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.

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.

In 1990, specific antituberculous chemotherapy can cure almost 100 p. cent of patients with pulmonary tuberculosis in France, provided practitioners follow strict therapeutic rules and patients' compliance with treatment is perfect. A single standard treatment is proposed for those patients whose tuberculosis has never previously been treated; it consists of a six months' course of isoniazid (5 mg/kg/day) and rifampicin (10 mg/kg/day); combined with ethambutol (20 mg/kg/day) and pyrazinamide (30 mg/kg/day) during the first two months. This treatment must be administered under regular medical supervision, and it must be prolonged for some time after cure has been obtained. In case of relapse or in some special situations (e.g. pregnant women, HIV positive patients, serofibrinous pleurisy, complex anatomico-clinical forms of the disease) treatment is more difficult, but it should always give favourable results.

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.