[Guidelines for respiratory infection: what are the objectives?].
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Biomedical subjects
Publications and source records attributed to M Murris-Espin.
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Between 1990 and 1995, 369 patients were investigated for obstructive sleep apnea syndrome (OSAS) by polysomnography. Among them, 248 patients with a mean Apnea-Hyponea index (AHI) of 37.7 per hour were treated by nasal continuous positive airway pressure (n-CPAP). Mean follow up was 39.5 +/- 20.4 months. In this group, 23 patients (9.2%) refused nCPAP immediately or after the first night and 39 (15.7%) gave up later. 15 patients (6%) died during the period of the study. The cumulative compliance reached 70% at 72 months. Non compliant patients usually gave up n-CPAP before the end of the first year. We compared the group of 150 patients always treated at the date of 31/12/95 with the group of 62 patients who refused nCPAP initially or gave up later. There was no difference in clinical parameters or polysomnographic data between the two groups. In 94 patients treated by nCPAP for more than a year we evaluated the outcome of AHI by a polysomnography performed after 72 hours of nCPAP cessation. Mean AHI of the group at this time was 38.2 +/- 20.3/h and was well correlated with the initial index (r = 0.41, p < 0.0001). However for 28 patients (29.7%) we observed, at the time of this second AHI determination, a variation (plus or minus) of at least 50% of the index. 6 patients, without any significative weigth loss, had an AHI below 5/h at this second determination. In this small group nCPAP was interrupted for 6 to 12 months, then another polysomnography was performed. At this time mean AHI was 42.4/h and clinical symptoms had reappeared in all patients. This study demonstrated that compliance to nCPAP in OSAS patients is good. No clinical or polysomnographic factors allow to predict non compliance. AHI is not modified by long term treatment with nCPAP.
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Rhinopharyngeal tuberculosis is a rare pathological condition. It is most often associated with lymph node and pulmonary lesions, but it may be an isolated finding. The authors report a recent case of an isolated rhinopharyngeal tuberculosis in a 64-year-old female. A review of the literature is presented. They emphasize the clinical presentation, that, in all aspects, may resemble a malignant tumour of the nasopharynx, as well as the difficulty of obtaining a pathological and bacteriological diagnosis.
In normal upper airways, nitric oxide is generated by the paranasal sinus epithelium and then diffuses into the nasal cavities. This study examined whether or not nasal NO concentration is affected by paranasal sinus inflammatory diseases. The influence of obstruction (nasal polyposis) and/or inflammation (allergy or chronic sinusitis) of the paranasal sinuses on nasal NO concentration was evaluated in nasal allergic (n=7 patients) or nonallergic (n=20) polyposis, nonallergic chronic sinusitis (n=10) and Kartagener's syndrome (n=6) and compared with control subjects (n=42). A score of alteration of the paranasal sinus (number of altered and occluded sinuses) was determined by a computed tomography scan. The nasal NO concentration in nasal nonallergic polyposis (150+/-20 parts per billion (ppb)) was significantly decreased compared with both controls (223+/-6 ppb, p=0.01) and polyposis with allergy (272+/-28 ppb, p<0.0001). In each group, the nasal NO concentration was inversely correlated with the extent of tomodensitometric alteration of the paranasal sinuses. In Kartagener's syndrome, the nasal NO concentration (14+/-2 ppb) was drastically decreased compared with all other groups, despite the presence of open paranasal sinuses. Thus, the nasal NO concentration in patients with nasal polyposis appeared to be dependent on both the allergic status and the degree of obstruction of the paranasal sinuses.
The relationship between infections of the respiratory tract and exacerbations of pulmonary symptoms in individuals with asthma is well established on clinical grounds. Patients having an acute attack of asthma often give a history of a "cold" before the onset of the exacerbation. The identification rate of viruses during exacerbations of asthma (10-30%) is much higher than the viral identification rate generally found during asymptomatic periods in asthmatics (3%). The mechanisms whereby upper respiratory viruses might induce or contribute to attacks of asthma are currently unknown: epithelial damage, increased cytokines releasability, mouth breathing.... Influenza vaccination is recommended in patients with chronic pulmonary diseases. However, bronchial hyperreactivity has been reported after influenza vaccination in asthmatics. Reactions to these vaccines may be due to non-immunogenic impurities, which are not present in the more recently developed subunit vaccines. In spite of the lack of double-blind studies between subunit and killed influenza virus vaccines, and because of the potential bad prognosis of influenza infection on airway obstruction, influenza vaccination should be recommended in asthmatics with stable respiratory function but influenza vaccination rate remains low.
