In chronic hepatitis B virus (HBV) infection, inflammation-associated cytokines including proinflammatory cytokines are involved in the development and progression of liver fibrosis. The liver is a source of many cytokines that may influence liver function. High-mobility group box 1 (HMGB1) was identified as an inflammatory cytokine. HMGB1 is present in nuclei of all mammalian cells and is released both through active secretion from various cells and by passive release from necrotic cells. Here we explore the relationship between HMGB1 plasma levels and liver fibrosis. HMGB1 serum levels, HBV-DNA, and ALT values were significantly higher in patients with chronic HBV than in controls. In addition, HMGB1 serum levels were significantly higher in patients with low fibrosis (fibrosis score 1-2) compared to those with high fibrosis (fibrosis score 3-4). In the present study, we have shown that HMGB1 is a noninvasive, repeatable, and convenient marker for distinguishing advanced fibrosis from low fibrosis in chronic HBV patients. We believe that the inhibition of HMGB1 may reduce inflammation, apoptosis, and fibrosis, and may stop the progression of chronic liver disease. Furthermore, we are of the opinion that fibrotic progression in chronic liver patients may be prevented by the inhibition of HMGB1, and that this substance can be a new means of following chronic HBV treatment.

Aim. We aimed to determine the relation of asymmetric dimethyl arginine (ADMA) levels to atherosclerotic vascular disease and inflammation markers in type 2 diabetes. Methods. We recruited 50 type 2 diabetic patients with atherosclerosis, 50 type 2 diabetic patients without atherosclerosis, and 31 healthy control patients into our study. We obtained fasting serum and plasma samples and measured HbA1c, fasting blood glucose, C-peptide, creatinine, total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, hsCRP, fibrinogen, erythrocyte sedimentation rate, total homocysteine, and ADMA levels. In addition, all of the patients were evaluated for carotid artery intima media thickness by ultrasound. We evaluated ADMA levels in healthy controls, diabetic patients with macrovascular complications, and diabetic patients without macrovascular complications and evaluated the relationship between ADMA levels and total homocysteine, inflammation markers, and macrovascular disease. Results. Mean ADMA values in non-MVD and control groups were significantly lower than in MVD group (0.39 ± 0.16, 0.32 ± 0.13, 0.52 ± 0.23, P < 0.05, resp.). These three variables (carotid intima-media thickness, inflammatory markers, and ADMA levels) were significantly higher in diabetes group than control (P < 0.05). Conclusion. There is a relationship between ADMA and macrovascular disease in type 2 diabetes, but further studies are needed to understand whether increased ADMA levels are a cause of macrovascular disease or a result of macrovascular disease.

Objective. We aimed to determine the effectiveness of endoscopic retrograde cholangiopancreatography (ERCP) in patients with inoperable perihilar cholangiocarcinoma and establish the incidence of cholangitis development following ERCP. Material and Method. This retrospective study enrolled patients diagnosed with inoperable perihilar cholangiocarcinoma who underwent endoscopic drainage (stenting) with ERCP. Patients were evaluated for development of cholangitis and the effectiveness of ERCP. The procedure was considered successful if bilirubin level fell more than 50% within 7 days after ERCP. Results. Post-ERCP cholangitis developed in 40.7% of patients. Cholangitis development was observed among 39.4% of patients with effective ERCP and in 60.6% of patients with ineffective ERCP. Development of cholangitis was significantly more common in the group with ineffective ERCP compared to the effective ERCP group (P = 0.001). The average number of ERCP procedures was 2.33 ± 0.89 among patients developing cholangitis and 1.79 ± 0.97 in patients without cholangitis. The number of ERCP procedures was found to be significantly higher among patients developing cholangitis compared to those without cholangitis (P = 0.012). Conclusion. ERCP may not provide adequate biliary drainage in some of the patients with perihilar cholangiocarcinoma and also it is a procedure associated an increased risk of cholangitis.

Background and objective Pediatric guidelines on the diagnosis of celiac disease (CD) have reported that the positivity of anti-endomysium antibodies in the presence of anti-transglutaminase antibodies (TGA) 10 times higher than normal is sufficient for the diagnosis. In this study, we aimed to evaluate whether this diagnostic process for children can also be applied to adult patients. Materials and methods We retrospectively examined patients aged >18 years who were diagnosed with CD. The results of serological tests and endoscopic biopsy were evaluated. Patients with more than one month of duration between celiac serology and endoscopy, those diagnosed with CD before admission, those on a gluten-free diet, and those with selective IgA deficiency were excluded from the study. Results A total of 269 patients were included in the study. TGA value was significantly higher in patients with villous atrophy (p<0.001) and positively correlated with mucosal damage (r=0.60, p<0.01). Considering the cut-off value of 100 U/mL (>10 ULN) for the TGA antibodies, in line with the criteria regulated by the European Society for Paediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) for the diagnosis of CD, the sensitivity was 71.64%, the specificity was 100%, and the positive predictive value (PPV) was 100%. When the cut-off value was taken as 29.42 U/mL, the sensitivity was 100% and the specificity was 99.5%. For a TGA cut-off value of 52.7 U/mL (5.27 ULN), which determines the presence of partial or complete villous atrophy in the evaluation made considering mucosal damage, the sensitivity was 90%, the specificity was 100%, and the PPV was 100%. Conclusion Based on our findings, TGA titers were highly effective in demonstrating CD-related mucosal damage. This study endorses a biopsy-free strategy in adult patients in line with the ESPGHAN criteria. Local validation of test-specific thresholds will ensure that this approach has a significant impact on adult patients.

