Nevin Oruc

University of Pittsburgh, Pittsburgh, PA, United States

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Publications (47)111.91 Total impact

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    ABSTRACT: Pancreas ductal adenocarcinoma (PDAC) is among tumors with unfavorable prognosis. The aim of this study was to determine potential prognostic factors in PDAC.
    Acta gastro-enterologica Belgica 06/2014; 77(2):229-34. · 0.58 Impact Factor
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    ABSTRACT: Sleep disorders (SDs) are common in cirrhotics and are often associated with hepatic encephalopathy. SDs negatively affect patients' daily activities and work efficiency. For this reason, early diognosis is important. The methods used for diagnosis of SDs are not practical and need longer periods of application and evaluation. In this study we aimed to investigate sleep disorders and related clinical parameters in liver cirrhosis and also want to investigate the using of Sleep Timing and Sleep Quality Screening questionnaire (STSQS), a simple form with a short application time, for diagnosis of SDs and its correlation with Pittsburg Sleep Quality Index (PSQI) form. Cirrhotic patients and age-matched healthy volunteers were enrolled. Patients were excluded from the study if they had neuropsychiatric disease or used excessive alcohol or drugs known to affect sleep. Both groups completed validated Turkish form of PSQI and STSQS. SD was defined as PSQI score (0-21) of >5 or STSQS≥5. 131 cirrhotic patients and 18 healthy volunteers were enrolled. SDs in cirrhotics and control group were detected 56.5% and 27.8% by PSQI, 49.6% and 16.7% by STSQS respectively, SDs is the most frequent in the Child C patients, and the least frequent in the Child A patients (p>0,05). No correlation was found between the MELD score and SDs. SDs were more common in cirrhotic patients with hypoalbuminemia and low hemoglobin levels. In addition, the patients with decompensated cirrhosis had more frequently SDs than the patients with compensated cirrhosis. In the patient group, sleep latency and total sleep time, sleep parameters were correlated with SDs. STSQS had statistical significant correlation with PSQI for diagnosis of SDs. SDs are common in cirrhotics and STSQS could be an appropriate and practical method for diagnosis of SDS in these patients. We can use it in cirrhotic patients at outpatient clinics. This article is protected by copyright. All rights reserved.
    Liver international: official journal of the International Association for the Study of the Liver 02/2014; · 3.87 Impact Factor
  • Pancreatology 01/2014; 14(3):S2. · 2.04 Impact Factor
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    ABSTRACT: Background We aimed to measure the diurnal changes of critical flicker frequency in healthy subjects and cirrhotic patients and to investigate their relationship with sleep disturbance. Methods Cirrhotic patients and healthy volunteers were included. All groups completed the Pittsburgh Sleep Quality Index and a simple sleep questionnaire. Sleep disturbance was defined as a Pittsburgh Sleep Quality Index score of >5. Critical flicker frequency was measured twice a day to detect diurnal abnormalities. Results Overall, 59 cirrhotic patients (54.2% males, Mean Age 59 ± 11 years) and 18 controls (39.9% males, Mean Age 58 ± 9 years) were included. Sleep disturbances were more common in cirrhotics (66.1%) than controls (38.9%, p < 0.05). In cirrhotics, the critical flicker frequency was not related to decompensation. The nocturnal values were higher than the morning values in cirrhotics (64.4%), but not in controls (p < 0.0001). Additionally, sleep disturbances were more common in cirrhotics who had higher nocturnal values (p < 0.05). Conclusions Changes in the diurnal critical flicker frequency were observed in cirrhotics but not in controls. Sleep disturbances in cirrhotics appear to be associated with deviations of the diurnal rhythm of critical flicker frequency rather than with clinical parameters such as the clinical stages of cirrhosis and the Model For End-Stage Liver Disease and Child–Pugh scores.
    Digestive and Liver Disease. 01/2014;
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    Journal of gastrointestinal and liver diseases: JGLD 03/2013; 22(1):8. · 1.86 Impact Factor
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    ABSTRACT: Myasthenia gravis is an antibody-mediated autoimmune disease at the neuromuscular junctions. It can be associated with many other autoimmune diseases. We report a case of acute presentation of autoimmune hepatitis with myasthenia gravis, thymoma, Hashimoto thyroiditis and connective tissue disorder.
