[HBV pol/S gene mutations in chronic hepatitis B patients receiving nucleoside/nucleotide analogues treatment]. / Nükleozid/nükleotid analogu tedavisi alan kronik hepatit B hastalarinda hbv pol/S geni mutasyonlari.

Chronic hepatitis B (CHB) is an important public health problem affecting over 240 million people all around the world. The aim of the treatment in chronic hepatitis B is to prevent progression to cirrhosis and liver cancer. Interferons (standard and peginterferon) (Peg-IFN) and nucleoside/nucleotide analogues (NAs) are widely used in the treatment of CHB. The use of long-term therapy can however result in drug resistant mutations, which can lead to treatment failure. In patients with chronic hepatitis B, in addition to primary drug resistance mutations in the pol gene, compensatory mutations were reported. The genom of HBV polymerase (pol) gene overlaps with the envelope (S) gene. Nucleoside/nucleotide analogue (NA) resistance mutations in the pol gene of HBV, either from selection of primary or secondary resistance mutations, typically result in changes in HBsAg. Recent studies have conferred a new acronym for these HBV pol/S gene overlap mutants; ADAPVEMs, for antiviral drug-associated potential vaccine-escape mutants. The aim of this study was to investigate clinically and epidemiologically significant HBV pol/S gene mutations in NA treated CHB patients. In the study, a total of 100 patients who received nucleoside/nucleotide analogue therapy for one year or more were included. The levels of HBV DNA from serum samples were detected by the commercial real-time PCR assay and the mutations of pol/S genes by direct sequencing. Sixteen samples with low HBV DNA levels (> 200 IU/ml) could not be interpreted by sequencing due to insufficient amplification. Of the remaining 84 patients that could be sequenced HBV pol gene of HBV, 53 (63.09%) were males and 31 (36.91%) were women and the mean age was 47 ± 14.99 years (range: 20-67). Primary/secondary drug mutations (rtM204I/V, rtI169S, rtL180M, rtT184L, rtA194V, rtM204I/rtL91I, rtQ149K, rtQ215H/S, rtN238D) were detected in 38 (45.2%) of the patients. Because of the HBV pol/S gene overlapping, in 27 patients immun-selected amino acid substitutions (sI110L, sT127P, sS114A, sT123A), in nine patients HBIg selected escape mutants (sP120R, sT123N, sE164D, sY134F, sQ129H, sT118A, sP127K), in seven patients vaccine escape mutants (sT126I, sP120S, sG145A, s S193L) and in one patient misdiagnosis of HBsAg (sT131I) were detected. In addition, antiviral drug-associated potential vaccine-escape mutants were detected in 13 (15.4%) patients. In patients with chronic HBV, NAs including commonly used lamivudine were observed to have the potential for ADAPVEM to emerge during treatment. It was concluded that after determination of antiviral drug resistance and ADAPVEMs replanning of treatment should be done in the NA treatment of patients with CHB.

H. pylori positivity and various pathological, endoscopic and clinical features correlated with each other.

OBJECTIVE: To investigate the relationship between dyspepsia symptom scores and endoscopic appearances, and histopathological findings and helicobacter pylori positivity in patients having dyspepsia symptom. METHODS: The study was conducted at the gastroenterology outpatient clinic of Adnan Menderes University, School of Medicine, Aydin, Turkey from April 2012 to July 2012 and comprised patients between 18-65 years of age who were admitted with dyspepsia. Glasgow dyspepsia severity scoring was done with questions posed orally to the patients. In histopathological evaluation of biopsy specimens according to Sydney criteria, chronic inflammation, activity, atrophy, intestinal metaplasia and helicobacter pylori parameters were used. Total number of eosinophils and number of mast cells were recorded. RESULTS: Of the 60 patients with dyspepsia, 38(63.3%) were female and 22(36.7%) were male. The degree of activation and severity of inflammation increased significantly with increasing helicobacter pylori positivity(r=0.459'p<0.0001; r=0.475'p<0.0001). A significant relationship was found between inflammation, activation and the number of mast cells (p<0.05).There was no relationship between helicobacter pylori intensity and the eosinophil count (r=0.171; p=0.093). There was also a statistically significant correlation between severity of inflammation and activation and the number of eosinophils (r=0.313;p=0.002;r=0.245;p=0.016). CONCLUSIONS: Mast cell density was seen to have a role in the inflammatory processes of helicobacter pylori infection.

