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Alpha-fetoprotein (AFP)-producing gastric cancer (AFPGC) is a rare, aggressive tumor. In the absence of metastasis in diagnosis, close observation and long-term follow-up is needed to monitor and slow its progress. We report a young patient who presented with nonbiliary pancreatitis. Upon finding Virchow’s nodule, we conducted tests and observed multiple lymph nodes and liver and pancreatic metastasis. We subsequently made a diagnosis of AFPGC. This study describes the different presentations of this rare but aggressive subtype of gastric cancer with a review of the literature.

Background: In this study, we aimed to evaluate the surgical outcomes after enucleation of esophageal leiomyomas and present the feasibility of enucleation using video-assisted thoracoscopic surgery. Methods: The medical records of 13 patients (8 males, 5 females; mean age 45.9 years; range, 30 to 69 years) who underwent open or thoracoscopic surgery for an esophageal leiomyoma between April 2007 and June 2019 were retrospectively reviewed. The patients were evaluated with regard to age, sex, presenting symptoms, duration of symptoms, size and localization of tumors, diagnostic methods, surgical methods, conversion to open surgery, morbidity and mortality, discharge time, and follow-up period. Results: Of the patients, four were operated via thoracotomy and nine via video-assisted thoracoscopic surgery. Enucleation was successfully completed with thoracoscopy in five patients. Four patients required conversion to thoracotomy. In the early postoperative period, two of these four patients developed complications and underwent re-thoracotomy. A solitary leiomyoma was detected in all, but one patient (multiple). The mean size of the tumors was 68.4 mm. Complications were seen in only one patient during follow-up and no recurrence was observed in any patient. Conclusion: Our study results indicate that thoracoscopic enucleation of esophageal leiomyoma is a safe, feasible, and effective technique in selected patients and conversion to open surgery can be easily done for any reason during the procedure.

Intestinal tuberculosis is an uncommon form of tuberculosis, and its diagnosis remains a challenge in patients with Crohn's disease. The clinical, endoscopic, radiologic, and histologic features of Crohn's disease and tuberculosis are remarkably similar, posing a diagnostic challenge. Accurate diagnosis of these two conditions remains vital to the decision on the treatment of the patients. Computerized tomography, endoscopic ultrasound (EUS), capsule endoscopy, balloon enteroscopy, ascitic fluid adenosine deaminase (ADA), tuberculosis polymerase chain reaction (TB-PCR), GeneXpert MTB/RIF assay (Cepheid, Sunnyvale, CA), and laparoscopy can be beneficial in the diagnosis of intestinal tuberculosis. Herein, we report a case where tuberculosis could not be documented, although the patient displayed lymphocytosis in ascites and weight loss. Laparoscopy was diagnostic and the patient benefited from the correct treatment.

Surgeries for obesity can lead to complications. Dumping syndrome is one such complication caused by the quick passage of hyperosmolar chyme from the stomach to the duodenum. Mild cases can be cured with dietary modification and medical treatment. However, refractory cases may need invasive treatment options, such as transoral outlet reduction or surgery. We successfully treated a 48-year-old female with dumping syndrome, using a combination of argon plasma coagulation and hemoclips to narrow the pyloric lumen. We suggest that this new technique could be a cheap and easily accessible alternative to surgery, especially in countries where the specialised devices needed to treat such cases are unavailable.

Hepatosteatosis, a common condition, is increasing in prevalence. It is typically associated with diet, alcohol consumption and obesity. In some cases, a rare genetic disease may be the underlying defect. Lipid storage myopathy (LSM) is a genetic disease caused by lipid metabolism defects. LSM often affects the muscles, heart and liver. Coenzyme Q, riboflavin or carnitine replacement can be beneficial in some cases. We describe a patient who presented with liver failure and was unresponsive to treatment. LEARNING POINTS Hepatosteatosis can be associated with genetic disease and not just diet. Lipid storage disease should be considered in patients presenting with liver disease with hypoglycaemia, muscle weakness and a family history. Lipid storage disease is a rare heterogeneous genetic condition that has no specific treatment and requires further research.

Human immunodeficiency virus (HIV) is a worldwide disease with an increasing number of cases globally. Initially, HIV cholangiopathy was often observed among such patients but has become rare after three decades because of the availability of new treatment options and potent antiretroviral drugs. Consequently, its occurrence now suggests drug resistance or disease progression. The relationship between cholangiocarcinoma and HIV remains unclear. We report the case of a patient with high-grade dysplasia of the ductus choledochus and uncontrolled disease which was treated with potent antiviral agents and bile duct dilatation. LEARNING POINTS HIV cholangiopathy should be kept in mind in an HIV-positive patient even if they are receiving combination antiretroviral therapy (cART); endoscopic retrograde cholangiopancreatography can provide symptomatic relief. Once HIV cholangiopathy is detected, close follow-up for cholangiocarcinoma is required. Opportunistic infections can cause cholangiocarcinoma in HIV-positive patients.

Aim: Our study aimed to examine the relationship of the visceral adiposity index (VAI) with clinical and histological parameters in biopsy-proven nonalcoholic fatty liver disease (NAFLD) cases and ...

In this retrospective study of real-life data, we aimed to determine the diagnostic accuracy in patients with choledocholithiasis of some current imaging modalities, including ultrasonography (US), computerized tomography (CT), magnetic resonance cholangiopancreatography (MRCP), and endoscopic retrograde cholangiopancreatography (ERCP). This study utilized a database of imaging records from 86 consecutive patients with ERCP-proven choledocholithiasis in a single-center outpatient clinic. Features of the stones found, namely number, size, localization, choledochal dilation and cholestasis, were determined using various imaging modalities and liver function tests (LFTs). Our study focused on a total of 86 patients (43 female; 43 male) who underwent the ERCP procedure. Hepatobiliary ultrasound was performed in 71 (82.6%); MRCP in 59 (68.6%); and CT in 13 (15.1%) patients. All 86 patients had choledocholithiasis: 59 (68.6%) with multiple stones and 21 (24.4%) with stones over 10 mm in diameter. Sensitivity for the presence of choledocholithiasis was 40.8% for US, 76.9% for CT, and 86.4% for MRCP, where ERCP was taken as the reference method. Even though US, CT, and MRCP are widely used as noninvasive imaging modalities for CL, in our real-life data their sensitivity for choledocholithiasis was lower than expected. MRCP is preferred when a nontherapeutic but only diagnostic evaluation is aimed for; however, while highly competent in establishing the level of choledochal dilation, it had a low yield in differentiating the localization, size, and number of the stone(s).

