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J Constans

Publications and source records attributed to J Constans.

At least 55 records · Page 3Linked to original sources
PubMed1999

[Inflammatory arteriopathy of the arms in the course of Horton disease. Report of six cases].

We report 6 cases of upper limb involvement in giant cell arteritis; upper limb involvement revealed the disease in 4 cases and clinical symptoms were present in 5 (upper limb pain, Raynaud's phenomenon). Upper limb pulses were not palpable and blood pressure unmeasurable in all. Duplex ultrasonography found signs of inflammatory arteriopathy in 4 cases (hypoechogenous halo of the arterial wall and acceleration of flow velocity). Arteriography was performed in 5 cases and showed long and regular stenoses. In the last case, arteriography was not done because the duplex exploration gave an easier diagnosis. With this technique, the diagnosis of upper limb involvement, frequent in autopsy series of giant cell arteritis, might be made more often. Corticosteroid therapy is indicated and surgery should be discussed only in emergency situations.

Aged↗
PubMed1999

Effects of heparin and related sulfated polysaccharides on tissue factor expression induced by mitogenic and non-mitogenic factors in human vascular smooth muscle cells.

Smooth muscle cells (SMCs) of the intima are generally quiescent and non proliferative. Their proliferation due to different stimulations occurs in myointimal hyperplasia and is regularly present in atherogenesis or after transluminal angioplasty leading to vascular occlusive stenosis. In the course of these pathologies, the Tissue Factor (TF) synthesis was upregulated and rapidly expressed at the membrane of the SMCs. Heparin is known to inhibit SMCs proliferation induced by FCS. We evaluated the inhibitory effect of heparin on the expression of TF induced by various mitogenic (FCS, PDGF-BB and EGF) and non-mitogenic (bacterial LPS) agents. Inhibition by heparin of SMCs proliferation induced by the same agonists was also determined. Quiescent human vascular SMCs from normal adult arteries were treated for 1 h by heparin and related sulfated polysaccharides before stimulation by the agonists. All the agonists up-regulated the expression of TF antigen and activity. TF expression induced by the growth factors was inhibited by heparin (IC 50: 10-30 microg/ml), and other sulfated polysaccharides (IC 50: 1-5 microg/ml). SMCs proliferation, late activation of the extracellular signal-regulated kinases (ERK1/2), and PKC activity were inhibited by heparin (IC 50: 30-50 microg/ml) in SMCs stimulated by FCS but not in SMCs treated by PDGF or EGF. In contrast, heparin had no effect on LPS-induced TF expression nor on LPS-induced PKC activation. These results indicate that, besides its well known effect on SMC proliferation, heparin displays an inhibitory effect on cell mediated blood clotting processes through regulation of the TF expression.

Adult↗
PubMed1999

[Hemorrhagic complications of antivitamin K. Report of 75 hospitalized patients].

Hemorrhagic complications are the most frequent complications of antivitamin K (AVK) treatments and can be life-threatening. We report 75 patients from a University Hospital. They were 40 males and 35 females (median age 74 years, 20-94), and were classified into 3 grades according to clinical picture: grade 1 (no surgery or transfusion, grade 2: surgery or blood transfusion needed, grade 3: death). 43 patients had grade 1 complications, 27 grade 2, and 5 grade 3 complications. The most frequent complications were muscular hematomas (36 patients), sub-cutaneous hematomas (14 patients), digestive bleeding (13 patients), hematuria (12 subjects). Eight patients had intracerebral bleeding, of whom 3 died. The treatment time was very variable (1 to 988 weeks). Only half patients had a prothrombin rate (PR) below 20% but two thirds had an INR above 5. This study showed that PR was a poor predictor of hemorrhagic complications. INR was a better parameter. For 15 patients, we considered that the indication was unadapted or questionable, among whom 2 died. This work suggests that the promotion of AVK prescription rules should go on.

Adult↗
PubMed1998

[Familial autoimmune hepatitis and C4 deficiency].

