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.

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.

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.

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.

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.

Biochemical and morphological characteristics of selenite-induced apoptosis in human hepatoma Hep G2 cells.

Selenium is a cellular growth inhibitor in many mammary tumor cells. To comprehend the mechanism for the selenium-induced cell death, we examined the effects of sodium selenite, which has been one of the most extensively investigated selenium compounds, in human hepatoma Hep G2 cells.Cell viability gradually decreased after treatment with sodium selenite within the concentration range of 10-50 microM. Low (10 mM) selenite has shown a high-percentage laddering pattern compared to the high (25 microM) cytotoxic selenium concentration in agarose gel electrophoresis. G2/M-phase enrichment was also concentration dependent. The most consistent transmission electron microscopic finding was the existence of large lysosomes. Based on these data, we hypothesize that sodium selenite predominantly shows its apoptotic effect over hydrogen selenite accumulation.

Leukotriene receptor antagonism in experimental acute pancreatitis in rats.

OBJECTIVES: Acute pancreatitis is a multifactorial disease caused by activation of several inflammatory mediators. Leukotrienes, beside other mediators, may be involved in acute pancreatitis. The aim of this study was to investigate the effects of 'zafirlukast', a leukotriene receptor antagonist, in acute pancreatitis and its relation with prostaglandin synthesis. METHODS: Eighty rats were randomly divided into eight groups. Acute pancreatitis was induced by subcutaneous injection of cerulein (20 microg/kg), four times at 1-h intervals. Zafirlukast (20 mg/kg) was applied intraperitoneally as a pretreatment. Prostaglandin synthesis was inhibited by low-dose indomethacin (5 mg/kg subcutaneously). Pancreatic histopathology, serum amylase activity and pancreatic myeloperoxidase activity were determined to assess the severity of pancreatitis. RESULTS: Zafirlukast pretreatment alone did not induce any inflammation and fatty necrosis in pancreatic tissue. However, it increased the histopathological score from 3.70 +/- 0.57 to 6.62 +/- 0.53 in rats with acute pancreatitis (P < 0.001). Fatty necrosis was especially prominent in the zafirlukast-treated acute pancreatitis group compared with the untreated group (2.62 +/- 0.26 versus 0.40 +/- 0.22, respectively; P < 0.001). Inhibition of prostaglandin synthesis by indomethacin partially suppressed the harmful effects of zafirlukast in acute pancreatitis. It decreased the pathological score (4.62 +/- 0.73) and fatty necrosis (1.50 +/- 0.32) in that group. CONCLUSION: Interestingly, leukotriene receptor antagonism by zafirlukast increased the pancreatic histopathological score and fatty necrosis in rats with acute pancreatitis. Blocking of cysteinyl leukotriene receptors might cause an induction of mediator synthesis via other pathways. Effects of leukotriene receptor antagonism on the pancreas must be evaluated extensively in further studies.

Infliximab: a new therapeutic agent in acute pancreatitis?

PURPOSE: Tumor necrosis factor alpha (TNF-alpha) has a central role in the pathogenesis of acute pancreatitis and related systemic complications. The aim of this study is to investigate the therapeutic effectiveness of monoclonal TNF antibody (infliximab) in acute edematous and severe necrotizing pancreatitis models in rats. METHODS: One hundred rats were randomly divided into 10 groups. Acute edematous pancreatitis (AEP) was induced by injection of cerulein 20 microg/kg 4 times subcutaneously at hourly intervals. Severe necrotizing pancreatitis (SNP) was induced by retrograde injection of 3% taurocholate into the common biliopancreatic duct. Infliximab 8 mg/kg was given via intravenous infusion. Serum amylase activity, pancreatic histopathology, myeloperoxidase enzyme activity (MPO), and pulmonary changes were assessed. RESULTS: Infliximab treatment significantly decreased serum amylase activity (11939 +/- 1914 U/L versus 3458 +/- 915 U/L, P < 0.001) and histopathologic score (4.1 +/- 0.5 versus 1.5 +/- 0.3, P < 0.001) in AEP. It also suppressed neutrophil infiltration and MPO activity of the pancreatic tissue. In SNP, infliximab treatment was found to decrease pathologic score (9.4 +/- 1.2 versus 3.6 +/- 0.8, P < 0.001) and serum amylase activity (20442 +/- 2375 versus 8990 +/- 1730, P < 0.01). It ameliorated both parenchymal and fatty tissue necrosis of the pancreas. Infliximab also alleviated alveolar edema and acute respiratory distress syndrome like pulmonary complications, but the difference was not significant. CONCLUSIONS: Chimeric TNF antibody, infliximab, should be evaluated for treatment of acute pancreatitis.

