James R. Panuska

Protocol therapy for acute asthma: Therapeutic benefits and cost savings☆

BACKGROUND To evaluate the therapeutic and financial benefits of protocol therapy for acute asthma using standard medications. MATERIALS AND METHODS This study employed a sequential design in which the influence of an asthma care path on hospital admissions, length of stay (LOS) in the emergency department, and return visits were evaluated for 1 year. This information was contrasted with similar data obtained from the 8 months immediately before the protocol was implemented (preprotocol) and a 12-month period after strict adherence to it had declined (admixture). RESULTS In all, 526 acute exacerbations of asthma were treated with the care path, and 429 and 558 episodes were evaluated during the preprotocol and admixture periods, respectively. There were no significant differences between the presenting clinical or physiologic features of any group. With the protocol, 77% of the patients resolved their symptoms within 1:47 +/- 0.02 hours:minutes of arrival in the emergency department with a 2% return rate within 24 hours. The algorithms used quickly identified those needing hospitalization. Patients not meeting the criteria for discharge after receiving the treatments employed typically did not resolve their symptoms for days (average hospital stay 4.1 +/- 0.2 days). Compared with the preprotocol period, the care path significantly reduced the LOS by 50 minutes, the number of urgent and intensive care unit admissions by 27% and 41%, respectively, and the frequency of return visits within 24 hours by 66%. Charges to patients and third-party payors decreased

Restricted replication of respiratory syncytial virus in human alveolar macrophages

395,000. When adherence to the protocol diminished, LOS, admissions, and returns rose significantly toward preprotocol values and the financial benefits were lost. CONCLUSIONS Asthma protocol therapy, based primarily upon aggressive use of sympathomimetics in association with serial monitoring of key indices of improvement, provides prompt and efficient relief for acute exacerbations of asthma. Such an approach yields significant financial benefit while quickly identifying individuals who require hospitalization, and it also detects physician practice patterns that can have potentially detrimental impacts on patient care.

Respiratory syncytial virus induces interleukin-10 by human alveolar macrophages. Suppression of early cytokine production and implications for incomplete immunity.

The cellular factors that regulate infection and replication of respiratory syncytial virus (RSV) in human alveolar macrophages were examined. RSV-exposed alveolar macrophages demonstrated a time-dependent expression of viral glycoproteins, maximal by 24 h post-infection resulting in infection of approx. 38% of the cells. Essentially all (33%) of these freshly isolated alveolar macrophages replicated RSV as shown by infectious centre assays. This RSV-permissive subpopulation of alveolar macrophages consisted primarily of major histocompatibility class II-expressing cells as determined by fluorescence-activated cell sorting. Re-infection of alveolar macrophages did not significantly alter the number of cells infected or capable of replicating RSV. However, in vitro differentiation of alveolar macrophages prior to infection resulted in a significant (P < 0.05), time-dependent decrease (approx. sevenfold) in the number of cells that replicated virus. The mechanism by which cellular differentiation restricted RSV replication is unknown. Production of defective interfering particles did not account for this decrease. Alveolar macrophages infected with RSV produce a variety of cytokines potentially contributing to this restricted viral replication. Pretreatment with several of these cytokines did not affect viral infection or replication. However, tumour necrosis factor (TNF alpha) significantly (P < 0.05) decreased viral replication but only by 30 to 60%. Thus RSV replication is reduced by in vitro differentiation of alveolar macrophages and, to a lesser degree, by pretreatment with TNF.