INTRODUCTION: Familial auto-immune hepatitis is unusual. We report a case in which hepatitis was associated with a deficiency in the C4 component of the complement. EXEGESIS: Type 1 auto-immune hepatitis A was diagnosed in a 38-year-old woman presenting with systemic lupus erythematosus. Her daughter had to undergo a splenectomy for immunologic thrombocytopenic purpura when she was 9 years old. When she turned 13, she further developed type 1 autoimmune hepatitis. During follow-up (4 and 8 years, respectively), both patients had a mild deficiency in C4. CONCLUSION: C4 deficiency is not only frequently observed in relatives of patients with auto-immune hepatitis, but also in familial systemic lupus. This abnormality may have had a crucial pathogenic role in these two patients.

Adolescent↗
PubMed1998

[Deep venous thrombosis in an adult with varicella].

INTRODUCTION: Some viral infections are associated with deep venous thrombosis. We report a case of deep venous thrombosis in an adult with varicella. He had neither known predisposing factors for thrombosis nor thrombophilia. EXEGESIS: Transient significant level of antiphospholipid antibodies and lupus circulating anticoagulant were observed. There was no evidence of thrombophilia. Deep venous thrombosis has been mostly associated with varicella in children. A transient protein S deficiency was present in almost all cases, though it was sometimes related to an anti-protein S antibody. This association is exceptional in adults. Some viruses such as herpesvirus and HIV are responsible for endothelium dysfunction, but this is still unclear in the case of varicella-zoster virus. CONCLUSION: In our observation, endothelium activation or antiphospholipid antibodies might be responsible for thrombosis.

Adult↗
PubMed1998

Autoantibodies directed against phospholipids or human beta 2-glycoprotein I in HIV-seropositive patients: relationship with endothelial activation and antimalonic dialdehyde antibodies.

BACKGROUND: We investigated the possible role of antiphospholipid (APA) and anti-human 2-glycoprotein I (beta2-GPI) antibodies (Ab) in thrombosis and atherosclerosis in human immunodeficiency (HIV)-positive patients, in whom they seem to be more frequent. METHODS: We measured APA and anti-beta2-GPI Ab in 58 HIV-positive patients together with markers of disease progression, circulating beta2-GPI, plasma lipids, biological markers of endothelial activation and integrity (plasma thrombomodulin, von Willebrand factor, vascular cell adhesion molecule 1) and with antimalonic dialdehyde antibodies (anti-MDA Ab). RESULTS: We found a 41% frequency of IgG APA in the HIV-positive patients. APA IgMs were rarely positive (7%), and anti-beta2-GPI IgGs were positive in 3-4% patients. There was no correlation between APA or anti-beta2-GPI Ab and the presence of opportunistic infections. Although plasma thrombomodulin, von Willebrand factor and vascular cell adhesion molecule 1 were significantly increased in the HIV-positive patients, APA was correlated only with vascular cell adhesion molecule 1, suggesting that APAs are correlated with endothelial activation but not with vascular endothelial lesions. A correlation between APA and anti-MDA IgG was demonstrated using multivariate analysis (r=0.542, P < 0.0001), suggesting a relationship between the targets of these antibodies. Finally, IgG APAs are frequent in HIV infection but are not correlated with biological markers of endothelial injury. CONCLUSION: Our results do not support a role for APA or anti-beta2-GPI in HIV-associated silent vascular endothelial damage. However, the role of these autoantibodies in clinically relevant thrombotic events should be investigated in HIV-positive patients.

Adult↗
PubMed1998

[Thrombosis of the inferior vena caval and right atrium in amoebic abscess of the liver].

Amoebic abscess of the liver is sometimes complicated by deep venous thrombosis but extension to the right atrium is rarely observed. The authors report the case of inferior vena caval thrombosis extending to the right atrium in a case of amoebic hepatic abscess. The patient was treated initially by antibiotherapy with metronidazole associated with intravenous anticoagulation. Rapid extension of the thrombus despite this treatment led to the initiation of thrombolysis. There were no embolic complications and the outcome was good. Apart from the rarity of this complication, this case poses the problem of the management of these patients. No previous reports of the use of thrombolysis were found in the medical literature. In the light of previous publications and the present case, the authors suggest investigation by CT scanning, echocardiography and venous Doppler ultrasonography in all cases of hepatic amoebic abscess.

