[Show abstract][Hide abstract] ABSTRACT: Background:
The specific antiviral T cells provide CC chemokine receptor 5 (CCR5) for the immune response during the hepatitis C virus (HCV) infection. Heterogenous and/or homozygous 32 base pair deletion in CCR5 gene (CCR5Δ32 bpdel) leads to reduced protein expression.
In the current case control study, we aimed to compare the histopathological findings of liver to the CCR5Δ32 bpdel mutation profiles, expression and some other clinical findings in patients with chronic HCV infection.
Materials and Methods:
Multiple Strip Assay reverse hybridisation and Real Time PCR techniques were used to determine the germline CCR5 mutations and immunohistochemical technique was used to evaluate the gene expression in targer tissue biopsies.
Target CCR5 WT/WT, WT/Δ32, and Δ32/Δ32 genotypes were observed in 91.4%, 8.6% and 0.0% for HCV positive patients and 98.3%, 1.7% and 0.0% for control group respectively. The histologic activity index (HAI) was significantly lower (4.0 ± 1.0) in the mutated group than the non-mutated group (5.7 ± 1.0). Decreased fibrosis levels were detected in HCV positive mutated group.
Results showed that CCR5 polymorphism was more frequent in HCV positive patients than in healthy population in Turkish population. Current results also showed that mutated CCR5 signalling pathway due to CCR5-Delta32 may potentially result in subtle reduction of HCV specifity to the drug responses due to the positive impact on liver inflammation, fibrosis levels and liver destruction in HCV infection.
[Show abstract][Hide abstract] ABSTRACT: In the current study we aimed to show the common YMDD motif mutations in viral polymerase gene in chronic hepatitis B patients during lamivudine and adefovir therapy. Forty-one serum samples obtained from chronic hepatitis B patients (24 male, 17 female; age range: 34-68 years) were included in the study. HBV-DNA was extracted from the peripheral blood of the patients using an extraction kit (Invisorb, Instant Spin DNA/ RNA Virus Mini Kit, Germany). A line probe assay and direct sequencing analyses (INNO-LIPA HBV DR v2; INNOGENETICS N.V, Ghent, Belgium) were applied to determine target mutations of the viral polymerase gene in positive HBV-DNA samples. A total of 41 mutations located in 21 different codons were detected in the current results. In 17 (41.5%) patients various point mutations were detected leading to lamivudin, adefovir and/ or combined drug resistance. Wild polymerase gene profiles were detected in 24 (58.5%) HBV positive patients of the current cohort. Eight of the 17 samples (19.5%) having rtM204V/I/A missense transition and/or transversion point mutations and resistance to lamivudin. Six of the the mutated samples (14.6%) having rtL180M missense transversion mutation and resistance to combined adefovir and lamivudin. Three of the mutated samples (7.5%) having rtG215H by the double base substituation and resistance to adefovir. Three of the mutated samples (7.5%) having codon rtL181W due to the missense transversion point mutations and showed resistance to combined adefovir and lamivudin. Unreported novel point mutations were detected in the different codons of polymerase gene region in the current HBV positive cohort fromTurkish population. The current results provide evidence that rtL180M and rtM204V/I/A mutations of HBV-DNA may be associated with a poor antiviral response and HBV chronicity during conventional therapy in Turkish patients.
Asian Pacific journal of cancer prevention: APJCP 09/2013; 14(9):5489-94. DOI:10.7314/APJCP.2013.14.9.5489 · 2.51 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Although alveolar echinococcosis (AE) can cause a serious disease with high mortality and morbidity similar to malign neoplasms. A 62-year-old woman admitted to a hospital located in Sivas, Turkey, with the complaints of fatigue and right upper abdominal pain. On contrast abdominal CT, a 54×70×45 mm sized cystic lesion was detected in the left lobe of the liver that was seen to extend to the posterior mediastinum and invade the diaphragm, esophagus, and pericardium. The cystic lesion was seen to be occluding the inferior vena cava and left hepatic vein at the level where the hepatic veins poured into the inferior vena cava. Bilateral pleural effusion was also detected. We discussed this secondary Budd-Chiari Syndrome (BCS) case, resulting from the AE occlusion of the left hepatic vein and inferior vena cava, in light of the information in literature.
