TASL Practice Guidance on the Clinical Assessment and Management of Patients with Nonalcoholic Fatty Liver Disease.

Nonalcoholic fatty liver disease (NAFLD) is a multisystem disease and is significantly associated with obesity, insulin resistance, type 2 diabetes mellitus, metabolic syndrome, and cardiovascular disease. NAFLD has become the most prevalent chronic liver disease in Western countries, and the proportion of NAFLD-related cirrhosis among patients on liver transplantation waiting lists has increased. In light of the accumulated data about NAFLD, and to provide a common approach with multi-disciplines dealing with the subject, it has become necessary to create new guidance for diagnosing and treating NAFLD. This guidance was prepared following an interdisciplinary study under the leadership of the Turkish Association for the Study of the Liver (TASL), Fatty Liver Special Interest Group. This new TASL Guidance is a practical application guide on NAFLD and was prepared to standardize the clinical approach to diagnosing and treating NAFLD patients. This guidance reflects many advances in the field of NAFLD. The proposals in this guidance are meant to aid decision-making in clinical practice. The guidance is primarily intended for gastroenterology, endocrinology, metabolism diseases, cardiology, internal medicine, pediatric specialists, and family medicine specialists.

The prevalence of metabolic-associated fatty liver disease in the Turkish population: A multicenter study.

Background and Aim: The objective of the present study was to investigate the prevalence of metabolic-associated fatty liver disease (MAFLD) in patients with dyspepsia. Materials and Methods: A total of 909 consecutive patients who presented with dyspepsia at 8 tertiary care centers in Turkey between March 2019 and December 2019 were included. Results: The median age was 47 years. Among them, 30.3% of the patients were obese, 18.8% had type 2 diabetes mellitus (T2DM), 35.1% had metabolic syndrome, 84.8% had dyslipidemia, and 23.9% had hypertension. The prevalence of MAFLD was 45.5%. Among the patients with MAFLD, the prevalence of obesity, T2DM, metabolic syndrome, dyslipidemia, and hypertension was 43.3%, 24.9%, 52.5%, 92.3%, and 31.9%, respectively. MAFLD was significantly associated with all of the metabolic comorbidities (p<0.001). The median Fibrosis-4 Index score of the MAFLD patients was 0.88 (range: 0.1-9.5). Of note, 53 patients with hepatic steatosis did not meet the MAFLD criteria. Conclusion: The results of the present study indicated that there was a significantly high prevalence of MAFLD observed in daily clinical practice in Turkey. Early diagnosis and prevention efforts should be implemented to reduce disease progression, and a region-based strategy is recommended.

Serum cystatin C measurement in differential diagnosis of intra and extrahepatic cholestatic diseases.

OBJECTIVE: Cystatin C is a very potent inhibitor of cysteine proteinases and, it has been clinically applied as a sensitive marker in monitoring of renal and liver functions. The aim of this study was to reveal whether cystatin C may be a useful marker for distinguishing intra- versus extrahepatic cholestasis. MATERIALS AND METHODS: Serum cystatin C concentrations were determined by nephelometric immunoassay using N latex cystatin C kit in 53 patients with cholestatic disorder that included 18 patients with intrahepatic cholestasis , 17 patients with malignant extrahepatic cholestasis , 18 patients with benign extrahepatic cholestasis. Serum cystatin C concentration was also determined in 20 healthy volunteers. RESULTS: Mean serum cystatin C concentration was 2.82 +/- 0.24 mg/l (SD) in patients with intrahepatic cholestasis, 2.05 +/- 0.15 mg/l in patients with extrahepatic malignant cholestasis, 1.37 +/- 0.13 mg/l in extrahepatic benign cholestatic patients and 0.93 +/- 0.24 mg/l in control group. Serum cystatin C concentrations in patients with cholestatic disease were significantly higher than those in the healthy controls (p < 0.001). Moreover, mean serum cystatin C concentration in patients with intrahepatic cholestasis was higher than those in extrahepatic cholestasis groups (p < 0.001). Serum cystatin C concentrations were significantly higher in patients with malignant xtrahepatic cholestasis than in patients with benign extrahepatic cholestasis p < 0.001). There were no correlations patients among serum cystatin C concentrations and serum levels of AST, ALT, ALP, GGT, total and conjugated bilirubin. CONCLUSION: Our results suggested that serum cystatin C level may be a potential biochemical marker both to point out an intrahepatic origin by excluding an extrahepatic source of cholestasis in patients with jaundice and to possibly differentiate bening and malignant extrahepatic cholestatic disorders.

