liver and adipose tissue of diabetic and obese suggesting its role in NAFLD. SPINK-1 also behaves as an acute phase reactant protein. Some genetic factors including the genetic variations in SPINK-1 protein have been linked to chronic pancreatitis and diabetes. We therefore hypothesized that SPINK-1 mutations might be a risk factor for the development of NAFLD. METHODS: Liver biopsy proven fifty NAFLD cases (20 steatohepatitis, 30 diffuse fatty liver disease and 44 healthy controls were included to the study. Liver function tests were measured. Body mass index was calculated. Insulin resistance was determined by using a homeostasis model assessment (HOMA-IR). Ultrasound evaluation was performed for each subject. Common genetic mutations in the third exon of SPINK-1 gene were analyzed by direct sequencing method. RESULTS: We found two cases with a SNP at N34S location in NAFLD group (allele frequency %4). One subject with diffuse fatty liver disease and other with liver cirrhosis due to NAFLD had N34S mutation. No SNPs were detected in healthy controls. In conclusions, in limited number of patients SPINK-1 mutations were not considered as a risk factor alone for NAFLD development.

Serum procalcitonin and CRP levels in non-alcoholic fatty liver disease: a case control study.

BACKGROUND: Both C reactive protein (CRP) and procalcitonin (PCT) are well known acute phase reactant proteins. CRP was reported to increase in metabolic syndrome and type-2 diabetes. Similarly altered level of serum PCT was found in chronic liver diseases and cirrhosis. The liver is considered the main source of CRP and a source of PCT, however, the serum PCT and CRP levels in non-alcoholic fatty liver disease (NAFLD) were not compared previously. Therefore we aimed to study the diagnostic and discriminative role of serum PCT and CRP in NAFLD. METHODS: Fifty NAFLD cases and 50 healthy controls were included to the study. Liver function tests were measured, body mass index was calculated, and insulin resistance was determined by using a homeostasis model assessment (HOMA-IR). Ultrasound evaluation was performed for each subject. Serum CRP was measured with nephalometric method. Serum PCT was measured with Kryptor based system. RESULTS: Serum PCT levels were similar in steatohepatitis (n 20) and simple steatosis (n 27) patients, and were not different than the control group (0.06 +/- 0.01, 0.04 +/- 0.01 versus 0.06 +/- 0.01 ng/ml respectively). Serum CRP levels were significantly higher in simple steatosis, and steatohepatitis groups compared to healthy controls (7.5 +/- 1.6 and 5.2 +/- 2.5 versus 2.9 +/- 0.5 mg/dl respectively p < 0.01). CRP could not differentiate steatohepatitis from simple steatosis. Beside, three patients with focal fatty liver disease had normal serum CRP levels. CONCLUSION: Serum PCT was within normal ranges in patients with simple steatosis or steatohepatitis and has no diagnostic value. Serum CRP level was increased in NAFLD compared to controls. CRP can be used as an additional marker for diagnosis of NAFLD but it has no value in discrimination of steatohepatitis from simple steatosis.

Use of activated protein C has no avail in the early phase of acute pancreatitis.