BACKGROUND: Cetirizine and ebastine are two second-generation histamine H1 antagonists undergoing evaluation for treatment of perennial rhinitis. OBJECTIVE: The clinical efficacy and safety of once daily cetirizine 10 mg were compared with ebastine 10 mg in patients with perennial allergic rhinitis in a 4-week, double-blind, parallel-group, randomized, multicenter study. METHOD: Two hundred fourteen patients (120 females, 94 males, aged 17 to 70 years, mean 31.2 years) were selected on the basis of perennial allergic rhinitis history, positive skin test for perennial allergens and a minimum rhinitis symptom score of 6/12. Patients recorded nasal symptom severity (nasal stuffiness, nasal discharge, sneezing, and itching) once daily on diary cards using a rating scale of 0 (none) to 3 (severe). Clinicians made an overall evaluation after 4 weeks of treatment. An intent-to-treat-analysis was performed comparing cetirizine (106 patients) and ebastine groups (108 patients). RESULTS: The individual and total baseline symptom scores were comparable in both treatment groups. During the first week, the percentage mean decrease in the total nasal symptom score from baseline (sum of nasal stuffiness, discharge, sneezing, and itching) was significantly higher for cetirizine 46.2% than for ebastine 32.8% (P = .037). After 4 weeks of treatment, total symptom score improvement was 53.7% for cetirizine and 44.7% for ebastine (P = .12), and the clinician's overall evaluation showed that the percentage of symptom-free patients was significantly higher for cetirizine 17.8% than for ebastine 6.9% (P = .02). Cetirizine also significantly improved nasal stuffiness. An associated antiinflammatory effect is suggested. Commonly reported drug-related side effects were similar in both groups. CONCLUSION: This study shows that both antihistamines, cetirizine 10 mg and ebastine 10 mg once a day, improved symptom scores of patients with perennial allergic rhinitis. Cetirizine, however, provided faster improvement and total relief in a greater number of patients after 4 weeks.
Metastatic pulmonary calcifications, unlike dystrophic calcifications, occur in the normal healthy lung. The radiological pattern is quite specific. The disease is commonly described in chronic renal failure with calcium disorders. The prognosis is totally unpredictable. In 1992, a 50 yr old man underwent a successful renal transplantation during the final stage of chronic renal failure. He subsequently developed asymptomatic diffuse nodular opacities, that were discovered in 1995. An open lung biopsy confirmed the diagnosis of metastatic pulmonary calcification. There was no calcium disorder in this patient. In contrast to the benign course of pulmonary calcification in most patients, some fulminant pulmonary calcifications complicating renal transplantation or hypercalcaemia have been described. Radiographic identification of such entities is important to permit correction of calcium disorders. Otherwise, the condition is a potentially progressive and fatal cause of respiratory failure.
Nocturnal oximetry can show nocturnal oxygen desaturation. This examination was proposed as an investigation for the early detection of the sleep apnoea syndrome (SAS). We have compared the results of nocturnal oximetry and polysomnography in 329 consecutive patients seen in the department of thoracic medicine for the early detection of the SAS between June 1990 and June 1995. The diagnosis of SAS was confirmed at the time of polysomnography using an hypopnoea/apnoea index (IAH) greater or equal to 15 per hour. Two parameters of oximetry were well correlated with IAH less than 15 per hour: if the mean oxygen saturation is greater than 92% and for less than five per cent of the time of the examination there was a saturation of less than 90%. The sensitivity was 89.7% and the specificity was 57.8%. Among the 48 false positive cases on oximetry 17 patients were found to be suffering from COPD and 31 patients were probably suffering from a syndrome of upper airways resistance or possibly from the hypoventilation obesity syndrome. Amongst the 22 false, negatives to oximetry 10 non COPD patients with an IAH of greater than 30 per hour and diurnal somnolence had important anomalies of the oro-pharyngeal pathway as the origin of their nocturnal apnoea. The 12 other false negatives were patients with moderate SAS with an IAH of between 15 and 20 per hour. Logistical analysis has shown the association of the two oximetric criteria (mean oxygen saturation or percentage of time with a saturation of less than 5%) with clinical criteria (body mass index and formation on diurnal somnolence from a questionnaire) would enable a probable diagnosis of SAS in 75% of cases. Our study shows that nocturnal oximetry used an early diagnosis test, associated with clinical and respiratory function data enables the number of requests for polysomnography to be reduced.