Gastrocolic fistula secondary to gastric diffuse large B-cell lymphoma in a patient with pulmonary tuberculosis.

Gastrocolic fistula secondary to primary gastric lymphoma is a very rare entity. On admission to outpatient clinics, it may be difficult to diagnose gastrocolic fistula, as its clinical symptoms are nonspecific. A 65-year-old man was presented with weight loss, nausea, vomiting, diarrhea, fatigue, foul-smelling eructation, and upper abdominal pain for the last 2 months. He had also been started antituberculosis drugs 2 months ago because of acid-resistant bacillus (ARB) positivity in sputum in a state hospital. Therefore, symptoms such as nausea and vomiting were attributed to the drugs used for tuberculosis. However, nausea and vomiting continued despite stopping the drugs. Upper endoscopical examination revealed a large crater on the posterior wall of gastric corpus. A large fistulous opening to the transverse colon was also identified during endoscopic examination. An upper gastrointestinal x-ray series demonstrated a fistula between the stomach and the transverse colon. Histopathological examination of the gastric biopsy was determined to be primary gastric diffuse large B-cell-type non-Hodgkin's lymphoma. In conclusion, persistent vomiting may suggest a probable gastrocolic fistula despite nonspecific clinical findings. In the literature, the present case represents the first report of a gastrocolic fistula due to gastric lymphoma in a patient with tuberculosis at its initial presentation.

Leptin levels in the differential diagnosis between benign and malignant ascites.

AIM: To evaluate the role of leptin levels in the differential diagnosis of ascites. METHODS: Ascitic leptin, TNFalpha and serum leptin levels were measured in 77 patients with ascites (35 with malignancies, 30 cirrhosis and 12 tuberculosis). Control serum samples were obtained from 20 healthy subjects. Leptin and TNFalpha levels were measured by ELISA. Body mass index (BMI) and percentage of body fat (BFM) by skin fold measurement were calculated for all patients and control groups. Peritoneal biopsy, ascites cytology and cultures or biochemical values were used for the diagnosis of patients. RESULTS: In patients with malignancies, the mean serum and ascites leptin levels and their ratios were significantly decreased compared to the other patient groups and controls. In tuberculosis peritonitis, ascitic fluid TNFalpha levels were significantly higher than malignant ascites and cirrhotic sterile ascites. BMI and BFM values did not distinguish between patients and controls. CONCLUSION: In patients with malignant ascites, levels of leptin and TNFalpha were significantly lower than in patients with tuberculous ascites.

Mutations in the S gene region of hepatitis B virus genotype D in Turkish patients.

The S gene region of the hepatitis B virus (HBV) is responsible for the expression of surface antigens and includes the 'a'-determinant region. Thus, mutation(s) in this region would afford HBV variants a distinct survival advantage, permitting the mutant virus to escape from the immune system. The aim of this study was to search for mutations of the S gene region in different patient groups infected with genotype D variants of HBV, and to analyse the biological significance of these mutations. Moreover, we investigated S gene mutation inductance among family members. Forty HBV-DNA-positive patients were determined among 132 hepatitis B surface antigen (HbsAg) carriers by the first stage of seminested PCR. Genotypes and subtypes were established by sequencing of the amplified S gene regions. Variants were compared with original sequences of these serotypes, and mutations were identified. All variants were designated as genotype D and subtype ayw3. Ten kinds of point mutations were identified within the S region. The highest rates of mutation were found in chronic hepatitis patients and their family members. The amino acid mutations 125 (M -> T) and 127 (T -> P) were found on the first loop of 'a'-determinant. The other consequence was mutation inductance in a family member. We found some mutations in the S gene region known to be stable and observed that some of these mutations affected S gene expression.

Relationship between liver injury and serum cytokeratin 18 levels in asymptomatic hepatitis B virus carriers and in patients with chronic hepatitis B infection.

