Misinterpretation of NSAID-induced Colopathy as Crohn’s Disease

Zusammenfassung

Die NSAR-induzierte Kolopathie mit Erosionen, Ulzera, Strikturen und Diaphragma-Bildungen ist zwar seit längerer Zeit bekannt, wird aber immer noch nicht selten endoskopisch und histologisch als „Morbus Crohn” fehlinterpretiert. Dies zeigt diese Kasuistik eines 39-jährigen Patienten mit blutiger Diarrhö und Stenose im Colon transversum, die histologisch als „vereinbar mit Morbus Crohn” gedeutet wurde. Die Glukokortikoidtherapie hatte jedoch nur Nebenwirkungen. Nach der operativen Therapie der Stenose persistierten die blutigen Diarrhöen, endoskopisch fanden sich wiederum Erosionen und Ulzera im Colon transversum. Auch die Umstellung der Therapie auf Azathioprin hatte nur Nebenwirkungen. Die konsiliarische Begutachtung der histologischen Präparate erbrachte dann die Verdachtsdiagnose einer NSAR-induzierten Kolopathie. Die Analyse der Krankengeschichte ergab, dass bei dem Patienten ein Morbus Bechterew bekannt war, der seit längerer Zeit mit Diclofenac behandelt wurde. Diese Kasuistik zeigt exemplarisch, dass die NSAR-induzierte Enterokolopathie bei Internisten, Gastroenterologen und Pathologen immer noch zu wenig bekannt und wegen des diskontinuierlichen endoskopischen und histologischen Befunds als „Morbus Crohn” fehlinterpretiert werden kann.

Abstract

Although NSAID-induced colonopathy characterised by erosions, ulcers, strictures and diaphragms has been known for quite some time, it is not infrequently misinterpreted endoscopically and histologically as Crohn’s disease. This is exemplified by the present case history of a 39-year-old man with bloody diarrhoea and a stenosis in the transverse colon that was histologically interpreted as ”consistent with Crohn’s disease”. Treatment with glucocorticoids, however, merely gave rise to adverse reactions. After surgical treatment of the stenosis, the episodes of bloody diarrhoea persisted, and endoscopy continued to reveal erosions and ulcers in the transverse colon. Changing treatment to azathioprine also failed to produce any positive response, merely causing side effects. Subsequent evaluation of the histological specimens by a consultant pathologist turned up the tentative diagnosis of NSAID-induced colonopathy. An analysis of the patient’s medical history revealed that he was suffering from Bechterew’s disease, for which he had long been taking diclofenac. This case history is a good example of the fact that NSAID-induced enterocolopathy is still too poorly recognised among internists, gastroenterologists and pathologists, and, on the basis of the discontinuous endoscopic and histological findings, is often misinterpreted as Crohn’s disease.

