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Resume Introduction Les effets indesirables (EI) psychiatriques des fluoroquinolones sont connus depuis longtemps, mais peuvent etre non diagnostiques. Ce travail analyse les cas notifies aux centres regionaux de pharmacovigilance. Methodes Les cas d'EI psychiatriques dus aux fluoroquinolones notifies entre janvier 1985 et juin 2002 ont ete extraits de la base de donnees nationale. Une analyse descriptive a ete faite, incluant : âge, sexe, nature de l'EI, fluoroquinolones en cause, gravite, evolution. Resultats En 17 ans, 590 cas ont ete notifies, concernant 273 hommes et 316 femmes (non precise dans un cas) ; l'âge moyen etait de 66 ans (mediane : 70 ans, extremes : 12–102 ans). Les principaux EI psychiatriques etaient : confusion (51 %), hallucinations (27 %), agitation (13 %), delire (12 %), insomnie (8 %), somnolence (4 %) (plusieurs EI pouvaient etre notifies pour chaque patient). Les molecules en cause etaient : ofloxacine (28 %), pefloxacine (27,5 %), ciprofloxacine (24,6 %), norfloxacine (18,5 %), levofloxacine (1,2 %), sparfloxacine (0,8 %), enoxacine (0,7 %), lomefloxacine (0,7 %) (total superieur a 100 % en raison de la presence de plusieurs fluoroquinolones dans certains cas). Les cas graves representaient 21,7 % des dossiers, essentiellement representes par des hospitalisations ou des prolongations d'hospitalisation. Dans 88,5 % des cas, il y a eu regression complete de l'effet (dans 9,5 % des cas, l'evolution etait en cours ou inconnue). Conclusion Le nombre de cas est relativement faible, mais la sous-notification est probablement importante. La possibilite de survenue de ce type d'EI doit donc etre presente a l'esprit, particulierement chez les sujets âges, ou la posologie des fluoroquinolones doit etre adaptee a la fonction renale.

To investigate the effects of selenium or beta-carotene supplementation in human immunodeficiency virus (HIV)-infected patients, who are known to have deficiencies of selenium and vitamin A, we evaluated the blood enzymatic antioxidant system, including superoxide dismutase (SOD), selenodependent glutathione peroxidase (GPX), and catalase (Cat); glutathione (GSH) status; and plasma selenium concentration. The placebo group consisted of 18 HIV-infected patients with no supplementation, the selenium group was composed of 14 patients receiving oral selenium treatment, and the beta-carotene group comprised 13 patients receiving oral beta-carotene supplementation. All groups were studied for 1 y. At the beginning of the study, a significantly higher SOD activity (P < 0.001) was observed in all HIV-infected patients compared with uninfected control subjects, and GPX activity at baseline was higher in the placebo (P < 0.004) and selenium (P < 0.014) groups than in the control subjects. These higher enzyme activities could be related to an increased synthesis of these enzymes in erythrocyte precursors under oxidative stress. Moreover, we observed significantly lower GSH values in all HIV-infected patients than in control subjects at the beginning of the study (P < 0.001). After selenium or beta-carotene supplementation, no significant difference was observed for SOD activity compared with baseline. On the contrary, GPX activity increased significantly after selenium treatment (P < 0.04 between 3 and 6 mo), whereas a slight increase was found after beta-carotene treatment. Similarly, a significant increase in GSH values was observed at 12 mo compared with baseline both after selenium supplementation (P < 0.001) and beta-carotene supplementation (P < 0.01). Because GPX and GSH play an important role in the natural enzymatic defense system in detoxifying hydrogen peroxide in water, selenium supplementation could be of great interest in protecting cells against oxidative stress. The lower efficiency of beta-carotene could be attributed to the seriousness of the pathology at the time of recruitment into the beta-carotene group.

