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Benzo[a]pyrene is a cigarette smoke component that is metabolized in the human body to the diol-epoxide derivative benzo[a]pyrene-trans- 7,8-dihydrodiol-9,10-epoxide (BPDE-I), which is the final carcinogen. BPDE-I binds covalently to DNA, producing BPDE-I-DNA adducts. A competitive immunoenzymetric assay was used to measure BPDE-I-DNA adducts in blood samples from 58 heavy smokers, 32 men and 26 women, attending a smoking cessation clinic. Cigarette consumption was evaluated based on urinary continine levels. None of the subjects worked in jobs involving exposure to polycyclic aromatic hydrocarbons (e.g., benzo[a]pyrene). Concentrations of BPDE-I-DNA adducts varied with cigarette consumption, ranging from 10.00 to 28.20 fmol/50 micrograms of DNA.

A 41-year-old female patient presenting with chylothorax was found to have pulmonary lymphangiomyomatosis. Recurrence led to parietal pleurectomy. Lung biopsy performed at surgery confirmed the histology diagnosis. Hormone treatment with medroxyprogesterone acetate was initiated immediately and administered via intramuscular injections each month. The treatment was continued for three years and regular clinical, functional and radiologic follow-up provided evidence of response: radiologic and functional stability were achieved at the cost of major secondary effects of hormone therapy. This rare, apparently hormone-dependent, disease raises the problem of the long-term benefit of treatment.

There have been few studies examining the relationship between NOD and mortality in patients with COPD and none examining this relationship in those patients with a daytime PaO2 greater than 60 mm Hg. Is NOD related to early death, and if so, should nocturnal supplemental oxygen be considered as therapy for altering survival? We examined survival in 169 COPD subjects. Two definitions were used to classify subjects as NOD and non-NOD, one considering episodic desaturation associated mainly with REM sleep (definition 1) and one considering greater than 30 percent of time in bed spent below an SaO2 of 90 percent (definition 2) to be significant. Survival corrected for age was significantly better in non-NOD subjects. However, when stratified for supplemental oxygen use, survival remained better only in subjects separated by definition 1. There was a trend toward increased survival in 35 oxygen-treated vs 38 non-oxygen-treated NOD subjects (definition 1), but this difference was not statistically significant.

The authors report the case of a patient with chronic obstructive pulmonary disease (COPD) whose renal function depends on the ventilatory pattern. The data appeared in opposition with the standard physiopathological notions with an improvement of renal function during mechanical ventilatory assistance and a degradation while spontaneous breathing. The authors suggest an original hypothesis based upon the increase of oxygen cost of breathing (OCB) with a redistribution of the intravascular blood flow to the diaphragm.

One hundred seventeen patients with severe chronic obstructive pulmonary disease whose PaO2 in a stable clinical state ranged from 41 to 59 mmHg, were included in a multicentric controlled study on the effects of long-term O2 therapy (LTO), and the results of the 3-month probationary period are given here. Arterial blood gases were checked every month in order to assess the stability of hypoxemia. Time 0 represented the beginning and T3 the end of the probationary period. Patients whose PaO2 at T3 was still between 41 and 59 mmHg could be accepted for the long-term study (Group A), whereas patients whose PaO2 had increased over 59 mmHg were excluded (Group B). Only 77 patients could be followed up regularly from T0 to T3 (40 patients were lost to follow-up, missed some visits, or suffered from acute exacerbations of the disease) and 23 of them had a PaO2 at T3 that exceeded 59 mmHg (Group B), allowing the inclusion of 54 patients (Group A) in the long-term study. Patients in Groups A and B did not differ with regard to pulmonary volumes, PaCO2 at T0 or a past history of right heart failure. Arterial O2 tension at T0 was slightly and significantly (p less than 0.02) lower in Group A (51.3 +/- 5.5 mmHg) than in Group B (54.5 +/- 3.8 mmHg), but there was an important overlapping of individual results from one group to another.(ABSTRACT TRUNCATED AT 250 WORDS)

The haemodynamic definition of chronic cor pulmonale is precapillary pulmonary artery hypertension (P.A.H.T.), which determines the long term prognosis of chronic respiratory failure (C.R.F.) due to chronic obstructive airways disease (C.O.A.D.). The essential element of the various causes for an increase in pulmonary arterial pressure (PAP) is an increase in pulmonary arterial resistance secondary to alveolar hypoxia. At the present time, only long term oxygen therapy at home seems capable of limiting the progression of P.A.H.T., with a favourable influence on survival as demonstrated by two recent Anglo-Saxon multicenter surveys. The value of new drugs which have been proposed as a complement to or even a replacement for oxygen therapy, such as Almitrine dimesylate and Nifedipine, is currently being evaluated.

