Search PubMed⌕ Search

Biomedical subjects

E Weitzenblum

Publications and source records attributed to E Weitzenblum.

At least 19 recordsLinked to original sources
PubMed2006

[Pleural effusion complicating a totally implanted venous device].

INTRODUCTION: Totally implanted venous devices (TIVD) are an essential tool for repeated intravenous treatments such as chemotherapy for cancer and antibiotics for cystic fibrosis. CASE REPORT: A woman of 76 years was treated for bronchiectasis, colonised by Pseudomonas aeruginosa, with courses of intravenous antibiotics. On account of poor peripheral veins a TIVD was implanted. The implantation and subsequent antibiotic injections were uncomplicated. Three years later a further course of antibiotics was prescribed. As no reflux of blood was obtained on puncturing the device the position of the catheter was checked radiologically. The patient complained of right shoulder pain following each infusion. The chest x-ray showed a pleural effusion. The sudden onset of the effusion, the absence of signs of infection and the patient's good clinical condition suggested pleural extravasation of the antibiotic infusion from the TIVD. Pleural aspiration yielded 1400 mls of watery fluid. Injection of contrast into the TIVD confirmed intra-pleural extravasation. CONCLUSION: When using a TIVD it is important to bear in mind the possibility of late pleural complications.

Aged↗
PubMed2005

[Pulmonary hypertension associated with disorders of the respiratory system].

Pulmonary hypertension associated with disorders of the respiratory system is defined by a pulmonary artery mean pressure above 20 mmHg at rest in stable disease. The most frequent form of precapillary pulmonary hypertension is associated with chronic obstructive pulmonary disease, because of its high prevalence. Pulmonary vascular remodeling occurs in the small pulmonary arteries and is due mainly to chronic alveolar hypoxia. Pulmonary hypertension associated with disorders of the respiratory system is usually mild to moderate, with resting pulmonary artery mean pressure ranging between 20 and 35 mm Hg. It may increase markedly during sleep, exercise or exacerbation of respiratory failure, however. Abrupt postload elevation can lead to right heart failure, an indisputable indicator of prognosis. Because the symptoms of pulmonary hypertension are minimal relative to those of the chronic hypoxic lung disease, noninvasive diagnosis is difficult, particularly in patients with chronic obstructive pulmonary disease. Oxygen therapy (at least 16 h/day) is currently the best treatment for this type of pulmonary arterial hypertension.

Disease Susceptibility↗
PubMed2005

[Physiological functional tests to evaluate pulmonary arterial hypertension].

INTRODUCTION: Pulmonary arterial hypertension (PAH) is a rare and complex disease, which requires careful diagnostic evaluation. STATE OF THE ART: Most patients have a mild decrease in lung volumes and a moderate decrease in carbon monoxide transfer factor. Mild to moderate arterial hypoxaemia, is often present, associated with a mild respiratory alkalosis. When hypoxaemia is severe, it may represent an intracardiac shunt. Right heart catheterisation is required to confirm the diagnosis and in most cases shows a significant elevation of pulmonary artery pressure due to an increase in pulmonary vascular resistance. The haemodynamic profile and the response to an acute pulmonary vasodilator challenge are determinants of prognosis. Finally, exercise capacity which is usually assessed by the six minute walk test provides an overall functional measure of disease severity, response to therapy, and progression. PERSPECTIVES: Functional evaluation of the heart using echocardiography will play an increasing role in the evaluation of PAH. CONCLUSIONS: Physiological measurements in PAH have several objectives. They form part of the diagnostic definition, allow the exclusion of other conditions and are tools for the assessment of severity, prognosis and response to therapy.

Adolescent↗
PubMed2004

[Coagulation disorders and arterial thromboembolic events in non-small-cell lung cancer. A case report].

Certain coagulation disorders can occur in patients with cancer and thromboembolic complications are frequent. We report the case of a 53-Year-old patient with metastatic adenocarcinoma of the lung treated with chemotherapy who presented several cerebral arterial thromboembolic events leading to death a few weeks after the initial diagnosis of cancer. This case illustrates the important role of certain satellite disorders related to coagulation activation: non-bacterial thrombotic endocarditis, disseminated intravascular coagulation, anti-phospholipid antibody syndrome. The role of anticancer chemotherapy as a favoring factor for thromboembolic events is also emphasized in patients with non-small-cell lung cancer.