Morbus Crohn - NSAR-Kolopathie - ischämische Kolitis

Crohn’s disease - NSAID-induced colonopathy - ischaemic colitis

References

• 1 Bjarnason I, Hayllar H, MacPherson A J. et al . Side effects of non steroidal anti-inflammatory drugs on the small and large intestine in humans.  Gastroenterology. 1993;  104 1832-1847
• 2 Langman M JS, Morgan L, Worrall A. Use of anti-inflammatory drugs by patients admitted with small or large bowel perforations and haemorrhage.  Br Med J. 1985;  290 347-349
• 3 Allison M C, Howatson A G, Torrance C J. et al . Gastrointestinal damage associated with the use of nonsteroidal anti-inflammatory drugs.  N Engl J Med. 1992;  327 749-754
• 4 Lanas A, Sekar M C, Hirschowitz B I. Objective evidence of aspirin use in both ulcer and nonulcer upper and lower gastrointestinal bleeding.  Gastroenterology. 1992;  103 862-869
• 5 Lanas A, Serrano P, Bajador E. et al . Evidence of aspirin use in both upper and lower gastrointestinal perforation.  Gastroenterology. 1997;  112 683-689
• 6 Wilcox C M, Alexander L N, Cotsonis G A. et al . Nonsteroidal anti-inflammatory drugs are associated with both upper and lower gastrointestinal bleeding.  Dig Dis Sci. 1997;  42 990-997
• 7 Holt S, Rigoglioso V, Sidhu M. et al . Nonsteroidal anti-inflammatory drugs and lower gastrointestinal bleeding.  Dig Dis Sci. 1993;  38 1619-1623
• 8 Wilson R G, Smith A N, Macintyre I MC. Complications of diverticular disease and non-steroidal and anti-inflammatory drugs: a prospective study.  Br J Surg. 1990;  77 1103-1104
• 9 Campell K, Steele R JC. Non-steroidal anti-inflammatory drugs and complicated diverticular disease: a case-control study.  Br J Surg. 1991;  78 190-191
• 10 Aldoori W H, Giovannucci E L, Rimm E B. et al . Use of acetaminophen and nonsteroidal anti-inflammatory diverticular disease in men.  Arch Fam Med. 1998;  7 255-260
• 11 Bombardier C, Laine L, Reicin A. et al . Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis.  N Engl J Med. 2000;  343 1520-1528
• 12 De Vos M, Cuvelier C, Mielanths H. Ileocolonoscopy in seronegative spondylarthopathy.  Gastroenterology. 1989;  96 339-344
• 13 Leirisolo-Repo H, Turunen U, Stenman S. High frequency of silent inflammatory bowel disease in spondylarthopathy.  Arthritis Rheum. 1994;  37 23-31
• 14 Smale S, Natt R S, Orchard T R. Inflammatory bowel disease and spondylarthropathy.  Arthritis Rheum. 2001;  44 2728-2736
• 15 Laine L, Connors L G, Reicin A. et al . Serious lower gastrointestinal clinical events with nonselective NSAID or coxib use.  Gastroenterology. 2003;  124 288-292
• 16 Graham D Y, Opekun A R, Willingham F F. et al . Visible small-intestinal mucosa injury in chronic NSAID users.  Clin Gastroenterol Hepatol. 2005;  3 1-2
• 17 Maiden L, Thjodleifsson B, Theodors A. et al . A quantitative analysis of NSAID-induced small bowel pathology by capsule enteroscopy.  Gastroenterology. 2005;  128 1172-1178
• 18 Stolte M, Karimi D, Vieth M. et al . Strictures, diaphragms, erosions or ulcerations of the ischaemic type in the colon should always prompt consideration of nonsteroidal anti-inflammatory drug-induced lesions.  World J Gastroenterol. 2005;  11 5828-5833
• 19 Brune K, Schweitzer A, Eckert A. Parietal cells of the stomach trap salicylates during absorption.  Biochem Pharmacol. 1977;  26 1735-1740
• 20 Rampton D S. Non-steroidal anti-inflammatory drugs and the lower gastrointestinal tract.  Scand J Gastroenterol. 1987;  22 1-4
• 21 Pihan G RC, Szabo S. Vascular injury in acute gastric mucosa damage. Mediatory role of leukotrienes.  Dig Dis Sci. 1988;  33 625-632
• 22 Davies N M. Toxicity of nonsteroidal anti-inflammatory drugs in the large intestine.  Dis Colon Rectum. 1995;  38 1311-1321
• 23 Wallace J LAKE, McKnight G W. A monoclonal antibody against the CK 18 leucocyte adhesion molecule prevents indomethacin-induced gastric damage in the rabbit.  Gastroenterology. 1991;  100 878-893
• 24 Davies N M, Wallace J W. Nonsteroidal anti-inflammatory drug-induced gastrointestinal toxicity: New insights into an old problem.  J Gastroenterol. 1997;  32 127-133
• 25 Appleyard C B, McCafferty D M, Tigley A W. et al . Tumor necrosis factor medication of NSAID-induced gastric damage: role of leucocyte adherence.  Am J Physiol. 1996;  270 G42-48
• 26 Rothlein R, Czajkowski M, Kshimoto T K. Intercellular adhesion molecule-1 in inflammatory response.  Chem Immunol. 1991;  50 135-142