Background and study aims The success rate of Helicobacter pylori (H. pylori) eradication with the classical triple therapy is gradually declining. In this study, we aimed to compare and assess the efficacies of six different eradication regimens including sequential protocols. Patients and methods Endoscopically confirmed nonulcer dyspepsia patients were enrolled. H. pylori presence was determined either histologically or by a rapid urease test. Treatment-naive patients were randomly assigned to an either one of three 10-day (OAC, OTMB, and OACB) or one of three sequential protocols (OA + OCM, OA + OCMB, and OA + OMDB) (O = omeprazole, A = amoxicillin, C = clarithromycin, T = tetracycline, M = metronidazole, B = bismuth, D = doxycycline). The eradication was assessed 6–8 weeks after the completion of the treatment by a 14C-urea breath test. Results In total, 301 patients were included. Fifty-two percent of the participants (n = 157) were female, and the mean age was 44.9 years (range = 18–70). The intention to treat (ITT) and per protocol (PP) eradication rate for each regimen is as follows: OAC (ITT = 61.2%, PP = 75%), OTMB (83.3%, 87%), OACB (76.5%, 79.6%), OA + OCM (72.3%, 73.9%), OA + OCMB (82.7%, 89.6%), and OA + OMDB (59.3%, 65.3%). Smoking significantly affected the eradication rate (P = 0.04). Conclusion In this study, OTMB and OA + OCMB were significantly superior to the triple therapy and succeeded to reach the eradication rate proposed by the Maastricht consensus (over 80%). These two bismuth-containing regimens could be considered for first-line therapy in the regions with high clarithromycin resistance.

Background/Aims Nonalcoholic fatty liver disease (NAFLD) is currently the most common chronic liver disease worldwide. Along with the increase in the incidence of NAFLD and associated obesity, an increase in gallbladder disease (GD) has been noted. This has led to the identification of a new disease entity called fatty GD. There is a gap in the literature on the dynamics of gallbladder function in patients with NAFLD. Methods An observational case-control study, a total of 50 patients with biopsy proven NAFLD without gallbladder stone/sludge and 38 healthy comparison subjects were enrolled. Fasting, postprandial gallbladder volumes (PGV), gallbladder ejection fraction (GEF), and fasting gallbladder wall thickness (FGWT) were measured by real-time 2-dimensional ultrasonography. Results Fasting gallbladder wall thickness, fasting gallbladder volumes and PGV were significantly higher in patients with NAFLD than control subjects (P < 0.001, P = 0.006, and P < 0.001, respectively). Gallbladder ejection fraction was significantly lower in the NAFLD group than the controls (P = 0.008). The presence of NAFLD was an independent predictor for GEF, PGV, and FGWT. Also, steatosis grade was an independent predictor for GEF, and GEF was significantly lower in the nonalcoholic steatohepatitis (NASH) subgroup than the controls. Conclusions Gallbladder dysfunction and increase in gallbladder wall thickness exists in asymptomatic (without stone/sludge and related symptoms) patients with NAFLD and are useful in identifying fatty GD. Measurement of these variables in NAFLD patients may be useful in identifying those at higher risk for GD.

Objective Low baseline viremia and an early treatment response predict the best outcomes in hepatitis B virus (HBV)-infected patients treated with nucleoside analogues with low barriers to resistance. The aim of this study was to assess the long-term results and effectiveness of lamivudine in patients with low baseline viremia and early virological treatment response. Methods In this multicenter, real-life setting study, 111 antiviral-naive patients with low baseline viremia (HBV DNA

Background/aims Ulcerative colitis (UC) and Crohn's disease are chronic inflammatory diseases. Genetic, immunologic, and microbial factors play an important role in their pathogenesis. Extracellular matrix protein 1 (ECM1), a gene related to mucosal barrier function, has been shown to be associated with UC. This study aims to determine the relationship between ECM1 gene rs3737240 single nucleotide polymorphism (SNP) and UC in a group of Turkish patients. Materials and methods Ninety-four UC patients and 120 healthy controls were enrolled in the study. ECM1 gene rs3737240 SNP genotyping was performed using the polymerase chain reaction-restriction fragment length polymorphism method. Results TT genotype was significantly more common in UC patients than in the healthy control group [p=0.034; odds ratio (OR) 2.34; 95% confidence interval (CI) 1.04-5.25]. The presence of C allele significantly lowered the UC risk (p=0.034; OR 0.42; 95% CI 0.19-0.95). TT genotype was significantly associated with azathioprine use in UC patients (p=0.037; OR 3.0; 95% CI 1.04-8.65). The C allele significantly reduced the probability of azathioprine use in UC patients (p=0.037; OR 0.33 CI 95% 0.11-0.96). No relation was found between rs3737240 SNP genotype and the phenotypical characteristics of UC patients. Conclusion The TT genotype of ECM1 gene rs3737240 SNP significantly increased susceptibility for UC and azathioprine use in UC patients in a Turkish population.

Nonalcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease. NAFLD is a complex disease and inflammation is a crucial component in the disease pathogenesis. Recent genome wide association studies in hepatology area highlighted significant relations with human leukocyte antigen (HLA) DQ region and certain liver diseases. The previous animal models also emphasized the involvement of adaptive immune system in the liver damage pathways. To investigate possible polymorphisms in the HLA region that can contribute to the immune response affecting the NAFLD, we enrolled 93 consecutive biopsy proven NAFLD patients and a control group consisted of 101 healthy people and genotyped HLA DQB1 alleles at high resolution by sequence specific primers-polymerase chain reaction. The mean NAFLD activity score (NAS) was 5.2 ± 1.2, fibrosis score was 0.9 ± 0.9, ALT was 77 ± 47.4 U/L, AST was 49.4 ± 26.3 U/L. Among 13 HLA DQB1 alleles analyzed in this study, DQB1*06:04 was observed significantly at a more frequent rate among the NAFLD patients compared to that of healthy controls (12.9 vs. 2 % χ2 = 8.6, P = 0.003, P c = 0.039, OR: 7.3 95 % CI 1.6–33.7). In addition, the frequency of DQB1*03:02 was significantly higher in the healthy control group than the NAFLD patients (24.8 vs. 7.5 %, χ2 = 10.4, P = 0.001, P c = 0.013, OR: 0.2, 95 % CI 0.1–0.6). NAFLD patients were grouped according to their fibrosis score and NAS. The distribution of DQB1 alleles over stratified NAFLD patients did not reveal any statistically significant relation. Taken together, immune repertoire of individuals may have an effect on NAFLD pathogenesis and therefore, in NAFLD, adaptive immunity pathways should be investigated.