    Hepatology Research 08/2012; 42(8):835-9. · 2.07 Impact Factor
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    ABSTRACT: Idiopathic chronic pancreatitis (ICP) is a complex inflammatory disorder associated with multiple genetic and environmental factors. In individuals without cystic fibrosis (CF), variants of CFTR that inhibit bicarbonate conductance but maintain chloride conductance might selectively impair secretion of pancreatic juice, leading to trypsin activation and pancreatitis. We investigated whether sequence variants in the gene encoding the pancreatic secretory trypsin inhibitor SPINK1 further increase the risk of pancreatitis in these patients. We screened patients and controls for variants in SPINK1 associated with risk of chronic pancreatitis and in all 27 exons of CFTR. The final study group included 53 patients with sporadic ICP, 27 probands with familial ICP, 150 unrelated controls, 375 additional controls for limited genotyping. CFTR wild-type and p.R75Q were cloned and expressed in HEK293 cells, and relative conductances of HCO(3)(-) and Cl(-) were measured. SPINK1 variants were identified in 36% of subjects and 3% of controls (odds ratio [OR], 18.1). One variant of CFTR not associated with CF, p.R75Q, was found in 16% of subjects and 5.3% of controls (OR, 3.4). Coinheritance of CFTR p.R75Q and SPINK1 variants occurred in 8.75% of patients and 0.38% of controls (OR, 25.1). Patch-clamp recordings of cells that expressed CFTR p.R75Q showed normal chloride currents but significantly reduced bicarbonate currents (P = .0001). The CFTR variant p.R75Q causes a selective defect in bicarbonate conductance and increases risk of pancreatitis. Coinheritance of p.R75Q or CF causing CFTR variants with SPINK1 variants significantly increases the risk of ICP.
    Gastroenterology 10/2010; 140(1):162-71. · 12.82 Impact Factor
  • The Turkish journal of gastroenterology: the official journal of Turkish Society of Gastroenterology 06/2010; 21(2):188-9. · 0.48 Impact Factor
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    ABSTRACT: Celiac disease is a gluten-induced enteropathy controlled by gluten restriction. Celiac disease is occasionally associated with T-cell lymphoma. We report a case with celiac disease who presented with duodenal ulcer-like symptoms and endoscopic findings. The persistent symptoms despite a strict diet led to the suspicion of an associated malignancy. Intensive evaluation revealed a case with celiac disease associated with B-cell lymphoma. Although B-cell lymphoma is rare, it should be kept in mind especially in female patients with persistent symptoms and refractory celiac disease.
    The Turkish journal of gastroenterology: the official journal of Turkish Society of Gastroenterology 06/2010; 21(2):168-71. · 0.48 Impact Factor
  • Journal of Hepatology - J HEPATOL. 01/2010; 52.
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    ABSTRACT: Human Cytochrome P450 (CYP) comprises a multigene family of microsomal enzymes that metabolize a wide variety of xenobiotics, including drugs and carcinogens. Although the a number of CYP enzymes were also detected in epithelial cells along the gastrointestinal tract, little is known about the expression of CYP genes in gastric tissue. In this study, the expression patterns of CYP isoforms was investigated in a total of 14 antral biopsy tissues obtained from the patients with either chronic gastritis (n = 6) or cancer (n = 8) by gene-specific real-time reverse transcriptase -PCR analyses. We employed primer sets specific for CYPs -1A1, -1A2, -2A6, -2B6, -2C, -2D6, -2E1, and -3A5. Among the isoforms CYP1A1, CYP2C and CYP2D6 gave rise to detectable mRNAs in all 14 gastric tissues while the mRNAs for the other CYPs were detected in some of the tissues. The expression patterns were compared to clinical parameters. There were no significant differences in the parameters between the two groups; however the mRNA expression of CYP2A6 was significantly higher in women than man (p < 0.05). Our data suggests that the CYP isoforms were independently expressed with respect to the pathological status in human gastric tissue.
