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C Conri

Publications and source records attributed to C Conri.

At least 73 records · Page 4Linked to original sources
PubMed1996

Lipoprotein(a) in 505 hospitalized patients with various pathological states: correlations with cardiovascular diseases and therapies.

OBJECTIVE: Our aim was to study the lipoprotein (a) (Lp(a)) levels in various pathological states. EXPERIMENTAL DESIGN: This investigation was prospective and included a healthy control group. SETTING: This study was carried out in two internal medicine and angiology services in teaching hospitals. PATIENTS: 505 patients were included with various diseases: 66 acute infections, 9 HIV infections, 25 cancers, 86 diabetes, 36 systemic diseases, 94 atheromatous vascular disease, 27 arterial hypertensions. A control group was composed of 21 healthy subjects. INTERVENTIONS: There was no therapeutic intervention but cardiovascular treatments were recorded. MEASURES: Serum Lp(a), total cholesterol, triglycerides, HDL-cholesterol, calculated LDL-cholesterol, apolipoproteins A-I and B were measured together with inflammatory parameters, serum creatinine, proteinuria, serum aminotransferase activity. RESULTS: There was no difference in Lp(a) levels between controls and each patient group. However, a correlation was found in systemic diseases between Lp(a) and C reactive protein (r = 0.371, p = 0.026) or serum albumin concentration (r = 0.453, p = 0.006). In hypertension, Lp(a) correlated with serum creatinine (r = 0.420, p = 0.03). In the whole patient population, Lp(a) was correlated with cholesterol (r = 0.156, p = 0.0001), apolipoprotein B (r = 0.215, p = 0.0001), age (r = 0.108, p = 0.015), arterial events (r = 0.174, p = 0.0001) and platelet anti-aggregant drugs (r = 0.169, p = 0.0001). CONCLUSIONS: Lp(a), was related to atheromatous events and in systemic diseases to inflammation, suggesting that Lp(a) might vary in some patients in a manner similar to acute phase proteins.

Adult↗
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↗
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

[Pneumopathy caused by amiodarone in internal medicine: 8 cases].

We report on eight cases of amiodarone pulmonary toxicity. Main clinical symptoms are acute/subacute dyspnea or progression in some cases. Amiodarone responsibility is difficult to ascertain. Several arguments can be presented: clinical symptoms with dyspnea and/or fever and/or cough, interstitial or in diffusing capacity for carbon monoxide, abnormal broncho-alveolar lavage cytopreparation smear with increased percentage of lymphocytes and polymorphonuclear leucocytes in typical cases; trans-bronchoscopic lung biopsy failed to provided information on amiodarone toxicity in the two patients where biopsy were performed. Differential diagnosis is an essential step to eliminate other possible causes ie pulmonary micro-organism infections, cancer or pulmonary oedema secondary to heart failure. In one case acute pulmonary toxicity occurred early, after introduction of amiodarone, with a proposed immuno-allergic mechanism. In other cases, chronic amiodarone deposition in the lungs can explain clinico-radiologic features. In six cases improvement was observed after discontinuation of therapy within a 6-months period.

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PubMed1993

Carcinoid heart disease: two cases of left heart involvement diagnosed by transthoracic and transoesophageal echocardiography.

We report two observations of significant left heart involvement in patients with the carcinoid syndrome 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 ileal 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.

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