Recent studies have suggested that bacterial overgrowth and endotoxemia along with its receptor, Toll-like receptor 4 (TLR-4), play a role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). The present study was designed to test and evaluate the TLR4 gene polymorphism in patients with NAFLD in comparison to healthy controls.A total of 119 patients [mean (standard deviation, SD) age 43.4 (11.5) years, 55.5% were males] with NAFLD and 80 healthy controls [mean (SD) age 40.9 (8.1) years, 67.5% were females)] were evaluated in terms of patient demographics, anthropometrics, blood biochemistry, liver histology, and ultrasonographic (USG) findings. Histological evaluation was performed in 111 patients, and blood samples were collected from 119 patients with NAFLD and 80 healthy persons. Allelic variants of TLR4 (Asp299Gly and Thr399Ile) were assayed by real-time PCR. Genomic DNA was amplified using FAM/VIC primers specific for allelic variants of TLR4 Asp299Gly and Thr399Ile with real-time PCR. Amplicons were analyzed with high-resolution melting on a Light Cycler 480 for detecting different melting patterns of polymorphic and wild-type alleles.The number of the subjects with heterozygous mutation at genotype 299 (Asp299Gly) was significantly lower in the NAFLD than in the control group (23.8 vs. 10.9%, P=0.027). Logistic regression analysis revealed that female gender [odds ratio (OR)=2.984, 95% confidence interval (CI) 1.561-5.360, P=0.001] and heterozygous (Asp299Gly) mutation at codon 299 (OR=2.998, 95% CI 1.325-6.783, P=0.008) were the significant predictors of higher likelihood of TRL4 gene polymorphism-related prevention of NAFLD.As the first-time-in-humans controlled study related to investigation of TLR4 gene polymorphism in NAFLD, our findings contribute to the available data that TLR-4 signaling is pivotal for the pathogenesis of NASH and indicate that the TLR4 codon 299 heterozygous gene mutation (Asp299Gly) in humans may have a preventive role against the genesis of NAFLD.

Chronic hepatitis B treatment with oral antiviral drugs is a long course. During this course, antiviral resistance is a serious issue, particularly, if genetically low barrier drugs are in use. Host immunity is accepted to have an effect on antiviral resistance development. The earliest clinical sign of drug resistance is virologic breakthrough. In this study, we aimed to investigate the relation between HLA-DQB1 alleles and virologic breakthrough events.The patient records at single institution hepatology clinic were reviewed. Local institution ethics committee approval was taken. The patients' demographic data, virologic parameters, treatment statues were noted. Patients who had received lamivudine or adefovir were recruited and grouped into two according to virologic breakthrough occurrence. Patients who were not compliant to the given treatment were excluded. Blood samples were taken for DNA extraction. HLA-DQB1 alleles were determined at high level by sequence-specific primers-polymerase chain reaction. The distribution of DQB1 alleles among groups was analyzed.One hundred ninety-eight patients were eligible for the study. Ninety-six of them had virologic breakthrough where 102 did not have. DQB1 0503 allele was more frequent in patients without breakthrough (28.4% vs. 12.4%, P=0.006). In univariate analysis, HBeAg seropositivity (P0.001), absence of cirrhosis (P=0.007), younger age (P=0.002) and higher pretreatment logDNA (P0.001) were related to breakthrough events. However, in multivariate analysis only logDNA (P0.001) and DQB1*0503 (P=0.02) allele revealed statistically significant relation with breakthrough events.Host immunity may have an effect on outcome during treatment with oral antiviral drugs. A patient with better immunologic profile may suppress the viral replication better and this may cause less resistance occurrence during treatment with genetically low barrier drugs.

Crohn's disease (CD) decreases fertility both directly, by inducing inflammation in the fallopian tubes and ovaries, and indirectly, through the surgical interventions and tubal adhesions associated with disease treatment. Anti-müllerian hormone (AMH) is a reliable indicator of ovarian reserve in women. We aimed to compare serum AMH levels between reproductive-age women with CD and healthy controls.Serum AMH levels were measured by ELISA in 35 women with CD and 35 age-matched healthy women controls.CD patients and controls were similar in terms of age, height, weight and BMI. Mean CD duration was 60 months. CRP, ESR and leukocyte counts were significantly higher in CD patients compared to the controls (p0.001, p=0.004 and p=0.04, respectively). AMH levels in CD patients (1.02 ± 0.72) were significantly lower compared to the controls (1.89 ± 1.80) (p = 0.009). Serum AMH levels in CD patients with active disease (0.33 ± 0.25) were significantly lower compared to CD patients who were in remission (1.53 ± 0.49) (p = 0.001). Serum AMH levels were similar in CD patients with a disease duration of less than 5 years (17 patients) and CD patients with a disease duration of greater than 5 years (18 patients) (p = 0.8). In CD patients, a negative correlation between CDAI and serum AMH levels was found (r = -0.718, p0.001). Serum AMH levels were similar in CD patients who had (6 patients) and had not undergone (29 patients) surgical treatment (p = 0.2).Serum AMH levels of reproductive-age women with CD were significantly lower compared to the controls. CDAI and AMH are inversely correlated.

Osteopontin is a secreted phosphorylated glycoprotein that is expressed by a variety of cell types and that mediates numerous and diverse biological functions. Osteopontin knockout mice are protected from obesity-induced hepatic steatosis. In the present study, we sought to investigate whether serum osteopontin concentrations are associated with liver histology in patients with nonalcoholic fatty liver disease.Serum levels of osteopontin were measured by enzyme-linked immunosorbent assay in 179 well-characterized patients with nonalcoholic fatty liver referred for liver histology and 123 control subjects.Serum osteopontin levels were markedly higher in patients with nonalcoholic fatty liver disease than in controls (p0.001). Multivariable analysis showed that osteopontin levels were strongly and independently associated with both portal inflammation (β=0.294, p0.01) and serum aminotransferase levels (aspartate aminotransferase: β=0.295, p0.01; alanine aminotransferase; β=0.285, p0.01).In summary, these data demonstrate that serum levels of osteopontin are elevated in nonalcoholic fatty liver disease and are a significant independent predictor of portal inflammation in this clinical entity.

