LETTERS TO THE EDITOR Ulcerative Colitis After Anesthesia with Desﬂurane and Sevoﬂurane To the Editor: The pathogenesis of inﬂamma- tory bowel disease (IBD) remains unknown, but is likely multifactorial. Suspected factors include genotype, immune system dysregulation, intesti- nal barrier dysfunction, and microbial ﬂora. 1 To our knowledge, no associa- tions between IBD and inhalational anesthetics have been reported. Here we describe a patient who underwent anesthesia on separate occasions with desﬂurane and sevoﬂurane and on each occasion developed bloody diarrhea of several weeks duration. The patient was subsequently diagnosed as having ulcerative colitis (UC). A 48-year-old man was admitted to our hospital with complaints of bloody diarrhea and weight loss. The patient said that he was having 12–13 episodes of diarrhea per day. His med- ical history was signiﬁcant for two sur- gical procedures. Two years prior to the present visit, at a hospital afﬁliated with ours, the patient had undergone nasal septo- plasty for obstructive sleep apnea. According to the discharge summary, desﬂurane was used as the surgical an- esthetic. The patient said that after the surgery he began to experience bloody diarrhea and went to a general practi- tioner who, without performing labora- tory tests, diagnosed the diarrhea as in- fectious and prescribed a week-long course of antibiotics. The bloody diar- rhea, however, persisted for 1 month The patient’s second operation was a lumbar discectomy that had been performed at our hospital 46 days prior to the present visit. During that operation sevoﬂurane was used. The patient said that on the day after sur- gery he began to have diarrhea. During the following 2 weeks the diarrhea increased in frequency and became bloody, and continued up to the time when he applied to our clinic. On physical examination the patient’s temperature was 38.5  C and his heart rate was 92 beats per minute. Other physical ﬁndings were normal except for a slight sensitivity to palpa- tion of the abdomen. Laboratory ﬁnd- ings were as follows: hemoglobin 9.9 g/dL, hematocrit 37%, leukocyte count 11.1  10 3 /mL, platelets 392,000/lL, glucose 104 mg/dL (normal 70–105 mg/dL), aspartate aminotransferase 8 IU/L (normal 5–40 IU/L), alanine ami- notransferase 7 IU/L (normal 5–40 IU/ L), alkaline phosphatase 101 IU/L (normal 80–280 IU/L), gamma glu- tamyl transferase 31 IU/L (normal 10– 50 IU/L), total protein 5.67 g/dL (nor- mal 6.3–8.4 g/dL), albumin 3.34 g/dL (normal 3.8–5.1 g/dL), erythrocyte sed- imentation rate 78 mm/h, and C-reac- tive protein 107 mg/dL (normal 0–8 mg/dL). Other laboratory ﬁndings were normal. Stool specimens were exam- ined for ova, parasites, Clostridium dif- ﬁcile toxin, and cytomegalovirus; none of these were found. Stool cultures showed no pathogenic bacteria. On colonoscopy, the mucosa in the descending colon, sigmoid colon, and rectum was edematous, granular, and fragile without interruption. In the lumen were seen mucus, exudates, and hemorrhagic secretions. The biopsy specimen showed inﬂammation at the lamina propria with inﬁltration by lym- phocytes, plasmocytes, and eosinophils. The goblet cells were few in number. Crypt abscesses and morphologic dis- tortion of the crypts were visible. The patient was diagnosed as having severe UC and was hospitalized for treatment with mesalazine (oral and enema, 4 g/day each) and prednis- olone (oral, 60 mg/day). By the ﬁfth day of treatment the patient’s fre- quency of defecation decreased to three per day, and blood and mucus were no longer apparent in the stools. One month later, follow-up colono- scopy showed mucosal healing. A literature search revealed that a connection between IBD and inhala- tional anesthesia might be provided by interleukin-17. Fujino et al 2 found that in patients with IBD interleukin-17 expression was increased in the mu- cosa and serum compared to normal controls. More recently, Tylman et al 3 reported that in patients undergoing anesthesia with either sevoﬂurane and fentanyl or propofol and remifentanil, plasma interleukin-17 levels decreased in both groups during surgery, but af- ter surgery the levels increased more rapidly in the sevoﬂurane group. The ﬁndings of these studies are difﬁcult to interpret, given that among the events that lead to UC, it is not yet clear whether interleukin-17 should be con- sidered a cause or an effect. 4 I. Yuksel, MD* B. Uﬂaz, MD † E. Erarslan, MD* S. Haznedaroglu, MD* M. Dogan, MD ‡ *Department of Gastroenterology † Department of Internal Medicine ‡ Department of Pathology Etlik _ Ihtisas Educational and Research Hospital, Ankara, Turkey REFERENCES 1. Kucharzik T, Maaser C, Lu ¨gering A, et al. Recent understanding of IBD pathogenesis: implications for future therapies. Inﬂamm Bowel Dis. 2006;12:1068–1083. 2. Fujino S, Andoh A, Bamba S, et al. Increased expression of interleukin 17 in inﬂammatory bowel disease. Gut. 2003;52:65–70. 3. Tylman M, Sarbinowski R, Bengtson JP, et al. Inﬂammatory response in patients undergoing colorectal cancer surgery: the effect of two different anesthetic techniques. Minerva Anestesiol. 2010 [Epub ahead of print]. 4. Sarra M, Pallone F, Macdonald TT, et al. IL- 23/IL-17 axis in IBD. Inﬂamm Bowel Dis. 2010;16:1808–1813. Copyright V C 2011 Crohn’s & Colitis Foundation of America, Inc. DOI 10.1002/ibd.21736 Published online 27 April 2011 in Wiley Online Library (wileyonlinelibrary.com). Inﬂamm Bowel Dis  Volume 17, Number 7, July 2011 E76