The Korean Journal of Parasitology 08/2013; 51(4):475-7. DOI:10.3347/kjp.2013.51.4.475 · 1.15 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To treat viral infection of chronic hepatitis C (CHC) is a main strategy to prevent progression of liver disease, and cancer. Some patients with CHC have failed to respond to the common antiviral therapy in different populations.
In the current study it was aimed to find out the possible role of multiple drug resistance gene1 (MDR1) in non-responder patients with CHC infection in Turkish population.
Peripheral blood-EDTA samples were used for total genomic DNA isolation. In total of 55 patients with chronic hepatitis C and positive results for genotype 1 [31 male (56.4%), 24 female (43.6%) and mean age-min-max; 56.9 ± 9.66 (39-71)]; 19 responder (34.5%), 21 non responder (38.2%), and 15 recurrence (27.3%) were included in the presented results. Functional MDR1 gene was genotyped by multiplex PCR-based reverse-hybridization Strip Assay method, and some samples were confirmed by direct sequencing.
Our results indicate that MDR1 gene polymorphism is strongly associated with non-responder patients and those with recurrent chronic hepatitis C during conventional drug therapy when compared to the responder patients. Homozygous of the TT genotype for MDR1 exon 26 polymorphism was at 2.0-fold higher risk of non-responder than patients with CC and CT.
The homozygous MDR1 3435TT genotype which encodes the xenobiotic transporter P-glycoprotein may be associated with a poor antiviral response in HCV chronicity during conventional therapy, and large-scale studies are needed to validate this association.
[Show abstract][Hide abstract] ABSTRACT: To evaluate the effect of hyponatraemia on pulmonary thromboembolism mortality rates.
The retrospective study was conducted at the Cumhuriyet University Medicine Faculty's Emergency Department, and involved the analysis of records related to all patients who were diagnosed with acute pulmonary thromboembolism between January 2005 and June 2011. Diagnoses were confirmed by pulmonary angiography, multi-slice computed tomography or high-probablity ventilation/perfusion scintigraphy. All patients (n=260) were over 16 years of age. SPSS 14 was used for statistical analysis.
Plasma sodium level, platelet count and hospitalisation time were significiantly lower among those who died (n=16; 6.29) (p<0.005, p<0.035, p<0.035). Pearson correlation analysis found a negative correlation between plasma sodium level and C-reactive protein, white blood cells and pulmonary artery pressure (r = -0.238, p<0.001; r = -0.222, p<0.001; r = -0.444, p<0.018 respectively). A positive correlation was found between plasma sodium level and hospitalisation time (r=0.130; p<0.039).
While mortality rates in hyponatraemic pulmonary thromboembolism patients increases, low plasma sodium is an easy parameter that should be kept in mind for the prognosis of pulmonary thromboembolism disease.
Journal of the Pakistan Medical Association 03/2013; 63(3):331-5. · 0.41 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Aim:
Oral anticoagulants are the most common used substance for treatment and prophylaxis of warfarin venous and arterial thromboembolic disorders in the world. Therapeutic index of warfarin is narrow. CYP2C9 is a hepatic microsomal enzyme and has a primary role in metabolism of warfarin and genetic variations of CYP2C9 may cause a serious effect on the response to warfarin in patients. The aim of this study was to determine the efficiency of CYP2C9 gene polymorphisms on drug metabolism in patients who had upper gastrointestinal system bleeding while using warfarin.
There was a total of 67 patients in this study, 37 of whom had upper gastrointestinal system bleeding when INR was above 3 while using warfarin (group 1), 30 of whom had no bleeding and INR was stable under 3 (group 2).
