No abstract

Behçet's disease (BD) is a systemic vasculitis of unknown aetiology. Its pathogenesis is related to endothelial cell dysfunction, humoral immune defects, and immune system dysregulation. The aim of this study was to investigate the possible role of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in the pathogenesis of BD. We also investigated whether disease activity, age, or duration of BD correlates with VEGF and bFGF. We studied 33 patients and 20 healthy controls. Vascular endothelial growth factor and bFGF serum levels were measured by enzyme-linked immunosorbent assay. We measured acute phase reactants, including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). The mean serum VEGF level was significantly higher in patients with BD (398.8+/-222.2 pg/ml) than the control group (193.0+/-122.4 pg/ml) (P=0.002). The levels were similar in both active and inactive BD (P=0.675) but did not correlate with disease duration, CRP, ESR, or age (P>0.05 for each). The bFGF was below detection limits in 18 of 33 patients with BD and ten of 20 controls, and its mean serum level was higher in BD patients (42.4+/-76.9 pg/ml) than controls (29.0+/-9.1 pg/ml), but this difference was not statistically significant (P=0.232). The bFGF levels were similar in both active and inactive BD (P=0.09) and, in patients, correlated with disease duration and CRP (r=0.58, P=0.02; r=-0.57, P=0.02, respectively) but not with ESR or age (P>0.05 for each). Vascular endothelial growth factor may be more important in the pathogenesis of BD than bFGF. Neither growth factor is an activity criterion or inflammatory marker in BD.

The levels of oxidants xanthine oxidase (XO), nitric oxide (NO), and malondialdehyde (MDA) and of the antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione reductase (GRD) were determined in plasma within 24 h after onset of hemorrhagic stroke in 17 patients (9 men and 8 women, aged 60.7+/-11.5 yr) and in 20 healthy controls (12 men and 8 women, aged 62.5+/-8.3 yr). Compared to controls, the plasma SOD and total superoxide scavenger activities (TSSA) were significantly lower and the NO levels were significantly higher among the stroke patients. XO showed a slight, nonsignificant increase in the patients, but the levels of MDA, NSSA, GRD, and GSH-Px did not show any significant differences between the two groups. The hemorrhage volume was negatively correlated with the initial score of the Glasgow Coma Scale and a positive correlation with lethal outcome, but it did not correlate significantly with any of the measured parameters. The results suggest that free radicals might play a role in the development of brain injury following brain hemorrhage.

Hepatitis C virus (HCV) and hepatitis G virus (HGV) belong to the same family of flaviviridea. A causative role of HCV infection in the pathogenesis of non-Hodgkin's lymphoma (NHL) has been discussed widely. Little is known about the possible association between NHL and HGV discovered recently. In this study, anti-HCV and HGV-RNA prevalence were investigated in a group of 70 patients with NHL. The results were compared to a control group of 70 age- and sex-matched healthy subjects. One patient in each group (1.4%) was found to be anti-HCV-positive; the difference was not statistically significant (P > 0.05). Five subjects in the patient group (7.1%) were positive for HGV-RNA, while a single subject was positive in the control group (1.4%); the difference was not statistically significant (P > 0.05). Odds ratios for anti-HCV and HGV-RNA were 1 and 5.30, respectively. Our findings suggest that neither HCV nor HGV are causative or contributing factors in the aetiopathogenesis of NHL.

Intercellular adhesion molecule-1 (ICAM-1) is a membrane-bound molecule primarily involved in cell-cell adhesive interactions of the immune system. It is a cytokine-induced glycoprotein involved in the recruitment of cells into tissues undergoing inflammatory responses. The levels of soluble ICAM-1 were measured in sera of patients with systemic lupus erythematosus (SLE) using sandwich enzyme-linked immunoassay. Serum levels (mean +/- SD) of soluble ICAM-1 (sICAM-1) were significantly higher in 24 patients with SLE than in 20 controls (372+/-42 ng/dL vs 231+/-29 ng/dL, P < 0.001). A statistically significant positive correlation was observed between sICAM-1 levels and SLE disease activity index (SLEDAI) score in SLE patients, and no correlation was found between sICAM-1 and CRP, SLEDAI and CRP, or SLEDAI and ESR in patient groups (P>0.05). These findings suggest that sICAM-1 measurement may serve as an additional serologic marker of disease activity in patients with SLE.

