Search

Resume Les auteurs rapportent l’observation d’un homme de 53 ans pris en charge pour pneumopathie hypoxemiante. Le lavage alveolaire objectivait une alveolite neutrophilique et les recherches d’agents infectieux etaient negatives. Une biopsie pulmonaire objectivait un discret œdeme endo-alveolaire et un infiltrat polymorphe dans les parois alveolaires moderement epaissies. Une antibiotherapie inefficace etait remplacee, apres 17 jours, par une corticotherapie. La symptomatologie clinique et radiologique s’ameliorait alors en quelques jours et la pneumopathie ne recidivait pas a l’arret des corticoides. A l’origine de cette pneumopathie, les auteurs incriminent la minocycline que recoit ce patient depuis 2 ans pour un rhinophyma. Ce traitement avait ete suspendu pendant quelques semaines et c’est apres sa reprise qu’etait apparue la pneumopathie. Les differentes manifestations cliniques des pneumopathies a la minocycline sont ensuite passes en revue : pneumopathies a eosinophiles, BOOP, pneumopathies d’hypersensibilite. Un seul cas de polynucleaires neutrophiles au lavage a ete anterieurement rapporte.

Hemostatic disorders can be found in approximately 90% of cancer patients, but clinical expression in only 15%. Hemorrhagic complications are more frequent in acute leukaemia; solid tumors are often associated with deep venous thromboses (DVP). Disseminated intravascular coagulation syndrome (DICS) can be latent or acute, and has various clinical presentations, occurring in the course of many serious conditions including cancer. Patients have higher morbidity and mortality. Irrespective of the etiology, DICS can be revealed by a wide variety of clinical manifestations, from mild biological hemostasis disorders, to intravascular or extravascular microthromboses or lethal hemorrhagic events. We report the case of a 45-year-old female with non-small-cell lung cancer with metastases at diagnosis. The patient developed and finally died of numberous thromboembolic events subsequent to DICS. This case illustrates some rather rare complications of DICS and offers the opportunity to discuss the main therapeutic goal in this situation, i.e. to modulate the disproportionate production of thrombin, inducing thromboses and/or hemorrhages by consumption of the cellular and plasmatic coagulation factors. This means a symptomatic and mostly etiologic treatment, especially chemotherapy which can in itself provoke thromboembolic events.

Pituitary metastases are rare and generally asymptomatic. We studied 5 patients with pituitary metastases from lung cancer, illustrating the different clinical features. These metastases were in these cases symptomatic with the manifestation being diabetes insipidus or visual field defect. Histological subtypes from our five patients were as well small cell or non small cell lung cancer. After diagnosis of pituitary metastasis, prognosis seems to be linked to the histological subtype and the stage of lung cancer, rather than to the presence of such metastases.

We report a clinical case of a persistent left superior vena cava discovered in a 50-year-old female patient when a port-a-cath was inserted. This already seldom malformation was associated with an arteria lusoria and polysplenia with left inferior vena cava with hemiazygos continuation, right-sided stomach, short pancreas, preduodenal portal vein and intestinal malrotation, but without any cardiac abnormalities.

We report the case of a 35-year-old woman in whom a systematic thoracic x-ray led to the diagnosis of unilateral hyperlucent lung due to a carcinoid tumor obstructing the main left bronchus almost completely. Injected computed tomography permitted diagnosis of left lung hypoperfusion and visualization of the tumor. After enlarged inferior left lobar resection, normal perfusion was observed six months later on the isotopic lung perfusion scan. Other reported causes of unilateral hyperlucent lung are discussed as well as pathophysiological mechanisms of lung hypoperfusion and hypoxic vasoconstriction.

