The real millennium bug

The real millennium bug

cough, then what is? A distal oesophageal-tracheobronchial reflex is the commonest pathogenetic mechanism by which reflux triggers cough, yet it is ma...

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cough, then what is? A distal oesophageal-tracheobronchial reflex is the commonest pathogenetic mechanism by which reflux triggers cough, yet it is manifested in only some patients with GORD. Oesophageal mucosal sensory receptor sensitisation, different response characteristics of oesophageal primary afferents, and a differential in the local release of protussive neurotransmitters in the tracheobronchial tree may all be important factors. However, these have not been investigated. Only recently have studies been undertaken to establish the anatomical existence and nature of the oesophageal-tracheobronchial reflex, as well as of the central “cough centre” which may also influence this reflex. The answer to the third question of what differentiates the responder from the non-responder is more easily addressed. In Allen and Anvari’s study, GOR was proven before surgery in all patients. Laparoscopic fundoplication resulted in an overall reduction in GOR symptoms, proportion of time spent at pH <4·0, and an increase in LOS tone. However, over 17% of patients still had persistent cough. The investigators correctly identify that cough may have multiple causes—several descriptive series have shown that multiple causes are present 18–62% of the time, and three disease processes may be responsible as much as 42% of the time.1 It is therefore important that chronic cough be assessed systematically, so that cough can be promptly diagnosed and treated, and so that unnecessary investigations and therapy can be avoided.The American College of Chest Physicians (ACCP) has recently published evidence-based guidelines for the evaluation of chronic cough in both immunocompetent and immunocompromised adults (figure).1 It would be an interesting exercise to analyse those patients whose cough responded to antireflux surgery, versus the non responders, based on the performance of the ACCP protocol. *Alvin J Ing, Meng C Ngu Depar tments of Thoracic Medicine and Gastroenterology, Concord Hopsital, Concord, NSW 2139, Australia 1 Managing cough as a defence mechanism and as a symptom: a consensus panel report of the American College of Chest Physicians. Chest 1998; 114: 133S–81S. 2 Irwin RS, French CL, Curley FJ, Zawacki JK, Bennett FM. Chronic cough due to gastro-oesophageal reflux: clinical, diagnostic and pathogenetic aspects. Chest 1993; 104: 1511–17. 3 Irwin RS, Curley FJ, French CL. Chronic cough: the spectrum and frequency of causes, key components of the diagnostic evaluation and outcomes of specific therapy. Am Rev Respir Dis 1990; 141: 640–47. 4 Allen CJ, Anvari M. Gastro-oesophageal reflux related cough and its response to laparoscopic fundoplication. Thorax 1998; 53: 963–68. 5 DeMeester T R ,B o n avina L, Lascone C, Courtney JV, Skinner DB. Chronic respiratory symptoms and occult gastro-oesophageal reflux: a prospective clinical trial and results of surgical therapy. Ann Surg 1990; 211: 337–45. 6 Giudicelli R, Dupin B, Surpas P, et al. Gastroesophageal reflux and respiratory manifestations: diagnostic approach, therapeutic indications and results. Ann Chir 1990; 47: 552–54. 7 Ing AJ, Ngu MC, Breslin ABX. Pathogenesis of chronic persistent cough associated with gastro-oesophageal reflux. Am J Respir Crit Care Med 1994; 149: 160–67. 8. Irwin RS, French CL, Curley FJ, Zawacki JK, Bennett FM. Chronic cough due to gastro-oesophageal reflux: clinical, diagnostic and pathogenetic aspects. Chest 1993; 104: 1511–17. 9 Irwin RS, Zawacki JK, Curley FJ, French CL, Hoffman PJ. Chronic cough as the sole presenting manifestation of gastro-oesophageal reflux. Am Rev Respir Dis 1989; 140: 1294–300. 10 Waring JP, Lacayo L, Hunter J, Katz E, Suwak B. Chronic cough and hoarseness in patients with severe gastroesophageal reflux disease: diagnosis and response to therapy. Dig Dis Sci 1995; 40: 1093 11 Meier JH, McNally PR, Punja M, et al. Does omeprazole improve respiratory function in asthmatics with gastro-oesophageal reflux ? A double blind, placebo-controlled crossover study. Dig Dis Sci 1994; 39: 2127–33.

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12 Harding SM, Richter JE, Guzzo MR, Schan CA, Alexander RW, Bradley LA. Asthma and gastroesophageal reflux: acid suppressive therapy improves asthma outcome. Am J Med 1996; 100: 395–405. 13 Ing AJ, Ngu MC, Breslin ABX. A randomised double-blind trial of ranitidine in patients with chronic persistent cough associated with gastro-oesophageal reflux. Am Rev Respir Dis 1992: 145 (suppl): A11. 14 Smyrnios NA, Irwin RS, Curley FJ. Chronic cough with a history of excessive sputum production. Chest 1995; 108: 991–97

The real millennium bug See page 995 The launch in London on World TB Day (Mar 24) of the charity TB Alert—which aims to increase awareness of tuberculosis and to support operational research in the worst affected countries—is an indicator of the heightened attention being given to tuberculosis. The Lancet’s contribution to World TB Day is the series of essays in this week’s issue. We thank John Grange and Alimuddin Zumla for suggesting essay topics and for their piece. The series sets out to examine the threat posed by tuberculosis to global health, to focus attention on the most vulnerable, and to offer hope of a way forward. The way forward advocated by WHO is directly observed therapy short-course (DOTS), now implemented in about 100 countries. 500 000 infectious cases were treated under DOTS in 1996, compared with 250 000 in 1994. When fully implemented, DOTS can achieve wonders, as exemplified by the BRAC-run programme in Bangladesh described by Mushtaque Chowdhury. Yet only a third of those treated by the avowedly “women-focused” BRAC programme are women, and in 1996 only 16·5% of infectious tuberculosis cases in Bangladesh were detected under the DOTS strategy. Although these local difficulties can probably be overcome, Dye and colleagues have calculated that, even if targets for case detection and cure under DOTS are met by 2010, “three-quarters of the worldwide tuberculosis burden would not be averted in the next 23 years”.1 As Alexander Pym and Stewart Cole note, “acknowledgement of the limitations of DOTS would help generate the political will needed to swiftly develop a new generation of tuberculosis-control strategies”. The best tuberculosis-control strategy is undoubtedly elimination of poverty. However, debt-interest repayments mean that poor countries often give back to the west at least as much as they receive in aid. Chifumbe Chintu and Alwyn Mwinga from Zambia suggest debt cancellation to free resources for tuberculosis control. In neighbouring Tanzania, debt-servicing payments for 1997 were $275 million—ie, a third of the government budget, or nine times expenditure on primary health care (http://www. oxfam.org/advocacy/papers/tanzania.htm, accessed March 15). Yet Tanzania is not scheduled to receive debt relief under the International Monetary Fund and World Bank Heavily Indebted Poor Countries initiative until 2002. This initiative is intended to assist the 41 countries with the highest debt burden. Although the resources freed by debt relief cannot be guaranteed to go into health care, if the blight of tuberculosis is not to continue well into the next millennium, the sustained government commitment called for under DOTS must include a commitment from western governments to give developing countries a chance to help themselves. John McConnell The Lancet, London WC1B 3SL, UK 1

Dye C, Garnett GP, Sleeman K, Williams BG. Prospects for worldwide tuberculosis control under the WHO DOTS strategy. Lancet 1998; 352: 1886-91.

THE LANCET • Vol 353 • March 20, 1999