    Hepato-gastroenterology 01/2010; 57(98):372-6. · 0.77 Impact Factor
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    ABSTRACT: Eradication rates of Helicobacter pylori have declined to unacceptable levels in recent years. New and effective treatment options are warranted both as a first and second line treatment. To test an effectiveness of modified sequential therapy with levofloxacin for H. pylori eradication in Turkey. Helicobacter pylori infected dyspeptic patients were included to the study. Subjects were treated with modified sequential therapy consisting of rabeprazole 20 mg b.i.d. and amoxicillin 1 g b.i.d., for 7 days followed by rabeprazole 20 mg b.i.d, levofloxacin 500 mg q.d. and metronidazole 500 mg b.i.d for the remaining 7 days. Sixty-three treatment naive patients and 37 previous treatment failures were enrolled to the study (59 F, 41 M, age: 21-80 years). There was five drop out. Helicobacter pylori eradication was achieved in 80 patients, intention-to-treat (ITT): 80% (95% CI: 71-87%) and per-protocol (PP): 84.2% (95% CI: 75-91%), totally. In treatment naive patients ITT and PP eradication rates were 82.5% (95% CI: 71-91%), and 86.7% (95% CI: 75-94%), respectively. As a second line treatment eradication was successful in ITT 75.7%.(95% CI: 59-88%), and PP 80% (95% CI: 63-92%).Mild side effects were reported by 8 patients (8.4%). Sequential therapy using "rabeprazole and amoxicillin 7 days followed by rabeprazole, metronidazole and levofloxacin for 7 days" is a new regimen with acceptable eradication rates in naïve patients in Turkey. Further modifications in the dose or duration of this new sequential therapy might increase its effectiveness as both first and second line treatment.
    Helicobacter 12/2009; 14(6):520-4. · 3.51 Impact Factor
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    ABSTRACT: Nuclear factor-kappaB (NF-kappaB) is a potent mediator in several steps of acute pancreatitis. Leflunomide is a novel immunomodulating drug that is also a potent inhibitor of NF-kappaB activation. The aim of this study was to investigate the effects of leflunomide pretreatment in severe necrotizing pancreatitis in rats. Fifty rats were randomly divided into 5 groups. Severe necrotizing pancreatitis was induced by retrograde injection of 3% sodium taurocholate into the common biliopancreatic duct. Leflunomide (10 mg/kg) was given intragastrically for 2 doses before the experiment. Serum amylase activity, pancreatic histopathologic condition, malondialdehyde level, myeloperoxidase enzyme activity, nitric oxide level, and pulmonary changes were assessed. Leflunomide pretreatment significantly ameliorated pancreatic hemorrhage, edema, and neutrophil infiltration and decreased histopathological score compared with the untreated severe necrotizing pancreatitis group (pathological score [mean +/- SEM]: 6.70 +/- 1.19 vs 12.36 +/- 1.08 in the leflunomide treated and untreated groups, respectively, P < 0.01). Pulmonary changes was decreased in the leflunomide treated group (3.90 +/- 0.45 vs 4.75 +/- 0.25, respectively). Change in pulmonary alveolar distention was significant. Although serum amylase levels also decreased, the difference was not significant (5922 +/- 3290 vs 15547 +/- 5090 U/mL). Leflunomide is a beneficial agent in the severe form of acute pancreatitis in rats and should be considered as a potential agent for treatment of acute pancreatitis.
    Pancreas 09/2009; 39(2):237-42. · 2.95 Impact Factor
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    ABSTRACT: Pancreatic renin-angiotensin system has been implied to play a role in the regulation of pancreatic functions and could be a new therapeutic target in acute pancreatitis. The aim of this study was to evaluate the therapeutic potential of angiotensin-converting-enzyme inhibition by captopril and angiotensin II type 1 receptor inhibition by L-158809 and losartan experimentally in acute pancreatitis. Rats were randomly divided into 15 groups. Acute edematous pancreatitis was induced by injection of cerulein 20microg/kg SC four times at hourly intervals. Severe necrotizing pancreatitis was induced by retrograde injection of 3% taurocholate into the biliary-pancreatic duct. Captopril, L-158809 and losartan were given intraperitoneally. Main outcome features: pancreatic pathology, pancreatic myeloperoxidase activity and serum amylase activity were assessed. Captopril decreased serum amylase (10,809+/-1867 vs. 4085+/-1028U/L, p<0.01), myeloperoxidase activity (3.5+/-0.5 vs. 1.5+/-0.1, p<0.05) and histopathological score (5.0+/-0.4 vs. 1.1+/-0.5, p<0.01) in acute edematous pancreatitis. In taurocholate induced severe necrotizing pancreatitis captopril ameliorated histopathological score (10.1+/-1.2 vs. 3.4+/-0.5, p<0.01), pancreatic parenchymal necrosis (4.5+/-0.6 vs. 0.0+/-0.0, p<0.001), fatty necrosis (2.8+/-0.9 vs. 0.1+/-0.1, p<0.01) and edema (2.1+/-0.3 vs. 1.4+/-0.3, p<0.05). However, L-158809 did not have similar beneficial effects on acute pancreatitis in rats while losartan decreased pancreatic parenchymal necrosis and neutrophil infiltration. This study not only demonstrated the differential effects of captopril, losartan and L-158809 in acute pancreatitis but also showed that there is still much to investigate about pancreatic renin-angiotensin system. Inhibition of angiotensin-converting enzyme should be evaluated carefully as a potential new therapeutic target in acute pancreatitis.