OBJECTIVES: Sepsis and acute pancreatitis have similar pathogenetic mechanisms that have been implicated in the progression of multiple organ failure. Drotrecogin alfa, an analogue of endogenous protein C, reduces mortality in clinical sepsis. Our objective was to evaluate the early therapeutic effects of activated protein C (APC) in a rat model of acute necrotizing pancreatitis. SUBJECTS AND METHOD: Acute necrotizing pancreatitis was induced by intraductal injection of 5% Na taurocholate. Hourly bolus injections of saline or recombinant human APC (drotrecogin alfa) was commenced via femoral venous catheter four hours after the induction of acute pancreatitis. The experiment was terminated nine hours after pancreatitis induction. Animals in group one (n=20) had a sham operation while animals in group two (n=20) received saline and animals in group three (n=20) received drotrecogin alfa boluses after acute pancreatitis induction. Pancreatic tissue for histopathologic scores and myeloperoxidase, glutathione reductase, glutathione peroxidase, and catalase activities were collected, and blood for serum amylase, urea, creatinine, and interleukin-6 measurements was withdrawn. RESULTS: Serum amylase activity was significantly lower in the APC treated group than the untreated group (17,435+/-432 U/L vs. 27,426+/-118 U/L, respectively). While the serum interleukin-6 concentration in the APC untreated group was significantly lower than the treated group (970+/-323 pg/mL vs. 330+/-368 pg/mL, respectively). CONCLUSION: In the early phase of acute pancreatitis, drotrecogin alfa treatment did not result in a significant improvement in oxidative and inflammatory parameters or renal functions.

Reabsorption of ascites and the factors that affect this process in cirrhosis.

Ascites is one of the main features of liver decompensation in cirrhosis, and it is considered to be a dynamic process. In this study, we aimed to (1) measure the reabsorption rate of ascites; (2) evaluate whether these findings were related to features of ascites, hemodynamics, and serum measurements; and (3) examine morphologic changes in the diaphragm of cirrhotic patients. In all, 42 cirrhotic patients with ascites were enrolled in the study to comprise our study group. Using the dextran 70 test, patient ascites volumes and reabsorption rates were measured. Biopsies from the peritoneal side of the diaphragm were also processed for scanning electron microscopy and lymphatic immunohistochemical studies from the cirrhotic patients and control cadavers. The mean ascites reabsorption rate was 4.5 +/- 4.5 (0.18-14.6) mL/min, which correlated significantly with the calculated ascites volume (r = 0.75, P < 0.001). The mean ascites viscosity was 1.07 +/- 0.07 (0.99-1.17) centipoise, which demonstrated a high degree of negative correlation with the ascites reabsorption rate (r = -0.77, P < 0.001). Patients with a history of spontaneous bacterial peritonitis had significantly lesser ascites reabsorption rates than patients without this particular history. The size of lymphatic stomata in scanning electron microscopy depictions was increased, and lymphatic lacunae were dilated in immunohistochemical studies in the cirrhotic patients with ascites. However, these findings were not uniform in every cirrhotic patient with ascites. The volume and viscosity of ascites seem to influence its reabsorption rate. Additionally, previous episodes of spontaneous bacterial peritonitis may be responsible for the decreased ascites reabsorption rates observed in certain patient populations.

Live donor liver transplantation for acute liver failure.

BACKGROUND: Acute liver failure (ALF) carries a high mortality unless urgent orthotopic liver transplantation (OLT) is performed on time. Live donors are utilized to treat this irreversible condition first in pediatric cases and then in adults. Herein, we aimed to report our experience with live donors for ALF in a country of a deceased donor organ donation rate is only 1.5 per million people. METHODS: Among the 245 live donor liver transplantations (LDLT) performed from June 1999 to December 2005, 14 of them (6%) were performed for ALF in 8 pediatric and 6 adult cases. Right lobes were harvested for the adult cases whereas left lateral segments were harvested for pediatric cases, except one child transplanted with a right lobe graft. The etiology of the disease was; acute hepatitis B in four cases, hepatitis A in three cases, Wilson disease two cases, autoimmune hepatitis in two cases, and was unknown in three cases. RESULTS: Three-year graft and patient survival is 79% for these series. Five of the six adult patients and six of the eight pediatric cases survived after transplantation. There was not any donor mortality or major morbidity. CONCLUSIONS: LDLT offers a safe and effective modality of treatment for ALF for both pediatric and adult patients to overcome the problem of organ shortage especially in countries where the chance of receiving an organ from a deceased donor is low.

Adefovir dipivoxil alone or in combination with lamivudine for three months in patients with lamivudine resistant compensated chronic hepatitis B.