Previous studies detected higher Golgi protein 73 levels in the serum of patients with chronic liver disease. The Beta-2 microglobulin levels were also observed to be higher in patients with chronic hepatitis B infection compared to the inactive carriers and the protein plays an important role in the response to viral infections. The aim of the present study was to assess the liver fibrosis through non-invasive methods in chronic hepatitis B patients. Three groups were included in the study. The first group comprised of the patients who were admitted to the Infectious Diseases and Clinical Microbiology clinic to undergo a liver biopsy, while the second group included the patients who were admitted inactive hepatitis B carriers. The third group comprised the healthy controls. The Golgi p-73 and Beta-2 microglobulin levels in the plasma were determined using the ELISA method. Beta-2 microglobulin level was highest in the patients group and the difference was statistically significant. No significant difference was observed between the carriers group and the group of healthy controls. The Golgi P-73 values were significantly higher in the patients group in comparison to both other groups. However, the mean Golgi p-73 value was also significantly higher in the carrier group compared to the control group. In patients who are followed up with the diagnosis of chronic hepatitis B and who have undergone biopsies as candidates for treatment, the Beta-2 microglobulin and Golgi p-73 values may be important markers since they indicate the extent of the liver damage.

Urinary 8-OHdG levels could be investigated in every patient with chronic gastritis, since it is a simple and completely noninvasive procedure. In patients with high levels of urinary 8-OHdG, endoscopic procedures or even pathological investigation may then be carried out, with the consideration that there is a high risk of intestinal metaplasia or atrophy.

DRESS syndrome is a life-threatening adverse reaction characterized by skin rashes, fever, leukocytosis with eosinophilia or atypical lymphocytosis, lymph node enlargement, and liver or renal dysfunctions. DRESS syndrome related to valproic acid use is very rarely observed. We present a case of DRESS syndrome induced by sodium valproate, which developed and progressed fatally in a brucellosis patient with a positive c-ANCA test. A 19-year-old female patient presented with fever, cough, jaundice, and rash all over her body. Brucella Coombs test was positive at 1:1280 titers, and the Rose Bengal test was also positive. The involuntary movements were thought to be due to chorea, and the patient was started on sodium valproate 500 mg 2 1, as well as streptomycin 1 g flk 1 1 and tetradox capsules 2 1 for the brucellosis and was discharged. DRESS syndrome was suspected in the patient, and she was taken off sodium valproate and tetradox; N-acetylcysteine, ceftriaxon, prednizolone, and support treatment were started. When sodium valproate is used on its own, it carries no risk of inducing DRESS syndrome. However, in the case presented, another co-morbidity such as brucellosis and c-ANCA positivity was present. We believe that the presence of further co morbidity not yet reported in literature is important from the perspective of the risk of valproate-induced DRESS syndrome. Therefore, if sodium valproate treatment is to be started in patients, especially those with co morbidity, they must be closely monitored with clinical and laboratory observations. At the slightest suspicion of DRESS syndrome, all medication should be ceased immediately and the patient should be placed under continuous observation.

BackgroundThe burn wound represents a susceptible site for opportunistic colonization by organisms of endogenous and exogenous origin. Diminishing appetite is known to occur in patients with burn infection, yet its underlying reason is not fully understood. We have examined the levels of nesfatin 1, a protein that we consider to be a potential new treatment target for the solution of appetite and nutrition problem in patients with burn infection.ObjectivesThe aim of the present study was therefore to examine nesfatin levels in patients with burn infection.Material and MethodsLaboratory values, medication and dietary records, and patient notes with diagnostic information of burn wounds patients who were admitted to the Division of Burn Treatment Center were obtained from the Erzurum Region Education and Research Hospital electronic database. Post-burn wound infection was objectively assessed by culturing wound homogenates from skin tissue. The main immediate inflammatory stress response parameters assessed were serum CRP concentrations, WBC counts, and blood nesfatin concentrations.ResultsScalding was the predominant cause of burns in both categories of patients. In 19 (61.3%) burn wound infection patients, the burns were due to a scald. A significant difference was found for the nesfatin, CRP, and WBC levels between the patients and the control group (P = 0.000). A significant difference was also determined between the nesfatin, CRP, and WBC figures at the time of hospitalization and at discharge from the hospital (P = 0.000). The most predominant bacterial isolate was Pseudomonas aeruginosa 16 (51.6%) followed by Methicilline resistant Staphylococcus aureus (MRSA) 7 (22.6%).ConclusionsWe showed that the serum nesfatin 1 level was significantly lower in the patients with burn than in the control group in our study. We considered that the central nesfatin 1 system should be taken into consideration, rather than the peripheric nesfatin 1 system, when considering the regulation of appetite in patients with burns and particularly those accompanied by infection. In other explanation of the observed negative correlation between nesfatin 1 and burn wound infection suggests that nesfatin 1 may indicate the possible contribution of nesfatin 1 to the energy homeostasis.