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Effect of naproxen on gastroesophageal reflux and esophageal function: a randomized, double-blind, placebo-controlled study.
Am J Gastroenterol. 1995 May; 90(5):754-7.AJ

Abstract

OBJECTIVES

Gastrointestinal symptoms, particularly pyrosis, complicate nonsteroidal anti-inflammatory drug (NSAID) use. NSAIDs cause esophageal injury, and H2 blockers are often prescribed for, and successfully control, NSAID-related symptoms. To determine whether NSAIDs can induce gastroesophageal reflux, we studied the effect of a commonly used NSAID, naproxen, on reflux parameters and esophageal function.

METHODS

Nine healthy volunteers (five males, four females, age 23-34 yr) were studied. After basal measurements were taken, the subjects randomly received naproxen 500 mg p.o. b.i.d. or placebo for 1 wk. On day 6, the subjects underwent esophageal manometry with a water-perfused system and Dent sleeve. Body pressures, contraction velocity, and duration of contraction were recorded in the distal 7 cm of the esophagus. The lower esophageal sphincter pressure (LESP) and number of transient relaxations (TLESRs) were monitored. This was followed by 24-h pH monitoring. The subjects then crossed over to the other drug after a minimum 14-day wash-out period.

RESULTS

No subject experienced any GI symptoms during the study. One subject developed reflux-induced symptoms a few months after completing the study and was excluded from the analysis. The total fraction of time (pH < 4) was 4.9 +/- 1.0% in the basal state, 5.5 +/- 1.4% on placebo, and 5.4 +/- 1.5% on naproxen. These differences were not significant. The number of reflux episodes and the esophageal clearance time were not affected by naproxen. The LESP in the basal state was 32.1 +/- 5.6 mm Hg, 32.3 +/- 4.2 mm Hg on placebo, and 29.9 +/- 3.3 mm Hg on naproxen (p = NS). The number of TLESRs per 30 minutes in the basal state was 3.5 +/- 0.9, 4.6 +/- 1.2 on placebo, and 5.8 +/- 1.0 on naproxen (p = NS). The speed and duration of contractions were not affected by naproxen. The excluded subject had marked basal reflux (total fraction of time pH < 4 = 10.7%), low LESP (8 mm Hg), and a marked increase in reflux on naproxen (total fraction of time pH < 4 = 53%).

CONCLUSIONS

Naproxen did not induce reflux in normal subjects, although reflux did increase in some subjects. Naproxen had no significant effect on motility parameters. Our data suggest that NSAIDs do not impair the anti-reflux barrier or induce reflux. Pyrosis experienced during NSAID use may not arise from the esophagus or may reflect altered esophageal sensitivity. A single subject with decreased LESP and asymptomatic increased acid exposure in the basal state had a marked increase in reflux on naproxen. This person subsequently developed symptomatic gastroesophageal reflux. The effect of NSAIDs on individuals with a propensity to reflux deserves further study.

Authors+Show Affiliations

Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Randomized Controlled Trial

Language

eng

PubMed ID

7733082

Citation

Scheiman, J M., et al. "Effect of Naproxen On Gastroesophageal Reflux and Esophageal Function: a Randomized, Double-blind, Placebo-controlled Study." The American Journal of Gastroenterology, vol. 90, no. 5, 1995, pp. 754-7.
Scheiman JM, Patel PM, Henson EK, et al. Effect of naproxen on gastroesophageal reflux and esophageal function: a randomized, double-blind, placebo-controlled study. Am J Gastroenterol. 1995;90(5):754-7.
Scheiman, J. M., Patel, P. M., Henson, E. K., & Nostrant, T. T. (1995). Effect of naproxen on gastroesophageal reflux and esophageal function: a randomized, double-blind, placebo-controlled study. The American Journal of Gastroenterology, 90(5), 754-7.
Scheiman JM, et al. Effect of Naproxen On Gastroesophageal Reflux and Esophageal Function: a Randomized, Double-blind, Placebo-controlled Study. Am J Gastroenterol. 1995;90(5):754-7. PubMed PMID: 7733082.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of naproxen on gastroesophageal reflux and esophageal function: a randomized, double-blind, placebo-controlled study. AU - Scheiman,J M, AU - Patel,P M, AU - Henson,E K, AU - Nostrant,T T, PY - 1995/5/1/pubmed PY - 1995/5/1/medline PY - 1995/5/1/entrez SP - 754 EP - 7 JF - The American journal of gastroenterology JO - Am. J. Gastroenterol. VL - 90 IS - 5 N2 - OBJECTIVES: Gastrointestinal symptoms, particularly pyrosis, complicate nonsteroidal anti-inflammatory drug (NSAID) use. NSAIDs cause esophageal injury, and H2 blockers are often prescribed for, and successfully control, NSAID-related symptoms. To determine whether NSAIDs can induce gastroesophageal reflux, we studied the effect of a commonly used NSAID, naproxen, on reflux parameters and esophageal function. METHODS: Nine healthy volunteers (five males, four females, age 23-34 yr) were studied. After basal measurements were taken, the subjects randomly received naproxen 500 mg p.o. b.i.d. or placebo for 1 wk. On day 6, the subjects underwent esophageal manometry with a water-perfused system and Dent sleeve. Body pressures, contraction velocity, and duration of contraction were recorded in the distal 7 cm of the esophagus. The lower esophageal sphincter pressure (LESP) and number of transient relaxations (TLESRs) were monitored. This was followed by 24-h pH monitoring. The subjects then crossed over to the other drug after a minimum 14-day wash-out period. RESULTS: No subject experienced any GI symptoms during the study. One subject developed reflux-induced symptoms a few months after completing the study and was excluded from the analysis. The total fraction of time (pH < 4) was 4.9 +/- 1.0% in the basal state, 5.5 +/- 1.4% on placebo, and 5.4 +/- 1.5% on naproxen. These differences were not significant. The number of reflux episodes and the esophageal clearance time were not affected by naproxen. The LESP in the basal state was 32.1 +/- 5.6 mm Hg, 32.3 +/- 4.2 mm Hg on placebo, and 29.9 +/- 3.3 mm Hg on naproxen (p = NS). The number of TLESRs per 30 minutes in the basal state was 3.5 +/- 0.9, 4.6 +/- 1.2 on placebo, and 5.8 +/- 1.0 on naproxen (p = NS). The speed and duration of contractions were not affected by naproxen. The excluded subject had marked basal reflux (total fraction of time pH < 4 = 10.7%), low LESP (8 mm Hg), and a marked increase in reflux on naproxen (total fraction of time pH < 4 = 53%). CONCLUSIONS: Naproxen did not induce reflux in normal subjects, although reflux did increase in some subjects. Naproxen had no significant effect on motility parameters. Our data suggest that NSAIDs do not impair the anti-reflux barrier or induce reflux. Pyrosis experienced during NSAID use may not arise from the esophagus or may reflect altered esophageal sensitivity. A single subject with decreased LESP and asymptomatic increased acid exposure in the basal state had a marked increase in reflux on naproxen. This person subsequently developed symptomatic gastroesophageal reflux. The effect of NSAIDs on individuals with a propensity to reflux deserves further study. SN - 0002-9270 UR - https://www.unboundmedicine.com/medline/citation/7733082/Effect_of_naproxen_on_gastroesophageal_reflux_and_esophageal_function:_a_randomized_double_blind_placebo_controlled_study_ L2 - http://www.diseaseinfosearch.org/result/2996 DB - PRIME DP - Unbound Medicine ER -