A 53-year-old man was treated for hypoxic pneumonia. Alveolar lavage revealed neutrophilic alveolitis and search for an infectious agent was negative. Lung biopsy revealed discrete endo-alveolar edema and polymorphous infiltration in moderately thickened alveolar walls. After 17 days, an ineffective antibiotic regimen was replaced by corticosteroids. Clinical and radiological signs improved in a few days and pneumonia did not recur after corticosteroid withdrawal. The most likely causal agent was minocycline which the patient had received for two Years for the treatment of rhinophyma. Minocycline had been interrupted several weeks when the pulmonary disorder developed after re-introduction of minocycline. Different clinical manifestations of minocycline-induced lung disease have been described including eosinophilic pneumopathy, bronchiolitis obliterans with organized pneumonitis, and hypersensitivity pneumonitis. There has only been one report of polymorphonuclear neutrophils observed in the lavage fluid.

Over the last decade, advances in our knowledge of allergens and in methods for determining their structure have given the clinician a molecular rather than macroscopic view of allergy. The prevalence of sensitization to different allergenic molecules is known for the principal pneumallergens. This knowledge is crucial for understanding the cross reactions between respiratory allergens. The main cross reactions are described here for pollen, mites, roaches, and mammals. In addition, the biological function of a certain number of respiratory allergens are known. Allergens with an enzymatic function, allergens with a transport function, allergens implicated in the regulation of muscle contraction, and allergens participating in the protein defense system have been identified. Potential factors underlying the allergenicity of airborne allergens are discussed: physical properties, structures, biological functions. The diversity of biological functions prohibits retaining a single specific function as a prerequisite for allergenicity; certain major allergens do not have a defined function. No structural form appears to be incompatible with the allergenic potential of a protein found in the environment.

We report the case of a 28-year old man suffering from rhinitis and asthma which appeared 8 years after exposure to different woods, especially abachi wood. Serial PEFR monitoring at work and away from work were consistent with occupational asthma. Spirometry showed an airway obstruction, and metacholine inhalation test was positive. Skin prick-tests performed with different woods were only positive to abachi wood extract. The search for specific IgE was positive to abachi wood (4, 98 KU/l, class 3). The diagnosis of occupational asthma caused by exposure to abachi wood was established, the mechanism underlying this asthma was IgE mediated. Despite respiratory protection measures, the patient had persisting symptoms and was laid off. The German service for social cover asked for an expert evaluation: specific nasal and inhalation provocation tests performed by exposure to fine abachi wood dust were positive. This is an observation with a double significance: first, although the mechanisms underlying wood occupational asthma remain largely unknown, an IgE mechanism for abachi wood was demonstrated; second, legislation is different in France and Germany where occupational asthma will only be acknowledged if inhalation tests are positive.

The differential diagnosis between infectious complications and tumor progression is sometimes difficult in patients given cytotoxic drugs. We report a case of diffuse interstitial lung disease induced by gemcitabine, a new agent used for the treatment of advanced-stage non-small-cell lung cancer.

We report a series of 19 cases of bronchiolitis obliterans with organized pneumonitis (BOOP) observed in two pneumology units at the Strasbourg University Hospital between July 1987 and June 1997. Mean patient age was 60 years. Clinical features included dry cough, exercise-induced dyspnea, and a flu-like syndrome in three-quarters of the cases. Standard chest x-ray showed a diffuse non-systemized alveolar syndrome with a air bronchogram in 18 cases and an interstitial syndrome in one-third of the cases. computed tomography of the thorax visualized bronchial dilatations by traction of the alveolar syndrome in one-third of the cases. Pulmonary function tests showed moderate restriction. Lymphocytes predominated in bronchio-alveolar lavage fluid. Pathology examination of surgical lung specimens (5 cases), transbronchial biopsies (5 cases) and scan-guided transparietal punctures (4 cases) provided the diagnosis. In 5 cases the diagnosis was based on the radiological and clinical presentation and favorable course on corticosteroid therapy. Recurrence was observed at corticosteroid withdrawal or dose reduction in 7 cases. In this series, bronchiolitis obliterans with organized pneumonitis was probably secondary to rheumatoid arthritis (1 case), breast radiotherapy (3 cases), and drugs (amiodarone: 1 case: sotalol: 2 cases: betaxolol: 1 case). An association with betaxolol has not been previously reported in the literature.

