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Oxidative stress is a frequent mechanism involved in the pathogenesis of bronchopulmonary disease. The cause can be exogenous, in particular related to to atmospheric pollution and tobacco smoke, or endogenous, related to mobilization of inflammatory cells (macrophages and polymorphonuclear neutrophils). In this general review, we present work demonstrating this oxidative stress and activation of inflammatory cells. We discuss the effect of oxidative stress on the bronchial tree and the need to maintain an adequate balance between oxidants and anti-oxidants. This reviews focuses on experimental studies proving the anti-oxidant effect of NAC on glutathione synthesis and on different pharmacological models. We then discuss human trials, initially experimental then in different bronchopulmonary pathologies related to oxidative stress. Acetaminophen intoxication and pulmonary fibrosis are models for use of NAC. Recent work on COPD appears to show a decrease in exacerbations, improvement in symptoms and quality-of-life, and perhaps a reduction in the alteration of ventilatory function.

Levofloxacine is a fluoroquinolone presenting good anti-pneumococcal activity, including against strains with reduced sensitivity to penicillin. Four randomized controlled studies have compared the efficacy of levofloxacine versus other antibiotics (amoxacillin-clavulanic acid, amoxicillin, ceftriaxone, ceftriaxone plus cefuroxime +/- erythromycin) for the treatment of acute community-acquired pneumonia in adults. Grouping the 1,738 analyzable patients in these four studies, a meta-analysis was performed on the sub-group of 275 patients with documented pneumococcal infection (86 with bacteriemia) in order to compare the efficacy of levofloxacine with that of the comparer antibiotics. The trials were homogeneous, allowing the meta-analysis. The overall rate of clinical success was 88.6% in the levofloxacine group and 86.7% in the comparer group. The interval of confidence for the difference in the rate of estimated clinical success was between -5.65% and +9.39%. Bacteriologically, the rate of eradication was 90.2% and 90.4% respectively with an interval of confidence for the difference between -7.83% and +7.36%. The results of this meta-analysis confirmed that the efficacy of levofloxacine for the treatment of acute community-acquired pneumococcal pneumonia is not inferior to that of the comparers; the interval of confidence for the difference in the estimated rate of success did not include the breaking point of non-inferiority (-10% set for the clinical studies) and included zero.

Every thromboembolic manifestation, especially in young subjects, calls for an aetiological study in which haemostasis is evaluated primarily with assays of physiological coagulation inhibitors: protein C, protein S and antithrombin III. Protein C deficiency is found in 6 to 7% of thromboembolic manifestations. We report the case of a 21-year old man who had phlebitis followed by pulmonary embolism without facilitating factors. Protein C level was 50% of normal value (0.50 IU/ml). The patient received heparin, subsequently replaced by oral anticoagulants after a long period of overlap between the two treatments. The outcome was favourable. Family investigation yielded a history of thromboembolic accidents in several members of the family, some of whom were protein C deficient (50% of normal value). Protein C synthesis is vitamin K-dependent. Protein C deficiency is transmitted as an autosomal dominant trait. Normal values range from 0.65 to 1.35 IU/ml. Clinically, 25% of the patients are said to be asymptomatic. The first thrombotic accidents occur in young subjects (mean age 29 +/- 14 years). Several points emerge from this case: full evaluation must be performed, especially in young subjects; family investigation consolidates the diagnosis and enables symptomatic protein C deficient patients to be treated and thrombotic manifestations to be prevented by effective anticoagulant therapy in high-risk situations; a prolonged period of heparin-oral anticoagulant overlap is needed to avoid cutaneous necrosis.

It is very uncommon to find several cases of sarcoidosis in the same family. In the majority of published reports, only 2 persons are involved in each family. Genetic predisposition is probably, but its true importance as compared with environmental conditions is uncertain owing to the lack of epidemiology studies. We report 3 cases of sarcoidosis in the same family. In 2 of these cases (2 black sisters) the clinical set up was similar, consisting of multivisceral sarcoidosis involving the lung and mediastinum, the skin and the peripheral lymph nodes and muscles, with poor general condition and dependence on, or resistance to corticosteroids. Although the two sisters lived in different countries for several years and despite the 4-year age difference between them, the disease began in both cases at the age of 40 years. The history of this family is exemplarily in favour of a genetic predisposition and suggests than the penetrance of genetic transmission is underevaluated. Systematic pulmonary clinical and radiological examinations performed in the relatives of patients with sarcoidosis might provide information on the true incidence of familial cases. Studies of the genetic equipment of these familial cases would perhaps constitute a line of research aimed at determining the pathogenesis of the disease.

