Intestinal metaplasia in an interposed colonic segment in distal esophagus

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Letters to the Editor

AJG – Vol. 95, No. 7, 2000

important bilateral eye accomodation impairment with conjunctival suffusion; a bilateral uveitis was diagnosed. Pomona Leptospira antibodies were markedly positive (1: 3200 at hemoagglutination test) and amoxicillin 2 g/day p.o. for 14 days was started. The patient completely recovered after 1 month, and is well 3 yr after. Leptospirosis is the most common zoonosis in the world (1). The clinical pattern of this disease is very atypical. It varies from subclinical infection, self-limited anicteric febrile illness with or without meningitis, to a severe and potentially fatal disease known as Weil’s syndrome, which is characterized by hemorrhage, renal failure, and jaundice (2). Leptospirosis may occur with two clinical patterns: the anicteric leptospirosis (80 –90% of all cases), and the icteric leptospirosis (5–10% of all cases) (2). Occupational activities (as in our case), recreational activities, living conditions, and seasonal weather conditions may be associated with a greater risk, and they may give a good hint as to the diagnosis (2). We stress the importance of evaluating an elevated blood bilirubin level without an increase of blood transaminase level (which was normal in our case). Leptospirosis infection determines an altered bilirubin excretion, but the exact mechanism is unknown (2). Pancreatitis may be evidenced in leptospirosis infection (1); in our case, the diagnosis of mild acute pancreatitis is possible for an important increase of blood lipase level, because this enzyme has a specificity for the pancreatitis’s diagnosis of 97–99% (3). We can confirm that mild acute pancreatitis without any detectable ultrasound morphology change of the pancreas may be present in leptospirosis, as previously reported (1). Giovanni Casella, M.D. Department of Medicine Desio Hospital Desio (Milan), Italy Loreno Florio Scatena, M.D. Department of Medicine Sarnico Hospital Sarnico (Bergamo), Italy

REFERENCES 1. Monno S, Mizushima Y. Leptospirosis with acute acalculous cholecystitis and pancreatitis. J Clin Gastroenterol 1993;16: 52– 4. 2. Farr RW. Leptospirosis—State of the art. Clin Infect Dis 1995; 21:1– 8. 3. Ventrucci M, Pezzilli R, Gullo L, et al. Role of serum pancreatic enzyme assays in diagnosis of pancreatic disease. Dig Dis Sci 1989;34:39 – 45. Reprint requests and correspondence: Giovanni Casella, M.D., Department of Medicine, Desio Hospital, P.zza Benefattori, 1 20033, Desio (Milan), Italy. Received Feb. 18, 1999; accepted Feb. 23, 2000.

Re: A Look Back— Discovery of Anesthesia TO THE EDITOR: Just a brief note on the discovery of anesthesia. Although I greatly admire what Dr. William Morton and Dr. John Warren did in 1846 when ether was administered for surgery, I think the record should be corrected to show that this was not the first use of ether in a surgical procedure. This was first done in Georgia 4 –5 yr earlier, and this is well documented. Robert E. Mitchell, Jr., M.D. Virginia Physicians, Inc. Richmond, Virginia Reprint requests and correspondence: Robert E. Mitchell, Jr., M.D., Virginia Physicians, Inc., 7605 Forest Avenue, Suite 211, Richmond, VA 23229. Received and accepted Dec. 20, 1999.