BACKGROUND AND STUDY AIMS: Apoptosis represents a well-known mechanism of cell death involved in most chronic liver injuries. Our aim was to investigate the serum fragment level of cytokeratin 18 (CK18), M30, in asymptomatic hepatitis B virus (HBV) carriers and patients with chronic hepatitis B (CHB) and to evaluate the relationship between serum M30 levels and the severity of hepatic injury. PATIENTS AND METHODS: Asymptomatic HBV carriers (n=169), patients with CHB (n=100), and healthy control subjects (n=43) were enrolled in the study. Serum CK18 (M30) levels were analysed in all subjects. Liver biopsy for histopathological assessment was performed in asymptomatic HBV carriers and in patients with CHB infection. RESULTS: Serum CK18 (M30) levels were significantly higher in asymptomatic HBV carriers (198.77±77.62U/L) than in healthy control subjects (146.92±40.18U/L). Patients with CHB (283.02±147.45U/L) had significantly higher CK18 (M30) levels than asymptomatic HBV carriers (p=0.001). The diagnostic efficacy of CK18 (M30) levels in distinguishing patients with HBeAg-negative CHB from asymptomatic HBV carriers was found to be moderate (c-statistics: 0.695), and the diagnostic cut-off value of CK18 (M30) was 262U/L (specificity: 85%, sensitivity: 48%, positive likelihood ratio: 3.35, and negative likelihood ratio: 0.60). There was a positive correlation between serum CK18 (M30) levels and histological activity index scores in asymptomatic HBV carriers and patients with CHB. CONCLUSIONS: Serum CK18 (M30) levels may be a valuable indicator in distinguishing asymptomatic HBV carriers from patients with HBeAg-negative CHB when considered together with ALT and HBV-DNA levels.

Preventative Effect of Vitamin E on Mast Cells in Carbon Tetrachlorideinduced Acute Liver Damage.

BACKGROUND: Preventing liver damage that might lead to cirrhosis is very important in the early stages of injury to that organ. The role of mast cells (MCs) in liver injuries has been long debated, and vitamin E is a well-known antioxidant used to treat those injuries. This study aimed to determine the protective role of vitamin E on MCs in injury to the liver that is triggered by carbon tetrachloride (CCl4). There is a correlation between MC deposits and improvement in fibrosis tissues. METHODS: To further examine this, 68 male Albino Wistar rats were divided randomly into five groups: the control group, the vitamin E group, the CCl4 group, the CCl4 + vitamin E group, and the vitamin E + CCl4 group. Malondialdehyde (MDA) analysis, MC counts, histopathological investigation, and statistical analyses were used to evaluate the findings. RESULTS: The administration of CCl4 resulted in an increase in the accumulation of MCs, degenerative parenchyma cells, MDA level, steatosis and inflammation. Additionally, proliferation of the bile ducts in the portal area and porto-portal and porto-central fibrosis were observed in the CCl4 group. In contrast, in the vitamin E group and in the groups administered a combination of vitamin E and CCl4, vitamin E prevented these increases. CONCLUSION: It was concluded that the significant decrease in the MC counts, in the level of MDA and the number of degenerative cells, as well as a decrease in the steatosis and inflammation scores showed that vitamin E could prevent liver injuries by protecting the organ's histological architecture. Finally, the results indicate that vitamin E has positive effects on liver injuries.

Argon plasma coagulation in the treatment of hemorrhagic radiation proctitis.

Hemorrhagic radiation proctosigmoiditis is a serious complication of pelvic radiation therapy. Pharmacotherapy is generally ineffective in the treatment of chronic radiation proctitis. Argon plasma coagulation is an effective, safe and well-tolerated therapy option for radiation proctitis. We report a case of hemorrhagic radiation proctosigmoiditis treated successfully with Argon plasma coagulation. We used argon plasma coagulation for mucosal coagulation in painting pattern set at 1.5 L/min and 60 W. After five therapy sessions with argon plasma coagulation, the patient's rectal bleeding and anemia resolved. After four months of argon plasma coagulation therapy, the patient is well and her endoscopic examination showed remarkable improvement of the vascular lesions. Blood transfusion requirement was resolved after therapy, and hemoglobin level increased from 8.2 g/dl to 11.5 g/dl. Argon plasma coagulation therapy may be useful as alternative treatment for hemorrhagic radiation proctitis. Future prospective controlled trials are necessary to confirm the efficacy of argon plasma coagulation in the treatment of radiation proctitis.

The efficacy, safety and tolerability of pantoprazole-based one-week triple therapy in H. pylori eradication and duodenal ulcer healing.

