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Acta Cardiologica 2010-Feb

Investigation of oxidant and antioxidant pathway changes in acute rheumatic fever.

Aðeins skráðir notendur geta þýtt greinar
Skráðu þig / skráðu þig
Krækjan er vistuð á klemmuspjaldið
Abdurrahman Uner
Ertan Sal
Murat Doğan
Fatih M Sanli
Mehmet Acikgoz
Mustafa Cemek
Erdal Peker
Eren Cagan

Lykilorð

Útdráttur

OBJECTIVE

The purpose of this study was to investigate the role of oxidant stress in the clinical process and pathogenesis of acute rheumatic fever (ARF).

METHODS

The study included 33 children with ARF and 20 healthy control subjects. The diagnosis of ARF was established according to the Jones Criteria. Malondialdehyde (MDA), reduced glutathione (GSH), alpha-tocopherol, ascorbic acid, retinol and beta-carotene levels were measured as markers of oxidative stress together with some antioxidant markers.

RESULTS

Our study includes 33 (19 male, 14 female) children with ARF and 20 (11 male, 9 female) healthy control subjects. The mean age ranged between 5-16 years and 5-15 years in the study and control groups, respectively. MDA was measured as 2.1 +/- 0.9 nmol/mL in the control group, 3.3 +/- 2.7 nmol/mL in the study group before treatment, and 2.1 +/- 1.2 nmol/mL after treatment. Blood GSH levels were 48.2 +/- 12.7 mg/dL in the control group, 24.7 +/- 16 mg/dL in the study group before treatment, and 40.6 +/- 21.3 mg/dL in the study group after treatment. MDA and GSH levels prior to the treatment were found to be significantly high and low as compared with the levels of the control group, respectively (P < 0.05, P < 0.001). After treatment, statistically important decrements and increments were determined in the levels of MDA (P < 0.05) and GSH (P < 0.01), respectively. Furthermore, alpha-tocopherol, retinol and beta-carotene levels prior to treatment in the study group, were significantly lower in comparison with control group levels (P = 0.05, P < 0.05, P < 0.01, respectively).

CONCLUSIONS

We suggested that tissue damage in ARF may not only occur in the presence of increased oxidative stress, but also as a consequence of decreased antioxidant markers.

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