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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. (c) 1996 American Society for Clinical Nutrition [ABSTRACT FROM AUTHOR]

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, H = 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 epitopc(s) autoantibody titres correlated strongly with systemic lupus activity measure (SLAM. r = 0.702, P = 00001), anti-nuclear antigen autoantibodies (ANA. r = 0.4, P=0029), IgG anti-cardiolipin (r=0.558, P = 003) and the steroid drug regimen (r = 0-52, P = 0004). 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. [ABSTRACT FROM AUTHOR]

We report two observations of significant left heart involvement in patients with the carcinoid svndrome assessed by transthoracic and transoesophageal echocardiography. Echocardiographic lesions of this kind have only been reported twice. In the present cases, there was mitral involvement with mitral regurgitation in one case and a mitro-aortic involvement with mitral and aortic regurgitation in the other. The mechanism of left heart lesions is unclear since in both cases no right-to-left cardiac shunt was present, as attested by colour Doppler and saline contrast transoesophageal echocardiography. The location of the primary tumour was unknown in one case and Heal in the other; no pulmonary metastasis was detected. The use of transoesophageal echocardiography might make it possible to detect left-sided cardiac-lesions more frequently since they were found in anatomical series, in 30% of patients with carcinoid syndrome. [ABSTRACT FROM PUBLISHER]

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). [ABSTRACT FROM PUBLISHER]

Introduction. – Distensibility is the ability of large elastic arteries to increase in diameter from diastole to systole. Pulse wave velocity (PWV) is one of the ways to measure this parameter. Several techniques, including QKd, are able to measure PWV.Purpose. – QKd is the time interval between the Q wave on EKG and auscultation of the second Korotkoffˈs sound at the brachial artery. QKd is measured by a specific apparatus that registers ambulatory blood pressure as well as EKG (normal > 200 ms). Arterial distensibility seems to be able to predict cardiovascular morbidity and QKd has been demonstrated to predict such morbidity in a sample of elderly hypertensives. Currently the relationship between QKd and prognosis is under investigation in systemic sclerosis (ERAMS study).Conclusion. – QKd is a noninvasive ambulatory method that measures arterial distensibility as well as blood pressure. [ABSTRACT FROM AUTHOR]

Abstract: Objective: The objectives of this article are to review the data about the consequences of thrombophilia testing and to think about its indications. Current knowledge and key points: The indications of congenital thrombophilic testing have extended since the discovery of prevalent abnormalities, such as mutations of factor V or II genes. However, thrombophilia does not result in a significant increase in the risk of recurrence unlike the spontaneous occurrence of thrombotic events. The factor V Leiden mutation is associated with a moderate increase in recurrence rate, while the G20210A mutation of factor II is not associated with a significant increase in recurrence. Regarding the decrease in natural anticoagulants is concerned, there is no definite conclusion, although the decrease in antithrombin is suspected of being associated with an increase in recurrence. Future prospects and projects: Finally, identification of a constitutional thrombophilia most often do not influence the therapeutic decisions unless some rare abnormalities are found, such as a decrease in antithrombin, homozygous mutations in factors V or II genes or associations of thrombophilia. One must remember that antiphospholipid antibodies must be searched because their impact on recurrences is well-known. Diagnostic work-up for thrombophilia is not useful after a distal or a superficial venous thrombosis (except for antiphospholipid antibodies in case of distal venous thrombosis). [Copyright &y& Elsevier]

Abstract: Introduction. – Painful bruising syndrome was described by Gardner and Diamond in 1955. It is marked by spontaneous bruising, without any biological abnormality, affecting young women with pathological mental context. Exegesis. – We report three observations with painful bruising syndrome. In a patient, psychotherapy induced improvement in dermatological and articular manifestations. In other case, placebotherapy made clinical symptoms go away for a prolonged period. Conclusion. – Some etiological hypotheses have been postulated for Gardner and Diamond syndrome. However, published cases speak in favour of psychogenic hypothesis. Somatic and psychological approach must be offered to these patients. [Copyright &y& Elsevier]

Increased vascular endothelial cell growth factor (VEGF) may be important in cardiovascular pathophysiology (perhaps relating to angiogenesis and collateral vessel development) and binds target endothelium via receptors such as Flt-1. We hypothesized that there would be increased levels of plasma VEGF and Flt-1 in patients with atherosclerosis and others with hyperlipidemia compared with controls, and a reduction in these factors with 3 months of lipid-lowering therapy. Twenty patients with uncomplicated hyperlipidemia but no atherosclerosis, 20 patients with hyperlipidemia plus clear atherosclerosis, and 40 matched controls were studied. Plasma VEGF was higher in patient groups than in healthy controls (p <0.01), but Flt-1 was not significantly altered. After lipid-lowering therapy, patients with uncomplicated hyperlipidemia had significantly reduced total cholesterol and VEGF (all p <0.05) but no significant change in Flt-1. Lack of a significant correlation between the von Willebrand factor and VEGF suggests the latter is unrelated to endothelial damage. Plasma VEGF that increases in patients with uncomplicated hyperlipidemia free of major underlying atherosclerosis and in patients with hyperlipidemia plus established atherosclerosis is reduced by successful lipid-lowering treatment. These findings may have implications for the pathophysiology and treatment of hyperlipidemia and atherosclerosis, and suggest an alternative mechanism (i.e., modulation of angiogenesis) by which lipid-lowering therapy may reduce cardiovascular events beyond lipid reduction alone. [ABSTRACT FROM AUTHOR]

Introduction. – The association between adult Henoch-Schonlein purpura and prostatic carcinoma is exceptional. We report a new case.Exegesis. – The diagnosis of prostatic adenocarcinoma, suspected because of prostatic induration is made after anatomopathological study. The patient has all the clinical (purpura, polyarthralgia), biological (circulating monocmonal IgA), and histological (leukocytoclastic vasculitis, with IgA and C3 deposits) criteria of Henoch-Schonlein purpura too. The simultaneous appearance of vasculitis and neoplasia is known. The association between adult Henoch-Schonlein purpura and malignant neoplasm like lung carcinoma or lymphoma exists too. The initial events leading to the development of these vasculitis could be tumor antigens or abnormal IgA production.Conclusion. – The simultaneous appearance of these two disease asks here the question of mechanisms implicated in these association. [Copyright &y& Elsevier]