We review the methods available for determining airborne pollen. In addition to the classical gravimetric and volumetric methods, new immunochemical techniques are also used for detecting allergenic pollen and measuring of the size of allergen-carrying particles. Pollen counts are available in France for 39 urban sites. In the last decade changes in the pollen environment have basically concerned higher counts from resinous trees in southern France and birch tree counts in northern France as well as a lesser role for ash trees. Among the recent acquisitions, it has been demonstrated that allergens are present in twigs and leaves, or even the bark of certain trees. Interactions with atmospheric pollution is better understood and could be a contributing factor to the increasing number of people allergic to pollen. Pollen allergens can be carried on particles of various sizes and immunochemical studies have demonstrated that gramineous pollen allergens can be carried on starch particles less than 3 mu in diameter. These recent studies would explain the apparent disagreement between pollen counts and the number of clinical manifestations.

The authors report the case of a patient with a pancreatic carcinoma who developed lung metastases mimicking a diffuse bronchiolo-alveolar carcinoma. Such features have already been described mostly with carcinomas of the digestive tract but also with breast, and head and neck carcinoma. Macroscopically and microscopically there is no difference between these lung metastases and a primitive bronchiolo-alveolar carcinoma. Identification of a surfactant protein might identify a primitive bronchiolo-alveolar carcinoma.

Specific bronchial provocation tests can confirm the diagnosis of occupational respiratory disease and also identify the causal agent of occupational asthma. The changes in French regulations established in 1993 which allow other agents to be recognized as causal in compensation for occupational diseases has increased interest in these tests. The different diagnostic methods used for occupational asthma are discussed here with special emphasis on limitations in each case: history taking, immunological investigations, respiratory function tests, measurement of peak flow during occupational activity and holidays, sequential measurements of non-specific bronchial hyperreactivity. The difficulty in standardizing specific provocation tests used for occupational asthma is related to the wide variety of causal agents which can be inhaled as gas, aerosols or powders. Because of the required precautions, these tests must be performed by specialized personnel in hospital units. There are also limitations to specific provocation tests. False positives require placebo tests and false negatives may result from insufficient identification of the causal agent. Exposure time may be too short or concentrations too low, and may depend on how long the causal agent has been evicted. Specific provocation tests may be avoided when the clinical history reveals a typical situation due to an agent known to cause occupational asthma and repeated peak flow measurements at the working site and/or immunological sensitisation tests provide objective evidence. But in a certain number of cases, specific investigations are required to obtain the precise etiological diagnosis required to evict the allergen rapidly and avoid chronic asthma.

There is a certain controversy over whether there is a relationship between passive smoking and bronchogenic cancer. The first epidemiology studies has found a small increase in the relative risk. Experimental work in animals have demonstrated that the smoke produced by a burning cigarette contains more cancerogenic agents than the smoke inhaled by a smoker. In man where only epidemiology studies are possible, the problem lies in quantifying exposure to passive smoking. Questionnaires or assay of markers such as CO and HbCO, thiocyanates, nicotine and its metabolite cotinine and certain adduits have been used. There are many possibilities for bias in such studies including classification of smokers among non-smokers, confounding factors (age, profession, eating habits), subjects' memory, and data collection errors. Meta-analyses have attempted to overcome the lack of power in many studies. Some of these meta-analyses have used correction factors to take into account publication bias. Meta-analyses have led to the conclusion that the risk for women exposed to their husband's tobacco smoke is somewhat increased compared with a non-smoking non-exposed population. The relative risk is about 2-fold higher and has been observed in Greece. The existence of a dose-intensity relationship has not been confirmed. Likewise, it is impossible to conclude concerning the role of passive smoking in children due to the small amount of data available.

