It is well-known within the medical community that frequent NSAID (Non-steroidal anti-inflammatory drugs) may cause stomach irritation in susceptible people. Here we see two studies that demonstrate the possible mechanism of action of such irritation (increased gastro-intestinal permeability), and the use of L-glutamine, a non-essential amino acid, as an agent to mitigate these negative side effects.
Korean J Gastroenterol. 2004 Nov;44(5):252-8.
[Effect of glutamine on the non-steroidal anti-inflammatory drug-induced bacterial translocation].
Ann JY1, Kim SJ, Han SP, Kim JW, Kim HJ, Do JH, Kim JG, Chang SK, Jeon WK.
NSAIDs induce gut damage throughout the entire gastrointestinal tract and bacterial translocation. The aim of this study was to examine if administration of glutamine was able to prevent the NSAID-induced gut damages and bacterial translocation in the animal models.
Rats were utilized into 5 groups; control group, diclofenac group, and diclofenac with glutamine 0.8, 1.6, and 3.2 g/kg/day group. The animals with glutamine were fed with L-glutamine for 4 days before diclofenac administration. Gut injury was induced by administration of a single dose of diclofenac (80 mg/kg orally). Intestinal permeability (24 hour urinary excretion of phenolsulfonphthalein), enteric aerobic bacterial counts, serum biochemical profiles and bacterial translocation to mesenteric lymph nodes, liver and spleen were measured.
Diclofenac caused the increase in intestinal permeability, enteric bacterial count, enteric protein and albumin loss and bacterial translocation. Administration of glutamine reduced the increase in intestinal permeability, protein losing enteropathy, enteric bacterial overgrowth and bacterial translocation induced by diclofenac.
Glutamine may have beneficial effects on NSAID-induced gut damage and bacterial translocation.
Aliment Pharmacol Ther. 1999 May;13(5):679-85.
Effect of glutamine on the intestinal permeability changes induced by indomethacin in humans.
Hond ED1, Peeters M, Hiele M, Bulteel V, Ghoos Y, Rutgeerts P.
Long-term non-steroidal anti-inflammatory drug (NSAID) intake may induce increased intestinal permeability, eventually resulting in enteropathy. Because increased permeability might be related to cell damage resulting from energy depletion, it was hypothesized that glutamine--the major energy source of the intestinal mucosal cell--might prevent permeability changes.
The 6-h urinary excretion of 51Cr-EDTA after an oral load of 51Cr-EDTA was used in this study as a measure for intestinal permeability. Healthy volunteers underwent a series of permeability tests: (i) basal test; (ii) test following NSAID (indomethacin); (iii) test following NSAID in combination with glutamine and/or misoprostol.
The NSAID induced increased permeability in all volunteers. Pre-treatment with glutamine (3x7 g daily, 1 week before NSAID-dosing) did not prevent the NSAID-induced increase in permeability. Multiple doses of glutamine close in time to NSAID-dosing resulted in significantly lower permeability compared to the NSAID without glutamine. Co-administration of misoprostol with the multiple-dose scheme of glutamine resulted in a further reduction in the NSAID-induced increase in permeability.
Glutamine decreases the permeability changes caused by NSAID-dosing when it is administered close in time, and misoprostol has a synergistic effect.