There was no difference in terms of warfarin dose used among the groups (p>0.05). Mutant genotype, INR and aspirin usage were found significantly different in the group with bleeding (p less 0.05). When analyzed in terms of drug interaction, there was no difference between the two groups (p>0.05). Logistic regression analysis was made in order to determine the risk factors that may cause bleeding. Aspirin usage (p= 0.016) and genetic polymorphism (p= 0.024) were related to the increased risk of bleeding.
CYP2C9*2 and CYP2C9*3 polymorphisms were related to the increase of excessive anticoagulation and bleeding risk in the patients who used warfarin.
[Show abstract][Hide abstract] ABSTRACT: BACKGROUND AND AIMS: After NADPH oxidase mediated radical formation, hypochloric acid (HOCl) is formed when Cl is used as a substrate by the myeloperoxidase enzyme. Myeloperoxidase is secreted from H2O2 activated leukocytes with polymorphic nuclei. The generation of HOCl also causes the formation of advanced oxidation protein products (AOPP) through damage to normal tissue and protein oxidation. AOPP has been identified as a marker of inflammation in many diseases. However, AOPP has not been investigated in ulcerative colitis. As a result of mucosal inflammation in ulcerative colitis, oxidative stress can occur. We aimed to determine whether plasma AOPP and oxidative stress markers are detectable in active ulcerative colitis. METHODS: The patient group consisted of 59 patients who were diagnosed with ulcerative colitis in the clinic by histology and endoscopy. The patients were hospitalised and treated in the Gastroenterology Department of Gazi University Medical Facility. The 59 patients were separated into active and inactive groups according to the endoscopic activation index (EAI). Group I consisted of 33 active ulcerative colitis patients, Group II consisted of 26 inactive ulcerative colitis patients and Group III consisted of healthy control subjects. The disease activity of these patients were measured using the Rachmilewitz EAI based on rectosigmoidoscopic or colonoscopic findings. Patients with EAI scores greater than 4 were scored as having active disease (Group I). Patients with EAI<4 were scored as being in disease remission (Group II). The control subjects (Group III) were 51 healthy individuals. The plasma AOPP levels were measured using a spectrophotometric method. RESULTS: There were no statistically significant differences in gender (P<0.22) and age (P<0.11) between the groups examined. The plasma AOPP level in Group I was 148.72±9.08μmol/L. The plasma AOPP level in Group II was 74.48±7.06μmol/L, and the plasma AOPP level in Group III was 64.93±2.55μmol/L. The AOPP levels in Group I were statistically different than in Group II and III (P<0.05). The AOPP levels were similar between Group II and Group III (P>0.05). The EAI value was 8.84±0.31 in Group I and 2.76±0.08 in Group II. There were statistically significant differences for EAI between groups (P<0.05). The correlation between AOPP and EAI in all patients with ulcerative colitis were statistically significant (P<0.05, r=0.61). The regression model in this correlation was statistically significant (y=49.68+10.75x, P<0.05). DISCUSSION: Based on our results, we suggest that AOPP could be used as a non invasive activation marker for ulcerative colitis patients.
[Show abstract][Hide abstract] ABSTRACT: Chanarin-Dorfman syndrome (CDS) is an autosomal recessive neutral lipid storage disease. It is very rare and characterized by ichtiosis, intracellular fat droplets in leucocytes (Jordan anomaly) and involvement of multiple tissues (skeletal muscle, central nervous system, bone marrow, eye and ear) mainly the liver. Our patients were diagnosed as CDS because they had ichtiosis, Jordon anomaly of leucocytes in peripheral blood smear, liver involvement and presence of homozygous 88 insertion C frame shift mutation on exon 4 of ABHD5/CGI-58 gene in genetic analysis. Our cases were two sisters. One of them developed severe steatohepatitis on age 19 and the other one was diagnosed as decompensated cirrhosis when she was 26 years old. We report here a new mutation in comparative gene identification-58 (CGI-58) gene causing syndactyly and steatohepatitis induced early cirrhosis.