Adenocarcinoma↗
PubMed2003

Polymorphism of the serotonin transporter gene and pulmonary hypertension in chronic obstructive pulmonary disease.

BACKGROUND: The serotonin transporter (5-HTT) is involved in the pulmonary artery smooth muscle hyperplasia that leads to pulmonary hypertension (PH). Because hypoxia and 5-HTT gene polymorphism control 5-HTT expression, we examined 5-HTT gene polymorphism and PH in hypoxemic patients with advanced chronic obstructive pulmonary disease (COPD). METHODS AND RESULTS: In 103 patients with COPD recruited in France (n=67) and the UK (n=36), we determined 5-HTT gene polymorphism and pulmonary artery pressure (PAP) measured during right heart catheterization (France) or Doppler echocardiography (UK). Ninety-eight subjects from the 2 countries served as control subjects. The distribution of 5-HTT gene polymorphism did not differ between patients and control subjects. In patients carrying the LL genotype, which is associated with higher levels of 5-HTT expression in pulmonary artery smooth muscle cells than the LS and SS genotypes, PH was more severe than in LS or SS patients. Mean PAP values in patients from France with the LL, LS, and SS genotypes were 34+/-3, 23+/-1, and 22+/-2 mm Hg (mean+/-SEM), respectively (P<0.01). Corresponding systolic PAP values in the UK were 40+/-3, 28+/-3, and 24+/-3 mm Hg, respectively (P<0.01). Compared with control subjects, platelet 5-HTT protein was increased in COPD patients in proportion to the hypoxemia level, and strong 5-HTT immunostaining was observed in remodeled pulmonary arteries from COPD patients. CONCLUSIONS: 5-HTT gene polymorphism appears to determine the severity of PH in hypoxemic patients with COPD. Because PH is an important prognostic factor in this disease, recognition of patients at risk for PH should be helpful in managing COPD.

Adult↗
PubMed2003

Allelic imbalance at loci containing FGFR, FGF, c-Met and HGF candidate genes in non-small cell lung cancer sub-types, implication for progression.

Fibroblast growth factors (FGF), hepatocyte growth factor (HGF) and their receptors, FGFR and c-Met, are essential components of the regulatory networks between the epithelium and mesenchyme in embryonic lung, but their respective roles in tumour growth are not clear. We performed allelotyping at loci containing the candidate genes FGFR-1-2-3-4, FGF-1-2-7-10, c-Met and HGF in 36 non-small cell lung cancer (NSCLC) (20 squamous-cell carcinomas (SQC) and 16 adenocarcinomas (ADC)), by surrounding each locus with two microsatellites (MS), as close as possible to the genes of interest. Unexpectedly, SQC and ADC were frequently altered at all of these loci, and SQC showed more simultaneously altered loci. In ADC, alterations at the 15q13-22 locus (FGF7 candidate gene) were significantly more frequent. Thus, these loci showed different patterns of molecular alterations between SQC and ADC. Finally, alterations at loci containing FGFR and HGF candidate genes were inversely correlated to the lymph node status in SQC and ADC, respectively.

Adult↗
PubMed2002

[Therapeutic management of primary pulmonary hypertension].

SEVERITY AND TREATMENT: The management of primitive pulmonary hypertension starts by the evaluation of its severity, based on the New York Heart Association's (NYHA) functional classification and right cardiac catheterization data. Hemodynamic criteria of poor prognosis are: an increase in right atrial pressure > 10 mm Hg, a decrease in cardiac output (cardiac index < 2.2 l/min/m2), an increase in pulmonary vascular resistance > to 20 mm Hg/l/min/m2, and saturation of the oxygen content in venous blood < 63%. These prognostic data will condition treatment. CALCIUM CHANNEL BLOCKERS: Are the only vasodilators that have demonstrated efficacy in primitive pulmonary hypertension (PPH). However, only 20% of patients respond to calcium blockers. To determine a positive response to these agents, a carbon monoxide inhalation test is required during right cardiac catheterization. Prescription of calcium channel blockers to non-responders is often responsible for adverse events, from enhanced dyspnoea to sudden death. Continuous intravenous infusion of epoprostenol has considerably improved the prognosis of PPH and related pulmonary hypertension (PH). Despite the constraints, such treatment should be proposed to NYHA functional class III and IV patients not responding to carbon monoxide tests, until new, equally efficient products have been launched on the market. If epoprostenol fails or provokes severe side effects, pulmonary or cardio-pulmonary transplantation should be envisaged.