Therapeutic plasma exchange for hypertriglyceridemia induced acut pancreatitis: the 33 cases experience from a tertiary reference center in Turkey.

BACKGROUND/AIMS: Hypertriglyceridemia (HTG) is the third most common cause of acute pancreatitis. In patients with severe HTG (TG level>1000 mg/dL), it may be beneficial to immediately lower the levels of triglyceride (TG) and chylomicrons. In this study, we present one of the largest case series on the use of therapeutic plasma exchange (TPE) for hypertriglyceridemia-induced acute pancreatitis (HTG-AP). MATERIALS AND METHODS: Overall, 33 patients who were admitted to our clinic for HTG-AP and underwent TPE between January 2007 and July 2017 were included in the study. Clinical data and outcomes and the reduction of triglyceride levels were examined retrospectively. RESULTS: The TG level decreased by 54.4%, and the total cholesterol level decreased by 52.1% after one TPE session. The TG decrease after the second TPE session was found to be 79.4%. There were 20 (60.6%) patients with mild acute pancreatitis, 10 (30.3%) patients with moderetaly severe acute pancreatitis, and 3 (9.1%) patients with severe acute pancreatitis based on the categorization according to the revised Atlanta criteria. Regarding local complications, the acute peripancreatic fluid collection was observed in 13 (39.4%) patients, acute necrotic collection was observed in 1 (3%) patient, walled-off necrosis was observed in 1 (3%) patient, and pancreatic pseudocyst was not observed in any patient. Mortality was not determined in patients with mild and moderately severe acute pancreatitis, and its rate was 33.3% in patients with severe acute pancreatitis. The overall mortality rate was 3%. No significant complications related to TPE were noted. CONCLUSION: TPE is a safe and helpful therapeutic treatment method for patients with HTG-AP and may be considered particularly in patients with severe acute pancreatitis.

Factor V Leiden G1691A, prothrombin G20210A, and MTHFR C677T mutations in Turkish inflammatory bowel disease patients.

BACKGROUND/AIMS: Patients with inflammatory bowel disease (IBD) have an increased risk for thromboembolic complications. We investigated the incidence of factor V Leiden G1691A, methylene tetrahydrofolate reductase (MTHFR) C677T, and prothrombin G20210A mutation in 27 Turkish IBD patients with no history of thromboembolic disease. METHODOLOGY: Twenty-seven patients, 22 with ulcerative colitis (UC) and 5 with Crohn's disease (CD), and 47 healthy were included to the study. The DNAs were obtained from peripheral blood by using pure polymerase chain kit. Then, factor V Leiden G1691A, which active protein C resistance positive, prothrombin G20210A and MTHFR C677T mutations were investigated in DNA by using LightCycler-Factor V Leiden G1691A mutation, Prothrombin G20210A and MTHFR C677T estimate kits. RESULTS: The heterozygote factor V Leiden G1691A mutation was detected in 3 (11.1%) patients with IBD and 2 (4.3%) controls (p > 0.05). The homozygote factor V Leiden G1691A mutation was not estimated among patients and controls. Heterozygote prothrombin G20210A mutation was detected in 2 (7.4%) patients with IBD and in 0 (0%) controls (p > 0.05). There was no homozygote prothrombin G20210A mutation in IBD and controls. Heterozygote MTHFR C677T mutation was 10 of 27 (37%) patients with IBD while 15 of 47 (32%) controls (p > 0.05). Homozygote MTHFR C677T mutation was detected in 4 patients (14.9%) with IBD and 3 (6.3%) controls (p > 0.05). CONCLUSIONS: Our study did not reveal any association between IBD and the most common hereditary thrombophilic factors and these mutations interfere with neither disease manifestations nor the thrombotic complications.