[Show abstract][Hide abstract] ABSTRACT: Ulcerative colitis (UC) is an inflammatory disease of the colonic mucosa. The presence of gene responsible for FMF, MEFV, which frequently causes inflammation, may aggravate the clinical course of UC. We aimed to determine the prevalence of MEFV mutations in UC patients and its impact on the clinical course. Four groups were formed as group 1 UC with distal disease, group 2 UC with pancolonic disease, group 3 UC with total colectomy, and group 4 Rheumatoid Arthritis (RA) patients. Eleven mutations of FMF gene were investigated. The mean age of group 1, 2, 3, and 4 were 46.7 ± 13.9, 43.8 ± 12.9, 44.8 ± 14.2, and 45.8 ± 10.9 years, respectively. The mutations were identified in 19 of the 54 UC patients (35.2%). Homozygous E148Q in 2 patients (3.7%) and heterozygous in 17 patients (31.5%) (E148Q 11.1%, M694V 5.6%, V726A 5.6%, K695R 1.8%, M680I 1.8%, and compound heterozygous 5.6%) were determined. Frequencies of MEFV mutations in group 1, 2, and 3 were 30, 27.3, and 58.3%, respectively. The mutations were identified in 3 of the 20 RA patients (15%). All of them were heterozygous. The rate of MEFV mutations were higher in group 3 than in group 4 (P = 0.018), and the number of attacks that were treated with steroid in all UC patients with mutation positive was higher than in mutation negative (P = 0.016). FMF gene mutations may be identified in UC patients up to 58.3%. It may be suggested that the UC patients with severe form should be identified for MEFV mutations before the judgment of colectomy.
Rheumatology International 03/2010; 31(7):859-64. DOI:10.1007/s00296-010-1380-y · 1.52 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To determine the association between Helicobacter pylori (H. pylori) and globus sensation (GS) in the patients with cervical inlet patch.
Sixty-eight patients with esophageal inlet patches were identified from 6760 consecutive patients undergoing upper gastrointestinal endoscopy prospectively. In these 68 patients with cervical inlet patches, symptoms of globus sensation (lump in the throat), hoarseness, sore throat, frequent clearing of the throat, cough, dysphagia, odynophagia of at least 3 mo duration was questioned prior to endoscopy.
Cervical heterotopic gastric mucosa (CHGM) was found in 68 of 6760 patients. The endoscopic prevalence of CHGM was determined to be 1%. H. pylori was identified in 16 (23.5%) of 68 patients with inlet patch. Fifty-three patients were classified as CHGM II. This group included 48 patients with globus sensation, 4 patients with chronic cough and 1 patient with hoarseness. All the patients who were H. pylori (+) in cervical inlet patches had globus sensation.
Often patients with CHGM have a long history of troublesome throat symptoms. We speculate that disturbances in globus sensation are like non-ulcer dyspepsia.
World Journal of Gastroenterology 01/2010; 16(1):42-7. DOI:10.3748/wjg.v16.i1.42 · 2.37 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Factors affecting diagnostic accuracy and comparison of patients in the follow-up period for negative outcomes are not thoroughly investigated in a randomized trial.
Our purpose was to compare diagnostic accuracy, complications, and number of interventions.
Prospective, unicentric, single-blind, randomized study.
Single tertiary referral university hospital.
One hundred twenty patients with intermediate risk for common bile duct (CBD) stones were randomized to either an EUS-first, endoscopic retrograde cholangiography (ERC)-second (n = 60) versus an ERC-only (n = 60) procedure.
EUS, ERC, sphincterotomy, and balloon sweeping of CBD when needed.
Sensitivity of EUS versus ERC, factors affecting diagnostic capability, complications, total number of endoscopic procedures.