Massive upper gastrointestinal bleeding is a life-threatening emergency which needs urgent intervention. Hematological malignancies are very rare causes of this type of bleeding and they usually originate from duodenum. In this case we present a gastric diffuse large B-cell lymphoma (DLBCL) causing massive upper gastrointestinal system bleeding. A 77-year-old male patient was admitted to emergency clinic with hematemesis and hematochezia. In physical examination patient was pale and sweaty; his vitals were unstable with a heart rate of 110 per minute and a blood pressure of 90/50 mmHg. His hemoglobin level was found 7.5 g/dL and he was transfused with one unit of packed red blood cells. After his vitals were normalized, gastroscopy was performed showing mosaic pattern in corpus and antrum mucosa and multiple ulcers in various sizes, largest being approximately 2 cm in diameter, higher than mucosa covered with exude mostly on corpus and large curvature. Biopsy results were reported as DLBCL. Gastric mucosa is involved in most of the DLBCL cases. Although not listed as a common cause of massive gastrointestinal bleeding DLBCL can cause life-threatening situations mostly because of its malignant nature.

Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and is one of the most common causes of chronic liver disease, worldwide. Lipoprotein-associated phospholipase A2 (Lp-PLA2) was recently characterized as a novel inflammatory biomarker that is correlated with several components constituting the metabolic syndrome.In this study, we determined the serum levels of Lp-PLA2 in patients with definite nonalcoholic steatohepatitis (NASH, n=25), borderline NASH (n=22), simple fatty liver (n=10), and healthy controls without evidence of liver disease (n=38). The levels of Lp-PLA2 were measured by enzyme-linked immunosorbent assay and compared in the four study groups. Moreover, concentrations of Lp-PLA2 were assessed in relation to the general characteristics of the study participants and the results of liver biopsy.Concentrations of Lp-PLA2 were significantly higher in patients with definite NASH (161.8±0.9 μg/L, P0.001), borderline NASH (135.4±47.7 μg/L, P=0.001), and simple fatty liver (132.4±46.2 μg/L, P=0.042) compared with healthy controls (86.2±40.7 μg/L). Furthermore, the serum Lp-PLA2 level was strongly associated to histological steatosis scores in patients with NAFLD (β=0.32, t=2.50, P=0.016).Although subject to future confirmation, our data suggest that Lp-PLA2 levels are elevated in NAFLD.

In this study, we aimed to investigate the relationship between the histological features of nonalcoholic fatty liver disease (NAFLD) and serum insulin-like growth factor-1 (IGF-1) and insulin-like growth factor-binding protein-5 (IGFBP-5) to determine the usefulness of this relationship in clinical practice.Serum samples were collected from 92 patients with biopsy-proven NAFLD and 51 healthy controls and serum levels of IGF-1 and IGFBP-5 were assayed by enzyme-linked immunosorbent assay.Serum IGFBP-5 levels were correlated with liver steatosis, fibrosis, and nonalcoholic steatohepatitis scores. IGF-1 levels were significantly decreased in patients with moderate-to-severe fibrosis compared with patients with no or mild fibrosis.Serum IGFBP-5 levels may be useful to differentiate both advanced fibrosis and definite nonalcoholic steatohepatitis from other NAFLD groups. Also, serum IGF-1 levels may be useful to differentiate advanced fibrosis in patients with NAFLD.

Eur J Clin Invest 2012; 42 (4): 411–418 Abstract Background Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome (MS). However, not all patients with the MS will develop NAFLD and not all patients with NAFLD have the MS. We sought to investigate the differences between patients with biopsy-proven NAFLD with and without the MS. Methods A total of 357 consecutive patients with biopsy-proven NAFLD were analysed. Of them, 216 patients had nonalcoholic steatohepatitis (NASH) and 96 a fibrosis score ≥ 2. The MS was defined as ≥ 3 of the ATP III criteria. Results A total of 214 patients with NAFLD met the criteria for the MS, while the remaining 143 did not. In NAFLD patients with the MS, homeostasis model of insulin resistance (P = 0·03; OR, 1·06; 95% CI, 1·023–1·25 per unit increase) and diabetes (P = 0·01; OR, 1·2; 95% CI, 1·1–2·4) were independent predictors of NASH. In NAFLD patients without the MS, the only variable independently associated with NASH was haemoglobin (P = 0·007; OR, 1·9; 95% CI, 1·4–3·6 per 50 g/L increase). Alanine aminotransferase (P = 0·03; OR, 1·04; 95% CI, 1·006–1·11 per 10 U/L increase) was an independent predictor of fibrosis ≥ 2 in NAFLD patients with the MS, while haemoglobin (P = 0·02; OR, 1·4; 95% CI, 1·2–1·9 per 50 g/L increase) was the only variable significantly associated with fibrosis ≥ 2 in NAFLD patients without the MS. Conclusions Increased haemoglobin in NAFLD subjects without MS should be considered in the selection of cases for histological assessment.

Summary Sirtuins are members of the silent information regulator 2 (Sir2) family, a group of Class III histone/protein deacetylases. There are 7 different sirtuins in mammals (SIRT1-7), of which SIRT1 is the best known and most studied. SIRT1 is responsible for the regulation of protein activation by means of deacetylating a variety of proteins that play important roles in the pathophysiology of metabolic diseases. Recently, it has been shown that SIRT1 plays key roles in the regulation of lipid and glucose homeostasis, control of insulin secretion and sensitivity, antiinflammatory effects, control of oxidative stress and the improvements in endothelial function that result due to increased mitochondrial biogenesis and β-oxidation capacity. Nonalcoholic fatty liver disease (NAFLD) is currently the most common liver disease, and it has been accepted as the hepatic component of metabolic syndrome. Recent studies have shown that SIRT expression in the liver is significantly decreased in an NAFLD model of rats fed a high-fat diet, and moderate SIRT1 overexpression protects mice from developing NAFLD. In addition to resveratrol, a natural SIRT1 activator, small-molecule pharmacologic SIRT1 activators have positive effects on metabolic diseases. These effects are particularly promising in the case of diabetes mellitus, for which phase studies are currently being performed. With this information, we hypothesized that the pharmacologic activation of SIRT1, which has been implicated in the pathogenesis of NAFLD, will be a potential therapeutic target for treating NAFLD. In this paper, we review the metabolic effects of SIRT1 and its association with the pathophysiology of NAFLD.

