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2009 | 5 | 2 | 102-107
Article title

Choroba refluksowa przełyku a astma oskrzelowa

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Title variants
EN
Gastro-oesophageal reflux disease and bronchial asthma
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EN PL
Abstracts
EN
Bronchial asthma and gastro-oesophageal reflux disease are often coexisting disease entities. Reflux is thought to be a potential factor stimulating or aggravating asthma. This hypothesis is based on both pathophysiological premises and clinical examinations. In an experimental study, it was indicated that the acidification of the lower part of the oesophagus causes an increase in bronchial reactivity. Several mechanisms are suggested to explain this phenomenon, of which the most essential are the nervous, inflammatory and microaspiration theories. It was also indicated that unspecific tests for bronchial hyperreactivity could induce reflux episodes, which argues for the role of asthma itself in inducing GERD. Weakening of anti-reflux mechanisms is brought about by an increase in negative pressure in the chest and the “air trap”, related to exacerbations of asthma, and also by some oral bronchodilating drugs, especially theophylline. Both diseases can interact with each other on the basis of a vicious circle, which result in therapeutic implications. However, there is no explicit data from randomised studies concerning the effectiveness of pharmacological and surgical anti-reflux treatment. The latest data from the literature does not prove the positive results of such a therapy in the group of difficult asthma, in which implementation of treatment with large doses of IPP has been recommended so far. There is still no convincing data concerning the role of non-acid and/or biliary reflux in asthma. It is necessary to improve and standardise diagnostic methods and therapeutic protocols allowing us to single out a group of patients in whom the anti-reflux therapy will bring the best effects for the control of asthma.
PL
Astma oskrzelowa i choroba refluksowa przełyku są często współwystępującymi jednostkami chorobowymi. Uważa się, że refluks stanowi potencjalny czynnik wywołujący lub zaostrzający astmę. Hipoteza ta opiera się zarówno na przesłankach patofizjologicznych, jak i badaniach klinicznych. W badaniach eksperymentalnych wykazano, że zakwaszanie dolnej części przełyku powoduje wzmożoną reaktywność oskrzeli. Powstało kilka teorii wyjaśniających to zjawisko, do najistotniejszych należą teoria nerwowa, zapalna i mikroaspiracji. Wykazano również, że nieswoiste testy nadreaktywności oskrzeli mogą indukować epizody refluksu, co przemawia za udziałem samej astmy w promowaniu GERD. Do osłabienia mechanizmów antyrefluksowych prowadzą związane z zaostrzeniami astmy wzrost ujemnego ciśnienia w klatce piersiowej oraz „pułapka powietrzna”, a także niektóre doustne leki rozszerzające oskrzela, zwłaszcza teofilina. Obie choroby mogą oddziaływać na siebie na zasadzie błędnego koła, co pociąga za sobą implikacje terapeutyczne. Nie ma jednak jednoznacznych danych z badań randomizowanych o skuteczności antyrefluksowej terapii farmakologicznej i chirurgicznej. Najnowsze dane z piśmiennictwa nie potwierdzają pozytywnych rezultatów takiej terapii w grupie astmy trudnej, w której dotąd rekomendowano wdrożenie leczenia dużymi dawkami IPP. Nadal brak jest przekonywających danych dotyczących roli niekwaśnego i/lub żółciowego refluksu w astmie. Konieczne jest udoskonalenie i standaryzacja metod diagnostycznych oraz protokołów terapeutycznych pozwalających wyodrębnić grupę pacjentów, u których terapia antyrefluksowa przyniesie najlepsze efekty dla kontroli astmy.
Discipline
Year
Volume
5
Issue
2
Pages
102-107
Physical description
References
  • 1. GINA Report, Global Strategy for Asthma Management and Prevention, Updated 2008. Chapter 1. Definition and overview: 1-9. Adres: www.ginasthma.org.
  • 2. Locke G.R. 3rd, Talley N.J., Fett S.L. i wsp.: Prevalence and clinical spectrum of gastroesophageal reflux: a population-based study in Olmsted County, Minnesota. Gastroenterology 1997; 112: 1448-1456.
