# Ingvar Bjarnason
**Ingvar Bjarnason** is known for defining NSAID enteropathy, developing the 51Cr-EDTA intestinal permeability test, and validating faecal calprotectin (protein in stool indicating intestinal inflammation) as a marker of intestinal inflammation.[18](https://www.meditsimple.com/practitioners/dr-ingvar-t-bjarnason/43414) [King's College London](https://www.edgepedia.org/kings-college-london)'s research portal lists his work under non-steroidal anti-inflammatory drug (NSAID) pharmacology, intestinal permeability, faecal calprotectin, inflammatory bowel disease, and cyclooxygenase 2.[1](https://kclpure.kcl.ac.uk/portal/en/persons/ingvar-bjarnason/) He has been described by his hospital profile as part of the team that discovered NSAID enteropathy, a small-intestinal disease affecting millions of people worldwide.[2](https://www.cromwellhospital.com/find-a-consultant/ingvar-bjarnason-consultant-gastroenterologist/)
| Fact | Detail |
|---|---|
| Signature work | Reviews "[Side effects of nonsteroidal anti-inflammatory drugs on the small and large intestine in humans](https://doi.org/10.1016/0016-5085(93)90667-2)" (Gastroenterology, 1993) and "[Intestinal permeability: An overview](https://doi.org/10.1016/0016-5085(95)90708-4)" (Gastroenterology, 1995); ["INTESTINAL PERMEABILITY AND INFLAMMATION IN RHEUMATOID ARTHRITIS: EFFECTS OF NON-STEROIDAL ANTI-INFLAMMATORY DRUGS"](https://doi.org/10.1016/s0140-6736(84)92739-9), *The Lancet*, 1984 |
| Key finding | NSAID enteropathy in 44% of 312 patients on long-term NSAIDs, by faecal calprotectin[4](https://gut.bmj.com/content/45/3/362) |
## Training and career
The Cromwell Hospital profile places his gastroenterology training at the MRC Clinical Research Centre at Northwick Park Hospital between 1981 and 1990.[2](https://www.cromwellhospital.com/find-a-consultant/ingvar-bjarnason-consultant-gastroenterologist/) A 1982 Clinical Science paper on in vitro intestinal permeability in jejunal biopsies, published from the Division of Clinical Cell Biology at the MRC Clinical Research Centre, records this early work.[5](https://doi.org/10.1042/cs063008p)
## Measuring intestinal permeability
Bjarnason's early work made small-intestinal injury measurable in humans. His 1986 Gut study of non-steroidal anti-inflammatory drugs and prostaglandins found a significant, stepwise increase in 24-hour urinary excretion of 51Cr-EDTA, a permeability probe, in proportion to each drug's potency for inhibiting cyclooxygenase: excretion rose from about 1.5% in controls to about 2% after aspirin, about 2.5% after ibuprofen, and about 4% after indomethacin. The paper proposed that increased 51Cr-EDTA absorption reflects loss of intestinal integrity from decreased prostaglandin production.[7](https://doi.org/10.1136/gut.27.11.1292) His 1991 Gut study addressed whether the damage is local or systemic: in about ten volunteers, a week of indomethacin (150 mg/day) raised 51Cr-EDTA permeation from 0.63 (0.09)% to 1.20 (0.14)%, while [nabumetone](https://www.edgepedia.org/nabumetone) (1 g/day) had no significant effect, suggesting the main damage is sustained during drug absorption or after biliary excretion rather than systemically; the permeability effect reversed within a week, although inflammation may persist for over 16 months after stopping NSAIDs.[8](https://doi.org/10.1136/gut.32.3.275)