Hydatid acute pancreatitis.

BACKGROUND/AIMS: Hydatid acute pancreatitis is a rare condition, mostly reported as case presentations. METHODS: A series of eight patients with hydatid acute pancreatitis, referred between January 1990 and January 2003, are reported. All patients presented acute pancreatitis confirmed with clinical presentation, radiologic examination and laboratory findings. All patients had elevated levels of blood amylase value (more than 500 U/L). Five patients (62%) had high bilirubin levels (2.1 to 3.4 mg/dl) during the initial hospitalization. Computed tomography findings revealed acute pancreatitis in four patients; two had associated pseudocyst formation. RESULTS: Endoscopic retrograde cholangiopancreatography was performed on all patients and revealed hydatid cystic material in the common bile duct secondary to cystobiliary rupture in all patients. All patients underwent endoscopic sphincterotomy that was performed after dilatation with extractor balloon, and hydatid material was removed in all. Six patients were operated on after the initial episode subsided. Drainage of the cyst, appropriate cavity management and T-tube drainage of the common bile duct was employed in all patients to control bile leakage after the operation. Scolices and hydatid membrane were detected during common bile duct exploration in all patients due to presentation of cystobiliary rupture. There was no mortality. Postoperative pulmonary infection and wound infection were encountered in one patient each. During two to 13 years' follow-up, one patient developed recurrent hydatid disease. Recurrent pancreatitis did not occur. CONCLUSIONS: Hydatid acute pancreatitis is a rare condition. However, it should be remembered in patients with abdominal pain, especially in endemic areas.

Characterization of the cellular response during apoptosis induction in cadmium-treated Hep G2 human hepatoma cells.

Cadmium is a toxic transition heavy metal of continuing occupational and environmental concern, with a wide variety of adverse effects on regulation of gene expression and cellular signal transduction pathways. Injury to cells by cadmium leads to a complex series of events that can culminate in the death of the cell. It has been reported that cadmium induces apoptosis in many cell lines. However, the morphological characteristics leading to apoptosis or subsequent regeneration in cells exposed to cadmium have not been clarified. We evaluated whether human hepatoma cells maintained in culture undergo apoptosis when exposed to cadmium. Cytotoxic activity of cadmium on Hep G2 cells determined using 3-[4,5-dimethylthiazol-2-yl]-2,5- diphenyltetrazolium bromide assay. A DNA ladder assay was performed by electrophoresis. Cell cycle analysis was quantified by flow cytometry. Nuclear morphology was studied by fluorescence microscopy after staining with propidium iodide and Hoechst 33342. Morphologic alterations in culture hepatocytes treated with CdCl2 were observed by transmission electron microscopy. We have demonstrated that apoptosis is a major mode of elimination of damaged HepG2 cells in cadmium toxicity and it precedes necrosis.

Trace elements analysis of ascitic fluid in benign and malignant diseases.

OBJECTIVES: To evaluate differences in ascitic fluid trace element concentrations which might be useful in discrimination between benign and malignant ascites. DESIGN AND METHODS: The concentrations of copper, zinc, magnesium and iron in ascitic fluid and venous blood in 17 patients were investigated. The relationship between these trace elements and type of disease were examined. Investigations were carried out in a group of 5 males and 5 females aged 54 to 77 yr who had cirrhosis ascites and in a group of 7 females aged 41 to 76 yr with ascites due to gynecologic neoplasms. RESULTS: The mean ascitic fluid and serum concentrations of copper were significantly higher in neoplastic diseases compared to benign disease states (118,43 vs. 97,50, 91,14 vs. 26.90) (p < 0,05 and p < 0,01 respectively). The zinc levels in ascitic fluid and serum were significantly different between the groups (p < 0,01). Neoplastic patients had significantly higher ascitic fluid magnesium levels than the benign disease group (2,17 vs. 1,55, p < 0,001). The serum levels of iron were significantly lower in the neoplastic diseases group (92, 28 vs. 255, p < 0, 01). In benign diseases the concentration of zinc in ascitic fluid correlated positively with ascitic fluid copper concentrations. The concentrations of zinc and iron in malignant ascites correlate positively with the magnesium concentrations. Statistically significant negative correlations were found between ascites zinc and magnesium and magnesium and copper in cirrhotic patients and magnesium and copper in malignant diseases. CONCLUSIONS: The results showed that zinc, magnesium and iron levels were significantly different between cirrhotic and neoplastic illness. Analysis of serum and ascitic fluid trace element composition may be helpful in identifying and distinguishing the malignant and nonmalignant ascites and provides useful information on processes regulating passage of blood components into the peritoneal cavity.

