Clinical usefulness of D-dimer tests in excluding pulmonary embolism is highly dependent upon age.
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Biomedical subjects
Publications and source records attributed to D Mottier.
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UNLABELLED: The aim of the study was to evaluate in general practice, in a large and unselected population of patients, the efficacy and safety of benazepril associated or not with hydrochlorothiazide (HCTZ) and to identify clinical and demographic predictive factors of antihypertensive efficacy. In this open uncontrolled study, 16,987 patients with mild to moderate hypertension were included by 5350 GPs. They received benazepril (BNZ) 10 mg once daily for 8 weeks. If sitting DBP remained > 90 mmHg after 4 weeks, HCTZ 12.5 mg once a day was then added for the last 4 weeks. RESULTS: In the intent to treat analysis, 54.5% of patients, after 4 weeks, and 80.6% of patients after 8 weeks, were controlled (DBP < 90 mmHg). Mean sitting DBP decreased from 100.5 +/- 5.5 mmHg (baseline) to 86.7 +/- 7.5 mmHg after 4 weeks and to 82.5 +/- 6.5 mmHg after 8 weeks. Mean SBP decreased from 169.5 +/- 13.1 mmHg to 150.5 +/- 12.5 mmHg after 4 weeks and to 145.0 +/- 10.9 mmHg after 8 weeks. Of the 16,900 patients included in the safety analysis, 853 (5.0%) dropped out of the study, 504 (3.0%) for adverse events (AE). The most frequent AE were: cough (3.5%), headache (0.9%), dizziness (0.8%), asthenia (0.6%) and nausea (0.5%). 13 deaths were observed during the study, mainly due to stroke or cancer. Six cases of raised serum creatinine level, 3 cases of angio-oedema and 2 cases of hepatitis were also reported. After 8 weeks of treatment, the main predictors of therapeutic response (DBP) were: recently discovered hypertension (86.3% of controlled DBP), regular exercise (85.5%) and age < 50 years (84.6%). Conversely: obesity, diabetes mellitus (77.9%), previously treated with several drugs (75.2%) and initial DBP > or = 105 mmHg (74.5%) were not predictive. Predictive factors emerging from logistic regression were : baseline DBP (< 105 mmHg), history of hypertension, body mass index, initial treatment of hypertension (no treatment--one drug--several drugs) and age. CONCLUSION: This large-scale study confirms, the antihypertensive efficacy and good tolerability of benazepril alone or associated with hydrochlorothiazide in general practice.
BACKGROUND: Low-molecular-weight heparin appears to be at least as effective and safe as standard, unfractionated heparin for the treatment of deep-vein thrombosis, but only limited data are available on the use of low-molecular-weight heparin to treat acute symptomatic pulmonary embolism. METHODS: We randomly assigned 612 patients with symptomatic pulmonary embolism who did not require thrombolytic therapy or embolectomy to either subcutaneous low-molecular-weight heparin (tinzaparin) given once daily in a fixed dose or adjusted-dose, intravenous unfractionated heparin. Oral anticoagulant therapy was begun between the first and the third day and was given for at least three months. We compared the treatments at day 8 and day 90 with respect to a combined end point of recurrent thromboembolism, major bleeding, and death. RESULTS: In the first eight days of treatment, 9 of 308 patients assigned to receive unfractionated heparin (2.9 percent) reached at least one of the end points, as compared,with 9 of 304 patients assigned to low-molecular-weight heparin (3.0 percent; absolute difference, 0.1 percentage point; 95 percent confidence interval, -2.7 to 2.6). By day 90, 22 patients assigned to unfractionated heparin (7.1 percent) and 18 patients assigned to low-molecular-weight heparin (5.9 percent) had reached at least one end point (P=0.54; absolute difference, 1.2 percentage points; 95 percent confidence interval, -2.7 to 5.1). The risk of major bleeding was similar in the two treatment groups throughout the study. CONCLUSIONS: Under the conditions of this study, initial subcutaneous therapy with the low-molecular-weight heparin tinzaparin appeared to be as effective and safe as intravenous unfractionated heparin in patients with acute pulmonary embolism.
BACKGROUND: The value of a risk factor analysis in the presence of a clinically suspected deep venous thrombosis (DVT) has been assessed mainly in inpatient populations. The aim of this prospective study was to evaluate the potential association between DVT and acquired circumstances suspected as risk factors, in a cohort of outpatients with a clinically suspected DVT. METHODS: Consecutive outpatients referred for a clinically suspected DVT, with recent clinical signs, not exceeding 1 week, were included. Before venography, all patients were interviewed by a trained physician to detect the presence of risk factors. RESULTS: From March 1992 to February 1994, 277 patients were included; venography was positive in 162 (58.4%). Five independent variables were significantly associated with the occurrence of DVT; in a multivariate analysis, 64.7% of patients were correctly classified; odds ratios for having DVT in the presence of these underlying conditions were respectively: 1.75 for age over 65 years, 1.68 for prior history of venous thromboembolism, 1.69 for high risk circumstances (any type of surgery or leg trauma within the past 3 months), 5.59 for malignancy, and 2.56 for varicose veins. CONCLUSIONS: In outpatients referred for a clinically suspected DVT, recognition of associated conditions might increase the certainty of the diagnosis.