The sensitivity and specificity of ERC were 75% (95% CI, 42%-93%) and 100% (95% CI, 95%-100%), respectively. The sensitivity and specificity of EUS were 91% (95% CI, 59%-99%) and 100% (95% CI, 95%-100%), respectively. EUS is more sensitive than ERC in detecting stones smaller than 4 mm (90% vs 23%, P < .01). Although not significant, there was a trend for an increased number of endoscopic procedures in the ERC group compared with the EUS group (98 vs 83). The post-ERC pancreatitis rate was 6 in 120 (5%) in all study patients, and the post-ERC pancreatitis rate in patients with an undilated CBD was 5 of 53 (9.43%). The independent factors for post-ERC pancreatitis are undilated CBD (risk ratio [RR] 6.320; 95% CI, 1.703-11.524, P = .009), allocation into the ERC group (RR 2.107; 95% CI, 1.330-3.339, P = .02), female sex (RR 1.803; 95% CI, 1.155-2.813, P = .03), and age less than 40 years (RR 1.888; 95% CI, 1.245-2.863, P = .01). Kaplan-Meier analysis revealed higher rate of negative outcome in the ERC group than in the EUS group (P = .049, log-rank test).
The EUS-first approach is not associated with further risk for subsequent endoscopic procedures. Patients with an undilated CBD should be investigated by the EUS-first approach to prevent post-ERC pancreatitis.
[Show abstract][Hide abstract] ABSTRACT: Achalasia may be associated with extraesophageal dysmotility. However, this relation is still poorly understood. In the present study, we used noninvasive real-time ultrasonography to examine the motility function of the gallbladder in the patients with achalasia.
Thirty-three achalasic patients and 33 healthy volunteers were included in the study. All subjects were investigated after 12 hours of fasting and 30 minutes after a standard test meal. Premeal and postmeal gallbladder volumes were used for calculation of the ejection fraction of the gallbladder and fasting gallbladder volume.
The mean fasting volume (18.52+/-1.45 vs. 24.63+/-1.84 cm; P<0.05) and ejection fractions of gallbladder (35.84+/-4.12 vs. 54.47+/-2.47; P<0.05) in the patients with achalasia were lower than the control group.
Such a finding may confirm the possible extraesophageal extension of primary achalasia. Achalasic patients have smaller gallbladders than do others. It could be speculated that it is congenital and/or achalasic patients' gallbladder has incomplete relaxation (as in the lower esophageal sphincter of the achalasia).
[Show abstract][Hide abstract] ABSTRACT: Introduction:
There have been several reported cases of lansoprazole-associated collagenous colitis (CC) reported in the literature but only 1 reported case of lansoprazole-associated lymphocytic colitis (LC) in the literature. Both CC and LC are considered inflammatory bowel diseases, but they are distinctly classified based on the condition of the colon, which is typically confirmed through biopsy.
A 52-year-old white male (Patient 1), with a height of 178 cm and weight of 75 kg, presented to Gazi University Hospital, Ankara, Turkey, with a 3-month history of abdominal pain and nonbloody, watery diarrhea. The patient reported receiving PO lansoprazole 30 mg/d to treat heartburn ~1 week prior to the onset of diarrhea. The patient's medical history revealed that he did not have any preexisting conditions, other than gastroesophageal reflux disease (GERD) for which lansoprazole was prescribed. The medical history report also revealed that the patient was not receiving any concomitant medications or treatments at the time. A colon biopsy confirmed LC. Additionally, a 43-year-old white female (Patient 2), with a height of 168 cm and weight of 61 kg, presented to the same facility with a 6-month history of nonbloody, watery diarrhea and mild lower abdominal cramping. The patient reported that initial onset began ~2 months after receiving a 10-day Helicobacter pylori eradication combination treatment regimen that included lansoprazole, amoxicillin, and clarithromycin, followed by lansoprazole monotherapy to treat GERD. The patient's medical history revealed no other concomitant medications were being adminstered at the time. A colon biopsy confirmed LC.
