Serkan Cerrah

Is HMGB1 a new indirect marker for revealing fibrosis in chronic hepatitis and a new therapeutic target in treatment

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.

The Role of Diminishing Appetite and Serum Nesfatin-1 Level in Patients with Burn Wound Infection

Background The 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. Objectives The aim of the present study was therefore to examine nesfatin levels in patients with burn infection. Material and Methods Laboratory 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. Results Scalding 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%). Conclusions We 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.

Should increased levels of urinary 8-hydroxydeoxyguanosine in chronic gastritis imply intestinal metaplasia or gastric atrophy?

Objectives: Helicobacter pylori (H pylori) infection induces chronic inflammation that can progress to gastric atrophy, intestinal metaplasia, and gastric adenocarcinoma. We have examined oxidative damage caused by Helicobacter pylori, metaplasia, and atrophy of gastric mucosal cells in patients with chronic gastritis by measuring their urinary 8-hydroxydeoxyguanosine (8-OHdG) levels. Methods: We recruited 77 outpatients with chronic gastritis, confirmed by endoscopic examination. H pylori status was evaluated by histology (modified Giemsa staining), the H pylori stool antigen test (n=20), and the 13C urea breath test (n=27), as described in the Maastricht consensus report. Results: The mean amount of 8-OHdG (&mgr;g/g creatinine) in 77 subjects was 18.07 ± 13.49 x 10-3 &mgr;g/g creatinine. The levels of urinary 8-OHdG in the H pylori-positive gastritis patients were also significantly higher than those in the H pylori-negative gastritis patients (P=0.003, respectively, 20.42 ± 13.33 x 10-3 &mgr;g/g creatinine, 13.16 ± 12.71 x 10-3 &mgr;g/g creatinine). The level of urinary 8-OHdG was markedly higher in patients with gastric atrophy and intestinal metaplasia than in those without (P=0.000, P=0.002, respectively). There were significant correlations between levels of urinary 8-OHdG and both the atrophy score (r=0.441, P=0.000) and the intestinal metaplasia score (r=0.436, P=0.000). Conclusions: 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.

Anti-cyclic citrullinated Peptide frequency in patients with chronic hepatitis C virus infection and effect of presence of systemic disease.

OBJECTIVE Patients with chronic hepatitis C virus (HCV) infection may show a variety of rheumatic symptoms and signs. Anti-cyclic citrullinated peptide (anti-CCP) is widely used as as a marker, particularly for rheumatoid arthritis (RA), and may be positive in some diseases that also cause arthritis, such as systemic lupus erythematosus, familial Mediterranean fever, Behçets disease, and psoriatic arthritis. MATERIALS AND METHODS Blood samples were obtained (in routine protocols) from 57 patients with chronic HCV infection from the Gastroenterology Clinic of Ataturk University and Infectious Disease Clinic of Erzurum Region Research and Education Hospital. Normal sera were obtained from volunteer blood donors at Ataturk University. RESULTS Anti-CCP antibodies were found in 5 chronic HCV patients with RA. The patient with the highest anti-CCP antibody level had RA. No patient in the control group was positive for anti-CCP antibodies. CONCLUSION Anti-cyclic citrullinated peptide (anti-CCP) antibodies should be measured frequently in patients with HCV and an additional systemic disease, such as end-stage chronic renal failure, chronic obstructive airway disease, and decompensated liver cirrhosis, to differentiate RA from non-RA arthropathy.