  • 3. Isolauri J., Laippala P: Prevalence of symptoms suggestive of gastro-oesophageal reflux disease in an adult population. Ann. Med. 1995; 27: 67-70.
  • 4. Osler WB.: The Principles and Practice of Medicine. Wyd. 8, D. Appleton, New York 1912: 628-631.
  • 5. Davis M.V: Relationship between pulmonary disease, hiatal hernia, and gastroesophageal reflux. N. Y. State J. Med. 1972; 72: 935-938.
  • 6. Sontag S.J., O’Connell S., Khandelwal S. i wsp.: Most asthmatics have gastroesophageal reflux with or without bronchodilator therapy. Gastroenterology 1990; 99: 613-620.
  • 7. Havemann B.D., Henderson C.A., El-Serag H.B.: The association between gastroesophageal reflux disease and asthma: a systematic review. Gut 2007; 56: 1654-1664.
  • 8. Harding S.M., Guzzo M.R., Richter J.E.: The prevalence of gastroesophageal reflux in asthma patients without reflux symptoms. Am. J. Respir. Crit. Care Med. 2000; 162: 34-39.
  • 9. Gatto G., Peri V, Cuttitta G. i wsp.: Gastroesophageal reflux symptoms are more frequent in patients with severe asthma. Gastroenterol. Int. 2000; 13: 139-142.
  • 10. Rey E., Elola-Olaso C.M., Rodriguez-Artalejo F. i wsp.: Prevalence of atypical symptoms and their association with typical symptoms of gastroesophageal reflux in Spain. Eur. J. Gastroenterol. Hepatol. 2006; 18: 969-975.
  • 11. Jaspersen D., Kulig M., Labenz J. i wsp.: Prevalence of extra-oesophageal manifestations in gastro-oesophageal reflux disease: an analysis based on the ProGERD Study. Aliment. Pharmacol. Ther. 2003; 17: 1515-1520.
  • 12. Mansfield L.E., Hameister H.H., Spaulding H.S. i wsp.: The role of the vague nerve in airway narrowing caused by intraesophageal hydrochloric acid provocation and esophageal distention. Ann. Allergy 1981; 47: 431-434.
  • 13. Schan C.A., Harding S.M., Haile J.M. i wsp.: Gastroesophageal reflux-induced bronchoconstriction. An intraesophageal acid infusion study using state-of-the-art technology. Chest 1994; 106: 731-737.
  • 14. Kjellen G.: Esophageal dysfunction and bronchial asthma. Prog. Pediatr. Surg. 1985; 18: 62-67.
  • 15. Wright R.A., Miller S.A., Corsello B.F.: Acid-induced esophagobronchial-cardiac reflexes in humans. Gastroenterology 1990; 99: 71-73.
  • 16. Harding S.M., Guzzo M.R., Maples R.V. i wsp.: Gastroesophageal reflux-induced bronchoconstriction: vagolytic doses of atropine diminish airway responses to esophageal acid infusion. Am. J. Respir. Crit. Care Med. 1995; 151: A589.
  • 17. Ing A.J., Ngu M.C., Breslin A.B.: Chronic persistent cough and clearance of esophageal acid. Chest 1992; 102: 1668-1671.
  • 18. Pisegna J.R.: GERD and its complications. The pathogenic relationship between symptoms and disease progression. Postgrad. Med. 2001; Spec No: 19-23.
  • 19. Fouad Y.M., Katz PO., Hatlebakk J.G., Castell D.O.: Ineffective esophageal motility: the most common motility abnormality in patients with GERD-associated respiratory symptoms. Am. J. Gastroenterol. 1999; 94: 1464-1467.
  • 20. Vandenplas Y., Hassall E.: Mechanisms of gastroesophageal reflux and gastroesophageal reflux disease. J. Pediatr. Gastroenterol. Nutr. 2002; 35: 119-136.
  • 21. Herve P, Denjean A., Jian R. i wsp.: Intraesophageal perfusion of acid increases the bronchomotor response to methacholine and to isocapnic hyperventilation in asthmatic subjects. Am. Rev. Respir. Dis. 1986; 134: 986-989.