A search of the literature using the MEDLINE database and all relevant English-language articles with key words lansoprazole and lymphocytic colitis, found that there were several cases of lansoprazole-associated CC reported and 1 reported case of lansoprazole-associated LC. Histologic findings from laboratory tests and colon biopsies confirmed diagnoses of LC in both patients in this case report. Patient 1 presented with diarrhea and cramping, which the patient reported had been ongoing for ~3 months, following lansoprazole administration. However, after lansoprazole was discontinued, the symptoms completely resolved within 7 days. Patient 2 presented with diarrhea and cramping, which had been occurring for ~6 months. That patient reported that initial onset commenced ~2 months after a 10-day H pylori eradication combination treatment regimen that included lansoprazole, amoxicillin, and clarithromycin, followed by lansoprazole monotherapy to treat GERD. However, after sulfasalazine (3 g/d) was prescribed for 2 months immediately upon diagnosis of LC, there was little improvement in the effort to control the diarrhea in this patient. After omeprazole 20 mg/d was substituted for lansoprazole, the patient's diarrhea ceased. Follow-up sigmoidoscopy 2 months later revealed normal mucosa and complete normalization of histologic findings. The patient remains diarrhea-free while on omeprazole. A causality assessment using the Naranjo adverse reaction algorithm produced scores of 6 for both patients, suggesting that LC was probably associated with lansoprazole treatment.
Here we report 2 cases of LC in patients probably associated with the administration of lansoprazole treatment. Complete remission occurred after lansoprazole was discontinued.
Current Therapeutic Research 09/2007; 68(5):360-366. DOI:10.1016/j.curtheres.2007.10.001 · 0.45 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Heterotopic gastric mucosa (HGM) is commonly seen in the upper esophagus during endoscopyand is generally considered a benign disease. A hyperplastic polyp and an adenocarcinoma arising in heterotopic gastric mucosa are quite rare occurences.
We present two cases: The first is a patient who suffered from dysphagia because of a large hyperplastic polyp that arose from HGM; the polyp was excised endoscopically. Secondly, we report a rare case of adenocarcinoma arising in HGM of the cervical esophagus.
Morphologic changes or malignant transformation can develop in the inlet patch. Therefore, gastroenterologists should be aware of the possibility of HGM just distal to the upper esophageal sphincter.
Journal of Medical Case Reports 02/2007; 1(1):127. DOI:10.1186/1752-1947-1-127
[Show abstract][Hide abstract] ABSTRACT: Hypertriglyceridaemia is a well known risk factor for acute pancreatitis. Hypertriglyceridaemia may be primary in origin or secondary to alcohol abuse, diabetes mellitus, pregnancy or use of drugs. In this case report, the cause of acute pancreatitis was tamoxifen. We report on a patient with tamoxifen-induced acute pancreatitis and hypertriglyceridaemia who was successfully treated with insulin infusion and long-term gemfibrozil.
Clinical Drug Investigation 02/2006; 26(5):297-302. DOI:10.2165/00044011-200626050-00007 · 1.56 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Cefoperazone is a third-generation cefalosporin that contains the N-methyl- thio-tetrazole (NMTT) side chain, which inhibits vitamin K-dependent carboxylation. Administration of NMTT-containing cefalosporins can cause alterations in the hepatic glutathione redox state, resulting in a dose-related increase in oxidised glutathione, which is responsible for the inhibition of microsomal reduction of vitamin K epoxide. In addition, cefoperazone is not metabolised and is excreted predominantly through the bile. In patients with hepatic impairment, the clearance of cefoperazone has been shown to be significantly reduced and the half-life prolonged. We report a case of choledocholithiasis related to a prolonged prothrombin time and INR secondary to cefoperazone therapy.
Clinical Drug Investigation 02/2006; 26(8):481-4. DOI:10.2165/00044011-200626080-00006 · 1.56 Impact Factor