European journal of respiratory diseases最新文献

This trial was performed in a randomized double-blind manner on four different days in 13 asthmatic patients in order to compare the bronchodilator efficacy of two different inhalation devices, Inspirease (IP) and Aerochamber (AC), to the conventional metered dose inhaler (MDI). The results showed that clenbuterol determined a significant FEV1 increase inhaled either via MDI or via IP and AC. IP caused a greater bronchodilatation than AC, 30 min after clenbuterol administration. IP caused a greater mean increase (P less than 0.05) in FEV1 than the MDI at all time intervals; AC provided an improvement in bronchodilator response over directly administered MDI. Such responses are only marginally clinically relevant when patients use MDI correctly. These devices are mainly indicated in patients with poor hand-lung coordination.

We report two patients with Churg-Strauss syndrome (CSS), who presented with life-threatening alveolar haemorrhage as the major manifestation of their disease. One improved on high doses of steroids and cyclophosphamide; the other deteriorated on prednisolone alone, but responded rapidly to the addition of cyclophosphamide and plasma exchange. On follow-up, neither showed further evidence of lung disease except for well-controlled asthma. Pulmonary haemorrhage is a well-recognised phenomenon in patients with other forms of systemic vasculitis, and CSS must now be considered in the differential diagnosis of such cases.

The diagnosis of bird breeder's lung (BBL) depends upon a range of epidemiological, clinical, radiological and immunological arguments. The simple detection of antibodies cannot constitute a pathognomonic criterion of BBL. We applied the enzyme-linked immuno-filtration assay (ELIFA) to the study of 50 sera chosen from 2509 samples taken from subjects exposed to avian antigens. The arc-IgAp was detected in all sera samples (n = 27) taken from symptomatic subjects (n = 16), but was only demonstrated 3 times out of 2466 samples taken from exposed asymptomatic subjects. The ELIFA method revealed IgG, IgM, IgA and IgE precipitating antibodies only in the case of clinically ill subjects. Finally, this technique demonstrated a second functional antigenic component (arc-P2) which preferentially induced specific immunoglobulins of different classes. Compared immunological profiles (CIP), established by ELIFA, seem to be highly significant for BBL, and correlate well with pathological symptoms and their evolution.

A new dosimeter nebulization method was studied in 10 asthmatics and 8 normal volunteers by delivering fixed doses of 99mTc-traced radioaerosol in 0.2 s periods of tidal breathing. Two separate inspiratory phases were studied with the onset of nebulization, when in the earlier phase 15% and in the later phase 60% of tidal volume was inhaled. Further, bronchodilator administration was analogically assessed in the asthmatics. In healthy subjects, the total lung deposition was 17% greater in the earlier phase (p less than 0.005) than in the later one. In asthmatics, the difference was not significant. The losses of aerosol outside the lower respiratory tract were minimized, in the mouthwashing 0.3% and in the exhaled air 1.4%. The onset of nebulization (early or late) had no significant effect on bronchodilation with salbutamol in asthmatics. We conclude that the present dosimeter method is useful for efficient delivery of radioaerosols and drugs, and for standardization of bronchoprovocation.

The degree of physical activity at the onset of spontaneous pneumothorax was evaluated retrospectively in 219 patients, predominantly smokers who had had this disease for the first time. More than 87% had been inactive at the onset of the symptoms. Moderate exertion was recorded in only 2%, and no patients were exerting themselves heavily when the symptoms began. The occurrence of spontaneous pneumothorax was unevenly (p less than 0.001) distributed over the day. In 9% the symptoms had their onset during quick movement--such as fastening a seat belt--without any effort. The inactivity or low activity at the onset of symptoms of spontaneous pneumothorax suggests that this condition is unrelated to muscle effort.

To study the origin of increased serum placental-like alkaline phosphatase (PLAP-like) activity in smokers, heat stable alkaline phosphatase activity was assayed from serum and bronchoalveolar lavage (BAL) fluid in 83 smoking and non-smoking patients. PLAP-like activity was increased in about 80% of the smokers, independently of the underlying lung disease. Isoenzyme activities in BAL fluid correlated (r = 0.631, p less than 0.001) with serum values. When adjusted for the albumin concentration, mean PLAP-like activity in BAL fluid was almost 1000-fold higher than that in serum, suggesting local synthesis of PLAP-like isoenzymes in the lungs. Although a direct dose-response effect was not observed, the values in serum and in BAL fluid tended to be higher in patients smoking over 10 cigarettes daily as compared to patients smoking less. In ex-smokers the results indicated that PLAP-like activity decreased to the level observed in non-smokers within 5 years after cessation of smoking. PLAP activity was L-leucine sensitive compatible with the Nagao-variant type of PLAP in almost all cases. In three patients the activity was due to the L-leucine resistant (true placental) isoenzyme.

The aim of this study was to investigate whether a direct causal relationship exists between gastro-oesophageal (GO) reflux episodes and bronchial asthma. Forty-two patients with moderate or severe asthma and pathological GO-reflux were examined using a 24-h pH test at a proximal and a distal level of the oesophagus. Respiratory symptoms and the use of extra beta-2 agonist metered dose inhaler were recorded in a standardized protocol, and peak expiratory flow (PEF) was recorded once an hour until the patient went to bed. No association was found between reflux at either the proximal or the distal level of the oesophagus and bronchial symptoms or PEF reductions. We conclude that GO-reflux does not play an important role as an immediate trigger factor in bronchial asthma.