  • 22. Hamamoto J., Kohrogi H., Kawano O. i wsp.: Esophageal stimulation by hydrochloric acid causes neurogenic inflammation in the airways in guinea pigs. J. Appl. Physiol. 1997; 82: 738-745.
  • 23. Kohrogi H., Hamamoto J., Kawano O. i wsp.: The role of substance P release in the lung with esophageal acid. Am. J. Med. 2001; 111 supl. 8A: 25S-30S.
  • 24. Wu D.N., Tanifuji Y., Kobayashi H. i wsp.: Effects of esophageal acid perfusion on airway hyperresponsiveness in patients with bronchial asthma. Chest 2000; 118: 1553-1556.
  • 25. Singh V, Aggarwal V, Bansal S. i wsp.: Effect of intraesophageal acid instillation on airway reactivity in patients with asthma. J. Assoc. Physicians India 2000; 48: 601-602.
  • 26. Boyle J.T, Tuchman D.N., Altschuler S.M. i wsp.: Mechanisms for the association of gastroesophageal reflux and bronchospasm. Am. Rev. Respir. Dis. 1985; 131: S16-S20.
  • 27. Mokhlesi B., Morris A.L., Huang C.F i wsp.: Increased prevalence of gastroesophageal reflux symptoms in patients with COPD. Chest 2001; 119: 1043-1048.
  • 28. Ekstrom T.K., Tibbling L.I.: Can mild bronchospasm reduce gastroesophageal reflux? Am. Rev. Respir. Dis. 1989; 139: 52-55.
  • 29. Moote D.W, Lloyd D.A., McCourtie D.R., Wells G.A.: Increase in gastroesophageal reflux during methacholine-induced bronchospasm. J. Allergy Clin. Immunol. 1986; 78: 619-623.
  • 30. Ekstrom T, Tibbling L.: Influence of theophylline on gastroesophageal reflux and asthma. Eur. J. Clin. Pharmacol. 1988; 35: 353-356.
  • 31. Crowell M.D., Zayat E.N., Lacy B.E. i wsp.: The effects of an inhaled B2-adrenergic agonist on lower esophageal function: a dose-response study. Chest 2001; 120: 1184-1189.
  • 32. Dent J.: Role and development of reflux disease symptom questionnaires. Eur. J. Gastroenterol. Hepatol. 2001; 13 (supl. 3): 23-25.
  • 33. Irwin R.S., Curley F.J., French C.L.: Difficult-to-control asthma. Contributing factors and outcome of a systematic management protocol. Chest 1993; 103: 1662-1669.
  • 34. Pehl C., Waizenhoefer A., Wendl B. i wsp.: Effect of low and high fat meals on lower esophageal sphincter motility and gastroesophageal reflux in healthy subjects. Am. J. Gastroenterol. 1999; 94: 1192-1196.
  • 35. Castell D.O.: Physiology and pathophysiology of the lower esophageal sphincter. Ann. Otol. Rhinol. Laryngol. 1975; 84: 569-575.
  • 36. Grater H.: Gastroesophageal reflux disease - extra-esophageal manifestations. Praxis (Bern 1994) 1998; 87: 1208-1212.
  • 37. Dent J., Brun J., Fendrick A.M. i wsp.; Genval Workshop Group: An evidence-based appraisal of reflux disease management - the Genval Workshop Report. Gut 1999; 44 supl. 2: S1-S16.
  • 38. Irwin R.S., Curley FJ., French C.L.: Chronic cough. The spectrum and frequency of causes, key components of the diagnostic evaluation, and outcome of specific therapy. Am. Rev. Respir. Dis. 1990; 141: 640-647.
  • 39. McGarvey L.P.A., Heaney L.G., Lawson J.T. i wsp.: Evaluation and outcome of patients with chronic nonproductive cough using a comprehensive diagnostic protocol. Thorax 1998; 53: 738-743.
  • 40. Ahmed T, Vaezi M.F.: The role of pH monitoring in extraesophageal gastroesophageal reflux disease. Gastrointest. Endosc. Clin. N. Am. 2005; 15: 319-331.