## NSAID enteropathy
NSAID enteropathy is inflammation and injury of the small intestine caused by NSAIDs. In his 1987 Acta Medica Scandinavica paper "The Pathogenesis and Consequence of Non Steroidal Anti-Inflammatory Drug Induced Small Intestinal Inflammation in Man", he argued that NSAIDs cause small intestinal inflammation in the majority of patients taking them regularly for more than a year, that the inflammation is preceded by increased permeability related to cyclooxygenase-inhibiting potency, and that concomitant prostaglandin administration reduces the permeability effect; he also proposed that the small intestine may be a greater source of morbidity than the stomach in NSAID users.[9](https://doi.org/10.3109/03009748709096722) His 2018 review in [Gastroenterology](https://www.edgepedia.org/gastroenterology) set out the mechanism: NSAIDs interact with phospholipids and uncouple mitochondrial oxidative phosphorylation, initiating biochemical changes that impair the gastrointestinal barrier, and the resulting increase in permeability leads to low-grade inflammation, erosions, and ulcers, with complications including bleeding, protein loss, stricture formation, and perforation.[10](https://pubmed.ncbi.nlm.nih.gov/29221664/)
Later studies confirmed the scale his group had reported. Capsule-endoscopy studies in the mid-2000s found small-bowel injury in 71% of arthritis patients taking non-selective NSAIDs for more than three months, against 10% of controls, and mucosal breaks in 13 of 16 patients (81%) who had used NSAIDs for over 12 months versus 4 of 12 (33%) non-users; other reviews put NSAID enteropathy in more than 60% of long-term users, mostly subclinical.[11](https://link.springer.com/article/10.1007/s00535-019-01657-8) • [12](https://www.sciencedirect.com/science/article/abs/pii/S088985530900034X)
## Faecal calprotectin
[Faecal calprotectin](https://www.edgepedia.org/faecal-calprotectin) is measurable in a single stool sample. His group validated it against the established method of faecal excretion of indium-111 labeled white cells in 47 patients taking NSAIDs, showing significant correlation and establishing the assay as a simple practical method for diagnosing NSAID enteropathy.[4](https://gut.bmj.com/content/45/3/362)
A 2025 observational study of 431 patients with functional bowel disorders found that NSAID prescriptions within 90 days of testing were associated with higher faecal calprotectin (57 versus 25 μg/g) and PPI prescriptions with higher levels (66 versus 23 μg/g), and that a level above 50 μg/g carried a higher likelihood of referral for colonoscopy (40% versus 19%), so these medications should be considered when interpreting results.[13](https://doi.org/10.1080/00365521.2025.2512368)
## COX-2 inhibitors and gut safety
In Bjarnason's double-blind crossover trial in about 30 healthy subjects, one week of indomethacin 50 mg three times daily significantly increased intestinal permeability (day-7-to-baseline 51Cr-EDTA/l-rhamnose ratio 1.53), while rofecoxib 25 mg or 50 mg daily did not differ from placebo, showing that selective COX-2 inhibition alone did not raise permeability in this setting.[14](https://gut.bmj.com/content/47/4/527) According to a 2018 review in *Gastroenterology*, although COX-1 and COX-2 are both involved in NSAID gastrointestinal damage, other COX-independent factors contribute, which remains the open mechanistic question in his own recent work.[10](https://pubmed.ncbi.nlm.nih.gov/29221664/)
## Representative work
Two reviews stand as his most representative contributions. **"[Side effects of nonsteroidal anti-inflammatory drugs on the small and large intestine in humans](https://doi.org/10.1016/0016-5085(93)90667-2)"** (Gastroenterology, 1993). **"[Intestinal permeability: An overview](https://doi.org/10.1016/0016-5085(95)90708-4)"** (Gastroenterology, 1995). His 1984 Lancet paper examined intestinal permeability and inflammation in rheumatoid arthritis and the effects of NSAIDs, and his 1987 Lancet paper reported blood and protein loss via small-intestinal inflammation induced by NSAIDs ([The Lancet](https://www.edgepedia.org/the-lancet), volume 330, issue 8561, pages 711–714).[15](https://doi.org/10.1016/s0140-6736(84)92739-9) • [16](https://doi.org/10.1016/0163-7258(94)90008-6)