Patients with systemic lupus erythematosus (SLE) are at risk of developing deep venous thrombosis (DVT). Should anticardiolipin antibodies (aCL) be detectable, this risk is significantly raised, particularly when these autoanti-bodies are cofactor-dependent. We conducted a cross-sectional study of consecutive unselected outpatients referred for clinical suspicion of DVT, as an attempt to address the following questions: firstly, were aCL antibodies associated with DVT in non-SLE patients? Secondly, was this association related to the cofactor dependence? From March 1992 to February 1994, 208 patients were enrolled in the study. Venography was positive in 110 patients (DVT patients), while the diagnosis of DVT could not be confirmed in the remaining 98 (referred to as disease controls). ACL was measured by ELISA, for IgG and IgM isotypes in two ways: fetal calf serum or bovine serum albumin were used as blocking agents to distinguish between cofactor-dependent and cofactor-independent antibodies. Positive aCL was defined as optical density (OD) values greater than the 95th percentile of OD distribution of 60 healthy controls. We found a high frequency of positive IgG aCL antibodies in both DVT patients and in disease controls (25.5 vs 23.5%). We suggest an association between IgM aCL and DVT. This association was, however, not dependent on the cofactor requirement.
BACKGROUND: Recent findings have demonstrated a high frequency of activated protein C resistance in patients suffering from deep venous thrombosis (DVT). This abnormality has been related to a mutation in the factor V gene (at nucleotide position 1,691, guanine to adenine [G-->A] substitution). AIM: To assess the frequency of the mutation in unselected inpatients with a proved DVT. To study the clinical characteristics of such patients. METHODS: All consecutive patients admitted to the hospital because of a clinical suspicion of DVT were eligible. Diagnosis of DVT with the help of venous ultrasound imaging or venography. Ventilation and perfusion lung scan was performed in all patients, and interpreted according to the Prospective Investigation of Pulmonary Embolism Diagnosis criteria; in patients with a low- or intermediate-probability lung scan, pulmonary angiography was requested. Polymerase chain reaction amplification was performed in patients with a proved DVT. A control group consisted of bone marrow volunteer donors. RESULTS: From July 1994 to November 1995, 165 patients were included. Thrombosis was considered as distal in 77 and proximal in 88; an associated pulmonary embolism (PE) was found in 75 patients. Of 165 patients, 24 (14.5%) showed the factor V gene mutation (95% confidence interval, 9.4 to 19.8); the mutation was present in 3.5% of 200 bone marrow volunteer donors; odds ratio for having DVT in the presence of the mutation was 4.1. No difference in the level of DVT, or the presence of an associated PE was observed according to the presence of the mutation. Patients with the mutation have a significantly more frequent history of DVT (p=0.04) and more previous reported episodes (1.1 vs 0.6; p=0.04). CONCLUSION: The factor V mutation is frequent in unselected DVT patients. No difference in the severity of the thrombosis episode was observed in these patients.
BACKGROUND: Plasma D-Dimer analysis, using ELISA assays, has demonstrated in previous studies a high sensitivity, suggesting its utility in excluding deep venous thrombosis (DVT). AIM: To assess the performance of a new rapid plasma D-Dimer ELISA measurement in suspected DVT patients with recent clinical signs, not exceeding one week. METHODS: A prospective study of patients admitted for a suspected recent DVT. Contrast venography or compression ultrasonography were performed within 24 h of admission. A new membrane based ELISA technique, which uses an immunofiltration and two complementary monoclonal antibodies was tested. Results were expressed as positive or negative. A standard plasma D-Dimer ELISA measurement was also performed. D-Dimer performances were assessed at the end of the study. RESULTS: 265/448 patients had a proven DVT (72 distal, 193 proximal). The sensitivity of the instantaneous method in the diagnosis of overall DVT is 92 +/- 3.4% (95% CI), and specificity is 36.6 +/- 6.9%. Positive predictive value is 67.7 +/- 4.8% and negative predictive value is 76.1 +/- 8.9%. Sensitivity and negative predictive values reach 97.9 and 94.3% in the diagnosis of proximal DVT, but only 76.3 and 79.7% in the diagnosis of distal DVT. Similar results are observed with the standard ELISA method. CONCLUSION: This new rapid plasma D-Dimer measurement appears highly sensitive, and could substitute the older ELISA methods. Both methods provide lower sensitivity in the case of a distal DVT location.
Contrast venography is the gold standard for the diagnosis of deep vein thrombosis in the lower limb extremities, but it fails to visualize deep veins like deep femoral vein and internal iliac vein. The internal iliac can be examined with duplex scanning if the technique and the examination conditions are correct. As reported in these two cases, thrombosis of these deep veins may lead to pulmonary embolism. The first case is a young female with venous thromboembolic disease in whom internal iliac vein thrombosis was documented only at the second examination. In the second case, deep femoral vein thrombosis appeared early in a comatose young male. This thrombosis may be classified as proximal muscular vein thrombosis. These two cases emphasize the importance of a duplex scanning examination performed with rigorous technique, whose the main limitation being examination conditions.
