[Homocysteine, vitamin B-12, folic acid and the cognitive decline in the elderly]. / Homocystéine, vitamine B12 et acide folique dans le déclin cognitif chez les personnes âgées.

Hyperhomocysteinemia is a risk factor for neurological diseases, but the underlying pathophysiology has not been adequately explained. Mild hyperhomocysteinemia, which is sometimes associated with a low plasma level of vitamin B9, B12 and folic acid, is responsible in the toxicity in neural cell by activating NMDA receptor. Indeed, even if vitamin supplementation has clearly proven its efficiency on lowering plasma levels of homocysteine, recent studies do not show any positive effect of vitamin therapy on cognitive function. The hypothesis that this therapy is inefficient has been recently reinforced by two randomized trials on the effects of vitamin supplementation. Several hypotheses still need to be explored: Mechanisms of homocysteine toxicity and that of total uselessness of vitamin supplementation; the possible need to complete the actual data with further, more powerful studies in order to prove the role of homocysteine in the development of neurodegenerative diseases and a clinical effect of vitamin therapy.

[Predictive value of the markers of inflammation in acute coronary syndromes]. / Valeur prédictive des marqueurs de l'inflammation au cours des syndromes coronaires aigus.

This prospective study aims to establish the association between markers of inflammation (CRP and fibrinogen) and the severity of coronary lesions in patients with acute coronary syndromes. For this purpose, Plasma CRP, fibrinogen and troponin I were measured upon admission in 143 consecutive patients presenting with an acute coronary syndrome who underwent subsequently coronarography . Mean age is 55.5+/-11.6 years. Sex Ratio is 3.61 in favour of men; 68% of our patients presented with acute myocardial infarction with ST segment elevation; 23% with an unstable angina and 9% with an acute myocardial infarction without ST segment elevation. 31 patients (24.4%) have not any significant coronary lesion. Mean CRP level in these patients is (6.82+/-8.2 mg/l) lower than that measured in patients with significant lesions (17.4+/-26.9 mg/l; p=0.02). In patients with pathologic coronarogram, we demonstrated that the mean CRP level is higher in patients heaving one or more lesion of at least 70% of diameter stenosis than that in patients with no significant lesions (21.28+/-30.45 mg/l vs 11+/-14.2 mg/l; p=0.05). The mean CRP level grows with the number of proximal and significant stenoses. (CRP level in patients with one significant stenosis: 11+/-14.2 mg/l vs 27.45+/-39.67 mg/l in patients heaving 3 lesions; p=0.02. CRP level in patients with one proximal lesion: 14.35+/-19.8 mg/l vs 50.33+/-65 mg/l in patients heaving 3 proximal lesions; p=0.007). Fibrinogen levels measured upon admission in patients having significant lesions are higher than those measured in patients with normal coronary arteries (4.7+/-1.81 mg/l vs 3.93+/-1.69 mg/l; p=0.02). Compared with that measured in patients having distal lesions, the fibrinogen level is higher in case of proximal and multiple coronary lesions. There is a significant gradual increase in fibrinogen levels with increasing of the number of proximal coronary lesions and the degree of diameter stenosis. Multivariate logistic regression analysis showed that a CRP level higher than 10 mg/l is an independent predictive factor of the presence of the presence of significant coronary lesions (p=0.006; OR = 8.62; CI=0.7 to 7.4). We conclude that high CRP and fibrinogen plasma levels are associated with extended, severe and proximal coronary lesions.