AIM: To analyze the relationship between the serum lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) levels and clinical and histopathological features of biopsy-confirmed nonalcoholic fatty liver disease (NAFLD) patients. METHODS: Fifty-three consecutive, biopsy-proven NAFLD patients (31 males and 22 females, mean age 42.5 +/- 9.6 years) and 26 age-and gender-matched, healthy controls (14 males and 12 females, mean age 39 +/- 10.7 years) were included. The patients with NAFLD were consecutive patients who had been admitted to the hepatology outpatient clinic within the last year and had been diagnosed with NAFLD as the result of liver biopsy. The healthy controls were individuals who attended the outpatient clinic for routine health control and had no known chronic illnesses. The histological evaluation was conducted according to the NAFLD activity scoring system recommended by The National Institute of Diabetes and Digestive and Kidney Diseases Nonalcoholic Steatohepatitis Clinical Research Network. The serum LOX-1 levels were measured using an ELISA kit (Life Science Inc. USCN. Wuhan, Catalog No. E1859Hu) in both patients and healthy controls. A receiver operating characteristic (ROC) curve analysis was used to identify the optimal cutoff value of LOX-1 and thereby distinguish between patients with nonalcoholic steatohepatitis (NASH) and healthy controls. A P-value < 0.05 was considered statistically significant. RESULTS: NAFLD and healthy control groups were similar in terms of age and sex. NAFLD patients consisted of 8 patients with simple steatosis (15%), 27 with borderline NASH (51%) and 18 with definitive NASH (34%). Metabolic syndrome was found in 62.2% of the patients with NAFLD. The mean serum LOX-1 level in biopsy-proven NAFLD patients was 8.49 +/- 6.43 ng/mL compared to 4.08 +/- 4.32 ng/mL in healthy controls (P = 0.001). The LOX-1 levels were significantly different between controls, simple steatosis and NASH (borderline+definite) cases (4.08 +/- 4.32 ng/mL, 6.1 +/- 6.16 ng/mL, 8.92 +/- 6.45 ng/mL, respectively, P = 0.004). When the cut-off value for the serum LOX-1 level was set at 5.35 ng/mL, and a ROC curve analysis was performed to distinguish between steatohepatitis patients and controls; the sensitivity and specificity of the serum LOX-1 level were 69.8% and 69.2%, respectively. CONCLUSION: The serum LOX-1 levels were significantly higher in NAFLD patients than in healthy controls. Additionally, the serum LOX-1 levels could differentiate between steatohepatitis patients and healthy controls.

The aim of the present study was to assess the influence of quercetine (QE) on liver regeneration after partial hepatectomy (PH) in rats. A total of 24 male Wistar albino rats were divided into three groups: sham-operated (SH), PH and PH+QE; each group contain 8 animals. The rats in QE-treated groups were given QE (15 mg/kg body weight) once a day i. p., for 7 days starting 3 days prior to hepatectomy operation. At 7 days after resection, liver samples were collected. The malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) levels were estimated in liver homogenates. Moreover, histopathological examination, mitotic index (MI), proliferating cell nuclear antigen labelling, proliferation index (PI), transferase-mediated dUTP nick end-labelling assay, apoptotic index (AI) were evaluated at 7 days after hepatectomy. As a result, QE significantly increased MI, PI, and significantly decreased AI in PH rats. Additionally, QE remarkably inhibited the elevation of MDA, restored impaired antioxidant SOD activity and GSH level, and also attenuated hepatic vacuolar degeneration and sinusoidal congestion. These results suggested that QE treatment had a beneficial effect on liver regenerative capacity of the remnant liver tissue after hepatectomy, probably due to its antioxidative, antiapoptotic and proliferative property.

Summary Background/Aim: Angiotensin converting enzyme (ACE) and angiotensin II (AT-II) have been suggested to play an important role in liver fibrogenesis. There is a significant relationship between inheritance of hightened expression of transforming growth factor β1 (TGF-β1) and AT-II and the development of progressive hepatic fibrosis. The purpose of this study was to investigate the effects of captopril, an ACE inhibitor and candesartan cilexetil, an AT-II type 1 receptor (AT1-R) blocker, on liver fibrosis induced in rats by carbon tetrachloride (CCl4) administration. Methods: rats were divided into 4 experimental groups: The first group was given CCl4 alone; the second was given both CCl4 and captopril (100 mg · kg · −1day−1); the third was given both CCl4 and candesartan cilexetil (8 mg · kg · −1day−1); fourth group was given 0.9% NaCl only. Seven weeks after initiating the treatment, indices of fibrosis were assessed. Results: Candesartan cilexetil treatment significantly reduced the fibrosis development. These inhibitory effects were not observed in the captopril-treated group. The mean fibrosis score was significantly lower in the CCl4/candesartan group compared with the group applied to CCl4 alone and the group applied to CCl4/captopril. Similarly, the number of α-smooth muscle actin positive cells was markedly suppressed by candesartan treatment. Conclusions: The results suggest that AT-II plays a pivotal role in hepatic fibrogenesis and candesartan significantly attenuates the progression of liver fibrosis. This drug may provide an effective new strategy for prevention of liver fibrosis. Its effectiveness should be investigated in chronic liver disease associated with progressive fibrosis.

Purpose: The purpose of this study was to assess the patterns of contrast enhancement of hepatic hemangiomas on gadolinium-enhanced MR fluoroscopy imaging prospectively. Method: Investigation was performed on a 0.3-T open MR unit. Gadolinium-enhanced MR fluoroscopy images were obtained in 24 patients with 28 hepatic hemangiomas. Each MR fluoroscopy image was obtained in 2 s and MR fluoroscopy lasted for 10–25 min for each investigation. Results: Three patterns of contrast enhancement were observed in 24 patients on MR fluoroscopy images. Four small lesions were not detected on MR fluoroscopy images. Uniform enhancement was seen in nine lesions (29%), peripheral nodular enhancement progressing centripetally to uniform enhancement was seen in nine lesions (29%), and peripheral nodular enhancement with persistent central hypointensity was seen in six lesions (22%). Conclusion: Enhanced MR fluoroscopy technique could obtain dynamic images of hepatic hemangiomas. It can be suggested as a useful technique for the showing of enhancement of hepatic hemangiomas, keeping in mind its low sensitivity in the diagnosis of small hemangiomas.

Sirtuins (SIRTs) are members of the silent information regulator-2 family and act as nicotinamide adenine dinucleotide (NAD+)-dependent histone/protein deacetylases. The de-acetylation of proteins and histones results in an up- or down-regulation of gene transcription and protein function. In recent years, the regulatory action of the deacetylation activity of SIRT1 has been shown to have a positive impact on the pathophysiological mechanisms of nonalcoholic fatty liver disease (NAFLD). Among the effects of SIRT1 are: its healing activity on insulin sensitivity, thereby ameliorating glycemic regulation; its mimetic activity on calorie restriction; its antihyperlipidemic activity on lipid homeostasis via the liver, adipose tissues and skeletal muscles; its antiinflammatory activities; its protective effects against cardiovascular events and endothelial dysfunction; its positive influence on autophagy, apoptosis and cancer; and finally, its anti-aging activity. The current approach for the treatment of NAFLD involves the treatment of etiological factors and recommendation of life-style changes including more physical activity and a low-calorie diet. However, there are no specific medical treatments for NAFLD. The therapeutic potential of SIRT1 activity in the treatment of NAFLD discovered in humans has been presented in this article. In this review, the potential effects of SIRT1 activation on NAFLD-related pathophysiological mechanisms and on the treatment of NAFLD are discussed.

