Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Università di Napoli, Secondo ateneo
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Monaldi Arch Chest Dis · Apr 1997
Randomized Controlled Trial Clinical TrialIneffectiveness of a four week treatment with the thromboxane synthetase inhibitor, imidazole salycilate, in reducing airway hyperresponsiveness to methacholine in asthmatics.
In a randomized, double-blind, placebo-controlled study, the acute and long-term effects of the reduction of thromboxane A2 (TxA2) synthesis on airway sensitivity and maximal airway narrowing in response to methacholine was evaluated in 12 subjects with mild-to-moderate stable asthma, using imidazole salycilate (IS), an anti-inflammatory drug which selectively inhibits the TxA2 synthetase. Dose-response curves with methacholine (MCh) were performed in basal conditions (baseline); 1-1.5 h after administration of 1,500 mg of IS or placebo (acute); at 15 and 30 days of treatment with 750 mg t.i.d. of IS or placebo; and after a 2 week period of run-off (45 days). The serum levels of thromboxane B2 (TxB2) were measured at the same time points, except after acute administration, in five patients from each group. ⋯ The initial provocative dose of methacholine causing a 20% fall in FEV1 (PD20) amounted to 27.0 +/- 1.5 micrograms in the IS group and 41.7 +/- 1.5 micrograms in the control group (geometric mean +/- GSEM) (NS). Despite a reduction of TxB2 serum levels with IS vs placebo at 15 days (24.9 +/- 8.5 vs 45.5 +/- 3.4 pg.mL-1; p < 0.05) and 30 days (27.0 +/- 6.3 vs 45.0 + 3.2 pg.mL-1; p < 0.05), MCh-induced bronchoconstriction, evaluated either as PD20 or maximal airway narrowing, did not change significantly during active treatment compared to placebo. These results show that prolonged reduction of thromboxane A2 synthesis does not improve airway sensitivity and limit maximal bronchoconstriction in asthmatic subjects, suggesting that thromboxane A2 per se does not play a substantial role in the pathogenesis of the airway hyperresponsiveness in human asthma.
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Monaldi Arch Chest Dis · Apr 1997
Randomized Controlled Trial Clinical TrialUtility of monitoring breathing during night hours in COPD patients undergoing long-term oxygen therapy.
We investigated the occurrence of nocturnal respiratory disorders during air and supplemental oxygen breathing in 16 patients with chronic obstructive pulmonary disease (COPD) undergoing long-term home oxygen therapy (LTOT). Following a first night of acclimatization, non-attended continuous nocturnal monitoring was performed for two successive nights in a randomized order. During one night patients breathed room air ("Air night"), and during the other they underwent LTOT ("O2 night") at the same protective O2 nasal flow rate set during waking hours in a resting state. ⋯ During the O2 night, compared to the Air night, mean (+/- SD) desaturation time decreased from 46 +/- 29 to 13 +/- 25%, while obstructive apnoea-hypopnoea duration increased from 6 +/- 8 to 9 +/- 7%, both expressed as percentage of total sleep time. The sleep apnoea/hypopnoea syndrome (SAHS) rate during the Air-night was 2 out of 16, both SAHS patients showing a reduction of apnoea-hypopnoea number.h-1 during the O2 night; whilst SAHS was noted in a further two patients during the O2 night. We conclude that Sp,O2 together with monitoring of breathing during the night, is potentially useful in patients with chronic obstructive pulmonary disease undergoing long-term oxygen therapy, not only when evaluating the O2 flow rate to be used during the night, but also for an understanding of the pathogenesis of nocturnal arterial oxyhaemoglobin desaturations, which may or may not be related to respiratory events.