Acid suppression in duodenal ulcer

A meta-analysis to define optimal dosing with antisecretory drugs

D. B. Jones, Colin Howden, D. W. Burget, G. D. Kerr, R. H. Hunt

Research output: Contribution to journalArticle

233 Citations (Scopus)

Abstract

Many different dosage schedules of antisecretory drugs for the treatment of duodenal ulcer are recommended. The relationship between degree of acid suppression and therapeutic efficacy has not been precisely defined for these drugs. We have examined the association between suppression of intragastric acidity and duodenal ulcer healing rates for a number of therapeutic regimens. For the H2 receptor antagonists alone, the most significant correlation with healing rates was with suppression of intragastric acidity at night (r=0-926; p=0-0001). When other classes of drug: high dose antacid, omeprazole and a synthetic prostaglandin (enprostil) were included in the analysis, the closest correlation was with suppression of total 24 hour intragastric acidity (r=0·91 1; p<00001). Stepwise linear regression analysis was used to investigate the relative contributions to healing of suppression of acidity during the day and night. Suppression of nocturnal acidity was found to be the single most important factor in explaining healing rates. No further benefit was obtained with daytime suppression for H 2 receptor antagonists; suppression of acidity at night accounted for 86·1 % of the observed variation in healing rates among different regimens of H2 receptor antagonists. When all classes of drugs were analysed, inclusion of daytime suppression produced a significant improvement in correlation over nocturnal suppression alone. Drug regimens providing potent suppression of nocturnal acidity produce the highest healing rates in controlled clinical trials. The healing rate for any dose regimen of an antisecretory drug can be predicted from a knowledge of its effect on intragastric acidity. For the H2 receptor antagonists, suppression of nocturnal acidity is the most relevant in this context. Moderate suppression of acidity achieves ulcer healing rates at four to eight weeks which are comparable with those seen with potent suppression at two to four weeks. Increasing degrees of suppression merely accelerate healing.

Original languageEnglish (US)
Pages (from-to)1120-1127
Number of pages8
JournalGut
Volume28
Issue number9
DOIs
StatePublished - Jan 1 1987

Fingerprint

Duodenal Ulcer
Meta-Analysis
Histamine H2 Receptors
Acids
Pharmaceutical Preparations
Enprostil
Synthetic Prostaglandins
Antacids
Omeprazole
Controlled Clinical Trials
Ulcer
Linear Models
Appointments and Schedules
Regression Analysis
Therapeutics

All Science Journal Classification (ASJC) codes

  • Gastroenterology

Cite this

Acid suppression in duodenal ulcer : A meta-analysis to define optimal dosing with antisecretory drugs. / Jones, D. B.; Howden, Colin; Burget, D. W.; Kerr, G. D.; Hunt, R. H.

In: Gut, Vol. 28, No. 9, 01.01.1987, p. 1120-1127.

Research output: Contribution to journalArticle

Jones, D. B. ; Howden, Colin ; Burget, D. W. ; Kerr, G. D. ; Hunt, R. H. / Acid suppression in duodenal ulcer : A meta-analysis to define optimal dosing with antisecretory drugs. In: Gut. 1987 ; Vol. 28, No. 9. pp. 1120-1127.
@article{e27c8377356a453e800cf63df9e0cfdd,
title = "Acid suppression in duodenal ulcer: A meta-analysis to define optimal dosing with antisecretory drugs",
abstract = "Many different dosage schedules of antisecretory drugs for the treatment of duodenal ulcer are recommended. The relationship between degree of acid suppression and therapeutic efficacy has not been precisely defined for these drugs. We have examined the association between suppression of intragastric acidity and duodenal ulcer healing rates for a number of therapeutic regimens. For the H2 receptor antagonists alone, the most significant correlation with healing rates was with suppression of intragastric acidity at night (r=0-926; p=0-0001). When other classes of drug: high dose antacid, omeprazole and a synthetic prostaglandin (enprostil) were included in the analysis, the closest correlation was with suppression of total 24 hour intragastric acidity (r=0·91 1; p<00001). Stepwise linear regression analysis was used to investigate the relative contributions to healing of suppression of acidity during the day and night. Suppression of nocturnal acidity was found to be the single most important factor in explaining healing rates. No further benefit was obtained with daytime suppression for H 2 receptor antagonists; suppression of acidity at night accounted for 86·1 {\%} of the observed variation in healing rates among different regimens of H2 receptor antagonists. When all classes of drugs were analysed, inclusion of daytime suppression produced a significant improvement in correlation over nocturnal suppression alone. Drug regimens providing potent suppression of nocturnal acidity produce the highest healing rates in controlled clinical trials. The healing rate for any dose regimen of an antisecretory drug can be predicted from a knowledge of its effect on intragastric acidity. For the H2 receptor antagonists, suppression of nocturnal acidity is the most relevant in this context. Moderate suppression of acidity achieves ulcer healing rates at four to eight weeks which are comparable with those seen with potent suppression at two to four weeks. Increasing degrees of suppression merely accelerate healing.",
author = "Jones, {D. B.} and Colin Howden and Burget, {D. W.} and Kerr, {G. D.} and Hunt, {R. H.}",
year = "1987",
month = "1",
day = "1",
doi = "10.1136/gut.28.9.1120",
language = "English (US)",
volume = "28",
pages = "1120--1127",
journal = "Gut",
issn = "0017-5749",
publisher = "BMJ Publishing Group",
number = "9",

