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Biomedical subjects

J Constans

Publications and source records attributed to J Constans.

At least 91 records · Page 5Linked to original sources
PubMed1995

[Effect of primary prevention of Pneumocystis carinii pneumonia on the inaugural clinical and biological presentation of AIDS: 624 cases (Aquitaine Cohort, 1985-1994)].

In a cohort of HIV-infected patients, this study compares the clinical and immunological features at the time of AIDS diagnosis of patients who either received primary Pneumocystis carinii prophylaxis (P+; n = 335) or who did not (P-; n = 289). Frequency of P carinii pneumonia was lower in P+ than in P- patients (14.9% vs 26.0%; p < 0.001). Conversely, toxoplasmic encephalitis, esophageal candidiasis, cytomegalovirus disease and M avium complex disease were more frequent in P+ patients. CD4+ count (median/mm3) at the time of AIDS diagnosis was lower in P+ than in P- patients: 22 vs 97 (p < 0.001); this suggests that early intervention delays the onset of AIDS for about one year. While searching for new prevention strategies against other opportunistic infections, efforts should be expanded to improve prophylaxis of P carinii pneumonia which remains in France the most frequent first AIDS-related illness.

AIDS-Related Opportunistic Infections↗
PubMed1995

Autoantibodies to malondialdehyde-modified epitope in connective tissue diseases and vasculitides.

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.

Adult↗
PubMed1995

Asymptomatic atherosclerosis in HIV-positive patients: A case-control ultrasound study.

Atherosclerosis has been reported in some HIV-positive subjects without any known risk factor. The purpose of the present study was to investigate cervical arteries, abdominal aorta and femoral arteries by B-mode ultrasonography and doppler in 30 HIV-positive subjects matched to 18 controls for sex, age, tobacco consumption and arterial hypertension. Although no haemodynamically or clinically relevant lesions were found, plaques occurred more often in patients than in controls (11 patients, 36.7% vs. 2, 11.1%; P = 0.05). Compared to the HIV-positive patients without plaques, those with plaques had a tendency to have decreased lower HDL cholesterol, higher tobacco consumption and lower CD4-cell count (77 +/- 85/mm3 vs. 220 +/- 202/mm3). The patients with plaques (but not those without plaques) had lower HDL cholesterol than controls (P = 0.03). Asymptomatic atherosclerosis seems to be more frequent in HIV-positive patients and is associated to lower HDL cholesterol.

Adult↗
PubMed1995

Circulating endothelial markers and ischemic status in peripheral occlusive arterial disease.

In 34 patients with peripheral occlusive arterial disease, circulating levels of endothelial cell markers were compared with the ischemic status. Unlike tissue plasminogen activator and plasminogen activator inhibitor, plasma levels of thrombomodulin were closely related to both transcutaneous oxygen pressure (p = 0.01) and the graded clinical stages of disease (p = 0.02). Levels of von Willebrand factor were correlated only with the transcutaneous oxygen pressure (p = 0.04). Since thrombomodulin and von Willebrand factor constitute markers of endothelial cell damage, the extent of endothelial injury would appear to be determined by the ischemic status.

Aged↗
PubMed1995

Relationship between endothelial tissue factor and thrombogenesis under blood flow conditions.

We have evaluated the relationship between the level of tissue factor (TF) expression by stimulated endothelial cells and thrombus formation under blood flow conditions. Cultures of human umbilical venous endothelial cells (HUVECs) were treated in order to express different levels of TF activity. They were stimulated for 4 h with either I) lipopolysaccharides (LPS, 10 micrograms/ml), II) recombinant interleukin 1 beta (IL1 beta, 50 UI/ml) or III) simultaneously with LPS and IL1 beta (LPS+IL1 beta). TF activity was low on confluent HUVECs or on the corresponding extracellular-matrix (ECM prepared by exposure of HUVECs to 0.1 N NH4OH). In contrast, it was high when HUVECs were stimulated with LPS or IL1 beta, and significantly higher (p < 0.05) with LPS+IL1 beta. The TF activity associated with the stimulated ECM was 2-fold higher (p < 0.05) than that expressed on the luminal surface of the stimulated HUVECs, irrespective of the agonist or combination of agonists used. These surfaces were exposed to non-anticoagulated human blood at a venous (50 s-1) and an arterial (650 s-1) wall shear rate in parallel-plate perfusion chambers for 5 min. Thrombus formation was morphologically quantified by measuring the deposition of platelets and fibrin. Fibrin deposition was also immunologically quantified. Fibrin deposition was related to the level of TF expression. Non-stimulated HUVECs and corresponding ECMs were not thrombogenic. The luminal surface of HUVECs stimulated with LPS or IL1 beta alone expressed low levels of TF activity and was a poor inducer of platelet deposition and fibrin deposition (< 15%) at 50 s-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Antithrombin III↗
PubMed1994

Plasma lipids in HIV-infected patients: a prospective study in 95 patients.