Administration, Oral↗
PubMed2002

[Alveolar hypoventilation in the obese: the obesity-hypoventilation syndrome].

The obesity-hypoventilation syndrome (or alveolar hypoventilation in the obese) is a new name for an old syndrome, Pickwickian syndrome. It is defined as chronic alveolar hypoventilation (PaO(2)<70 mmHg, PaCO(2) > 45 mmHg) in obese patient with a body mass index > 30 kg/m(2) who have no other respiratory disease explaining the gas anomalies. The large majority of obese subjects are not hypercapnic, even in case of severe obesity. There are three principal causes explaining alveolar hypoventilation in obese subjects: high cost of the work of respiration, dysfunction of the respiratory centers, repeated episodes of nocturnal obstructive apnea. The obesity-hypoventilation syndrome is generally found in males aged over 50 years. Exercise-induced breathlessness is a constant finding. Diagnosis is often made after an episode of severe respiratory failure. Associated diseases favored by obesity are frequent: diabetes, high blood pressure, heart disease. By definition, there is a hypoxemia-hypercapnia syndrome persisting after an acute episode. Spirography usually demonstrates moderate volume restriction. Pulmonary hypertension is frequent but not constant. Obesity-hypoventilation syndrome must be distinguished from obstructive sleep apnea, although the two conditions are often associated. Obstructive sleep apnea may be absent in certain patients with obesity-hypoventilation syndrome (we have had several cases) and inversely, obesity is not observed in certain patients with obstructive apnea. It should be recalled that the term Pickwickian syndrome designates obesity-hypoventilation syndrome (with or without obstructive apnea) and not obstructive sleep apnea syndrome.

Hemodynamics↗
PubMed2002

[Long-term oxygen therapy for chronic respiratory failure. Rationale, indications, modalities].

Long-term oxygen therapy (LOT) has become quite popular over the last 20 years due to better knowledge of the beneficial effect (improved life expectancy, improved quality of life, stabilization of the pulmonary hypertension) and to technological progress (concentrators, liquid oxygen). Ambulatory techniques have greatly contributed to the widespread use of oxygen therapy as has the decision of the French National Health Insurance System to reimburse this costly treatment. Almost all the studies devoted to the clinical and functional aspects of LOT have concerned patients with chronic obstructive pulmonary disease (COPD). By extension, it is generally accepted that LOT is warranted in other forms of respiratory failure (diffuse fibrosis, cyphoscoliosis, cystic fibrosis, etc.) when blood gas criteria similar to those retained for COPD are present: PaO(2)<=55 mmHg during stable periods with control measurements at lest 3 weeks apart; PaO(2) between 56 and 60 mmHg if there is also an elevated red cell count or pulmonary hypertension, signs of cor pulmonale ou frank hypoxemia during sleep. These consensus indications are widely accepted but other indications remain controversial: should LOT be prescribed for moderate hypoexmia (PaO(2) >=60 mmHg), exercise-induced hyoxemia alone, sleep hypoxemia alone? Appropriate studies are lacking so systematic prescription of LOT cannot be recommended in these three situations. The duration of LOT should be >=16 h/d, and if possible >=18 h/d. It has been established that objective results (life expectancy, improvement in pulmonary hypertension) are better for longer daily treatment. Patient compliance is however often insufficient. In addition to education, the best way to improve patient participation is to strive for improved quality of life with oxygen therapy (portable device, liquid oxygen) in these patients.

Home Care Services↗
PubMed2002

[COPD].

Explore the source record for details and available documents.

Humans↗
PubMed2001

"Natural history" of pulmonary hypertension in a series of 131 patients with chronic obstructive lung disease.

