Asthma management: evidence based studies and their implications for cost-efficacy.

This review attempts to infer a cost-effective strategy for the management of bronchial asthma based on evidence from randomized controlled trials. Acute severe asthma should be treated with short-acting inhaled beta-agonists followed by a short course of oral steroids. Decisions on hospital admission should be made within 1 to 2 hours and prolonged treatment in emergency departments avoided. A comprehensive educational and drug optimizing program will prevent chronic illness and relapse. Educational programs should be brief but intensive, supervised by asthma specialists and incorporate self monitoring of symptoms plus written action plans. Peak expiratory flow monitoring should not be mandated for all patients. Inhaled corticosteroids (ICS) are the most cost-effective drugs for the long term prevention of asthma. ICS should be started at low doses. If the symptoms of asthma are not well controlled by moderate doses of ICS, high dose ICS treatment should be avoided and add on medication prescribed instead. Oral bronchodilators are less expensive add on medication than long-acting inhaled beta-agonists.

Detection of Mycobacterium tuberculosis in sputum, pleural and bronchoalveolar lavage fluid using DNA amplification of the MPB 64 protein coding gene and IS6110 insertion element.

Two gene sequences specific for Mycobacterium tuberculosis were evaluated for the diagnosis of pulmonary tuberculous (PTB) in pleural fluid (PF), bronchoalveolar lavage fluid (BAL) and sputum (Sp). The 240 bp sequence (nts 460-700) coding for the MPB 64 protein coding gene and the 123 bp IS6110 insertion element present in multiple copies in the mycobacterial genome were amplified using the polymerase chain reaction. Fifty-nine clinical specimens were studied. The diagnosis of PTB was confirmed by positive M. tuberculosis cultures in 14 specimens, and by the presence of characteristic histological features of granuloma and Langerhan's giant cells on pleural biopsy in 3 PF specimens through cultures for M. tuberculosis were negative. The remaining 42 specimens were obtained from patient's with non-tuberculosis pulmonary infections or malignancy, and these served as negative controls. Our results showed that the IS6110 insertion element and MPB 64 gene sequence were detected in all 14 culture positive PTB cases, although detection of the latter sequence required both DNA amplification and oligonucleotide hybridization. There was however one false positive specimen with the MPB 64 detection protocol. More importantly, both the MPB 64 sequence and IS6110 insertion element protocols were unable to detect M. tuberculosis DNA in the 3 PF samples diagnosed by histological characteristics on pleural biopsy and culture negative. We conclude that DNA amplification for M. tuberculosis-specific sequences is a useful method for rapid diagnosis of PTB in culture positive specimens. However, the false negative results with TB culture negative cases of tuberculosis pleurisy, limits its usefulness for the diagnosis of tuberculous pleurisy.