Background/Aims: We sought to examine whether the presence of gallstone disease (GD) in patients with biopsy-proven nonalcoholic fatty liver disease (NAFLD) is associated with liver fibrosis and histological nonalcoholic steatohepatitis (NASH) score. Methods: We included 441 Turkish patients with biopsy-proven NAFLD. GD was diagnosed in the presence of sonographic evidence of gallstones, echogenic material within the gallbladder with constant shadowing and little or no visualization of the gallbladder or absence of gallbladder at ultrasonography, coupled with a history of cholecystectomy. Results: Fifty-four patients (12.2%) had GD (GD+ subjects). Compared with the GD- subjects, GD+ patients were older, had a higher body mass index and were more likely to be female and have metabolic syndrome. However, GD+ patients did not have a higher risk of advanced fibrosis or definite NASH on histology. After adjustment for potential confounding variables, the prevalence of GD in NAFLD patients was not associated with significant fibrosis (>= 2) (odds ratio [OR], 1.06; 95% confidence interval [Cl], 0.53 to 2.21; p=0.68) or definite NASH (OR, 1.03; 95% Cl, 0.495 to 2.12; p=0.84). Conclusions: The presence of GD is not independently associated with advanced fibrosis and definite NASH in adult Turkish patients with biopsy-proven NAFLD.

Background/Aims: To evaluate the association between insulin resistance and hepatic fibrosis in patients with chronic hepatitis C.Materials and Methods: A total of 104 chronic hepatitis C patients were included in this non-interventional, open-label, observational, multicenter, cross-sectional study conducted at 20 gastroenterology clinics in Turkey. The primary end point was the correlation between stage of hepatic fibrosis and insulin resistance evaluated via the homeostasis model of assessment-insulin resistance index. Confounders of hepatic fibrosis and insulin resistance were the secondary end points.Results: The mean age of patients was 52.8 years; 65.4% were female. Type 2 diabetes was present in 6.8% and insulin resistance noted in 38.0% of patients. Further, 45.7% of the patients had mild (A0/A1) and the remaining had moderate/severe (A2/A3) hepatic necroinflammatory activity. Patient distribution according to Metavir fibrosis stage was as follows: F0/F1 (57.0%); F2 (6.5%); F3 (23.7%); and F4 (12.9%). A univariate analysis revealed significant positive correlations between Metavir fibrosis stage and insulin resistance (r=0.297; p=0.007). Logistic regression analysis showed that significant predictors of insulin resistance were high alanine transaminase levels (odds ratio, 0.97; 95% confidence interval, 0.944-0.997) and liver fibrosis stage (odds ratio, 0.114; 95% confidence interval, 0.021-0.607).Conclusion: Our findings revealed significant associations between insulin resistance and hepatic fibrosis. © 2014 by The Turkish Society of Gastroenterology.

Mitochondrial neurogastrointestinal encephalomyopathy is an autosomal recessive multisystem disorder caused by thymidine phosphorylase deficiency. The disease is characterized clinically by ptosis, progressive external ophthalmoparesis, severe gastrointestinal dysmotility, peripheral neuropathy, leukoencephalopathy, and mitochondrial abnormalities. Herein, we describe a patient with mitochondrial neurogastrointestinal encephalomyopathy who presented intestinal pseudoobstruction.

AIM: To investigate serum insulin-like growth factor-binding protein 5 (IGFBP-5) levels and intestinal IGFBP-5 expression in patients with Crohn’s disease (CD). METHODS: We analyzed the serum concentrations and intestinal expression of IGFBP-5 in 42 patients with CD, of whom 26 had endoscopically or radiologically proven stricture formation. Nine of the 42 patients had active disease, with a Crohn’s disease activity index > 150. Serum IGFBP-5 levels were analyzed in 20 healthy controls matched by sex and age to the CD patients. Serum IGFBP-5 was measured using an enzyme-linked immunosorbent assay. Intestinal tissue was obtained from patients through endoscopic biopsies. IGFBP-5 expression was detected using immunohistochemistry and was scored semiquantitatively. RESULTS: The median serum IGFBP-5 concentrations of CD patients were significantly lower compared with healthy controls [median 7.2 (IQR: 5.5-11.3) ng/mL vs 11.3 (8.0-44.6) ng/mL, P < 0.001]. There was no significant difference between median serum IGFBP-5 levels in CD patients with or without stricture formation [6.9 (5.5-11.3) ng/mL vs 7.8 (5.3-10.1) ng/mL, P = 0.815]. The serum IGFBP-5 levels were not significantly different between patients with active disease and inactive disease [7.2 (6.5-7.6) ng/mL vs 7.2 (5.5-11.3) ng/mL, P = 0.890]. However, a significant correlation was observed between serum IGFBP-5 levels and platelet count (PLT) (r = 0.319, P = 0.0395). No significant correlation was found between tissue IGFBP-5 immunohistochemical staining intensity scores and serum IGFBP-5 levels. No significant difference was found when comparing the serum IGFBP-5 levels among the patients with different tissue IGFBP-5 staining scores (absent/very weak, weak, moderate or strong). There was a significant correlation between tissue IGFBP-5 staining scores and white blood cell count (r = 0.391, P = 0.01) and PLT (r = 0.356, P = 0.021). CONCLUSION: Our results indicate that serum IGFBP-5 concentrations were lower in CD patients compared to healthy controls regardless of disease activity or the presence of stricture formation.