OBJECTIVE: Recently, proton pump inhibitor (PPI)-based triple therapy has been recommended as a first line treatment in the eradication of Helicobacter pylori. The aim of this open, multicentre trial was to investigate the efficacy, safety, tolerability and the ulcer healing rate of a triple regimen consisting of pantoprazole 40 mg, clarithromycin 500 mg and amoxicillin 1000 mg twice daily for 7 days, in the eradication of H. pylori in patients with duodenal ulcer in Turkey. RESEARCH DESIGN AND METHODS: H. pylori infection was assessed by histological examination and rapid urease test at baseline and 4 weeks after the completion of the therapy. Seventy-seven patients were enrolled, 5 were excluded due to various reasons and 72 completed the entire course of the trial. RESULTS: H. pylori eradication was confirmed in 49 of these patients; the eradication rate was 68% by per-protocol analysis and 63.6% by intention-to-treat analysis. The ulcers were completely healed in 61 patients (85%) at the second endoscopic examination. Drug compliance was excellent (97.3%) and there were no serious adverse events. CONCLUSION: Pantoprazole-based 1-week triple therapy was well tolerated and the ulcer healing rate was high (85%). Relatively low H. pylori eradication rates may be attributed to rising antibiotic resistance over recent years. A large scale, comparative study with other PPI-based regimens is warranted based on the results of this open study with the pantoprazole-based regimen.

Antioxidant capacity and nitric oxide in patients with hepatic cirrhosis.

This study investigated the relationship between the antioxidant capacity of blood and the serum level of nitric oxide (NO) in patients with hepatic cirrhosis. The study included 20 patients with compensated cirrhosis (group I), 30 with decompensated cirrhosis (group II), and 30 healthy controls (group III). The serum levels of NO, albumin, bilirubin, and uric acid, and the erythrocyte activity of superoxide dismutase (SOD) were measured in all groups. The mean erythrocyte SOD activity (5.94 +/- 3.21 U/mg protein) and serum NO level (25.19 +/- 8.15 micromol/L) in group I were similar to those of controls (6.86 +/- 2.47 U/mg protein and 21.67 +/- 6.51 micromol/L, respectively). However, erythrocyte SOD activity in group II was significantly lower than in groups I and III and mean serum NO level was significantly higher in group II than in groups I and III. In regard to non-enzymatic antioxidants, the mean serum albumin level was lower and the mean serum total bilirubin level was higher in group II than in groups I and III. As expected, group I had higher mean serum total bilirubin level than the control group. Correlation analysis showed that erythrocyte SOD activity in cirrhotic patients was negatively correlated with their serum levels of NO. These results suggest that disturbances of antioxidative mechanisms may diminish hepatic resistance to oxidative stress, thereby contributing to the development of fibrogenesis.

Oxidative stress and enzymatic antioxidant status in patients with nonalcoholic steatohepatitis.

Oxidative stress is an important pathophysiological mechanism in nonalcoholic steatohepatitis (NASH). To assess whether there are relationships between oxidative stress and antioxidant enzymes in the development of NASH, we investigated oxidative stress by measuring serum malondialdehyde (MDA) and nitric oxide (NO) and antioxidant status by measuring serum glutathione (GSH), glutathione peroxidase (GSH-Px), glutathione reductase (GR), and superoxide dismutase (SOD). The study included 18 patients (13 men, 5 women; mean age 42 yr) with biopsy proven NASH and 16 healthy volunteers (10 men, 6 women; mean age 38 yr). Serum levels of MDA, NO, GSH, GSH-Px, GR and SOD were determined by spectrophotometric methods. Serum levels (mean +/- SD) of MDA (6.7 +/- 1.6 vs 2.8 +/- 1.7 nmol/ml, p 0.0001), NO (135 +/- 28 vs 113 +/- 35 mmol/L, p 0.04), GSH (919 +/- 137 vs 770 +/- 128 mmol/L, p 0.003) were increased in patients with NASH vs controls. Serum levels of GSH-Px (1063 +/- 152 vs 1000 +/- 94 U/L) and GR (47 +/- 22 vs 40 +/- 21 U/L) were not singnificantly different in the patients vs controls. However, the serum level of SOD (1.24 +/- 0.32 vs 1.51 +/- 0.37 U/ml, p: 0.04) was significantly decreased. Impaired antioxidant defense mechanisms may be an important factor in the pathogenesis of NASH. Treatment approaches that affect the antioxidant enzymes may be beneficial in patients with NASH.

