La Clinica terapeutica · 2007
[Hyperhomocysteinemia, oxidative stress, endothelial dysfunction in postmenopausal women].
Аннотация на английскомСтатьяНазвание и аннотация: Перевод пока не подготовлен
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Pulvirenti D, Signorelli S, Sciacchitano S, Di Pino L, Tsami A, Ignaccolo L, Neri S
Аннотация
AIM: Menopause seems to accelerate the development of atherosclerosis and cardiovascular diseases. Several studies show a significant correlation between elevated homocysteine serum levels and increased cardiovascular risk. Oxidative stress is involved in the pathophysiology of endothelial dysfunction and atherosclerosis. Our study aim was to assess the correlations between intima-media thickness, homocysteine serum levels and oxidative stress both in fertile and postmenopausal women.
MATERIALS AND METHODS: We have investigated 34 fertile women (mean age = 42 +/- 2 yrs; BMI = 21 kg/m2 and 34 postmenopausal women (48 +/- 3 yrs; BMI = 22 +/- 2 kg/m2).
RESULTS: Results show increased levels of homocysteine, oxidative stress and intima-media tickness (IMT) in postmenopausal women. having a positive correlation with IMT.
CONCLUSIONS: The positive correlations between serum levels of homocysteine and IMT in postmenopausal women reinforce the idea that a hyperhomocysteinemia may play a role in the progression of atherosclerosis. The lack of estrogens could be a pathophysiologic risk factor for endothelial damage via an augmented oxidative stress. Clin
MATERIALS AND METHODS: We have investigated 34 fertile women (mean age = 42 +/- 2 yrs; BMI = 21 kg/m2 and 34 postmenopausal women (48 +/- 3 yrs; BMI = 22 +/- 2 kg/m2).
RESULTS: Results show increased levels of homocysteine, oxidative stress and intima-media tickness (IMT) in postmenopausal women. having a positive correlation with IMT.
CONCLUSIONS: The positive correlations between serum levels of homocysteine and IMT in postmenopausal women reinforce the idea that a hyperhomocysteinemia may play a role in the progression of atherosclerosis. The lack of estrogens could be a pathophysiologic risk factor for endothelial damage via an augmented oxidative stress. Clin