The tachykinin substance P (SP) is present in lung sensory nerve endings and may be released after neurogenic stimulation. Its role in the pathogenesis of asthma is still unclear. Nevertheless, it may play a major role in airway neurogenic inflammation. Alveolar macrophages are the predominant cells of the airway space and are involved in various types of airway inflammation. We studied guinea pig alveolar macrophage response to SP and other related peptide (C- and N-terminal sequences, NK1-receptor agonist) stimulation. Alveolar guinea pig macrophages were recovered by bronchoalveolar lavage (BAL). Macrophage reactive oxygen intermediate (ROI) production was studied by luminol-dependent chemiluminescence with several concentrations of SP and related peptides. Eicosanoid synthesis after stimulation was evaluated by thin-layer chromatography (TLC) and enzyme-linked immunosorbent assay (ELISA). SP, C-terminal sequence, and NK1-receptor agonist significantly increased ROI production by alveolar macrophages (P < 0.01). NK1-agonist and C-terminal sequence modified arachidonic acid metabolism and induced a significant increase in prostaglandin (PG)D2 synthesis (211% and 66%, respectively). We concluded that SP and related peptides directly affect guinea pig alveolar macrophages by inducing the production of inflammatory metabolites.
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Invasive pulmonary aspergillosis (API) is a necrotising pneumonia generally occurring in profoundly immunodepressed subjects. These observations were based on four patients in the intensive care unit, suffering from chronic respiratory failure (IRC), without profound immunodepression. After a pathophysiological and clinical review, a focus on the diagnostic methods permits one to stress on the reliability, in this type of patient, of the evidence from direct examination of aspergillus filaments in the bronchoalveolar lavage (LBA) or protected bronchial brushings, taking account of the weak value of routine culture of spit or bronchial aspiration in IRC in whom patients are frequently colonised. These four cases permit one to discuss the factors which predispose to the development of API outside the usual immune suppression: IRC itself, by the disorder of mucociliary function, which it leads to; repeated antibiotic therapy which destabilises the saprophytic flora; viral infections which would be responsible for transitory immunodepression. But it is above all steroid therapy which seems to be the major factor favouring the development of API without producing profound immunodepression but probably because it inhibits phagocytosis of aspergillus spores. In these circumstances it is necessary to make an early diagnosis and to use fibre optic bronchoscopy with protected sampling and bronchoalveolar lavage with a complete microbiological. Only early treatment allows one to contemplate a cure.
OBJECTIVE: This study was undertaken in order to evaluate the impact of pharmacokinetics on the toxicity of oral etoposide administered daily for 21 days. METHODS: The daily dose was 50 mg/m2. Thirty-two patients 24 males and eight females, 36 76 years old, treated for various tumour types), were evaluated. Blood samples were obtained on day 1 for all patients, and on day 21 for 16 patients. Plasma etoposide concentrations were determined by high-performance liquid chromatography, and etoposide plasma protein binding by equilibrium dialysis. RESULTS: On day 1, the mean value (with coefficient of variation for interindividual variability) for the unbound fraction (fu), area under the concentration versus time curve (AUC), and unbound AUC was 9.8% (59%), 34 mg x h/l (39%), and 3.5 mg x h/l (92%), respectively. The ratio between AUC on day 1 and day 21 ranged between 0.5 and 1.8 (mean 0.9, with CV 33%). The plasma trough unbound concentrations and the unbound AUCs both corresponding to the first administration were significantly higher in the 11 patients who had a severe neutropenia than in the 21 patients who had no or moderate toxicity. However, total etoposide concentrations did not differ between these two groups. A limited sampling strategy using the NONMEM program and a database of 89 patients previously studied was performed. The optimal sampling schedule (i.e. 1, 4, and 24 h after oral etoposide administration) allowed to obtain the AUC accurately on day 1. CONCLUSION: Individual adjustment of oral etoposide based on unbound pharmacokinetics after the first administration appears relevant and feasible.