Therapeutic effect of oral recombinant human granulocyte macrophage-colony stimulating factor in radiotherapy-induced esophagitis.

BACKGROUND/AIMS: Radiation-induced esophagitis is one of the most important early side effects of irradiation of chest, and head and neck malignancies. This condition often leads to interruption of radiotherapy for several days. An effective treatment for reducing the incidence and severity of this complication has not yet been found. We aimed to investigate the therapeutic effect of rhGM-CSF on radiation-induced esophagitis in the patients with chest or head and neck malignancies. METHODOLOGY: Ninety-seven patients with chest or head and neck malignancies who had not previously received radiation therapy, were treated with radiotherapy, concurrent or sequential chemoradiotherapy. Forty-eight patients who had grade 1, 2 or 3 esophagitis symptoms according to Radiation Therapy Oncology Group radiation morbidity score, underwent upper gastrointestinal endoscopy. In the patients with grade 3 esophagitis (according to Kuwahata's scoring system) rhGM-CSF was administered for 5-10 consecutive days as an oral solution. RESULTS: Endoscopic examinations showed grade 3 esophagitis in 26 of these patients according to Kuwahata's score. Twenty-five patients with grade 3 esophagitis were given rhGM-CSF therapy. Radiotherapy was continued in 23 patients. After the rhGM-CSF therapy, esophagitis had regressed from grade 3 to grade 0 in 10 (43%), from grade 3 to grade 1 in 8 (35%), and from grade 3 to grade 2 in 3 patients (12%). Two patients (9%) did not respond to rhGM-CSF therapy. Twenty-one patients (91%) completed planned radiotherapy without interruption. CONCLUSIONS: In patients with radiation-induced esophagitis, ulcerated esophageal mucosa healed with local granulocyte macrophage-colony stimulating factor administration in median 8 days without radiotherapy interruption.

Serum thrombopoietin levels in patients with chronic hepatitis and liver cirrhosis, and its relationship with circulating thrombocyte counts.

BACKGROUND/AIMS: Thrombocytopenia in chronic liver diseases may be related to deficient production of thrombopoietin. The aim of this study was to measure serum thrombopoietin levels and to examine the relationship between serum thrombopoietin concentration, circulating platelet counts and clinical stage of the disease in patients with chronic hepatitis and liver cirrhosis. METHODOLOGY: The study included 18 patients with chronic hepatitis, 48 with liver cirrhosis and 27 healthy volunteers. Serum thrombopoietin levels were measured by enzyme-linked immunosorbent assay. Additionally, serum albumin levels, prothrombin time, circulating platelet counts and spleen volume index were determined. RESULTS: Mean serum thrombopoietin level (100.96 +/- 41.67 pg/mL) in the chronic hepatitis group was similar to that of the healthy group (97.60 +/- 43.99 pg/mL), however serum thrombopoietin levels in patients with liver cirrhosis (69.60 +/- 30.23 pg/mL) were lower than patients with chronic hepatitis and controls (p < 0.05 for both). In patients with liver cirrhosis, serum thrombopoietin levels were found to be decreased as the disease progressed (80.99 +/- 24.85 pg/mL in patients at Child-Pugh stage A, 67.92 +/- 39.37 in patients at stage B and 57.62 +/- 21.09 pg/mL in patients at stage C). Cirrhotic patients had increased prothrombin time (17.12 +/- 3.52 sec) and spleen volume index (94.38 +/- 26.48 cm2), and decreased serum albumin level (3.11 +/- 0.56 g/dL) and platelet counts (102,368 +/- 30,653/mm3) when compared to both chronic hepatitis and control groups. Thrombocytopenia was found in 31 (65%) of the patients with liver cirrhosis. In patients with liver cirrhosis, while there was a positive correlation between serum thrombopoietin and albumin levels (r = 0.36, p = 0.004), no correlation was found between platelet counts and serum thrombopoietin level, and spleen volume index. CONCLUSIONS: The findings reveal that serum thrombopoietin levels are normal in patients with chronic hepatitis, but in patients with liver cirrhosis, serum thrombopoietin levels decrease, as degree of cirrhosis progresses. The impaired production of thrombopoietin may contribute to the development of thrombocytopenia in advanced stage of liver disease.

