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Biomedical subjects

N A Martelli

Publications and source records attributed to N A Martelli.

13 recordsLinked to original sources
PubMed2003

Once-daily budesonide/formoterol in a single inhaler in adults with moderate persistent asthma.

Patients with moderate persistent asthma (n = 523; mean FEV1 77.4%) not fully controlled with inhaled corticosteroids (ICS; 400-1000 microg/day) were randomized to receive either once-daily budesonide/formoterol (160/4.5 microg, two inhalations); or twice-daily budesonide/formoterol (160/4.5 microg, one inhalation); or budesonide (400 microg) once-daily for 12 weeks. Once-daily dosing was administered in the evening and twice-daily dosing was administered in the morning and evening. All patients received twice-daily budesonide (200 microg) during a 2-week run-in. Compared with budesonide alone, change in mean morning and evening peak expiratory flow was greater in the once-daily budesonide/formoterol group (27 and 171 min(-1), respectively; P < 0.001) and twice-daily budesonide/formoterol group (23 and 24 l min(-1), respectively; P < 0.001). Night awakenings, symptom-free days, reliever-use-free days and asthma-control days were all improved during once-daily budesonide/formoterol therapy vs. budesonide (P < or = 0.05). Similar improvements were also seen with twice-daily budesonide/formoterol (P < or = 0.05). The risk of a mild exacerbation was reduced after once- and twice-daily budesonide/formoterol vs. budesonide (38% and 35%, respectively; P < 0.002). All treatments were well tolerated. Budesonide/formoterol, once- or twice-daily, in a single inhaler improved asthma symptoms and exacerbations compared with budesonide. In the majority of patients with moderate persistent asthma requiring ICS and long-acting beta-agonists, once-daily formoterol/budesonide provided sustained efficacy over 24 h, similar to twice-daily dosing.

Administration, Inhalation↗
PubMed1994

[Chronic obstructive pulmonary disease].

Several meetings of chest specialists were held in order to update basic knowledge on Chronic Obstructive Pulmonary Disease (COPD) and to establish guidelines regarding its prevention and treatment. This Consensus was prompted by the important morbidity and mortality due to COPD. Pulmonary emphysema, chronic bronchitis and asthma may evolve into COPD when developing chronic, persistent, non reversible airflow obstruction. Its pathologic features, physiopathology, pulmonary function derangements and clinico-radiological picture are summarized. Early detection and prevention accomplished through smoking cessation are essential to stop health damage due to this condition. Strategies directed to smoking cessation are described. Once COPD is established, inhaled bronchodilators (IB)--anticholinergics, beta-2 agonists or both--might be useful. Teophylline is indicated additionally when no improvement is obtained with IB. Inhaled steroids (IE) may stop progression of airways obstruction; they are recommended in patients who remain symttomatic and/or with severe airflow obstruction (FEV1 less than 50% predicted) despite treatment with beta-2 adrenergics and teophylline. Vaccination against influenza and pneumococcal pneumonia is suggested. Other medications (antibiotics, psychoactive drugs, alpha-1 antitrypsine, respiratory stimulants) or surgical interventions, including lung transplantation, might be of help in certain circumstances. In patients with physiotherapy, supplementary nutrition, muscle retraining, prolonged oxygen therapy and, eventually, noninvasive mechanical ventilation might improve survival and quality of life. Acute decompensations leading to respiratory failure should be promptly detected and treated with oxygen, IB, teophylline, corticosteroids, antibiotics and, eventually, mechanical ventilation. The main role of public education in disease prevention is emphasized. Moreover, patient and family education is essential for adequate treatment of COPD.

Humans↗
PubMed1986

Asthma, cardiac arrhythmias, and albuterol aerosol.

Twenty asthmatic patients clinically free of heart disease were studied for the possible arrhythmogenic action of albuterol (salbutamol). Two puffs of either albuterol or placebo were inhaled four times per day on two consecutive days and continuous ECG recordings obtained during each 24-hour period. Sixteen patients had atrial extrasystoles, four with albuterol, one with placebo, and 11 with both drugs. The extrasystoles/hour were 6.55 (23.75 SD) with albuterol and 8.37 (33.82) with placebo, a nonsignificant difference. Ventricular extrasystoles were shown in 11 patients, two with albuterol, two with placebo, and seven during both treatments. The extrasystoles/hour were 2.57 (6.36) and 3.10 (7.61) with albuterol and placebo, respectively. This difference was not significant. These findings suggest that therapeutic doses of albuterol aerosol in asthmatic patients without evidence of heart disease and severe hypoxemia should not be considered a cause of cardiac arrhythmias.

Adult↗
PubMed1979

Bronchial and intravenous provocation tests with indomethacin in aspirin-sensitive asthmatics.

In an attempt to elucidate the mechanisms involved in analgesic-induced asthma, I performed bronchial and intravenous challenge tests with indomethacin in 5 aspirin-sensitive asthmatics. Bronchial challenge with less than 2 mg of indomethacin elicited bronchoconstriction that developed immediately in most cases, reached its macimum at a mean time of 64 min, and was over within 2 to 4 h. The time sequence of the reaction after intravenous challenge was similar to that after bronchial challenge, except that to obtain a comparable degree of bronchoconstriction it was necessary to administer at least twice the inhaled dose. Inhalation of disodium cromoglycate during bronchoconstriction inhibited the reaction within 8.6 +/- 5.7 min, regardless of the route of challenge. This suggests that sequential mast cell degranulation with liberation of chemical mediators is the mechanism responsible for bronchoconstriction in analgesic-induced asthma.

Adult↗
PubMed1977

Inhibition of aspirin-induced bronchoconstriction by sodium cromoglycate inhalation.

Five patients with asthma and severe aspirin hypersensitivity were challenged on separate days with increasing doses of aspirin given by mouth, starting with 5 mg, until a reduction in FEV1 greater than 15% was obtained. Sodium cromoglycate in doses of 20-40 mg inhibited the bronchoconstrictive reaction not only when inhaled before the challenge but also after it, at a time when progressive reduction in FEV1 values was taking place. According to these results, it seems reasonable to postulate sequential mast cell degranulation and liberation of mediators of anaphylaxis as the mechanism through which aspirin induces bronchoconstriction in aspirin-sensitive asthmatics. The differences between bronchial provocation tests and oral challenge with aspirin are stressed.

Adolescent↗