SUMMARY Malondialdehyde (MDA), a peroxidative end-product released during polyunsaturated fatty acid degradation, reacts strongly with lysine residues of cellular proteins. MDA-modified proteins become immunogenic and may elicit specific autoantibody formation. We hypothesized that systemic diseases in which inflammatory events occur, could be an interesting model for studying oxidative stress. A few studies have suggested that MDA-modified proteins may exist in systemic diseases, and that autoantibodies to MDA-modified structures might reflect this oxidative process. Autoantibodies to MDA-modified epitope(s) were therefore assayed in sera of patients with systemic lupus erythematosus (SLE, n = 29), scleroderma (SCL, n = 11), giant cell arteritis (GCA, n = 11), periarteritis nodosa (PAN, n = 10), rheumatoid arthritis (RA, n = 9), and healthy subjects (HS, n = 32). Significantly increased anti-MDA-modified epitope(s) autoantibodies were found in patients with SLE and also in other systemic diseases such as PAN and SCL. Autoantibodies to MDA-modified epitope(s) were predominantly of IgM isotype, with low levels of IgG and no IgA activity. In SLE, anti-MDA-modified epitope(s) autoantibody titres correlated strongly with systemic lupus activity measure (SLAM, r = 0·702, P = 0·0001), anti-nuclear antigen autoantibodies (ANA, r = 0·4, P = 0·029), IgG anti-cardiolipin (r = 0·558, P = 0·03) and the steroid drug regimen (r = 0·52, P = 0·004). Autoantibodies to MDA-modified epitope(s) may reflect oxidative modifications occurring in systemic diseases, and might be useful as clinical markers of SLE activity if further investigated.

We report a case of mitochondrial myopathy (MM), assessed by histological and biochemical studies. This illness was diagnosed in a 69-year-old patient with myocardiopathy revealed by ventricular arrhythmias. The originality of this case lies in the patient's age, the mode of onset and the biochemical features (i.e. normal mitochondrial enzymatic complexes but very low respiration when using glutamate as a substrate).

Background In systemic lupus erythematosus (SLE), disease severity may be related to factors such as endothelial cell damage. Objectives We tested the hypothesis that anti-endothelial cell antibodies (AECA) and plasma markers of endothelial cell dysfunction would be related to disease severity in SLE. Methods Accordingly we measured AECA by human umbilical vein endothelial cell binding, endothelial markers von Willebrand factor, soluble thrombomodulin, soluble E-selectin by ELISA, and disease severity by SLEDAI and SLICC/ACR in 35 patients with SLE. Results Despite high levels of IgG AECA (p Conclusion We conclude that IgG AECA seem to be related to disease activity in SLE, possibly in a pathogenic role. Conversely, plasma markers of endothelial cell damage seem to be an epiphenomenon and may only be related to excess inflammation in these patients.

Objectives. To evaluate the distensibility of large arteries in patients with systemic sclerosis (SSc). Design. Prospective case-control study including unselected patients with SSc. Setting. One cardiology and two internal medicine units in a teaching hospital. Subjects. Eighteen patients with SSc and controls matched for age, sex, height, weight and 24-h ambulatory blood pressure (BP). Intervention. The timing of Korotkoff's sounds (QKD interval), a newly described noninvasive ambulatory method was used to measure arterial distensibility during 24 h. Main outcome measures. Two endpoints were used: QKD 100–60 (normalized for a heart rate of 100 beats min-1 and a systolic BP of 100 mmHg) and the slope of QKD against pulse pressure. Results. The patients with SSc had a lower slope of QKD against pulse pressure than the controls (median 0.55, range 0–1.21, versus 0.92, range 0.5–1.34, respectively; P=0.003), and a lower QKD 100–60 (medians/ranges respectively 191 [162–216] and 203 [169–231]; P=0.01). Conclusions. These results indicate that arterial distensibility of large arteries is decreased in SSc.

Objective: To investigate red blood cell (RBC) and plasma fatty acids (FA) in HIV-positive patients in relation to oxidative stress and nutritional or immunologiical status. Design and Methods: FA, plasma selenium, vitamins A and E were measured in 95 patients divided into four groups according to CD4 cells. Results: Poly- and di-unsaturated FA (PUFA, DUFA) decreased and saturated FA (SFA) increased in RBC in the patients below 400/mm3 and in plasma in the patients below 50/mm3 RBC SFA correlated to CD4 cells, PUFA to MDA. Unlike vitamin E, plasma vitamin A and selenium decreased in most groups. Plasma SFA and MUFA correlated negatively to selenium and PUFA and DUFA to vitamin E. No correlation was found between PUFA and nutritional markers. Conclusion: FA seem to be modified during HIV infection by oxidative stress and disease evolution, but not by denutrition.