}

TY - JOUR

T1 - Acid suppression in duodenal ulcer

T2 - A meta-analysis to define optimal dosing with antisecretory drugs

AU - Jones, D. B.

AU - Howden, Colin

AU - Burget, D. W.

AU - Kerr, G. D.

AU - Hunt, R. H.

PY - 1987/1/1

Y1 - 1987/1/1

N2 - Many different dosage schedules of antisecretory drugs for the treatment of duodenal ulcer are recommended. The relationship between degree of acid suppression and therapeutic efficacy has not been precisely defined for these drugs. We have examined the association between suppression of intragastric acidity and duodenal ulcer healing rates for a number of therapeutic regimens. For the H2 receptor antagonists alone, the most significant correlation with healing rates was with suppression of intragastric acidity at night (r=0-926; p=0-0001). When other classes of drug: high dose antacid, omeprazole and a synthetic prostaglandin (enprostil) were included in the analysis, the closest correlation was with suppression of total 24 hour intragastric acidity (r=0·91 1; p<00001). Stepwise linear regression analysis was used to investigate the relative contributions to healing of suppression of acidity during the day and night. Suppression of nocturnal acidity was found to be the single most important factor in explaining healing rates. No further benefit was obtained with daytime suppression for H 2 receptor antagonists; suppression of acidity at night accounted for 86·1 % of the observed variation in healing rates among different regimens of H2 receptor antagonists. When all classes of drugs were analysed, inclusion of daytime suppression produced a significant improvement in correlation over nocturnal suppression alone. Drug regimens providing potent suppression of nocturnal acidity produce the highest healing rates in controlled clinical trials. The healing rate for any dose regimen of an antisecretory drug can be predicted from a knowledge of its effect on intragastric acidity. For the H2 receptor antagonists, suppression of nocturnal acidity is the most relevant in this context. Moderate suppression of acidity achieves ulcer healing rates at four to eight weeks which are comparable with those seen with potent suppression at two to four weeks. Increasing degrees of suppression merely accelerate healing.

AB - Many different dosage schedules of antisecretory drugs for the treatment of duodenal ulcer are recommended. The relationship between degree of acid suppression and therapeutic efficacy has not been precisely defined for these drugs. We have examined the association between suppression of intragastric acidity and duodenal ulcer healing rates for a number of therapeutic regimens. For the H2 receptor antagonists alone, the most significant correlation with healing rates was with suppression of intragastric acidity at night (r=0-926; p=0-0001). When other classes of drug: high dose antacid, omeprazole and a synthetic prostaglandin (enprostil) were included in the analysis, the closest correlation was with suppression of total 24 hour intragastric acidity (r=0·91 1; p<00001). Stepwise linear regression analysis was used to investigate the relative contributions to healing of suppression of acidity during the day and night. Suppression of nocturnal acidity was found to be the single most important factor in explaining healing rates. No further benefit was obtained with daytime suppression for H 2 receptor antagonists; suppression of acidity at night accounted for 86·1 % of the observed variation in healing rates among different regimens of H2 receptor antagonists. When all classes of drugs were analysed, inclusion of daytime suppression produced a significant improvement in correlation over nocturnal suppression alone. Drug regimens providing potent suppression of nocturnal acidity produce the highest healing rates in controlled clinical trials. The healing rate for any dose regimen of an antisecretory drug can be predicted from a knowledge of its effect on intragastric acidity. For the H2 receptor antagonists, suppression of nocturnal acidity is the most relevant in this context. Moderate suppression of acidity achieves ulcer healing rates at four to eight weeks which are comparable with those seen with potent suppression at two to four weeks. Increasing degrees of suppression merely accelerate healing.

UR - http://www.scopus.com/inward/record.url?scp=0023617192&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023617192&partnerID=8YFLogxK

U2 - 10.1136/gut.28.9.1120

DO - 10.1136/gut.28.9.1120

M3 - Article

VL - 28

SP - 1120

EP - 1127

JO - Gut

JF - Gut

SN - 0017-5749

IS - 9

ER -