The prognostic value and the evolution of pulmonary hypertension (PH) in patients with markedly hypoxemic chronic obstructive pulmonary disease (COPD), treated or not with long-term oxygen therapy (LTOT), has been extensively investigated. However, little is known in patients with mildly or moderately hypoxemic COPD not requiring LTOT. Therefore, we assessed the evolution of pulmonary hemodynamics in 131 patients with stable COPD by performing two right heart catheterizations at a mean (+/- SD) time interval of 6.8 +/- 2.9 yr. At inclusion (T0), no patient had PH (i.e., the mean pulmonary artery pressure [Ppa] at rest was < 20 mm Hg). Group 1 included 55 patients without exercising PH and group 2 included 76 patients with exercising PH, defined by a pulmonary arterial pressure (Ppa) > 30 mm Hg during a steady-state 40-W exercise. Group 2 patients compared with group 1 patients had a significantly higher resting Ppa (16 +/- 3 mm Hg versus 14 +/- 2 mm Hg, p = 0.001). At the second catheterization, 33 (25%) patients (9 of 55 in group 1, 24 of 76 in group 2, p = 0.048) showed a resting Ppa > 20 mm Hg, but PH was generally mild, ranging from 20 to 42.5 mm Hg. The mean Ppa at second evaluation was 16 +/- 5 mm Hg in group 1 and 19 +/- 7 mm Hg in group 2 (p = 0.01). The patients who developed resting PH at the second catheterization (T1) had higher resting and exercising Ppa (p = 0.001 and p = 0.002, respectively), and significantly lower resting and exercising Pa(O(2)) (p = 0.005 and p = 0.012, respectively) at T0. Logistic regression analysis showed that resting and exercising Ppa were independent predictors (at T0) for the subsequent development of PH (p = 0.029 and p = 0.027, respectively). The patients who developed resting PH (T1) had a significantly worsening of Pa(O(2)) (from 63.5 mm Hg at T0 to 60 mm Hg at T1, p = 0.047), whereas the Pa(O(2)) as a mean was stable in the remainder (69.5 mm Hg at T0 and T1). These results show the following. The progression of Ppa over time in patients with COPD with mild to moderate hypoxemia is rather slow, the average change for the group as a whole being of + 0.4 mm Hg/yr. Only about 25% of patients with COPD with mild to moderate hypoxemia and without resting PH at the onset will develop PH during a 6-yr follow-up. The patients with exercising PH at the onset have a significantly increased risk of developing PH over time. Only resting and exercising Ppa at the onset are independently related to the subsequent development of PH. However, in individual cases, the models of linear or logistic regression do not allow a pertinent prediction of the level of Ppa or the presence of PH at the second right heart catheterization.

Blood Pressure↗
PubMed2001

Outcome of COPD patients with mild daytime hypoxaemia with or without sleep-related oxygen desaturation.

The aim of the present study was to compare the evolution of pulmonary haemodynamics and of arterial blood gases in chronic obstructive pulmonary disease (COPD) patients with mild-to-moderate hypoxaemia, with or without sleep-related oxygen desaturation. COPD patients with daytime arterial oxygen partial pressure in the range 56-69 mmHg were included prospectively. Sleep-related oxygen desaturation was defined as spending > or = 30% of the nocturnal recording time with arterial oxygen saturation <90%. From the 64 patients included, 35 were desaturators (group 1) and 29 were nondesaturators (group 2). At baseline (t0), patients with sleep-related desaturation had a significantly higher daytime (mean +/- SD) arterial carbon dioxide partial pressure (Pa,CO2) (44.9 +/- 4.9 mmHg versus 41.0 +/- 4.1 mmHg, p=0.001) whereas mean pulmonary artery pressure (mPAP) was similar in the two groups. After 2 yrs (t2) of follow-up, 22 desaturators and 14 nondesaturators could be re-evaluated, including pulmonary haemodynamic measurements. None of the nondesaturator patients became desaturators at t2. The difference between the two groups in terms of daytime Pa,CO2 was still present at t2. The mean changes in mPAP from t0 to t2 were similar between the two groups, as were the rates of death or requirement for long-term oxygen therapy (American Thoracic Society criteria) during follow-up of up to 6 yrs. The presence of sleep-related oxygen desaturation is not a transitional state before the worsening of daytime arterial blood gases, but is a characteristic of some chronic obstructive pulmonary disease patients who have a higher daytime arterial carbon dioxide partial pressure. Such isolated nocturnal hypoxaemia or sleep-related worsening of moderate daytime hypoxaemia does not appear to favour the development of pulmonary hypertension, nor to lead to worsening of daytime blood gases.

Adult↗