## Honours and what remains open
The field he established remains active: a 2025 comprehensive review in the Indian Journal of Gastroenterology still treats NSAID enteropathy as a frequently underdiagnosed condition of the small intestine caused by extended NSAID use.[17](https://link.springer.com/article/10.1007/s12664-025-01886-1) The unresolved question framed in his own 2018 review is the contribution of COX-independent factors to NSAID gastrointestinal damage.[10](https://pubmed.ncbi.nlm.nih.gov/29221664/)
## References
1. Ingvar Bjarnason, King's College London research portal. https://kclpure.kcl.ac.uk/portal/en/persons/ingvar-bjarnason/
2. Professor Ingvar Bjarnason - Consultant Gastroenterologist. Cromwell Hospital. https://www.cromwellhospital.com/find-a-consultant/ingvar-bjarnason-consultant-gastroenterologist/
3. Qualifications - Professor Ingvar Bjarnason. http://ingvarbjarnason.com/4.html
4. High prevalence of NSAID enteropathy as shown by a simple faecal test. Gut, 1999. https://gut.bmj.com/content/45/3/362
5. In Vitro Determination of Intestinal Permeability in Jejunal Biopsies. Clinical Science, 1982. https://doi.org/10.1042/cs063008p
6. About Prof. Bjarnason. http://www.ingvarbjarnason.com/2.html
7. Effect of non-steroidal anti-inflammatory drugs and prostaglandins on the permeability of the human small intestine. Gut, 1986. https://doi.org/10.1136/gut.27.11.1292
8. Importance of local versus systemic effects of non-steroidal anti-inflammatory drugs in increasing small intestinal permeability in man. Gut, 1991. https://doi.org/10.1136/gut.32.3.275
9. The Pathogenesis and Consequence of Non Steroidal Anti-Inflammatory Drug Induced Small Intestinal Inflammation in Man. Acta Medica Scandinavica, 1987. https://doi.org/10.3109/03009748709096722
10. Mechanisms of Damage to the Gastrointestinal Tract From Nonsteroidal Anti-Inflammatory Drugs. Gastroenterology, 2018. https://pubmed.ncbi.nlm.nih.gov/29221664/
11. Current knowledge on non-steroidal anti-inflammatory drug-induced small-bowel damage. Journal of Gastroenterology, 2019. https://link.springer.com/article/10.1007/s00535-019-01657-8
12. Nonsteroidal Anti-Inflammatory Drugs and Lower Gastrointestinal Complications. https://www.sciencedirect.com/science/article/abs/pii/S088985530900034X
13. Prescription of NSAIDs and proton pump inhibitors are associated with increased faecal calprotectin levels. Scandinavian Journal of Gastroenterology, 2025. https://doi.org/10.1080/00365521.2025.2512368
14. COX-2 inhibition with rofecoxib does not increase intestinal permeability in healthy subjects. Gut, 2000. https://gut.bmj.com/content/47/4/527
15. https://doi.org/10.1016/s0140-6736(84)92739-9
16. https://doi.org/10.1016/0163-7258(94)90008-6
17. From pain relief to mucosal grief: A comprehensive review of NSAID enteropathy. Indian Journal of Gastroenterology, 2025. https://link.springer.com/article/10.1007/s12664-025-01886-1
18. Dr Ingvar T. Bjarnason: Book Online - MeditSimple. https://www.meditsimple.com/practitioners/dr-ingvar-t-bjarnason/43414
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*Topic: Encyclopedia › Life and health › Life and health scientists › Medical and health researchers › Gastroenterology and hepatology researchers › Luminal gastroenterologists › Intestinal disease researchers*
*Initially written Sep 20, 2026 · Reviewed: Sep 25, 2026; Sep 30, 2026 · Edited: Sep 25, 2026 · Last review: Sep 30, 2026*
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