Evaluation of hepatic functions and biliary dynamics in patients with liver cirrhosis by quantitative scintigraphy.

BACKGROUND/AIMS: Aim of the study is to determine the changes in hepatocyte and gallbladder motor functions, and biliary dynamics in patients with liver cirrhosis. METHODOLOGY: The study group consisted of 17 patients with liver cirrhosis (12 males, 5 females) who were diagnosed by clinical, laboratory and histopathologic findings. Control group consisted of 20 healthy persons (14 males, 6 females). Quantitative hepatobiliary scintigraphy was performed by using Tc99m-Mebrofenin i.v. and dynamic images were obtained and evaluated quantitatively by computer. Maximum excretion time of radiodiagnostic agent by liver (Tmax) and half excretion time of radio-diagnostic agent from liver (T 1/2), gallbladder filling time, gallbladder ejection fraction and the transit time of bile to duodenum were determined. RESULTS: Mean values of Tmax was 25.76 vs. 12.40 min, T 1/2 was 37.55 vs. 23.15 min, gallbladder filling time was 53.35 vs. 30.57 min, and transit time of bile to duodenum was 39.88 vs. 25.00 min in the patients and control group, respectively. These values increased significantly in the patient group (p < 0.05) compared to controls. Mean gallbladder ejection fraction was 37.55% in the patient group and 41.84% in the control group without any statistical significance (p > 0.05). The incidence of gallbladder stone was 29.41% in the cirrhosis group and 5% in the control group (p < 0.05). CONCLUSIONS: The quantitative hepatobiliary scintigraphy is a simple and reliable method in evaluation of hepatic functions and biliary dynamics in cirrhotic patients. Although the incidence of gallbladder stone is significantly increased in cirrhotic patients, it seems that a stone in the gallbladder does not affect the gallbladder motor functions.

Serum ubiquitin levels in patients with nonalcoholic steatohepatitis.

BACKGROUND/AIMS: Nonalcoholic steatohepatitis is increasingly recognized as the most common liver disease in patients with elevated liver enzymes. In the pathophysiology of nonalcoholic steatohepatitis, the first step is the lipid accumulation in the liver causing steatosis, the second step involves the endotoxins, cytokines and environmental toxins causing oxidative stress and lipid peroxidation, in time leading to steatohepatitis. Ubiquitin is a molecular chaperone that plays a major role in the degradation of intracellular proteins. Ubiquitin proteasome system is also considered as a cellular defense mechanism that removes damaged proteins generated by oxidative stress. In order to search for the role of ubiquitin in the pathogenesis of nonalcoholic steatohepatitis, serum levels of ubiquitin were studied in patients with nonalcoholic steatohepatitis for the first time in the literature, to our knowledge. METHODOLOGY: Eighteen patients with biopsy proven nonalcoholic steatohepatitis diagnosis (13 males and 5 females with a mean age of 41) and 16 healthy volunteers as a control group (11 males and 5 females, with a mean age of 38) were included in the study. Serum ubiquitin levels were studied by ELISA method. RESULTS: The mean serum ubiquitin level (14.13 +/- 1.46 micrograms/mL) in patients with nonalcoholic steatohepatitis was significantly elevated compared to that of the control group (7.66 +/- 0.40 micrograms/mL) (p < 0.001). No correlation was found among serum ubiquitin levels and hepatic steatosis, inflammation and fibrosis. CONCLUSIONS: Increased serum ubiquitin levels may show that the ubiquitin proteasome pathway actively participates in defending against oxidative stress in nonalcoholic steatohepatitis. Serum ubiquitin concentration may be a marker predicting the intracellular cytoprotective response against oxidative stress rather than the degree of liver damage in pathogenesis of nonalcoholic steatohepatitis. Ubiquitin proteasome system based therapies may have a place in the treatment of patients with nonalcoholic steatohepatitis in the future.

Colon carcinoma with synchronous subcutaneous and osseous metastasis: a case report.

Colon cancer usually metastasizes initially to regional lymphatics and later through the bloodstream. Hematogenous metastasis usually includes the liver, lungs, and brain. In colorectal cancer, osseous and/or subcutaneous metastasis without liver metastasis is a very uncommon event. We present here a case of colon adenocarcinoma, which synchronously metastasized to facial and other subcutaneous tissue and to bone within a short period after definitive therapy. Although such a pattern is uncommon, diagnostic biopsy for any new or suspicious lesion of the skin and bone scintigraphy for symptomatic patients should be done for patients with a colorectal cancer history.