Venous thromboembolism is a frequent and potentially severe ailment in medical patients; the clinical signs are unreliable and as early detection of the thrombosis process by non-invasive techniques is not available, prevention appears to be an alternative. Careful definition of the medical situations at risk from venous thromboembolism is necessary. Age, prior history of venous thromboembolism, and immobilization constitute high risk circumstances. Analysis of the published studies advocates prevention in three circumstances: myocardial infarction, stroke and intensive care. In other cases, further controlled studies, randomized versus placebo, are needed.
INTRODUCTION: We describe 3 cases of hyperimmunoglobulinemia D syndrome (hyper-IgD syndrome). CASES REPORT: As the 2 first cases are conventional with an onset in childhood, the third one appeared later suggesting possibility of acquired syndrome. The 3 cases presented with one or several skin eruptions during febrile attacks. COMMENTS: Up to now, 64 cases of this syndrome have been described. Skin lesions are observed in 80 p. 100 of patients. In this particular clinical context, they must lead to the diagnosis. This 3 cases and the review of literature show that skin manifestations are polymorphic, transient, not very symptomatic and not correlated to IgD rates. Histological examination may reveal urticarial reaction with leucocytoclasic vasculitis, where IgD could directly or not interact.
Sera from patients with giant cell arteritis and/or polymyalgia rheumatica were tested for the presence of IgG, IgM and IgA antibody to endothelial cells (AEC), cardiolipin (ACL) and phosphatidylethanolamine (APE) using enzyme-linked immunosorbent assays. There were strong correlations between ACL and APE, but also between AEC and ACL IgM (p < 0.02) and between AEC and APE IgA (p < 0.003). Inhibition of AEC binding was achieved by absorption onto EC, but ACL and APE binding was also significantly reduced. In contrast, the binding of AEC antibody could not be inhibited by incubation with CL. Our data suggest that AEC constitute a heterogeneous population of autoantibodies.
This study was designed to assess the risk of associated pulmonary embolism according to the level of deep venous thrombosis. From March 1992 to March 1994, 328 patients were referred to medical units for suspected deep venous thrombosis, with recent clinical signs, less than a week. Each patient underwent contrast venography and/or duplex ultrasounds of lower extremities, ventilation and perfusion lung scan within 48 hours and angiography in case of low or intermediate pulmonary embolism probability. Diagnosis of deep venous thrombosis was confirmed in 155 patients; location was distal in 41, proximal in 114; an associated pulmonary embolism was found in 66 patients (10 with distal, 56 with proximal deep venous thrombosis); odds ratio was 2.99 (95% Cl: 1.2-3.13). Significantly higher risk of associated pulmonary embolism when deep venous thrombosis involves proximal veins is confirmed, but as many as 10 out of 41 patients with distal thrombosis also had an associated embolism. Management of both distal and proximal deep venous thromboses appears identical.
The value and role of clinical findings in the diagnosis of pulmonary embolism were analysed in the three steps of clinical reasoning: firstly, they lead the physician to suspect the diagnosis; however, no sign or association of clinical signs allow confirmation or infirmation of the diagnosis; they are simply a guide to diagnosis; secondly, they contribute to the exclusion of a number of differential diagnoses, with the help of simple complementary investigations such as blood gases, electrocardiograms and chest X-ray; finally, when grouped together and expressed in terms of probability, clinical data are essential for the interpretation of pulmonary scintigraphy and for assessing the indications of further investigations.
Nine dual-fluorescence combinations were used to enumerate T-cell subsets in 112 human immunodeficiency virus type 1-infected patients. Two blood samples were analyzed, with a 6-month interval between the tests, in 53 of these 112 patients. The alteration in CD4 over this period of time correlated with the change in CD8 and CD8S6F1 (P < 0.02 and P < 0.01), irrespective of the disease stage. Two groups of patients were defined by the CD8S6F1 subset at the first normal levels. Changes in numbers of CD4, CD4CD45RA, and CD4CD29 were significantly higher in group B than in group A patients. The absolute count of CD8S6F1 could thus serve as an indicator of the ensuing depletion of the CD4 population, as well as the CD4 subsets.
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We report the case of an elderly woman with severe dysautonomic orthostatic hypotension in whom a deficit in dopamine B hydroxylase has been established. In the literature, such a deficit has been described in six young adults with long standing symptoms of postural hypotension. This enzyme catalyses the conversion of dopamine to noradrenaline. In our elderly patient, noradrenaline and adrenaline were undetectable in the plasma, but plasma dopamine was detectable. Treatment with the synthetic amino acid, DL-threo-dihydroxyphenylserine, which is converted to noradrenaline by dopa-decarboxylase, resulted in a significant increase in blood pressure. The mechanism of this acquired deficit is not elucidated.
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