We studied clinical and laboratory effects of 3 months of lamivudine with adefovir combination and adefovir dipivoxil (AD) alone in the treatment of patients with lamivudine-resistant hepatitis B virus (HBV) infection. Eligible patients were hepatitis B surface antigen-positive men and women with compensated liver disease who were given lamivudine at least more than 6 months and had HBV polymerase gene mutation. Patients were assigned to receive adefovir 10 mg/day (Group 1) or adefovir 10 mg once daily and lamivudine 100 mg once daily combination during first 3 months, and then stopped lamivudine and continued adefovir (Group 2). Median age was 48 years (34 males and 20 females, and 35 were HBeAg-negative). Baseline median ALT, AST, and HBV DNA levels were 66 IU/l, 49 IU/l, and 6.7 log(10) copy/ml, respectively. Median adefovir therapy time and ALT normalization time were 9 and 3.5 months, respectively. There was no significant difference between groups according to the baseline HBV DNA, ALT, HBe Ag status, age, gender, and lamivudine resistance time. Virological and biochemical responses were similar in both groups during therapy. Two patients (8%) had ALT flare more than five times upper limit of normal without any clinical decompensation in Group 1. Mild ALT elevation according to baseline levels were found in 8 (27.6%) and 4 (17.4%) patients, respectively, in Group 2 and Group 1, and no statistically significance between two groups. In conclusion, this study showed that it is not necessary to continue lamivudine therapy while switching to AD therapy. Adefovir alone is effective in the treatment of patients with lamivudine resistant HBV infection and compensated liver disease, without significant clinical and laboratory flares. However, it is not easy to say that switching to AD with cessation of lamivudine is safe, because the study population is not enough for precise conclusion and resistance may be a considerable problem against AD in patients using long-term treatment.

Liver fibrosis is associated with decreased peripheral platelet count in patients with chronic hepatitis B and C.

Thrombocytopenia is a common complication of chronic liver diseases, but its pathogenesis is not clear. Although generally attributed to hypersplenism, other factors should also be considered. We investigated the relationship between the peripheral platelet count and the degree of fibrosis in patients with chronic viral hepatitis. In an effort to avoid the effects of hypersplenism, we excluded patients with splenomegaly and/or bi- or pan-cytopenia. Seven hundred eighty-four patients (265 chronic viral hepatitis C and 519 chronic viral hepatitis B) were included in the study. Univariate analysis showed that the peripheral platelet count had a negative correlation with fibrosis score, necroinflammatory activity, and age in both groups. In multivariate analysis, the peripheral platelet count had a similar correlation with the fibrosis score and age, but not with necroinflammatory activity, in both groups. The peripheral platelet count decreased more significantly in females with chronic hepatitis C but not in the chronic hepatitis B group. In conclusion, a decrease in peripheral platelet count may be a sign of an increase in the degree of fibrosis during the course of chronic viral hepatitis B and C and factors other than hypersplenism may play a role in this decrease in the peripheral platelet count.

Liver biopsy: is the pain for real or is it only the fear of it?

Although percutaneous liver biopsy (PLB) has very low mortality and morbidity rates, it often is considered painful and frightening by the patients. This study was designed to grade the intensity of pain expected before the procedure and experienced during the procedure, and whether there is any correlation between pain and the emotional state of the patient. A total of 118 consecutive patients (aged 19-68 (mean, 44) years), who were undergoing PLB for the first time, were included in the study. Visual Analogue Scale (VAS) was used before the procedure, after the procedure to grade the degree of pain expected, and the degree of the pain experienced respectively. All the patients were evaluated by a questionnaire for their personality and emotional situation by using the Minnesota Multiphasic Personality Inventory Somatization Sub-scale (MMPI-SS). Mean VAS score for expected pain before the procedure was 60+/-20 and for the pain experienced during the procedure was 22+/-16 (P < 0.0001). Although the expected pain scores of female patients were significantly higher than males (66+/-22 vs. 55+/-17; P=0.003), there was no difference between female and male patients in the experienced pain scores. The procedure of PLB is expected to be more painful than it really is by the patients, especially by females. Calming the patients by informing them about the procedure and their diseases will probably diminish the expected pain.