Paraneoplastic cholestasis associated with prostate carcinoma.

Paraneoplastic syndromes associated with prostate carcinoma are very rare. We report a patient with prostate carcinoma and cholestatic jaundice without biliary obstruction, hepatic involvement or infectious etiology. In the literature, only one case of idiopathic cholestatic jaundice with prostate carcinoma has been reported and a paraneoplastic etiology was suggested. In our case, cholestasis rapidly regressed with chemotherapy and the patient is well at six months of follow-up. Paraneoplastic cholestasis should be kept in mind in the absence of biliary tract obstruction, hepatic involvement or infectious etiology.

Serum levels of acute phase proteins in patients with nonalcoholic steatohepatitis.

BACKGROUND/AIMS: A simple and practical method of detecting the degree of the inflammatory response during the development of nonalcoholic steatohepatitis has not been developed to date. In this study the serum levels of acute phase proteins in patients with nonalcoholic steatohepatitis and whether these levels had any relationship with histopathological findings in the liver were evaluated. METHODS: The study included 18 patients with NASH diagnosed by liver biopsy (13 males and five females with a mean age of 44 years) and 16 healthy volunteers as a control group (11 males and five females, with a mean age of 40 years). The serum levels of C-reactive protein, C-reactive ceruloplasmin, ferritin, transferrin, alpha-1-acid glycoprotein, alpha-2-macroglobulin, alpha-1-antitripsin, albumin, haptoglobulin and lipoprotein (a) were determined by nephelometric method in both groups. In patients with nonalcoholic steatohepatitis, liver histopathology was assessed using a modified scoring system based on the classification defined by Brunt. RESULTS: Serum C-reactive, ferritin, alpha-2-macroglobulin and ceruloplasmin concentrations in patients with nonalcoholic steatohepatitis were significantly higher than those of the control group (p=0.0001, p=0.001, p=0.007, p=0.01 respectively), but serum transferrin, albumin, haptoglobin, alpha-1-acid glycoprotein, alpha-1-antitripsin and lipoprotein (a) levels were not different. There was no difference in C-reactive protein levels regarding the degree of hepatic steatosis and inflammation and the stage of liver fibrosis. Acute phase proteins had no correlation with liver histology. CONCLUSIONS: Measurement of serum C-reactive protein, ferritin, ceruloplasmin and alpha-2-macroglobulin levels may be useful in assessing patients at risk of nonalcoholic steatohepatitis and those with high C-reactive protein and ferritin but normal transferrin should be considered for liver biopsy.

Transnasal endoscopy is preferred by transoral endoscopy experienced patients.

BACKGROUND & AIMS: Both unsedated transoral endoscopy (TOE) and sedated TOE have some drawbacks in clinical practice. Unsedated transnasal endoscopy (TNE) has been suggested as an alternative to both methods. This study aimed to determine the advantages of TNE in patients who have previously undergone unsedated conventional TOE. METHODS: Patients who had received an unsedated TOE in the last 12 months and were scheduled for a second upper endoscopy were included. They were randomized to undergo either unsedated TOE, using a standard endoscope, or unsedated TNE, using an ultrathin endoscope. Post-procedure, patients were asked to complete a questionnaire to assess pain, discomfort and acceptability of the procedure, and to compare the current procedure with their previous unsedated TOE. Endoscope insertion rate, procedure duration, and side-effects were recorded. RESULTS: Each group included 50 patients. With the exception of nasal pain, the tolerability and acceptance were significantly greater in the unsedated TNE group. Significantly more TNE patients (82%) found the current endoscopic procedure to be better than their previous TOE when compared with patients who had received a second TOE (12%). A repeat procedure was significantly more acceptable for TNE patients when compared to the TOE group (68% vs.16%). The duration of endoscopy was significantly shorter in TOE than in TNE (p<0.05). Endoscope insertion failed in 4% and mild epistaxis was observed in 4% of TNE patients. CONCLUSION: Unsedated TNE was better tolerated in endoscopy experienced patients when compared with unsedated TOE. The majority of patients found TNE more acceptable and preferable to TOE, suggesting that TNE should become a more common practice in clinics when applicable.