Current opinion in pulmonary medicine
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This review emphasizes the mechanisms responsible for maximum expiratory airflow limitation in acute and chronic persistent asthma. The phenomenon of acute but reversible loss of lung elastic recoil during acute asthma is reviewed, although no plausible physiologic explanations are offered. The authors have recently studied adult chronic, stable asthmatics with persistent forced expiratory volume in 1 second less than 80% predicted, despite optimal polytherapy. ⋯ Work in progress indicates that persistent reduced maximum expiratory airflow may be present for at least 12 +/- 4 years (mean +/- SD) and suggests possible early loss of lung elastic recoil. These observations provide a challenge to the concept of intrinsic airway narrowing resulting from airway remodeling as the major cause of expiratory maximum expiratory airflow limitation in chronic, moderate asthma and severe, persistent asthma. No morphologic or physiologic abnormalities readily explain the chronic, persistent loss of lung recoil.
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The clinical assessment of the probability of pulmonary embolism is a key step in proposed diagnostic strategies for pulmonary embolism, because the interpretation of noninvasive test results is conditional on the pretest probability derived from the presence or absence of clinical factors. The past year has brought important progress in the general area of clinical prediction of pulmonary embolism with the publication of two new simple clinical prediction rules. ⋯ Although these clinical prediction rules are perhaps only slightly better than the estimates of experienced clinicians, they provide an explicit method for estimating the probability of PE as an adjunct to diagnostic testing. Further validation work is now needed to assess how well these new prediction rules perform in settings other than the derivation sites.
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Patients sustaining traumatic injuries are at high risk for the development of venous thromboembolism. The reported incidence of deep venous thrombosis in trauma patients ranges from 20 to 90%. The reported incidence of pulmonary embolism in trauma patients varies between 2.3 and 22%. ⋯ Contraindications arising from associated injuries often limit the potential options for prophylaxis in patients with trauma. Large prospective randomized studies are needed to determine the most effective means of prophylaxis in trauma patients, who have a wide range of both isolated and combined injuries. Future studies should also address the duration of prophylaxis because many trauma patients remain immobile for an extended time.
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Recent advances in cellular and molecular biology have furthered the understanding of several genetic diseases, including cystic fibrosis. Mutations that cause cystic fibrosis are now understood in terms of the specific molecular consequences to the cystic fibrosis transmembrane conductance regulator (CFTR) protein expression and function. This knowledge has spawned interest in the development of therapies aimed directly at correcting the defective CFTR itself. ⋯ Opportunities for protein-repair therapy appear to be vast and range from naturally occurring compounds, such as isoflavonoids, to pharmaceuticals already in clinical use, including aminoglycoside antibiotics, butyrate analogues, phosphodiesterase inhibitors, and adenosine nucleotides. Future therapies may resemble designer compounds like benzo[c]quinoliziniums or take the form of small peptide replacements. Given the heterogeneity and progressive nature of cystic fibrosis, however, optimal benefit from protein-repair therapy will most likely require the initiation of combined therapies early in the course of disease to avoid irreparable organ damage.
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Review
The art and science of continuous positive airway pressure therapy in obstructive sleep apnea.
Despite the high prevalence of obstructive sleep apnea (OSA) syndrome, no ideal therapy has emerged to date. Based on recent randomized trials, continuous positive airway pressure (CPAP) therapy is the treatment of choice. Although CPAP can prevent pharyngeal collapse in virtually all patients who choose to wear it, poor patient adherence with treatment limits its effectiveness. ⋯ Patient adherence with CPAP can be improved with optimization of mask comfort, heated humidification, and intensive support and education. For those who remain poorly compliant, alternative therapies such as autotitrating devices and oral positive airway pressure can be considered. Further research into the basic mechanisms underlying OSA will be required for new therapeutic targets to develop.