A cerebrovascular event after single-dose administration of recombinant factor VIIa in a patient with esophageal variceal bleeding.

Upper gastrointestinal bleeding (UGIB) is a life-threatening complication of cirrhosis that develops from esophageal varices in almost 70% of patients. The mortality rate from the bleeding episodes is reported to be 30% [1-4]. Standard management of UGIB of cirrhotic patients is vasoactive therapy combined with endoscopic procedures such as endoscopic sclerotherapy and band ligation [5]. Currently, it is reported that recombinant activated fVIIa (Novoseven, NovoNordisc) can correct the prothrombin time in decompensated cirrhotic patients and also can be used safely in Child's B and C cirrhotic patients with UGIB [6-8]. Herein, we describe the first case report in the literature of a cerebrovascular event after the administration of a single dose of fVIIa in a cirrhotic patient with esophageal variceal bleeding.

Results of endoscopic management of anastomotic biliary strictures after orthotopic liver transplantation.

BACKGROUND/AIMS: Anastomotic biliary strictures are common biliary complications after orthotopic liver transplantation. We assessed the success of endoscopic retrograde cholangio-pancreaticography (ERCP) in the treatment and outcome of post-liver transplantation anastomotic biliary strictures in a university hospital, retrospectively. METHODS: Thirty-three ERCPs were performed in 20 of 162 adult liver transplant recipients with duct to duct anastomosis. RESULTS: In five patients, ERCP failed because the stricture could not be passed with guidewire. Four patients were treated with balloon dilatation only; two of them are recurrence-free with a follow-up of 24 and 8 months. Eleven patients had balloon dilatation and plastic stent placement as their primary treatment modality. In six of them, the anastomosis remained patent for the rest of the follow-up (22+/-13 months). Five patients had stricture recurrence after first stenting which necessitated re-stenting; four of them required a third, and three had a fourth stenting. CONCLUSIONS: Endoscopic balloon dilatation and stenting are safe and effective means of treatment of anastomotic biliary strictures following liver transplantation.

Hyperhomocysteinaemia and factor V Leiden mutation are associated with Budd-Chiari syndrome.

OBJECTIVES: Budd-Chiari syndrome (BCS) is characterized by hepatic venous outflow obstruction and may be caused by various prothrombotic disorders. We aimed to study the role of hyperhomocysteinaemia, factor V Leiden mutation and G20210A prothrombin gene mutation in the pathogenesis of the syndrome. METHODS: Thirty-two patients (16 male, 16 female, aged 19-45 years) with angiographically verified BCS and 33 age-matched and sex-matched voluntary healthy controls (15 male, 18 female, aged 19-45 years) were included into the study. Factor V Leiden and prothrombin gene mutations were determined in extracted DNA from peripheric mononuclear cells, using a light cycler amplification system. Plasma homocysteine levels were measured by fluorescence polarization immunoassay. RESULTS: The homozygote factor V Leiden mutation was diagnosed in four BCS patients and the heterozygote mutation was diagnosed in five. The frequency of the mutant allele was 20.3% in BCS patients and 7.6% in the controls (P < 0.05). There was no significant difference in prothrombin gene mutation frequency between the two groups. Serum homocysteine levels were significantly higher in the BCS group than in the controls (16.4 +/- 8.8 vs 11.0 +/- 2.7 micromol/l; P < 0.01). BCS patients with the mutant factor V Leiden allele have significantly higher levels of serum homocysteine (22.1 +/- 13.3 vs 14.4 +/- 5.9 mumol/l; P < 0.05). CONCLUSIONS: Hyperhomocysteinaemia, especially when associated with the factor V Leiden mutation, is an important risk factor for the development of BCS.

