8-Iso-prostaglandin F2α as a potential biomarker in patients with unipolar and bipolar depression.

OBJECTIVE: Previous studies have shown that the disturbance of redox homeostasis plays a role in the pathogenesis of mood disorders. It is currently unclear whether oxidative stress parameters can be used as biomarkers (state vs. trait). The aim of the present study was to investigate oxidative stress markers in patients with major depressive disorder (MDD) and bipolar disorder (BP) in acute depressive episodes and remission, and healthy individuals. PATIENTS AND METHODS: Thirty-two patients with a diagnosis of MDD, 32 patients with a diagnosis of BP and 32 matched healthy controls were included in the study. We measured the serum levels of markers of oxidative damage, including 8-hydroxy-2'-deoxyguanosine (8-OHdG), 8-Iso-prostaglandin F2α (8-iso-PGF2α; 8-isoprostane), and malondialdehyde (MDA), and also serum activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and glutathione reductase (GR) in both acute and remission phase, and in control group. RESULTS: After controlling for the effects of age, sex, body mass index, and smoking status, serum 8-iso-PGF2α levels were significantly higher in both patient groups compared to controls, regardless of disease phase. The activities of GPX and GR were significantly lower in the acute phase in MDD patients compared to controls. Serum GR activity was lower in both acute and remission phase in MDD compared to BP. CONCLUSIONS: Our results suggest that both MDD and BP are associated with a disturbed redox balance with a particularly pronounced increase in serum 8-iso-PGF2α levels in both groups and the presence of glutathione metabolism disorders in MDD patients. Further research is needed to confirm the importance of oxidative stress parameters as potential biomarkers of MDD and BP.

Hepatitis C virus-related hepatocellular carcinoma and liver cirrhosis.

PURPOSE: The aim of this study was to compare patients with hepatocellular carcinoma (HCC) associated with hepatitis C virus (HCV) infection with patients with liver cirrhosis associated with HCV virus infection. METHODS: Forty-five patients were prospectively analyzed, all with HCV infection. Patients were divided into 2 groups. The first group consisted of 21 patients with histologically proven HCC and the second one consisted of 24 patients with liver cirrhosis without HCC. PCR was carried out in order to diagnose active HCV infection and HCV genotyping. RESULTS: There was no statistically significant difference in the structure of the compared groups of patients in relation to sex and age. In 76.19% of the patients with HCC cirrhosis preceded HCC, while 23.81% of the patients had chronic hepatitis. The prevalence of genotypes in the HCC group was 1a in 4.76%, 1b in 80.95% and 2a in 14.29%. In the group with liver cirrhosis 1a was detected in 20.83%, 1b in 45.83%, 2a in 12.50%, 2b in 4.17% and 3a in 16.67% of the patients. The prevalence of genotype 1b was significantly higher among HCV RNA positive patients with HCC compared to the group with liver cirrhosis and HCV RNA positive patients (x(2)=4.48; p=0.034). In the group where cirrhosis preceded HCC, genotype 1b was found in 75% of the cases, genotype 2a in 18.75%, and genotype 1a in 6.25%. Genotype 1b was detected in 100% of patients with chronic hepatitis and HCC. CONCLUSION: The role of HCV infection in the development of HCC has not been fully clarified. Most authors evaluate the role of individual genotypes in the pathogenesis of HCC. This study has shown that the dominant genotype found in patients with HCC is 1b.

Coagulation status and the presence of postoperative deep vein thrombosis in patients undergoing laparoscopic cholecystectomy.

BACKGROUND: Venous thromboembolism is a relevant social and health care problem because of its high incidence among patients who undergo surgery (20-30% after general surgical operations and 50-75% after orthopedic procedures), its pulmonary embolism-related mortality rate, and its long-term sequelae (postthrombotic syndrome and ulceration), which may be disabling. This study aimed to determine the coagulation status and the presence of postoperative deep vein thrombosis (DVT) in patients undergoing laparoscopic (LC) and open cholecystectomy (OC). METHODS: Prospectively, 114 patients were randomized into two groups. group 1 (58 patients undergoing LC) and group 2 (56 patients who are undergoing OC). The coagulation parameters (prothrombin time [PT], partial thromboplastin time [PTT], D-dimer, prothrombin F1 + 2, antithrombin III, and factor VII) were monitored preoperatively and during the operation, then 24 and 72 h after the operation. The patients in both groups underwent color duplex scan examination preoperatively, then 3 and 7 days after surgery to establish the presence of DVT. None of the patients in either group received thrombosis prophylaxis. RESULTS: In the LC group, postoperative DVT developed in four patients (6.9%; in the calf veins of 3 patients and in the popliteal vein of 1 patient). In the OC group, nine patients (16.07%) had postoperative DVT (in the calf veins of 7 patients and in the popliteal and femoral veins of 2 patients). The plasma levels of monitored parameters in the patients of both groups were altered, but the difference between the groups was not statistically significant. For the patients in both groups who experienced DVT, only the decrease of factor VII had statistical significance (p < 0.05). CONCLUSIONS: The incidence of postoperative DVT among the patients who underwent OC was higher than among the patients who underwent LC (p < 0.05). The decrease in factor VII among the patients who underwent surgery could be a potentially useful parameter indicating the patients at high risk for developing DVT.