    Experimental and toxicologic pathology: official journal of the Gesellschaft fur Toxikologische Pathologie 07/2009; 62(4):353-60. · 1.43 Impact Factor
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    ABSTRACT: Procalcitonin and C-reactive protein are two acute-phase reactant proteins, although procalcitonin is a more specific marker for bacterial infections. Procalcitonin level might also be helpful to predict the disease activity of inflammatory bowel disease. This study aimed to compare the diagnostic value of serum procalcitonin and C-reactive protein as indicators of disease activity in inflammatory bowel disease. Patients admitted to the inflammatory bowel disease inpatient clinic with suspected inflammatory bowel disease who had not yet been treated with immunosuppressive treatments were included. Disease activity, white blood cell count, sedimentation rate, serum procalcitonin and C-reactive protein levels were evaluated in 45 newly diagnosed inflammatory bowel disease patients (9 Crohn's disease and 36 ulcerative colitis). Fifty healthy volunteers were analyzed as a control group. Crohn's disease patients had higher procalcitonin and C-reactive protein levels than healthy controls (Procalcitonin: 0.143+/-0.081 vs. 0.065+/-0.008 ng/ml, p<0.05; C-reactive protein: 29+/-7.5 vs. 2.9+/-0.5 mg/dl, p<0.001, respectively). Ulcerative colitis patients also had slightly higher procalcitonin levels and significantly higher C-reactive protein levels than controls (Procalcitonin: 0.107+/-0.042 ng/ml; C-reactive protein: 23+/-5.5 mg/dl). Two Crohn's disease patients had procalcitonin value above 1 ng/ml. Receiver operating characteristic curve analysis demonstrated that C-reactive protein is the best marker of disease activity in inflammatory bowel disease while procalcitonin has low sensitivity and specificity. Serum procalcitonin levels were highly correlated with serum C-reactive protein but no other disease activity parameters. Although still within normal ranges, procalcitonin levels were slightly elevated in Crohn's disease but not in ulcerative colitis patients compared to healthy controls. Serum C-reactive protein is a reliable marker for disease activity in inflammatory bowel disease. Procalcitonin has no diagnostic value in determining disease activity.
    The Turkish journal of gastroenterology: the official journal of Turkish Society of Gastroenterology 04/2009; 20(1):9-12. · 0.48 Impact Factor
  • Endoscopy 02/2009; 41 Suppl 2:E198. · 5.74 Impact Factor
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    ABSTRACT: Both C reactive protein (CRP) and procalcitonin (PCT) are well known acute phase reactant proteins. CRP was reported to increase in metabolic syndrome and type-2 diabetes. Similarly altered level of serum PCT was found in chronic liver diseases and cirrhosis. The liver is considered the main source of CRP and a source of PCT, however, the serum PCT and CRP levels in non-alcoholic fatty liver disease (NAFLD) were not compared previously. Therefore we aimed to study the diagnostic and discriminative role of serum PCT and CRP in NAFLD. Fifty NAFLD cases and 50 healthy controls were included to the study. Liver function tests were measured, body mass index was calculated, and insulin resistance was determined by using a homeostasis model assessment (HOMA-IR). Ultrasound evaluation was performed for each subject. Serum CRP was measured with nephalometric method. Serum PCT was measured with Kryptor based system. Serum PCT levels were similar in steatohepatitis (n 20) and simple steatosis (n 27) patients, and were not different than the control group (0.06 +/- 0.01, 0.04 +/- 0.01 versus 0.06 +/- 0.01 ng/ml respectively). Serum CRP levels were significantly higher in simple steatosis, and steatohepatitis groups compared to healthy controls (7.5 +/- 1.6 and 5.2 +/- 2.5 versus 2.9 +/- 0.5 mg/dl respectively p < 0.01). CRP could not differentiate steatohepatitis from simple steatosis. Beside, three patients with focal fatty liver disease had normal serum CRP levels. Serum PCT was within normal ranges in patients with simple steatosis or steatohepatitis and has no diagnostic value. Serum CRP level was increased in NAFLD compared to controls. CRP can be used as an additional marker for diagnosis of NAFLD but it has no value in discrimination of steatohepatitis from simple steatosis.