Two-year interferon therapy with or without ribavirin in chronic delta hepatitis.

UNLABELLED: The only beneficial agent for the treatment of chronic delta hepatitis (CDH) is interferon (IFN). However, there is no consensus on the best dosage or duration of IFN therapy. As ribavirin (RBV) increases the sustained response when added to IFN in chronic hepatitis C, probably because of its immunomodulatory effect, we aimed to investigate the efficacy of 2-year IFN treatment and whether RBV had any additive effect to IFN in CDH. METHODS: Patients (n = 31) with CDH were randomized with a 1:2 ratio as 10 patients (3 females/7 males, age 39 +/- 9) receiving IFN monotherapy (9 MU IFN-alpha2a three times weekly) and 21 patients (8 females/13 males, age 38 +/- 11) receiving IFN plus RBV for 2 years (IFN at the same dosage and RBV at 1000-1200 mg/day). Alanine transferase normalization and hepatitis delta virus (HDV) RNA negativity at the end of treatment and at the end of the follow-up period (at least 6 months following 2-year treatment) were primary endpoints of the study. In addition, virological response and biochemical response were determined separately. RESULTS: Eight of 31 patients (25%) had cirrhosis in liver biopsies. Six patients from the IFN monotherapy group and 12 patients from the combination group had biochemical response. Five patients from the IFN monotherapy group and 11 patients from the combination group had virological response at the end of therapy. Two patients from the IFN group and five patients from the combination group had sustained biochemical response at the end of the follow-up period. Hepatitis B virus (HBV) activations with HBV DNA positivity were observed in two patients (one from the IFN monotherapy group, one from the combination group). Two patients (20%) in the IFN group and five patients (23.5%) in IFN plus RBV group remained as virological responders at the end of the follow-up period (P > 0.05). None of the patients with liver cirrhosis were responsive at the end of the follow-up period. CONCLUSION: Almost 20% of the patients with CDH were responsive to 2-year IFN treatment at the end of the follow-up period and no additional effect of RBV was observed. Patients with advanced liver disease failed to respond to treatment.

Endoscopic injection therapy of bleeding Dieulafoy lesion of the stomach.

BACKGROUND/AIMS: Dieulafoy's lesion is a rare cause of upper gastrointestinal bleeding and is potentially life threatening. The aim of this study is to determine the clinical features of these lesions and the efficacy of the endoscopic injection sclerotherapy in patients with Dieulafoy's lesion. METHODOLOGY: Between January 1994 and December 2001, twenty-eight patients with upper gastrointestinal bleeding due to Dieulafoy's lesion were treated by endoscopic injection sclerotherapy. Efficacy of endoscopic therapy and clinical findings of these cases were analyzed. RESULTS: The study group consisted of 22 male (78.5%) and 6 female (21.5%) patients with a mean age of 57 years (range 22-82 years). Significant comorbidity was present in 22 (78.5%) patients. Hemoglobin values of the patients ranged from 5.4-10.3 g/dL at hospitalization. The median transfusion requirement was 5 (range 0-12) units. Dieulafoy's lesion was observed in the proximal half of stomach in 25 cases (89.3%), in the antrum in 2 cases (7.1%) and in the angulus in 1 case (3.5%). Endoscopic injection sclerotherapy was successful in stopping the bleeding in 26 out of 28 patients (92.8%). CONCLUSIONS: Dieulafoy's lesions mostly affect the proximal stomach and cause serious upper gastrointestinal bleeding. Endoscopic injection sclerotherapy is an effective and a safe therapeutic method for Dieulafoy's lesion.

Management of fatty liver disease with vitamin E and C compared to ursodeoxycholic acid treatment.