Clinical and biochemical features and therapy responses in primary biliary cirrhosis and primary biliary cirrhosis-autoimmune hepatitis overlap syndrome.

BACKGROUND/AIMS: Primary biliary cirrhosis and autoimmune hepatitis are two main immune-mediated liver diseases. Some patients display characteristics of both diseases, so called overlap syndrome. The aims of this study were to investigate and to compare the clinical and laboratory features and responses to therapy in primary biliary cirrhosis and overlap syndrome. METHODOLOGY: Twenty-three patients with primary biliary cirrhosis (21 females, 2 males; median age: 50 years) and 20 with primary biliary cirrhosis-autoimmune hepatitis overlap syndrome (18 females, 2 males; median age: 44 years) were included in the study. All patients with primary biliary cirrhosis were treated with ursodeoxycholic acid. Of patients with overlap syndrome, 16 were treated with ursodeoxycholic acid and 4 with ursodeoxycholic acid plus prednisolone. Histological findings laboratory and clinical data were compared at the baseline and at the 2nd year of treatment. RESULTS: Fatigue and pruritus were the most frequent and comparable symptoms in each group. Serum ALT, AST, gamma-glutamyl transpeptidase, total protein, globulin and gammaglobulin levels were higher in patients with overlap syndrome than those in patients with primary biliary cirrhosis. At the end of the 2nd year of the treatment, ALT normalization was achieved in 12 (52%), alkaline phosphatase in 7 (30%) patients with primary biliary cirrhosis. One of the non-responders to ursodeoxycholic acid therapy had the histological findings of overlap syndrome in her control biopsy. Fibrosis score deteriorated in 50% of the patients. Of ursodeoxycholic acid-treated overlap syndrome patients, 11 completed 2 years of treatment. Three patients were biochemically non-responsive and prednisolone was added to their regimen. Of the remaining 8 patients, 7 (64% of total patients) had normal ALT. Three patients had worse fibrosis score comparing the onset of the treatment. Six of 7 (86%) patients who were given ursodeoxycholic acid plus prednisolone including ursodeoxycholic acid-non-responsives had normal ALT and 2 of 6 biopsy-controlled patients display deterioration of their fibrosis score. CONCLUSIONS: Biochemical tests tended to be higher in patients with overlap syndrome comparing to those with primary biliary cirrhosis. Response to ursodeoxycholic acid treatment in patients with overlap syndrome was comparable with that obtained in primary biliary cirrhosis. Therefore it should be the first-line treatment. Non-responsive patients may benefit from the use of ursodeoxycholic acid plus prednisolone combination.

Serum, pleural effusion, and ascites CA-125 levels in ovarian cancer and nonovarian benign and malignant diseases: a comparative study.

OBJECTIVES: Cancer antigen-125 (CA-125) is not a specific tumor marker and it is synthesized by normal and malignant cells of different origins. Recently it has been shown that various diseases are associated with increased CA-125 levels, especially in the presence of serosal fluid. The aim of this study is to investigate serum and fluid CA-125 levels in patients with different diseases. METHODS: A total of 133 patients and 23 healthy control cases were included in the study and divided into eight groups on the basis of disease and the presence of fluid in the serosal cavities. Serum and serosal fluid CA-125 levels were measured by a commercial enzyme immunoassay kit at the same time. Comparisons among the groups were made. RESULTS: Abnormal levels of serum CA-125 were observed in 76% of ovarian cancer patients; 96% in patients with ascites and 56% in patients without ascites. Moreover, elevated serum CA-125 levels were detected in 52% of patients with hepatic diseases, in 100% of patients with nongynecologic peritoneal carcinomatosis, and in 87% of patients with pleural effusion. Serum and fluid CA-125 levels were significantly higher in cases of ovarian cancer with ascites than in the other groups (P < 0.01). A positive correlation between serum CA-125 levels and ascites amounts was observed in cases of ovarian cancer with ascites (P < 0.01, r = 0.81). Furthermore, no correlation was observed between ovarian mass volume and serum CA-125 levels in ovarian cancer patients with stage I disease without ascites (P = 0.08, r = 0.48). CONCLUSIONS: Although CA-125 levels may be considered a sensitive tumor marker in patients with epithelial ovarian cancer, it was determined that high serum CA-125 levels were closely related to the presence of serosal fluids and serosal involvement, whatever the origin is. These results should be considered in the interpretation of CA-125 elevation in patients with ovarian cancer.