AIM: To investigate changes in serum ghrelin and obestatin levels before and after Helicobacter pylori (H. pylori) eradication. METHODS: A total of 92 patients presenting with symptoms of dyspepsia were enrolled in the study. Upper endoscopy was performed on all patients and used to diagnose H. pylori infection according to the presence of characteristic histopathological findings; seventy patients were diagnosed with H. pylori infection and the remaining 22 non-infected patients were classified as healthy controls. H. pylori eradication was accomplished by administering the classical triple therapy drug regimen, consisting of lansoprazole 30 mg bid, amoxicillin 1 g bid, and clarithromycin 500 mg tid for 14 d. The eradication of H. pylori was assessed with C14-urea breath test, which was performed at eight weeks after treatment. Levels of serum active ghrelin and obestatin were assessed at beginning of the study (prior to treatment) and after eight weeks. The levels were comparatively analyzed between the H. pylori negative control group, the H. pylori eradicated group, and the H. pylori non-eradicated group. RESULTS: A total of 92 patients, 50 females and 42 males with a mean age of 38.2 ± 11.9 years (range: 19-64), were analyzed. H. pylori eradication success was achieved in 74.3% (52/70) of H. pylori positive patients. The initial levels of ghrelin in the H. pylori positive and control cases were 63.6 ± 19.8 pg/mL and 65.1 ± 19.2 pg/mL (P = 0.78), respectively, and initial obestatin levels were 771 ± 427 pg/mL and 830 ± 296 pg/mL (P = 0.19), respectively. The difference between the initial levels and the week 8 levels of ghrelin and obestatin in the control group was insignificant [4.5% (P = 0.30) and -0.9% (P = 0.65), respectively]. The difference between the initial and week 8 levels of ghrelin and obestatin in the H. pylori non-eradicated group were also insignificant [0.9% (P = 0.64) and 5.3% (P = 0.32), respectively]. The H. pylori eradicated group had a greater change in obestatin levels when compared to the control and the non-eradicated groups (148 ± 381 pg/mL vs -12 ± 138 pg/mL and -72.8 ± 203 pg/mL, respectively, P = 0.015), while decreases in ghrelin levels were insignificant (-7.2 pg/mL vs -1.4 pg/mL and -1.9 pg/mL, respectively, P = 0.52). The ghrelin/obestatin ratio for the initial and week 8 levels changed significantly in only the H. pylori eradicated group (0.11 vs 0.08, respectively, P = 0.015). For overweight patients (as designated by body mass index), we observed significant increases in obestatin levels in the eradicated group as compared to non-eradicated group (201 ± 458 pg/mL vs -5 ± 81 pg/mL, respectively, P = 0.02). In the H. pylori-eradicated group, the levels did not differ between the sexes for ghrelin (-6.3 ± 26.9 pg/mL vs -8.0 ± 24.0 pg/mL, respectively, P = 0.97) or obestatin (210 ± 390 pg/mL vs 96 ± 372 pg/mL, respectively, P = 0.23). CONCLUSION: Serum levels of ghrelin decreased while obestatin levels increased in H. pylori eradicated subjects, especially in overweight and male patients.

Currently, nonalcoholic fatty liver disease (NAFLD) itself has been accepted as an atherosclerotic risk factor and related to increased cardiovascular disease risk. In this study, we aimed to investigate the relationship of epicardial fat thickness (EFT), a parameter associated with atherosclerosis in recent years, with carotid artery intima-media thickness (C-IMT), another parameter of subclinical atherosclerosis.We investigated 57 patients with biopsy-proven NAFLD and 30 age-matched and sex-matched controls. EFT was obtained by transthoracic echocardiography and C-IMT was evaluated by an ultrasonographic measurement using a linear type B-mode probe.EFT and C-IMT were significantly higher in NAFLD patients compared with the controls (EFT: 0.58 ± 0.18 vs. 0.36 ± 0.17 cm, P0.001 and C-IMT: 0.64 ± 0.1 vs. 0.52 ± 0.1 mm, P0.001, respectively). We found a statistically significant correlation between EFT and BMI, C-IMT, waist circumference, homeostasis model assessment of insulin resistance, and nonalcoholic steatohepatitis scores in both groups. Stepwise regression analysis showed that C-IMT (β=0.36, t=2.86, P=0.006) and waist circumference (β=0.3, t=2.44, P=0.018), in the order they entered into the model, were independent predictors of EFT in patients with NAFLD.Our findings indicate that EFT and C-IMT were significantly higher in patients with NAFLD compared with the controls and waist circumference and C-IMT are independent predictors for EFT in patients with NAFLD.

In this study, we aimed to evaluate the endothelial functions in patients with nonalcoholic fatty liver disease (NAFLD). In this observational case–control study, a total of 51 patients with NAFLD in study group and a total of 21 with age- and sex-equivalent individuals in control group were enrolled. In both patients and control groups, levels of asymmetric dimethylarginine (ADMA), systemic endothelial function (brachial artery flow-mediated dilation) (FMD) and carotid artery intima-media thickness (C-IMT) were measured. FMD and C-IMT were evaluated by vascular ultrasound. Plasma levels of ADMA were measured by ELISA. C-IMT was significantly higher in patients with NAFLD group than control group (0.67 ± 0.09 vs. 0.52 ± 0.11 mm, P < 0.001). The average C-IMT measurements were found in groups of control, simple steatosis, and NAFLD with (borderline and definite) NASH as 0.52 ± 0.11, 0.63 ± 0.07, and 0.68 ± 0.1 mm, respectively. The differences between groups were significant (P < 0.001). Measurement of brachial artery FMD was significantly lower in patients with NAFLD group compared to control group (7.3 ± 4.8 vs. 12.5 ± 7.1 %, P < 0.001). FMD measurements in groups of control, the simple steatosis, and NAFLD with NASH as 12.5 ± 7.1, 9.64 ± 6.63, and 7.03 ± 4.57 %, respectively, and the differences were statistically significant (P < 0.001). The increase in C-IMT and decrease in FMD was independent from metabolic syndrome and it was also more evident in patients with simple steatosis and NASH compared to control group. There was no significant difference between the control and NAFLD groups in terms of plasma ADMA levels (0.61 ± 0.11 vs. 0.69 ± 0.37 μmol/L, P = 0.209). Our data suggested that NAFLD is associated with endothelial dysfunction and increased earlier in patients with atherosclerosis compared to control subjects.

Nonalcoholic fatty liver disease (NAFLD) is among the most common causes of chronic liver disease in many countries, and its prevalence is increasing. NAFLD is often considered to be a hepatic component of metabolic syndrome, and studies have established that insulin resistance plays a major role in the pathogenesis of NAFLD. Treatments for NAFLD primarily target insulin resistance. Interestingly, the most common environmental cause of insulin resistance is diet. This article examines the correlations between NAFLD and diet and provides some diet recommendations based on the most current data available.