Antiphospholipid/cofactor antibodies are detected in only 60% of patients with systemic lupus erythematosus (SLE) with thrombosis.1 Therefore, we studied thrombophilia factors and their relation with thrombosis in patients with SLE. Forty eight consecutive patients with SLE were included (39 women, 9 men), 15 with and 33 without past thrombosis (Th and NTh group, respectively). Twenty thrombotic events were identified: 17 deep venous and 1 arterial thrombosis, 2 osteonecrosis. Both groups had comparable clinical, biological, therapeutic data, and mean (SD) SLE disease activity index (SLEDAI) (5 (4.6) v 5.3 (4.8)). Patients were examined at least one month after thrombosis (>3 months in 11 out of 15). The following parameters were determined: protein C, total and free …

Plasma antioxidant status can be evaluated by selenium, retinol and a-tocopherol. The present study concerns 89 HIV-1 positive patients. The plasma level of selenium was determined by PIXE (proton-induced X-ray emission analysis) and by measurement of levels of vitamins A and E by HPLC. The data were compared to controls; among the HIV-1 patients, significant differences were found for plasma selenium between groups selected on the basis of the CD4 lymphocyte count. Differences were also observed for plasma retinol between the HIV-1 patients and the control subjects. Correlations with other nutritional and immunological parameters were shown.

Hyperchomocysteinaemia is a vascular risk factor. However few data are available as regards the efficacy of vitamin supplementation on the course of hyperhomocysteinaemia-related vascular disease. Since homocystein induces vascular endothelium cell dysfunction in vitro, we investigated the effect of vitamin supplementation on plasma soluble thrombomodulin (sTM) concentration, a marker of endothelium injury. The diagnosis of hyperhomocysteinaemia was assessed by oral L-methionin load. Homocysteinaemia was measured before and 6 hours after the load. The sTM concentration was measured while fasting before and 3-months after supplementation with 5 mg folic acid and 250 mg vitamin B6. The difference between fasting and post-load homocystein concentration decreased from 43.9+/14.9 mol/I before supplementation to 28.1+/-9.4 mol/I after a 3-monthslong supplementation. Then a 37% decrease was obtained in the post load rise in homocysteinaemia. 14 from the 17 patients (82%) no longer had detectable hyperhomocysteinaemia after the 3-months supplementation. The concentration of sTM decreased from 43.6+/19.8 ng/ml to 30.7+/I I ng/ml (p=0.005). After supplementation for 3 months with folic acid and vitamin B6, a significant decrease was obtained in sTM. This may reflect a decrease in injury of the vascular endothelium, sTM might be a useful marker to assess the efficacy of supplementation regiments on hyperhomocysteinaemia-related vascular disease.

We report the case of a 64 year-old woman who had pulmonary fibrosis and sicca syndrome for 4 years and in whom vascular purpura occurred, leading to the diagnosis of C hepatitis related cryoglobulinemia. The nosologic links between diseases are discussed.

Proton induced X-ray emission (PIXE) analysis, following enrichment by APDC-MIBK extraction, is used to measure chromium concentration in blood plasma from patients submitted to selective coronary artery cineangiography. The yield of the chromium preconcentration is determined with carrier-free 51Cr. From the catheterism results the patients are classified into three populations: coronary artery disease (CAD), heart disease (HD) and normal arteries (N). The first two groups, CAD and HD, have significantly lower chromium concentrations than does the group with normally patent arteries. The present analytical method and the results obtained provide an interesting contribution to the difficult problem of chromium determination in biological media.

Clinicopathologic findings are reported of a woman with plane xanthomatosis, multiple myeloma (IgGĸ) and normolipemia. Plasma lipoproteins were bound to the monoclonal immunoglobulin. The complex was separated by ultracentrifugation, then the proteins were measured by radial immunodiffusion and laser immunonephelometry. Monoclonal IgGĸ interact with the low-density lipoproteins. The literature about the association between normolipemic or hyperlipemic xanthomatosis and myeloma was reviewed and the physiopathology of this association discussed. Several hypotheses are suggested but, at present, it is shown that lipoprotein-paraprotein complexing in some patients may be due to autoantibody activity of the myeloma protein against serum lipoprotein; immune complexes interfere with normal lipoprotein catabolism resulting in xanthomas and normolipemia or hyperlipemia.