Oxidative status and the response to pegylated-interferon alpha2a plus ribavirin in chronic genotype 4 HCV hepatitis.

Oxidative stress may play a pathogenic role in chronic hepatitis C (CHC). The present study examined the oxidative status in plasma of patients with CHC who received pegylated interferon and ribavirin therapy. The following groups were included: (1) sustained virological response (28 patients), (2) null response (26 patients), (3) breakthrough (24 patients), (4) relapse (24 patients), (5) spontaneous cure (23 patients) and (6) twenty five normal subjects as a control group. Markers of oxidative stress including plasma malondialdehyde, nitric oxide, reduced glutathione, total antioxidant capacity and uric acid as well as serum ALT, AST, alkaline phosphatase, total bilirubin, albumin, prothrombin time were studied. The study indicated significant decline in reduced glutathione and total antioxidant capacity and markedly elevated levels of malondialdehyde and nitric oxide in all groups compared with the controls. Null response group had the highest levels of malondialdehyde and nitric oxide. Nitric oxide was significantly higher in those with null response compared with all other groups and with control subjects. Uric acid was significantly higher in spontaneous cure group compared with all other groups and with the controls. We concluded that CHC patients had increased oxidative stress. The oxidative status in plasma of these patients was not changed by antiviral therapy. The study also showed an important contribution of nitric oxide in null response patients. High serum uric acid did not interfere with the response and/or did not predict the response to antiviral therapy.

Anti-apolipoprotein A-I antibodies and paraoxonase 1 activity in Systemic Lupus Erythematosus.

Systemic lupus erythematosus (SLE) patients have an increased risk of atherosclerosis. Identification of at-risk patients and the pathogenesis of atherosclerosis in SLE remain elusive. Paraoxonase 1 (PON1) and anti-apolipoprotein A-I antibody (anti-Apo A-I) appear to have a potential role in premature atherosclerosis in SLE. The aim of this work was to study PON1 activity and anti-Apo A-I antibody in SLE female patients and to demonstrate their relations to disease activity as well as disease related damage. Forty SLE female patients and 40 apparently healthy volunteers were included. Anti-Apo A-I antibodies levels and PON1 activity levels were assessed. Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) and systemic Lupus International Collaboration Clinics (SLICC)/American College of Rheumatology (ACR) damage index were preformed in all patients. Compared with controls, SLE patients showed significantly lower PON1 activity and significantly higher titers of anti-Apo A-I. Anti-Apo A-I antibody titers correlated inversely with PON1 activity. Elevated titers of anti-Apo A-I antibody and reduced PON activity were related to increased SLEDAI and (SLICC/ACR) damage index scores. We concluded that there is decreased PON1 activity and formation of anti-Apo A-I antibodies in female patients with SLE. SLE-disease activity assessed by SLEDAI and SLE disease related organ damage assessed by SLICC/ACR damage index are negatively correlated with PON1 activity and positively correlated with anti-Apo A-I antibodies. PON1 activity and anti-Apo A-I antibodies might be involved in the pathogenesis of atherosclerosis in SLE patients.

A comparative study on efficacy of UVA1 vs. narrow-band UVB phototherapy in the treatment of vitiligo.

BACKGROUND/PURPOSE: Narrow-band ultraviolet B (NB-UVB) is considered the most effective and safe initial treatment for moderate-to-severe vitiligo but phototoxicity and possible carcinogenicity are the reported side effects. Ultraviolet A1 (UVA1) phototherapy has overlapping biological effects to NB-UVB and is relatively free of side effects associated with other phototherapy regimens. METHODS: Forty patients with vitiligo were included in this prospective, randomized controlled comparative clinical trial. Twenty patients received NB-UVB and 20 received UVA1 three times weekly for 12 weeks. The UVA1 group was divided into two subgroups. Ten patients received moderate and 10 received low dose of UVA1. Serum samples were collected before and after 36 sessions to assess soluble interleukin 2 receptor level. Patients were clinically evaluated before therapy then monthly according to Vitiligo Area Scoring Index (VASI) and Vitiligo European Task Force (VETF) scores. In addition, extent of response was determined by a blinded dermatologist comparing before and after therapy photographs. Pattern of response and side effects were recorded. RESULTS: NB-UVB was superior to UVA1 with a significant difference in blinded dermatological assessment (P<0.001), percentage change in VASI score (P<0.001) and percentage change in VETF area score (P=0.001). No significant difference in side effects was observed between both groups. Comparing UVA1 subgroups, better response in moderate-dose group was found as regard to percentage change in VASI (P<0.001) and percentage change in VETF area score (P=0.001), while no significant difference was found in blinded dermatological assessment (P=0.121). CONCLUSION: NB-UVB phototherapy remains to be an effective and safe therapeutic option in vitiligo. Response to UVA1 in vitiligo seems to be dose dependent and seems to be of limited value in treatment of vitiligo as a monotherapy. Further studies combining it with other lines of therapy such as systemic steroids may prove beneficial.

The role of liver in leptin metabolism in experimental nephrotic syndrome.

Leptin is a hormone influencing food intake, energy expenditure and body weight. It is produced by adipocytes, exerts its effects on brain, endocrine pancreas and other organs by activating trans-membrane receptors and is cleared from plasma mainly by the kidneys. Several studies have suggested that leptin's effects on metabolism are mediated by the liver. Our aim was to evaluate the role of the liver in the metabolism of leptin by comparing the serum leptin level in the portal vein with that in inferior vena cava and to study the relationship between leptin and lipoprotein levels in healthy and nephrotic rats. Experimental nephrotic syndrome was conducted in rats by intraperitoneal injection of the supernatant from the kidney suspension obtained by previous unilateral nephrectomy of the same rat and complete Freund's adjuvant. There was a highly significant rise in leptin and lipid profile levels in the nephrotic rats compared with the normal rats. A highly significant increase in leptin in the inferior vena cava was detected compared with the level in the portal veins of nephrotic rats, while insignificant difference was observed in normal rats. This work has stressed the role of liver in leptin and lipid metabolism in nephrotic rats.