Aim: Celiac disease (CD) is considered to be a risk factor for chronic kidney disease (CKD) but there is no study determining the prevalence of CD, among patients with CKD. We aim to determine the prevalence of CD in patients with CKD. Materials and methods: Anti-endomysial IgA (EMA) antibody was screened in patients with CKD (glomerular filtration rate

Background/Aims. The aim of this study was to compare the effects of ursodeoxycholic acid (UDCA) alone and UDCA plus domperidone on dissolution of solitary or multiple gallstones.Methods. Fifty-three patients with cholesterol gallstones were randomized into three treatment groups: group I () was given UDCA (15 mg/kg/day) alone and group II () was treated with domperidone (30 mg/day) in addition to UDCA. The control group () was followed without a medical treatment. Gallbladder volumes and ejection fractions were measured sonographically in all patients before and after treatment.Results. After 12 months of treatment, stone dissolution was found in 9 (40.9%) of the patients in group I and 7 (38.8%) of the patients in group II. The difference was statistically significant compared to controls in both treatment groups () but the two groups did not show a difference between each other (). All the patients that achieved dissolution had multiple gallstones except for one patient with a solitary stone in group I. Neither monotherapy of UDCA nor the combination with domperidone affected the ejection fraction of gallbladder.Conclusions. Combination with domperidone did not potentiate the efficacy of UDCA. It has been observed that both UDCA alone and UDCA plus domperidone treatment did not affect ejection fraction of gallbladder.

BACKGROUND/AIMS Fibrinogen-like protein 2 (fgl2), has recently been identified as a new member of the fibrinogen-like family of proteins. In this study we assayed plasma levels of fgl2 in patients with biopsy proven non-alcoholic fatty liver disease (NAFLD) and examined their association with clinical, biochemical and histological phenotypes. METHODOLOGY Levels of plasma fgl2 were measured by enzyme linked immunosorbent assay and compared between the study groups. Moreover, concentrations of fgl2 were assessed in relation to the general characteristics of the study participants and the results of the liver biopsy. RESULTS Levels of fgl2 were significantly higher in patients with definite non-alcoholic steatohepatitis (NASH) (788±190pg/mL, p

Background: Increased serum concentrations of pigment epithelium-derived factor (PEDF) have been linked to the metabolic syndrome in the general population. However, the relationship between serum PEDF and nonalcoholic fatty liver disease (NAFLD), a hepatic manifestation of the metabolic syndrome, remains unknown. Methods: We assayed serum PEDF levels in 156 patients with biopsy-proven NAFLD and 103 nonsteatotic control subjects who were matched for age and sex. The association between levels of PEDF and clinical, biochemical, and histological phenotypes was examined. Results: NAFLD patients had significantly higher serum PEDF levels (1.97 +/- 0.50 mu g/mL) than control subjects (1.51 +/- 0.49 mu g/mL, Student's t test, P

Background and Aims. We aimed to investigate the prevalence of Giardiasis in patients with dyspepsia and patients with diabetes mellitus. Methods. 400 patients and 100 healthy persons were included in this clinical prospective study. The number of patients in each group was equal, 200 dyspeptic and 200 diabetic, respectively. The antigen of G. lntestinalis was determined in the stool specimens by ELISA method. Results. The frequency of Giardiasis was 7% in dyspeptic and 15% in diabetic patients. There was no positive results in any of the healthy persons. There was a significant difference in prevalence rate of Giardiasis between patients with dyspepsia and diabetes mellitus (P<0.05). Conclusions. These results revealed that the prevalence of Giardiasis in dyspepsia and with diabetes mellitus was high in our country. This is the first study investigating the prevalence of Giardiasis in diabetic patients. To investigate Giardiasis in diabetic patients, who have dyspepsia or not, may be a good approach for public health.

Research suggests the presence of mild-to-moderate iron overload in patients with nonalcoholic fatty liver disease (NAFLD). The role played by hepcidin, the master regulatory hormone of systemic iron metabolism, in the pathogenesis of NAFLD remains controversial. The aims of this study were to: (1) Evaluate serum hepcidin levels in patients with biopsy-proven NAFLD and age- and sex-matched controls and (2) identify the potential associations of hepcidin with the clinical and biochemical characteristics of the study participants.Serum levels of hepcidin were measured by enzyme-linked immunosorbent assay and compared in 88 patients with NAFLD (56 males and 32 females; mean age, 44 ± 11 years) and 88 controls (51 males and 37 females; mean age, 43 ± 12 years). Moreover, concentrations of hepcidin were assessed in relation to the general characteristics of the study participants and the results of liver biopsy.Serum levels of hepcidin were significantly higher in patients with NAFLD (63.5 ± 19.5 ng/mL, P0.001) compared with controls (32.7 ± 8.3 ng/mL). Multivariable regression analyses in patients with NAFLD showed that hepcidin levels were positively associated with total cholesterol (β=6.9, t=3.3, P0.01) and triglycerides (β=1.4, t=2.4, P0.05), but not with iron parameters, histological staging, and pathological characteristics of NAFLD.Although subject to future confirmation, our data suggest that hepcidin levels are elevated in NAFLD and could be associated with lipid parameters in this setting.

Objective: To identify the demographic and clinicopathological characteristics of patients diagnosed with nonalcoholic fatty liver disease (NAFLD) and the risk factors for fibrosis based on histopathological findings in East-Southeastern Anatolia regions in Turkey. Subjects and Methods: The study included a total of 93 patients diagnosed with NAFLD from 5 different centers. Histopathological findings were evaluated by dividing them into four categories using Matteoni classifications. Cases with fibrosis were further evaluated using Brunt classifications. Results: The patients with a nonalcoholic fatty liver were in the 3rd and 4th decade age groups. The mean age was 38 years, 76% of the patients were male, 85% were overweight, 37% were obese, 18% had type 2 diabetes mellitus, and 80.6% had hyperlipidemia. A multiple regression analysis showed that age, type 2 diabetes mellitus, and aspartate aminotransferase (AST) levels were linked with the severity of the disease. Of the 93 patients, 55 (59.1%) had fibrosis, of which 10.8% were classified as severe. The severity of fibrosis was significantly higher in obese patients. Conclusions: The risk factors for severity of NAFLD included advanced age, type 2 diabetes mellitus and serum AST level, while the risk factor for the severity of fibrosis was obesity.

Malignant fibrous histiocytoma occurs most commonly in the extremities and trunk, but rarely in the visceral organs. Malignant fibrous histiocytoma of the small intestine is an extremely rare condition. To our knowledge, only ten cases of primary tumors involving the small intestine have been described up to now. Among them only one case has been reported to lead to intussusception. This case report documents the appearance of a storiform-pleomorphic type primary malignant fibrous histiocytoma of the ileum, which led to intussusception, in a 58-year-old man with a 3-month history of dyspepsia, weight loss, general fatigue, and nonspecific abdominal pain. The patient was well with no sign of disease at 8 months after surgery. The clinical and pathologic characteristics of malignant fibrous histiocytoma of the small intestine as found in the literature are also reviewed.