As the number of proteins recognized as causing allergic respiratory diseases increases, new aero allergens have appeared in the animal and vegetable realms, both in home and professional environments. Lepidoglyphus destructor and Blomia tropicalis, two mites found in storage areas, are particularly important in agricultural areas and in homes. Over the last ten years, the frequency of reactions to cockroaches has also increased in several countries. The allergenicity of non-biting insects is a frequent cause of allergy in certain countries including Japan. Chironomides cause respiratory diseases in professional and outdoor environments. The important role of Alternaria, a mold, in producing severe asthma has also been demonstrated. The pathophysiology of pollen-induced asthma has been shown to result from pollen allergens carried by particles less than 5 microns in diameter. Cyprus and ash tree pollen also cause an increasing number of pollinoses and flowers can cause rhinitis and asthma. Respiratory allergy to Ficus benjamina inaugurated a new type of allergies caused airborne allergens from non-pollinating plants. Allergy to latex raises a particular problem for health care workers. The immunochemical structures of the major and minor airborne allergens are now better known and the homologous structures of different allergens largely explains certain cross-reactions. In the future, recombinant allergens will probably be used to better understand the role of allergens in inducing and maintaining the allergic reaction and should help in our approach to diagnosis and therapy.

Isocyanate-induced occupational asthma is a model of experimental asthma related to the environment. Many of its features are identical with those of allergic asthma by sensitization to air-borne allergens. Exposure to isocyanate before the first symptoms of asthma varies from a few weeks to several years. The prevalence of isocyanate-induced asthma has been estimated at 5 to 25%. Atopy is found in less than 30% of the cases. A significant increase of HRBNS can be demonstrated in most patients, but it may be absent. It may also fluctuate with the working periods or after a bronchial provocation test with isocyanate. Elimination of this compound reduces the HRBNS level in only one quarter of the cases. Delayed or biphasic reactions are frequent: 30 to 60% depending of the authors. An early diagnosis followed by total elimination may result in complete cure, but more than 50% of the patients remain symptomatic and with HRBNS. An IgE-dependent mechanism can be demonstrated in about 20% of the cases. The course of isocyanate-induced asthma is interesting in that the same phenomena are probably observed in chronic asthma resulting from repeated exposures to environmental allergens.

The authors describe the methodology of allergen challenge tests, with special attention to some particular aspects, such as the allergenic extracts and their biological activity, and the methods used in aerosol administration and in measurements of bronchial obstruction. They present the results of their personal experience, concerning interindividual variations in a sensitized population and the reproducibility of the immediate reaction revealed by dose-response curves. Comparisons of allergen tests with exposure to allergens under physiological conditions are discussed. In occupational asthma the exposure tests sometimes constitute the only diagnostic method, owing to ignorance of the responsible mechanisms and to the multiplicity of incriminated substances. However, these tests are not without danger and must be performed by well-trained medical and paramedical teams.

Recurrence of thoracic sarcoidosis after spontaneous regression is extremely rare. Its existence is proven by two new cases associating sarcoidosis with L ofgren 's syndrome and sarcoid in skin scars, the latter facilitating the recognition of the presence of thoracic disease. Surveillance of the behaviour of scars forms part of routine examinations in the sarcoid patient. Even when there has been total spontaneous regression, subsequent clinical and radiological follow-up every two years must be continued.

Although on the increase overall, the actual prevalence of occupational asthma is difficult to assess because of variations seen according to periods, countries, jobs, and the agents responsible. In the authors' experience, this prevalence is slightly less than 10%. Three principal mechanisms, sometimes present together, not always elucidated: immunological, reflex and irritative, are responsible for such asthma. Whilst a positive diagnosis raises few problems, the aetiological diagnosis is difficult and involves two stages: recognition of the occupational characteristic of the asthma and attribution of this asthma to an allergen or substance in the occupational environment. Skin tests and in vitro tests, but above all exposure tests, make an important diagnostic contribution. Personal examples are used to illustrate the principal aetiological factors in occupational asthma of animal, vegetable or chemical origin.