BACKGROUND/AIMS: Despite a proposed role of oxidative stress in the pathogenesis of nonalcoholic steatohepatitis, antioxidant approaches have not been investigated sufficiently in the therapy of nonalcoholic steatohepatitis. Our aim was to determine whether vitamin E plus C therapy is effective in normalization of liver enzymes compared to ursodeoxycholic acid treatment in patients with fatty liver disease. METHODS: This was an open-labeled, prospective, randomized study enrolling patients with histologically proven fatty liver disease who had chronically elevated alanine aminotransferase, despite a three-month reducing diet. Patients consuming alcohol (more than 20 g/day) were excluded. The patients were randomly prescribed either oral vitamin E (600 IU/day) plus vitamin C (500 mg/day) or ursodeoxycholic acid (10 mg/kg/day). Patients were randomized as two groups to receive vitamin E plus vitamin C combination (28 patients, 10 F) or ursodeoxycholic acid treatment (29 patients, 13 F). RESULTS: There was no significant change in body mass index before and after the treatment in both groups. At the end of six months of therapy, serum aspartate aminotransferase and aminotransferase levels significantly decreased in both treatment options. Vitamin E and C combination was more efficacious on serum aminotransferase levels than ursodeoxycholic acid, but the difference was not significant. Alanine aminotransferase decreased to normal levels in 17 of 27 (63%) and in 16 of 29 patients (55%), respectively, in the two groups. Gamma-glutamyl transpeptidase decreased in patients receiving ursodeoxycholic acid, but no change was obtained in the vitamin-treated patients. CONCLUSIONS: Vitamin E plus C combination treatment is a safe, inexpensive and effective treatment option in patients with fatty liver disease, with results comparable to those obtained with ursodeoxycholic acid. Since more effective new therapeutic options are lacking, patients with fatty liver disease should be encouraged to take vitamin E and C supplements, which are safe and affordable.

Induction of apoptosis by fatty acid ethyl esters in HepG2 cells.

Fatty acid ethyl esters (FAEEs) are esterification products of ethanol and fatty acids which have been found particularly in the organ damaged by ethanol abuse. To evaluate any effect of FAEEs on HepG2 cells, we added FAEEs to cell culture medium. Electrophoresis of DNA from HepG2 cells exposed to 18.5 microM ethyl palmitate (EP) and 10.6 microM ethyl stearate (ES) for 24 h revealed a smear which is typical of non-specific degradation by DNA ladder assay. Apoptosis was characterized by electron microscopy, flow cytometry revealed that the cell cycle of HepG2 cells was perturbed by exposure to FAEEs. In the present study we demonstrate that treatment of HepG2 cells with EP and ES induces apoptosis, as well as perturbing the cell cycle as the number of cells in the G(2)/M and S phases decreased.

Interferon-lamivudine combination is no better than lamivudine alone in anti-HBe-positive chronic hepatitis B.

BACKGROUND AND AIMS: Results of studies using lamivudine and interferon combination in the treatment of chronic hepatitis B are not consistent or conclusive. This study aimed to evaluate the efficacy of interferon plus lamivudine use versus single lamivudine in anti-HBe-positive chronic hepatitis B. METHODS: Eighty patients were treated with either lamivudine or lamivudine plus simultaneously started interferon. Patients were assigned in groups according to random allocation rule. Lamivudine was given 150 mg/day for 96 weeks in each group; interferon was administered 10 MU three times a week for 24 weeks in the combination therapy group. RESULTS: Alanine aminotransferase (ALT) normalization was achieved earlier in patients treated with lamivudine alone. At the end of treatment, there was no difference between the groups with respect to HBV DNA negativity, ALT normalization and breakthrough rate. Histological improvement was remarkable in each group, but fibrosis score and necro-inflammatory activity were much lower in lamivudine-treated patients. CONCLUSIONS: Addition of interferon to the lamivudine regimen does not increase the effectiveness of the treatment. Considering the side effects of interferon treatment, this combination seems not to be convenient for anti-HBe-positive chronic hepatitis B.