| Home
> Table
of Contents > Original
/ Research Articles |
| |
| |
| |
Does The
Treatment for H. pylori + GORD Improve Asthma Control?
S Shyamsunder, Kumar Menon, Sameer
Sawant, SV Joshi, HL Dhar |
| |
Silent gastro-oesophageal
reflux disease co-exists with and worsens asthma by multiple
mechanisms. This study was conducted in 25 subjects to see the
effect of anti H. pylori in moderate persistent asthma in about
25 subjects and the results showed significant improvements
in peak flow rates as compared to standard therapy in moderate
persistent asthma. Therefore treatment for H.. pylori may result
in improved early asthma control. |
| |
| INTRODUCTION |
Asthma is a chronic inflammatory pulmonary
disorder that is characterized by reversible obstruction
of the airways. Underlying cause of the increasing prevalence
of asthma is unknown. Important aspects of asthma include
airways hyperresponsiveness and bronchoconstriction. Airways
hyperresponsiveness refers to an increased tendency of
the asthmatic airways to react to a variety of stimuli
that would not cause a response in a normal airway. These
asthma triggers can cause an asthma attack in an inflamed
airway. One of the prominent trigger factor is the acid
reflux which is considered to be a nightmare for the asthmatics.
Gastro-oesophageal reflux disease often
called “reflux”, “reflux oesophagitis”
or sometimes inaccurately referred to as “hiatus
hernia”. Gastro-oesophageal reflux is the term used
to describe a backflow of acid from the stomach into the
oesophagus. Almost everyone experiences GI reflux at sometime.
The usual symptom is heart burn, an uncomfortable burning
sensation behind the breastbone commonly occurs after
a meal. In some individuals reflux is frequent or severe
enough to cause more significant problems as trigger aggravate
certain other conditions like an episode of asthma in
known asthmatics. The role of H. pylori in the pathogenesis
of GORD is controversial. Some studies have indicated
a protective role1-5 whereas others fail to show different
H. pylori infection rates in patients with and without
Gastro-oesophageal reflux.6-8 There are also studies which
indicate worsening or development of GORD after eradication
of H. pylori in duodenal ulcer patients,9 although others
reported improvement of reflux symptoms after cure of
infection.10 Our aim was to study the improvement in asthma
and GORD symptoms after eradication of H. pylori. |
| |
| Material and Methods |
Patients presenting to our outpatient
department of the tertiary care centre with moderate to
severe persistent asthma were screened out of which twenty-five
patients were enrolled.
Asthma and severity were defined as per
the guidelines issued by the National Heart, Lung and
Blood Institute (NHLBI) USA. They were randomly allotted
to two groups. In group I, standard treatment based on
the same guidelines were given using inhaled salmeterol,
inhaled fluticasone, with spacer. Patients with allergic
rhinitis were treated with nasal steroids and anti histamines.
In group II, in addition to standard treatment patients
were treated with a 2-week course against H. pylori consisting
of 4 drug regime of Omeprazole, Metronidazole, BismuthSubcitrate
and Doxycycline at therapeutic dose for 10 days. Pulmonary
function test was done prior to initiating the therapy
and predicted values for FVC, FEV1 and FEV1/FVC were derived
followed by Wrights peakflow meter reading every 2nd,
4th, 6th and 8th week intervals.
Wrights peakflow meter reading measurements
were done blinded to the group the patients belonged to.
Predicted values for PEFR were calculated based on age
and height of the patient.
The patients were surveyed about their
reflux symptoms with specific questionnaire and response
categories were provided. |
| |
| Questionnaire |
The questions were designed to assess the severity
of asthma symptoms, the severity of GOR symptoms both
heartburn and regurgitation as well as complaints of cough,
its duration, frequency, etc and to determine whether
asthma symptoms worsened and patients had to use the b-agents
inhaled during symptomatic reflux.
All subjects were questioned to determine whether they
suffered from heartburn. Heartburn was described to them
as a burning sensation or pain and discomfort in the chest
after meals or when lying down.
They were asked whether their cough worsened or had shortness
of breath, wheeze, nocturnal symptoms and dyspnoea either
during the day or at night.