Background: Environmental pollution exposes humans to toxic substances. Herein we present 5 family members aged20-54 years that were poisoned by liquid mercury.Case Reports: Case 1 presented to our clinic with cough, fever, and night sweats. The patient had neutropenia, anemia,and pneumonia, rapidly developed acute respiratory distress syndrome (ARDS), and died on day 4 of hospitalization.Her WBC count was 0.4 × 10³ mm-3 (normal range: 4.3-10.3 × 103 mm-3) and Hb was 10.8 g dL–1 (normal range: 11.5-16.0 g dL–1). Case 2 presented with bicytopenia; the leukocyte count was 1.3 × 103 mm-3 (normal range: 4.3-10.3 × 103mm-3) and the PLT count was 88 × 103 mm-3 (normal range: 150-400 × 103 mm-3). Cases 2 and 3 had toxic peripheralneuropathy. The PLT count in case 3 was 123 × 103 mm-3 (normal range: 150-400 × 103 mm-3). Cases 4 and 5 presentedwith fatigue and headache; these 2 patients did not have positive findings, apart from high levels of mercury in theblood. We have written informed consent.Conclusion: We think that heavy metal exposure—although rare—should be considered in patients that present withnumerous symptoms involving multiple systems, including the cardiovascular, respiratory, and neurological systems.The present report is unique in that in describes mercury poisoning in 5 members of the same family.

Although both chronic active hepatitis-B (CAH-B) and liver cirrhosis (LC) are characterised by various degrees of inflammation and hepatocyte necrosis, in advanced stage cirrhosis, marked fibrosis develops and inflammation and tissue necrosis diminishes. In this study, we aimed to investigate serum tumour necrosis factor-alpha (TNF-alpha) concentration in patients with CAH-B and LC and its relationship to disease activity. Serum samples were taken from 30 patients with CAH-B and 30 with LC at different stages of the disease. TNF-alpha concentrations were measured by the ELISA technique. Results were compared with those of 30 healthy controls. Mean plasma TNF-alpha levels were found as 2.47 +/- 2.98, 0.8 +/- 1.21 and 0.72 +/- 1.08 pg/ml in CAH-B, LC and control groups, respectively. TNF-alpha levels were significantly higher in CAH-B group than LC and control groups (p <0.01 and p < 0.05, respectively). Although mean plasma TNF-alpha level of cirrhotic patients at Child-A stage was markedly high (3.31 +/- 0.15), no significant difference has been found between LC and control groups (p > 0.05). TNF-alpha concentrations were positively correlated with hepatitis activity index (Knodell's score) in CAH-B group whereas negatively correlated with Child-Pugh score in LC group (r =0.73, p < 0.01 and r = -0.42, p < 0.05, respectively). Our study showed that TNF-alpha level increases in patients with CAH-B correlated with histologic activity index. So it can be used to evaluate disease activity. Additionally, marked reduction of TNF-alpha concentration in advanced cirrhosis suggested that TNF-alpha production is determined by hepatic damage and inflammation.

Objective: To report a case of brucella infection presenting with thrombotic thrombocytopenic purpura (TTP) that responded well to plasma and antimicrobial treatment infusion. Case Presentation and Intervention: A 51-year-old man with moderate confusion, depressed mood and dysarthria was admitted. He was chronically ill, with fever (38.5°C), anemia, jaundice and petechial-purpuric skin lesions. Neurological examination revealed diminished consciousness with a Glasgow coma scale score of 7 and +1 neck rigidity. The hemoglobin and platelet counts were decreased and reticulocyte index, erythrocyte sedimentation rate, as well as serum lactate dehydrogenase and renal dysfunction were elevated. TTP was a possible diagnosis and the patient responded well to plasma infusion and antimicrobial treatment. Conclusion: This report shows that therapy of underlying infection together with plasma infusion may be a successful treatment option for brucellosis-induced TTP.