Moving from Evidence-Based Medicine to Evidence-Based Health

While evidence-based medicine (EBM) has advanced medical practice, the health care system has been inconsistent in translating EBM into improvements in health. Disparities in health and health care play out through patients’ limited ability to incorporate the advances of EBM into their daily lives. Assisting patients to self-manage their chronic conditions and paying attention to unhealthy community factors could be added to EBM to create a broader paradigm of evidence-based health. A perspective of evidence-based health may encourage physicians to consider their role in upstream efforts to combat socially patterned chronic disease.     

Moving from Ulcer Disease to Reflux Oesophagitis

Most vertebrates have spiral bacteria that have adapted to persist in the mucus layer of the gastric mucosa. Similarly, in underdeveloped societies, most humans acquire Helicobacter pylori in childhood, and this infection persists for the person‘s lifetime, unless the mucosa develops atrophic gastritis. In the developed world, major changes have occurred in the prevalence of H.pylori over the past 50-100 years: the elderly population mostly has the bacterium, but very few children or young adults are infected. These changes in prevalence of H. pylori mean that the developed world is moving from peptic ulcer disease towards reflux oesophagitis.     

Exclusive mutations related to isoniazid and ethionamide resistance among Mycobacterium tuberculosis isolates from Korea.

SETTING: The single base change at the 94th codon of inhA has been referred to as the event that confers resistance on the drugs isoniazid (INH) and ethionamide (ETH) in Mycobacterium smegmatis and M. bovis. From this observation, it has been anticipated that some of the INH-resistant clinical isolates of M. tuberculosis would carry missense mutations in the same region of the gene. However, few polymorphisms have been identified in this region among INH-resistant isolates. OBJECTIVE: To understand the molecular basis for M. tuberculosis resistance to INH and ETH. DESIGN: The sequence polymorphism at the 94th codon of inhA among M. tuberculosis isolates from Korea was analyzed by polymerase chain reaction (PCR) cloning and sequence analysis. RESULTS: No nucleotide change at the 94th codon of inhA was detected in any of the 24 INH-resistant isolates analyzed in this study. On the other hand, a point mutation was found exclusively at the regulatory region flanking a putative ribosome-binding site of the inhA locus in 14 isolates. Interestingly, all the mutations were of the same kind, which substitutes C to T. Among 14 isolates, 12 were resistant to INH as well as to ETH, while two were resistant to INH only. DISCUSSION: It seems that mutations previously found at the 94th codon of inhA have no particular relationship with the mechanism involved in the resistance of M. tuberculosis to INH and/or ETH. On the other hand, the resistance mechanism of M. tuberculosis to INH/ETH may involve an altered level of InhA, an expression which may have been influenced by the sequence change in the regulatory region of the inhA locus.