Experimental obstructive jaundice results in oxidized low-density-lipoprotein accumulation in surgical wound of rats.

INTRODUCTION: Mounting evidence suggests that impaired wound healing is a well-defined consequence in obstructive jaundice and, as redox-regulated processes are relevant to wound healing, it is not unreasonable to suppose that oxidative stress associated with lipid peroxidation in cholestasis might be a systemic phenomenon probably comprising all tissues and organs, including wounds. The aim of the present investigation was to analyse the lipid peroxidation status of surgical wounds, in terms of oxidized low-density-lipoprotein (oxLDL) accumulation in experimental obstructive jaundice. METHODS: Sixteen Wistar-Albino rats weighing 200-230 gr were randomly divided into two groups. Group I (n = 8) was designed as the prolonged obstructive jaundice group and was subjected to bile duct ligation. Group II (Sham-control, n = 8) rats underwent laparotomy alone and bile duct was just dissected from the surrounding tissue. Histopathological evaluation, immunohistochemical screening and immunoflourescent staining of the surgical wound was conducted to the bile-duct ligated rats and control group on the 21st postoperative day. RESULTS: Wound healing was found to be impaired in jaundiced rats histopathologically. When compared with the control group, significant positive oxLDL staining and intracellular accumulation of TNF-alpha, IL-2 and IL-6 was detected in the wound sections of the prolonged obstructive jaundice group. CONCLUSION: Our present data is the first in the literature, indicating significant oxLDL accumulation in surgical wounds of cholestatic rats, which might be one of the results of systemic oxidative stress leading to deficient healing capacity as a consequence of persistent inflammation.

Plasma levels of tumor necrosis factor-alpha and interleukin-6 in obsessive compulsive disorder.

AIM: Recent research implicated place of an immune mechanism in the pathophysiology of obsessive-compulsive disorder (OCD). Despite increasing evidence involvement of cytokine release in OCD, results of the studies are inconsistent. The aim of this study was to evaluate the plasma levels of the cytokines; tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in OCD patients. METHODS: Plasma concentrations of TNF-alpha and IL-6 were measured in 31 drug-free outpatients with OCD, and 31-year age and sex-matched healthy controls. TNF-alpha and IL-6 concentrations in blood were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: Both TNF-alpha and IL-6 levels showed statistically significant increases in OCD patients compared to controls (P < .000, P < .001, resp.). In addition, the age of onset was negatively correlated with TNF-alpha level (r = -.402, P = .025) and duration of illness was weakly correlated with IL-6 levels (r: .357; P: .048) in patients group. CONCLUSION: OCD patients showed increases in TNF-alpha and IL-6 levels compared to the healthy controls. This study provides evidence for alterations in the proinflammatory cytokines which suggest the involvement of the immune system in the pathophysiology of OCD.

Effect of hyperthyroidism and propylthiouracil treatment on liver biochemical tests.

Liver biochemical test (LBT) changes can be commonly observed in hyperthyroid patients. Those kinds of changes could also be observed because of propylthiouracil (PTU) therapy. We prospectively evaluated LBT changes because of PTU use for 1 year in patients who had been diagnosed with hyperthyroidism first. We studied 64 patients who had been diagnosed with hyperthyroidism. These patients took at least 1-year PTU treatment. We analysed LBT at diagnosis and after 2 and 12 months of treatment with PTU. Prior to PTU treatment, 30 (46.8%) of the 64 patients had at least one LBT abnormality. We observed at least one LBT abnormality in 11 (32%) patients after 2 months and nine (26%) patients after 12 months of treatment with PTU in 34 patients whose CBT were normal before treatment. We did not observe any deterioration in clinical picture and bilirubin levels. Elevated serum LBT during the pretreatment and PTU treatment period is common and usually transient and asymptomatic. PTU could be used for long times by lowering the dose and close follow-up in patients who have elevated LBT during the pretreatment and after PTU treatment period.

Common variable immunodeficiency in an adult with recurrent pneumonia.

