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Abstract
The pathogenesis of Henoch-Schönlein Purpura (HSP) is still controversial. The aim
of our study was to investigate the role of oxidative stress and cyclooxygenase (CO)
pathway products in the pathogenesis of HSP. In order to investigate this, malondialdehyde
(MDA) levels, indicating lipid peroxidation, prostaglandin E (PGE)-like activity as
inflammatory mediator and vitamin E (vit-E) levels indicating anti-oxidant status
were studied in a group of 10 children with HSP (five girls and five boys, aged 6–21
years, mean 10.7 years), both in the acute and recovery phase of the disease and in
five age and sex-matched healthy children as a control group. The patients were also
grouped into low and high clinical score groups. Plasma levels of MDA and PGE-like
activity were significantly elevated in the active phase of HSP compared to the recovery
phase. Vit-E levels were significantly reduced in the active phase compared to the
recovery phase. The plasma levels of PGE-like activity of the patients obtained in
the active phase were significantly higher than the levels of the control group, whereas
the levels of the recovery phase were significantly lower than in the control group.
No such difference between the controls and MDA and vit-E levels in the patient group
was shown. No correlation between the clinical scores and the parameters studied could
be found. Our findings indicate that oxidant stress and CO pathway products may play
a role in the pathogenesis of HSP.
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Article info
Publication history
Accepted:
July 17,
1998
Received:
July 7,
1998
Identification
Copyright
© 1998 Published by Elsevier Inc.