Adult↗
PubMed1998

Effect of the antioxidants selenium and beta-carotene on HIV-related endothelium dysfunction.

Patients infected with HIV are at increased risk of atherosclerosis, and have evidence of endothelium dysfunction. The hypothesis was tested that HIV-related endothelium dysfunction is related to loss of antioxidants. This was done by the supplementation of the antioxidants selenium and beta-carotene. We supplemented the diet of 10 HIV-seropositive subjects with 100 microg selenium daily, 11 subjects with 30 mg beta-carotene twice daily while 15 subjects were not supplemented. Plasma was obtained at outset and after a year, and tested by ELISA for endothelial cell, platelet and inflammatory markers. The non-supplemented patients experienced increases in von Willebrand factor and soluble thrombomodulin (both p <0.01). There were no changes in any of the indices in the patients taking selenium or beta-carotene. Increased von Willebrand factor and soluble thrombomodulin in the non-supplemented patients imply increased damage to the endothelium over the year of the study. Therefore we interpret the lack of increase in the patients taking antioxidants as evidence of the protection of the endothelium by these agents.

Antioxidants↗
PubMed1997

[Dilated cardiomyopathy and selenium deficiency in AIDS. Apropos of a case].

Cardiac-related death of HIV-positive patients is not rare. The etiology of AIDS-associated dilated cardiomyopathies often remains unknown, even at autopsy. We report an observation associated to a severe deficit in selenium. The patient had been diagnosed as HIV-positive 2 years before. He presented Pneumocystis carinii pneumonia then Cryptococcus meningitis. Two months later he was hospitalized for pancreatitis and cachexia. He presented global heart failure that lead to death. No microorganism was found in myocardium at autopsy but plasma selenium was dramatically decreased (24 micrograms/L). The deficit in selenium has been associated to a dilated cardiomyopathy in non-AIDS patients. HIV-positive patients have an early decrease in plasma selenium, this concentration is dramatically decreased in malnourished patients. Selenium deficit might be the cause of some of the AIDS-related dilated cardiomyopathies and selenium supplementation might be useful in these patients.

Acquired Immunodeficiency Syndrome↗
PubMed1997

[Assay of plasma thrombomodulin in systemic diseases].

Membrane thrombomodulin (TM) is a very efficient natural anti-thrombin glycoprotein with anticoagulant properties expressed on endothelial cell surface. Circulating plasmatic thrombomodulin (TMp) detected by enzyme immunoassay in plasma is considered as a cell marker of endothelial injury. The TMp levels are increased in many conditions (diabetes mellitus, atheromatous disease...). In cases of collagen vascular diseases, where vascular endothelium damage is suspected, TMp is increased particularly in systemic lupus erythematosus (SLE) and systemic sclerosis (SSc). It is noteworthy that the TMp level is correlated with disease activity. Since TMp is a non specific marker of endothelial damage, it may be of interest as a useful marker for the supervision of these diseases. Further studies are needed on larger series. TMp level change during spontaneous evolution or under treatment will help determine wether TMp is a predictor and prognostic marker of these systemic diseases.

Acute Disease↗
PubMed1997

Alteration of arterial distensibility in systemic sclerosis.

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.

Adult↗
PubMed1997

Soluble adhesion molecules and endothelial cell damage in HIV infected patients.

Endothelial damage is present in HIV infection but our understanding of markers and mechanisms is incomplete. We found increased levels of markers of endothelial cell damage such as von Willebrand factor (vWf), soluble thrombomodulin (sTM) and adhesion molecule E-selectin in 90 subjects seropositive for HIV relative to healthy controls. sTM was strongly raised in those patients with the lowest CD4+ cell count (p < 0.001), but levels of vWf increased at each incremental fall in CD4+ cell count and the two indices correlated significantly (r = -0.485, p < 0.001). vWf correlated strongly with levels of the inflammatory cytokines tumor necrosis factor (TNF-alpha) and alpha interferon (IFN-alpha) but sTM correlated only weakly with IFN-alpha. We suggest that increased vWf is largely the result of inflammatory stimulus of the endothelium but that sTM is found only in those patients with more severe disease, and so truly represents endothelial damage.

Adolescent↗