The present study aimed to determine plasma lipid levels in 95 HIV-infected patients divided into four groups according to the CD4 lymphocyte counts comparatively to a control group of 20 HIV-negative normolipidaemic subjects. A relationship between lipidic abnormalities and immune or nutritional status was also investigated. The patients below 200 CD4 lymphocyte mm-3 (groups 1 and 2) had significantly lower total cholesterol than the controls. The patients below 400 CD4 lymphocytes mm-3 (groups 1, 2, 3) had significantly higher triglycerides and Lp(a) but lower LDL-cholesterol than the controls. In all HIV-positive patients, whatever their CD4 lymphocyte count, HDL-C and apoA1 were lower than in the controls. By multivariate analysis triglycerides were positively correlated to acute opportunistic infections and to interferon-alpha levels, while cholesterol was negatively correlated to TNF-alpha, and LDL-C was positively correlated to albuminaemia. The latter parameter was the only lipidic value to correlate with nutritional markers. The contamination route, or the presence of wasting, was not correlated to any lipidic disorder.

Acquired Immunodeficiency Syndrome↗
PubMed1994

[Idiopathic periaortic fibrosis: a difficult diagnosis in internal medicine].

Peri-aortitis retroperitoneal fibrosis is characterized by a reaction of a variable inflammatory nature while constricting the organs crossing the retroperitoneal space, notably the ureters and the blood vessels. It is difficult to diagnose such a rare disease. We bring about here six cases of periaortic retroperitoneal fibrosis diagnosed from systemic, digestive, urinary or vascular signs. Early diagnosis is often difficult and is shown to be established after an average of three months investigation. The average age of these patients, all of the male sex, is 58 years old (54 to 90). In the six cases this disease appears to be idiopathic even though in two cases it is associated to giant temporal arteritis and polymyalgia rheumatica. TDM remains the best diagnostic tool to point out the existence of this fibrosis, to observe its evolution and to investigate for any extension of the disease. The etiology of this fibrosis remains a mysterious one; however an immunologic origin has been suggested. Medical treatment by corticosteroids is often successful but the long term evolution of the disease is still uncertain.

Aged↗
PubMed1993

Levels of plasma thrombomodulin are increased in atheromatous arterial disease.

The plasma thrombomodulin (TM) level depends on the integrity of the endothelium and the clearance of the molecule. In several different pathological conditions, plasma TM levels increase with damage to the endothelium. We studied plasma TM levels in patients with various localizations of atheromatous arterial disease who had normal serum creatinine levels. Two groups of patients had a single symptomatic localization, which was either peripheral occlusive arterial disease (POAD) or ischemic heart disease (IHD) and a third group of patients had multiple symptomatic localizations (polyvascular). We compared the plasma TM levels with the plasma levels of other specific markers of endothelial cell activation such as: prostacyclin (PGI2), tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1). Plasma TM levels were significantly increased in all three individual groups and when all patients were considered (total patients), as compared with normal controls. When all patients were considered, there was a significant positive correlation between plasma TM levels and t-PA and between plasma TM levels and PGI2. A significant positive correlation was also found between the plasma TM levels and PAI-1 for patients with POAD. Thus, our findings suggest that an increased influx of TM into the plasma may be caused by endothelial cell damage in patients with atheromatous arterial disease. However in our study, the plasma TM levels obtained were similar for all three types of atheromatous arterial disease. Though plasma thrombomodulin is a marker of endothelial cell injury, it cannot be of a clinical interest until its levels are related to the extend of the atheromatous lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Gm haplotype distribution in Amerindians: relationship with geography and language.

A review is made of the Gm haplotype distribution in 60 groups of Eskimos, North, Central and South American Indians, totaling 22,808 individuals. Differences were observed in the shapes of the distribution of Gm*ag and the other markers. Nearly identical values for FST and average heterozygosities were obtained in the North+Central/South comparisons. North-South and Southwest/Northeast clinal differences were observed in the Americas using correspondence factorial analysis. The two haplotypes mainly responsible for these differences are Gm*axg and Gm*abOst. When the populations are classified by language groups, besides the recognized differences between Eskimos and Athabaskan (Na-Dene) speakers compared with Amerinds, others are found. For instance, Uto-Aztecan speakers of the United States and Mexico differ in Gm frequencies from the Nuclear Chibchan, Macro-Arawak, and Carib speakers of Central and South America. The notion of a homogeneous Amerind genetic pool does not conform with these and other results.

Computers↗