    BMC Gastroenterology 02/2009; 9:16. · 2.11 Impact Factor
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    ABSTRACT: The renin-angiotensin system (RAS) has been implied in the pathogenesis of various diseases including acute and chronic pancreatitis. Angiotensin-converting enzyme (ACE) is the key enzyme in activating the RAS. Deletion (D)-type polymorphism in the 16th intron of the ACE gene has been associated with higher serum levels of the enzyme. Inhibition of ACE was found to ameliorate acute pancreatitis in animal models suggesting that ACE plays a role in pathogenesis and progression of acute pancreatitis. Objectives were to investigate the occurrence of the ACE insertion/deletion (I/D) polymorphism in acute pancreatitis patients and its association with the severity of the disease. Seventy-nine acute pancreatitis patients and 95 healthy controls were evaluated. Acute pancreatitis cases were grouped as mild or severe according to the Atlanta criteria. Main outcome measure: The presence of the ACE I/D polymorphism. ACE gene I and D allele frequency of patients (44% and 56%) were similar to controls (45% and 55%, respectively). There were no significant differences in severity of pancreatitis between patients with the ACE-insertion or ACE-insertion/deletion versus ACE-deletion genotypes. The ACE gene deletion polymorphism is neither a risk factor for development of acute pancreatitis nor contributes to the severity of disease or development of complications.
    HPB 02/2009; 11(1):45-9. · 1.94 Impact Factor
  • Endoscopy 02/2009; 41 Suppl 2:E206. · 5.74 Impact Factor
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    ABSTRACT: Primary biliary cirrhosis is an autoimmune liver disease that is strongly influenced by poorly defined, complex genetic factors. Alterations of the renin-angiotensin system have been implicated in the pathogenesis of various diseases. A deletion polymorphism of a 287-bp fragment of intron 16 of the angiotensin converting enzyme gene allele results in higher levels of circulating enzyme. Angiotensin converting enzyme deletion genotype has been linked to hypertension and sarcoidosis and has been reported to regulate liver fibrosis in HCV-mediated liver disease. We investigated the frequency of the Angiotensin converting enzyme gene insertion/deletion polymorphism in primary biliary cirrhosis patients. 52 biopsy-proven primary biliary cirrhosis patients and 98 healthy controls were evaluated. Angiotensin converting enzyme insertion/deletion polymorphism was detected by polymerase chain reaction amplification of a genomic DNA fragment on intron 16 of the angiotensin converting enzyme gene. Clinical phenotype of primary biliary cirrhosis was verified with positive anti-mitochondrial antibody or M2 antibody, demonstration of cholestatic liver enzymes, and staging of liver biopsy. The differences between these variables among different genotypes were noted. There was no significant difference in genotypes and allele frequency between the primary biliary cirrhosis group and controls. The D allele frequency was 54% in primary biliary cirrhosis cases and 55% in controls (p=ns). Furthermore, there was no significant difference in clinical features between patients with angiotensin converting enzyme-insertion or insertion/deletion genotypes vs. patients with angiotensin converting enzyme-deletion genotype. In our limited sample, the angiotensin converting enzyme deletion genotype did not make a significant contribution to the pathogenesis or progression of primary biliary cirrhosis.
    The Turkish journal of gastroenterology: the official journal of Turkish Society of Gastroenterology 01/2009; 19(4):250-3. · 0.48 Impact Factor

Publication Stats

176 Citations
111.91 Total Impact Points


  • 2004–2010
    • University of Pittsburgh
      • School of Medicine
      Pittsburgh, PA, United States
  • 2004–2009
    • Pamukkale University
      • Faculty of Medicine
      Denisli, Denizli, Turkey
  • 2001–2009
    • Ege University
      • • Faculty of Medicine
      • • Department of Gastroenterology
      İzmir, Izmir, Turkey
  • 2008
    • Adnan Menderes University
      • Department of Gastroenterology
      Güsel Hissar, Aydın, Turkey