Question regarding regurgitation were asked like return
of stomach contents or acid to the mouth or choking like
sensation. Current asthma medication were recorded along
with prior treatment for asthma as well as for any other
illnesses. Subjects were also asked past history of any
diseases, family history and history of smoking or tobacco
consumption in any form. |
| |
| Results |
Demographic data have been shown in
Table 1. Average age of control group was 49 ±
14 years and 39 ± 12 years. Both groups were well
matched in terms of baseline PEFR (Group 1 - 60% ±
10 vs. 52% ± 11 Group 2; p = 0.06). Per cent improvement
in PEFR was significant from 2nd to 8th week after treatment
in the group 2 (H pylori) compared to the group 1 (standard
asthma) as shown in Table 2 and Fig. 1
 |
 |
| |
Fig. 1 : Percentage improvement in PEFR from baseline. |
| |
 |
|
| |
| Discussion |
Gastro-oesophageal reflux (GOR) is a potential trigger
of asthma. The oesophagus and lung interacts through a
variety of mechanisms. Oesophageal acid induced broncho
constriction can be provoked by a vagally mediated reflux,
whereby acid in the distal oesophagus produces airway
responses, by natural enhancement of bronchial reactivity,
whereby oesophageal acid augments airway infection may
be common in asthmatics, and worsen airway disease. Treatment
for H. pylori may result in improved early asthma control. |
| |
References
| 1. |
Schwizer W, Thumshirn M, Dent J, et
al. Helicobacter pylori and symptomatic relapse of
Gastro-esophageal reflux disease : a randomised control
trial. Lancet 2001; 357 : 1738-42. |
| 2. |
O’cornner HJ. Review article
Helicobacter pylori and Gastroesophageal reflux disease
- clinical implication and management. Ailment Pharmacol
Ther 1999; 13 : 117-27. |
| 3. |
Wu JC, Sung JJ, Ng EK, et al. Prevalence
and distribution of Helicobacter pylori in gastroesophageal
reflux : a study from the East. Am J Gastroenterol
1999; 94 : 1790-94. |
| 4. |
Werdmuller BF, Loffeld RJ. Helicobacter
pylori infection has no role in the pathogenesis of
reflux esophagitis. Dig Dis Sci 1997; 42 : 103-05. |
| 5. |
Vicari JJ, Peek RM, Falk GW, et al.
The seroprevalence of cagA-positive Helicobacter pylori
strains in the spectrum of gastroesophageal reflux
disease. Gastroenterology 1998; 115 : 50-7. |
| 6. |
Newton M, Bryan R, Burnham
WR, et al. Evaluation of Helicobacter pylori in reflux
esophagitis and Barrett’s oesophagus. Gut 1997;
40 : 9-13. |
| 7. |
Hackelsberger A, Schultze
V, Gunther T, et al. The prevalence of Helicobacter
pylori gastritis in patients with reflux esophagitis;
a case control study. Eur J Gastroenterol Hepatol
1998; 10 : 465-68. |
| 8. |
Csendes A, Smok G, Cerda
G, et al. Prevalence of Helicobacter pylori infection
in 190 control subjects and in 236 patients with gastroesophageal
reflux, erosive esophagitis or Barrett’s esophagus.
Dis Esophagus 1997; 10 : 38-42. |
| 9. |
Labenez J, Blum AL, Bayerdorffer
E, et al. Curing Helicobacter pylori infection in
patients with duodenal ulcer may provoke reflux esophagitis.
Gastroenterology 1997; 112 : 1442-47. |
| 10. |
Malfertheiner P, Veldhuyezen
van Zanpen S, Bent J, et al. Does cure of Helicobacter
pylori infection induce heartburn? Gastroenterology
1998; 114 : A0870. |
| 11. |
Susan M, Harding MD. Gastroesophageal
reflux, Asthma and mechanism of interaction. Am J
Med 2001; Dec 3 III Suppl 8A8S-12S. |
| 12. |
Susan M Harding, Joel E
Richter. The role of Gastrooesophageal reflux in chronic
cough and Asthma. Chest 1997; 111 : 1389-1402 |
| 13. |
Harding M, Ritcher EJ,
Guzzo RM, et al. Asthma and Gastrooesophageal Reflux
: Acid suppressive therapy improves asthma outcome.
Am J Med 1996; 100 : 395-405 |
| 14. |
Peters, Kuipers, Ganesh,
et al. The influence of Helicobacter pylori on oesophageal
acid exposure in GERD during acid suppressive therapy.
Ailment Pharmacol Ther 1999; 13 (7) : 921-36.. |
| 15. |
Mc Coll KE. Motion - Helicobacter
pylori worsens GERD : arguments against the motion.
Can J Gastroenterol 2002; 16 (9) : 615-7. |
| 16. |
Naoki Chiba, Sander Jo
Veldhuyzen, Van Zanten, et al. Treating Helicobacter
pylori infection in primary care patients with uninvestigated
dyspepsia : the canadian adult dyspepsia empiric treatment
- Helicobacter pylori positive (cadet-Hp) randomised
controlled trial. BMJ 2002; 324 : 1012-16. |
| |
|
|
SLEEP APNOEA INCREASES RISKS IN GENERAL ANAESTHESIA
Patients with obstructive sleep apnoea are at high risk of complications when having general anaesthesia. Den Herder and colleagues say that undiagnosed sleep apnoea is common. Obesity (especially large neck circumference), increasing age, being male, and alcohol consumption predispose to sleep apnoea.
BMJ, 2004; 329 : 955. |
|
| |
|
| |
|