Intestinal Metaplasia in an Interposed Colonic Segment in Distal Esophagus TO THE EDITOR: We wish to report a unique case of intestinal metaplasia found in the colon after colonic interposition for the esophagus. At age 46 yr, this female patient developed massive hematemesis due to severe erosive esophagitis and underwent esophagectomy with colonic interpositioning. She subsequently developed heartburn symptoms and 3 yr later underwent fundoplication surgery. She had recurrence of symptoms 13 yr after the fundoplication. At that time a 24-h pH probe study done while the patient took famotidine 20 mg p.o. b.i.d. showed significant acid reflux, with a Deemester score of 92.8 (normal, i.e., the 95th percentile for the normal population, is ⬍14.7). On esophagogastroduodenoscopy (EGD) 1 yr later, 17 yr after the colonic interpositioning surgery, raised salmoncolored areas were seen in the interposed colon. Histopathology of the biopsy specimens revealed small intestinal metaplasia. The patient was treated with omeprazole 20 mg p.o. b.i.d. One year later, a second EGD showed similar findings, with islands of salmon-colored mucosa extending from 24 to 36 cm from the incisors, well within the interposed colonic segment. Biopsies from these areas revealed a mixture of gastric metaplasia and small intestinal metaplasia (Fig. 1). Colonoscopy was normal, other than for surgical shortening. The patient’s medical history was unremarkable other than her history of esophageal surgery. She did not smoke or drink alcohol. The occurrence of intestinal metaplasia in an interposed colonic segment in the distal esophagus has not been described before. A previous study from Finland described histological features of colonic mucosa 5 months to 15 yr after colon interposition for esophageal disease (1). In most study patients the graft mucosa was macroscopically and

AJG – July, 2000

Letters to the Editor

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small intestinal metaplasia, such as villous histology and Paneth cell hyperplasia, often occur in patients with inflammatory bowel disease (3). Our case demonstrates that gastroesophageal reflux can induce gastric and intestinal metaplasia in colonic mucosa, as it can in squamous mucosa of the esophagus. Intestinal metaplasia of the colon must occur uncommonly, given that it is visible endoscopically and has not been reported previously. It is not known whether intestinal metaplasia in colonic mucosa predisposes to adenocarcinoma, but no cancers have been reported in this setting. Anurag Soni, M.D. Amjad N. Awan, M.D. Richard M. Feddersen, M.D. David E. Johnston, M.D. Department of Medicine Department of Pathology Division of Gastroenterology University of New Mexico Health Sciences Center Albuquerque, New Mexico

REFERENCES 1. Isolauri J, Helin H, Markkula H. Colon interposition for esophageal disease: Histologic findings of colonic mucosa after a follow-up of 5 months to 15 years. Am J Gastroenterol 1991; 86:277– 80. 2. Farahvash MJ, Janney CG, Salimi Z, et al. Jejunized colon in carcinoid tumor. Am J Gastroenterol 1994;89:429 –33. 3. Dundas SA, Dutton J, Skipworth. Reliability of rectal biopsy in distinguishing between chronic inflammatory bowel disease and acute self-limiting colitis. Histopathology 1997;31:60 – 6. Reprint requests and correspondence: David E. Johnston, M.D., Division of Gastroenterology, ACC-5, University of New Mexico School of Medicine, 2211 Lomas Boulevard NE, Albuquerque, NM 87131-5271. Received Jan. 3, 2000; accepted Mar. 3, 2000.

Figure 1. Gastric and small metaplasia in colonic neoesophagus (original magnification ⫻400). Top: Hematoxylin and eosin. Gastric foveolar type cells (black arrow) with optically clear mucin droplet are contrasted with basophilic intestinal type goblet cells (white arrows). Middle: Mucicarmine stain. Lower: Alcian blue stain. Goblet cells (white arrows) are positive for acidic mucin, whereas gastric foveolar cells (black arrows) are negative. Not illustrated is a PAS stain for neutral mucin, which was moderately to strongly positive in the foveolar cells.

microscopically normal, except for inflammatory changes found in a few patients. No patients had evidence of gastric or intestinal metaplasia of interposed colon. Jejunal-type metaplasia of the colon has been described as a rare complication of metastatic carcinoid tumor (2). Some features of

Abnormal Activation of Transcription Factor NF-␬B Involved in Steroid Resistance in Chronic Inflammatory Bowel Disease TO THE EDITOR: Glucocorticoids are widely used as immunosuppressive agents in inflammatory diseases such as chronic inflammatory bowel disease (IBD). However, although glucocorticoids are highly effective, up to 29% of patients with severe ulcerative colitis fail to respond to steroids (1). This steroid resistance is not due to defects of the glucocorticoid receptor (GR) or abnormalities in steroid absorption. Thus, the molecular mechanism underlying steroid unresponsiveness remains unknown. The effects of steroids result largely from the inhibition of cytokine synthesis upon binding to the GR. Recently, it has