Primary immunodeficiency syndromes are rarely diagnosed among adults. Common variable immunodeficiency (CVID) is a congenital immunological disorder characterized by defective antibody production. In this report, we describe a 35-year-old male suffering from a common variable immunodeficiency, referred to us because of a lobar pneumonia. He had a history of recurrent pulmonary infections, which was present months before presentation, suggesting hypogammaglobulinemia. We found a severe hypogammaglobulinemia, which confirmed the diagnosis of CVID. His immunoglobulin profiles upon admission before infusion of immunoglobulin (normal ranges) were: IgG < 1.41 (8-17) g/l, IgA 0.25 (0.85-4.9) g/l, IgM 0.182 (0.5-3.7) g/l, and IgE < 2 (< 120) IU/ml. His HLA profiles were HLA A2 A26, B18 B38, Cw7, DR11 and DQ7 DQ9. He was treated with intravenous immunoglobulin. After this regimen, his IgG was maintained at > 6.0 g/L. On follow up, he has been free of opportunistic infections. In conclusion, CVID should be considered in the differential diagnosis of recurrent pneumonia in adults.

IL-6 levels in gingival crevicular fluid (GCF) from patients with non-insulin dependent diabetes mellitus (NIDDM), adult periodontitis and healthy subjects.

Cytokines play an important role in the pathology associated with chronic inflammatory diseases. One of these cytokines, interleukin 6 (IL-6) is a major mediator of the host response to tissue injury, infection and bone resorption. In the present study, gingival crevicular fluid (GCF) level of IL-6 was determined in patients with non-insulin dependent diabetes mellitus (NIDDM) with periodontitis, adult periodontitis, and healthy controls by use of an enzyme linked immunosorbent assay (ELISA). Twenty-four NIDDM patients with periodontitis, twenty-four adult periodontitis and twenty-four healthy controls were selected for the study. GCF sampling was performed on the vestibular aspects of maxillary incisors and canine teeth. Plaque index (PI), gingival index (GI), gingival bleeding time index (GBTI), probing depth (PD) and probing attachment levels (PAL) were recorded from each sampling area and also the entire dentition. NIDDM and adult periodontitis patients had numerous sites with radiographic evidence of alveolar bone resorption, loss of attachment and pocket depth greater than 3 mm. The mean GCF IL-6 level was 2.43 +/- 0.97 ng/ml in NIDDM patients, 1.31 +/- 0.92 ng/ml in adult periodontitis and 0.62 +/- 0.58 ng/ml in healthy subjects, respectively (p < 0.05). GCF IL-6 levels were markedly higher in NIDDM and adult periodontitis groups compared to the healthy controls. No correlation was found between GCF IL-6 levels and all clinical parameters. These findings suggested that GCF IL-6 levels were significantly higher in the area of inflammation and periodontal destruction locally. The high IL-6 levels in NIDDM patients might be due to different microbial flora in periodontal pockets and altered immune system. Future studies are needed to evaluate the complex interaction among IL-6 GCF levels, host response and local microbial environment in the NIDDM patients.

Comparison of sputum and serum eosinophil cationic protein (ECP) levels in nonatopic asthma and chronic obstructive pulmonary disease.

The aim of the present study was to investigate whether sputum eosinophil cationic protein (ECP) concentrations could be a useful marker in the differential diagnosis between intrinsic asthma and chronic obstructive pulmonary disease (COPD). For this purpose total blood eosinophil counts were obtained and concentrations of serum and sputum ECP from 10 nonatopic asthmatics with a mild attack and 9 COPD patients with acute exacerbation were measured by radioimmunoassay. Mean serum ECP concentration was 54.3 +/- 23.0 micrograms/L in the asthmatic group and 83.3 +/- 79.2 micrograms/L in the COPD group (p: n.s.). In the group of asthmatics mean sputum ECP level was 984.5 +/- 1245.5 micrograms/L/g sputum and in the COPD group it was 417.5 +/- 363.5 micrograms/L/g sputum. There was no significant difference in sputum ECP levels between patients with asthma and COPD. We conclude that neither sputum nor serum ECP levels are useful markers in differential diagnosis of asthma attack and acute exacerbation of COPD.