In a multicenter trial conducted with patients suffering from chronic bronchopathy, Biostim, an immunomodulating compound of biological origin has been studied using the double-blind placebo-controlled method for prevention of respiratory tract infections. One hundred and ten patients from 10 french pneumology health centers entered the study. The treatment was administered at random in three sequences of 8 days a month for 3 months (2 mg/day the first month, 1 mg/day the second and third months). Patients were separated into 2 groups regarding severity of the disease: group I (non complicated chronic bronchitis); group II (obstructive chronic bronchitis with or without respiratory failure). Patients were examined during 6 months with a monthly appraisal of number, duration and treatment clinically defined infectious episodes. The study of propensity to infections with respect to severity of the disease in patients given placebo showed a significantly lower number of infectious episodes in group I when compared to group II. In the group I (patients suffering from simple chronic bronchitis), no significant difference could be noted between placebo and Biostim but, at all events, the low frequency of episodes makes it difficult to evidence a protective effect in such a group. In contrast, with patients presenting a high infectious risk (group II), one can observe in Biostim treated patients compared with placebo group a significant decrease of infectious episodes and a larger number of patients standing free of episodes throughout the whole period of trial. Tolerance to Biostim has revealed itself satisfactory.

Several immunologic abnormalities exist in patients with active sarcoidosis. Impairment of in vivo and in vitro cellular immunity is well known. Humoral immunity disorders are characterized by increase in polyclonal serum immunoglobulin, existence of circulating immune complexes and auto-antibodies. In the serum, these abnormalities are nearly the same than disorders observed during auto-immune diseases. We report 2 cases of patients where active sarcoidosis was associated with auto-immune disease. Then we discuss the relationship which could exist between the 2 types of diseases. The first patient was a woman (aged 66 years). She presented an active sarcoidosis and clinical symptoms of sclerodermia. The second patient, a man (aged 24 years), presented active sarcoidosis diagnosed 4 years ago. He had never received any treatment. Thrombopenic purpura occurred suddenly and needed steroid therapy. Antibodies to platelets were found in the serum. These associations raise some questions: 1) are they only fortuitous? such cases are rare but their frequency is perhaps underestimated; 2) could any common abnormalities of the immune response explain the emergence of the 2 diseases? 3) could one of the diseases favour emergence of the other? This hypothesis seems possible only if sarcoidosis is the initial disease. Eventually these associations also raise difficult therapeutic problems and must incite to explore precisely the immunity of patients with active sarcoidosis.

The authors discuss the epidemiological problems of legionnaire's disease. Although Legionella is known to proliferate in watery environments, the origin and extension of sporadic cases and the factors responsible for bacterial spread remain unclear. The problem of prevention has also to be resolved.

A series of 125 CT-guided thoracic punctures performed over a 20-month period is reported. The only complications were pneumothorax in 14 cases, 5 of which were drained, and 1 case of hemomediastinum. For the diagnosis of malignancy the sensitivity of the method was 82%, its specificity 100% and its effectiveness 74%. The level of sensitivity rose to 86% in the last 90 cases. This method is an additional contribution to exploration of the lungs. In trained hands it gives rise to few complications and should result in a histological diagnosis in a large number of cases.

The authors report the 3 first cases of human syngamosis due to Mammomonogamus sp. in La Guadeloupe (French West Indies). After a review of the papers published on the previous 79 world-wide cases, they point out that this parasitic disease is restricted to the West Indies/South America area, and discuss the problem of the contamination mode; they claim that chronic cough is a constant signal symptom which suggests syngamosis in subjects who are native from, or have travelled in the endemic area.