The commercial availability of high-dose inhaled corticosteroid preparations for the treatment of asthma offers an occasion for reviewing the different mechanisms of action of glucocorticoids notably glucocorticoids, notably their interference with lipocortin protein synthesis and arachidonic acid metabolism. A favourable effect on bronchial hyper-reactivity and on delayed hypersensitivity reactions has also been observed. The problems raised by the various preparations responsible for varying degrees of systemic activity, the difficulties inherent in the use of inhalers and the side-effects of these products are discussed. The effectiveness and safety of the current high-dose inhaled preparations are emphasized.

Allergy reactions may be regarded as resulting from exposure to allergens of subjects who are genetically predisposed to synthesize IgE. The presence of allergens in the environment is necessary to acquire sensitization. With some allergens, sensitization seems to develop very rapidly. The introduction or presence in the environment of certain allergens, such as house dust mites, may increase the prevalence of asthma. Despite conflicting reports, in atopic subjects exposure to pet animals also is a risk factor. Introducing foreign proteins prematurely into infant's food has been considered a factor that facilitates the development of allergic diseases. Contact with occupational allergens results in allergic manifestations in less than one-third of the subjects exposed, which suggests that genetic factors play a predisposing role. Beside exposure to allergens, non-specific environmental factors, such as chronic inhalation of tobacco smoke or atmospheric pollutants (e.g. ozone, SO2, NO2, particles of burnt fuels) might contribute to sensitization. The part played by viral infections (RSV or influenza virus) in the triggering of allergic diseases has often been reported. Interactions between irritants and allergens may encourage the development of respiratory allergy.

A prospective study of clinical, cutaneous and biological sensitivity to the common air-borne allergens was conducted over a 16-year period in a total of 3,962 patients who reported to a hospital consultation for respiratory allergy. The study confirmed certain widely recognized semiological features, but it did it on the basis of a real population with a large number of subjects and therefore was a true textbook of allergology with a live material. In addition, the study benefited from the major advantage of computer data processing: an accurate and rapid analysis. Yet some uncertainties and omissions remained concerning answers to certain questions, but such gaps are inherent in the natural subjectivity of allergic patients and their doctors.

Serum levels of angiotensin conversion enzyme (A.C.E.) are increased in 60 to 80% of cases of sarcoidosis. A.C.E. levels were measured as part of the initial assessment of 70 patients with the disease, with repeated measurements in 18 of them. The subsequent course of sarcoidosis was evaluated over a minimum period of 7 months, in relation to initial serum A.C.E. levels. A high serum A.C.E. level is indicative of the secretion of the cells of the epithelioid and giant cell granuloma and reflects the activity of the disease at the particular time without providing any definite prognostic information. Study of 6 patients treated with corticosteroids showed that serum A.C.E. levels rose again when treatment was reduced or stopped in 4 of them, this renewed rise appearing to precede the radiological recurrence. Whilst the prognostic value of alveolar lymphocytosis is greater than that of serum A.C.E. levels in sarcoidosis, measurement of serum A.C.E. is easier in the context of therapeutic surveillance.

Forty-five patients with severe, poorly controlled asthma, including 23 corticosteroid-dependent patients, were treated with a preparation of beclomethasone dipropionate aerosol delivering 250 mcg per puff. The daily dose ranged from 1000 to 2000 mcg. The mean follow-up period was 14 +/- 7 months, and 11 patients have now been followed up for more than 2 years. Forty-two patients were improved, and total withdrawal of continuous steroid therapy could be achieved in 13 cases. Treatment remained effective in long term use, provided a minimum of 1000 mcg/day was given. However, despite clinical improvement the obstructive syndrome persisted in 65% of the patients.