Two uses of intermittent positive pressure can be distinguished: one supports inhalotherapy and the other longterm assisted ventilation. The apparatus can be connected to the patient either through mouth-piece or by tracheostomy. The main factors involved in the indication of assisted ventilation are the number of acute failures, hypoxemia, hypercapnia, cor pulmonale. In our department, 53 patients were kept under prolonged supervision before a decision was made to use assisted ventilation or not. This attitude seems absolutely necessary. An oxygen test of several hours provides very useful information. Finally, the authors review the indication of various ventilation methods (tracheostomy, oral) in relation to different chronic respiratory insufficiency etiologies (ie., chronic obstructive broncho-pneumonia, restrictive syndrome).

22 patients (4 female, 18 male) suffering from severe chronic obstructive respiratory failure (IRCO), were given artificial ventilation because of a super-imposed acute respiratory failure (IRA). The object of this study was to compare different methods of weaning patients from the ventilators using either intermittent mandatory ventilation (IMV) or an automatically triggered ventilation (VAD). Both blood gases in the acute phase and the functional data collected before the acute exacerbation failed to show any statistical difference between the two groups. The reduction of ventilation in the group of patients weaned by the technique of IMV did not appear statistically significant as shown by the following facts : controlled ventilation (IMV : 2.45 +/- 2.06 days; VAD : 4.72 +/- 3.89 days) : total duration of ventilation (IMV : 7.35 +/- 2.15; VAD : 8.54 +/- 6.56 days). The PaO2 of the subjects weaned by the technique IMV appeared higher before extubation (P less than 0.02) than the PaO2 obtained after weaning on VAD. In patients presenting with an acute exacerbation of chronic obstructive respiratory failure secondary to a bronchial infection the different techniques of weaning used (whether VAD or IMV) appear identical as regards the total duration of ventilation.

Serial blood gas measurement must be made for at least three months following an acute exacerbation of chronic obstructive pulmonary disease, to secure stable arterial oxygen tension (PaO2) values. The borderline indications of oxygen therapy concern the patients who have PaO2 over 8 kPa (60 mmHg), but have nocturnal hypoxaemia and/or pulmonary hypertension. The indications of specific drugs such as almitrine are still subject to discussion. The presence of obstructive sleep apnoeas together with ventilatory troubles related to chronic obstructive lung disease (overlap syndrome), is associated with many diagnostic and therapeutic problems.

Forced expiratory volume in the first second (FEV1) and serum theophylline levels were measured comparatively in 26 patients with stable bronchial asthma after a 240 mg theophylline infusion. The mean (+/- s.e.m.) elimination half-life and clearance of theophylline were 6.37 +/- 2.03 hours and 0.78 +/- 0.31 ml/min/kg respectively. A bronchodilator response (more than 20% increase in FEV1) was obtained in 17 patients whose pretreatment FEV1 was less than 30% of predicted normal values. No significant bronchodilator response was obtained in the other patients. There was no relationship in responders between changes in FEV1 and simultaneous serum theophylline levels. Maximal ventilatory response was apparent 1 to 2 hours only after the theophylline peak concentration.

The effects of oxygen administration were studied in 10 patients with severe obstructive lung disease. Sleep variable and gas exchanges were measured during two nights: one when they were breathing environmental air, the other when they were receiving oxygen. Carbon dioxide saturation and partial pressure measured by the transcutaneous method were continuously recorded. Sleep was perturbed in all patients, but despite wide interindividual variations its amount and quality were improved by oxygen. None of the patients had sleep apnoea syndrome. Oxygen administration was accompanied by a nocturnal increase in carbon dioxide pressure that was about twice as high as that observed under environmental air. Thus, in patients with chronic obstructive lung disease without concomitant infection suppression of the hypoxic stimulus by oxygen therapy seems to result in an increase in carbon dioxide partial pressure identical with the increase produced by sleep alone. Correlations between diurnal and nocturnal oxygen saturation and carbon dioxide partial pressure indicate that patients with the highest degree of hypoxia and hypercapnia in daytime have the most severe nocturnal blood gas disorders.

The influence of nocturnal oxygen therapy on ventilatory disorders and sleep abnormalities was evaluated in 5 male, non-obese patients with advanced chronic obstructive pulmonary disease (COPD). All had hypoxia, severe airway obstruction (FEV1 less than 1 l) and pulmonary arterial hypertension at rest; 3 had PaCO2 values above 50 mmHg. Polygraphic recordings were taken throughout the night, the patients breathing either air or oxygen, they included EEG, electromyography of chin muscles, eye movements, O2sat., thoraco-abdominal mechanics and nasal flow. Improvement in the quality of sleep under oxygen was observed in all patients, with an increase from 6.1% (air) to 14.6% (oxygen) in the R.E.M. (Rapid Eye Movement) sleep phase duration to total sleep duration ratio, and an increase from 8 to 12 in the number of episodes of apnoea (arrest of nasal flow greater than 10 sec). Oxygen also had a favourable influence on the number and amplitude of O2 desaturation phases (delta O2sat. greater than 4%) and on the time spent in desaturation, which decreased from 5.12% (air) to 3.7% (oxygen). Correction of the hypoxaemic episodes was partial in those R.E.M. sleep phases when these episodes were most severe and occurred in the absence of apnoea.