  • 41. Kahrilas P.J.: The changed role for esophageal pH monitoring. Eur. J. Gastroenterol. Hepatol. 2001; 13 (supl. 3): 29-30.
  • 42. Orr W.C., Craddock A., Goodrich S.: Acidic and non-acidic reflux during sleep under conditions of powerful acid suppression. Chest 2007; 131: 460-465.
  • 43. Maton P.N.: Omeprazole. N. Engl. J. Med. 1991; 324: 965-975.
  • 44. Field S.K., Sutherland L.R.: Does medical antireflux therapy improve asthma in asthmatics with gastroesophageal reflux? A critical review of the literature. Chest 1998; 114: 275-283.
  • 45. Jiang S.P, Liang R.Y., Zeng Z.Y. i wsp.: Effects of antireflux treatment on bronchial hyper-responsiveness and lung function in asthmatic patients with gastroesophageal reflux disease. World J. Gastroenterol. 2003; 9: 1123-1125.
  • 46. Kiljander TO., Salomaa E.R., Hietanen E.K., Terho E.O.: Gastroesophageal reflux in asthmatics: a double-blind, placebo-controlled crossover study with omeprazole. Chest 1999; 116: 1257-1264.
  • 47. dos Santos L.H., Ribeiro I.O., Sanchez P.G. i wsp.: Evaluation of pantoprazol treatment response of patients with asthma and gastroesophageal reflux: a randomized prospective double-blind placebo-controlled study. J. Bras. Pneumol. 2007; 33: 119-127.
  • 48. Bocskei C., Viczian M., Bocskei R., Horvath I.: The influence of gastroesophageal reflux disease and its treatment on asthmatic cough. Lung 2005; 183: 53-62.
  • 49. Gibson PG., Henry R.L., Coughlan J.L.: Gastroesophageal reflux treatment for asthma in adults and children. Cochrane Database Syst. Rev. 2003; (2): CD001496.
  • 50. Littner M.R., Leung F.W, Ballard E.D. 2nd i wsp.; Lansoprazole Asthma Study Group: Effects of 24 weeks of lansoprazole therapy on asthma symptoms, exacerbations, quality of life, and pulmonary function in adult asthmatic patients with acid reflux symptoms. Chest 2005; 128: 1128-1135.
  • 51. Kiljander TO., Harding S.M., Field S.K i wsp.: Effects of esomeprazole 40 mg twice daily on asthma: a randomized placebo-controlled trial. Am. J. Respir. Crit. Care Med. 2006; 173: 1091-1097.
  • 52. Leggett J.J., Johnston B.T, Mills M. i wsp.: Prevalence of gastroesophageal reflux in difficult asthma: relationship to asthma outcome. Chest 2005; 127: 1227-1231.
  • 53. American Lung Association Asthma Clinical Research Centers; Mastronarde J.G., Anthonisen N.R., Castro M. i wsp.: Efficacy of esomeprazole for treatment of poorly controlled asthma. N. Engl. J. Med. 2009; 360: 1487-1499.
  • 54. Gold B.D.: Asthma and gastroesophageal reflux disease in children: exploring the relationship. J. Pediatr. 2005; 146 (supl.): S13-S20.
  • 55. Sontag S.J., O’Connell S., Khandelwal S. i wsp.: Asthmatics with gastroesophageal reflux: long term results of a randomized trial of medical and surgical antireflux therapies. Am. J. Gastroenterol. 2003; 98: 987-999.
  • 56. Shimizu Y., Dobashi K., Kobayashi S. i wsp.: A proton pump inhibitor, lansoprazole, ameliorates asthma symptoms in asthmatic patients with gastroesophageal reflux disease. Tohoku J. Exp. Med. 2006; 209: 181-189.
  • 57. Galmiche J.P., Zerbib F, Bruley des Varannes S.: Review article: respiratory manifestations of gastroesophageal reflux disease. Aliment. Pharmacol. Ther. 2008; 27: 449-464.
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article
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bwmeta1.element.psjd-42378e96-0e70-4f6a-896c-c4ab3a52dfdf
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