dysplasia and invasive adenocarcinoma arising in Barrett’s esophagus.Am J Clin Path 1987;87:301–12.

3. Pascal RP, Clearfield HR. Mucoepidermoid (Adenosquamous) carci-noma arising in Barrett’s esophagus. Dig Dis Sci 1987;32:428–32.

4. Smith RRL, Hamilton SR, Boitnott JK, et al. The spectrum of carci-noma arising in Barrett’s esophagus. Am J Surg Path 1984;8:563–73.

5. Kahrilas PJ, Kishk SM, Helm JF, et al. Comparison of pseudoachalasiaand achalasia. Am J Med 1987;82:439–46.

6. Parkman HP, Cohen S. Malignancy-induced secondary achalasia. Dys-phagia 1994;9:292–6.

7. Tucker HJ, Snape WJ, Jr., Cohen S. Achalasia secondary to carcinoma:Manometric and clinical features. Ann Intern Med 1978;89:315–8.

8. Sandler RS, Bozymski EM, Orlando RC. Failure of clinical criteria todistinguish between primary achalasia and achalasia secondary totumor. Dig Dis Sci 1982;27:209–13.

9. Carter M, Deckmann RC, Smith RC, et al. Differentiation of achalasiafrom pseudoachalasia by computed tomography. Am J Gastroenterol1997;92:624–8.

10. Deviere J, Dunham F, Rickaert F, et al. Endoscopic ultrasonography inachalasia. Gastroenterology 1989;96:1210–3.

11. Ziegler K, Zimmer T. The role of endoscopic ultrasonography inesophageal motility disorders. Endoscopy 1992;24(suppl 1):338–41.

BOTH MASSIVE UPPER AND LOWERGASTROINTESTINAL HEMORRHAGE SECONDARY

TO TUBERCULOSIS

Eliathamby Kuganeswaran, M.D., Owen J. Smith, M.D.,Stella G. Quiason, M.D., Wendell K. Clarkston, M.D.,Prashant K. Pandya, D.O., and William DePond, M.D.

University of Missouri-Kansas City School of Medicine,Kansas City, Missouri

We report a case of gastrointestinal tuberculosis, presentingwith both massive upper and lower gastrointestinal bleedingthat required two emergency operations. Massive bleeding israre in gastrointestinal tuberculosis because of associatedobliterative endarteritis. Tuberculosis should be considered inthe differential diagnosis of massive gastrointestinal bleedingin the appropriate clinical setting even in an immunocompe-tent patient. (Am J Gastroenterol 1999;94:270–272. © 1999 byAm. Coll. of Gastroenterology)

INTRODUCTION

The incidence of tuberculosis has been increasing in recentyears in the United States. This results from an increasing numberof HIV-infected patients and immigrants. Although gastrointestinaltuberculosis is a relatively infrequent disease in the United States,cases continue to occur. Massive GI bleeding from tuberculosis israre because of associated obliterative endarteritis. We report anunusual case of gastrointestinal tuberculosis presenting with bothmassive upper and lower gastrointestinal hemorrhage, requiringtwo emergency operations.

CASE REPORT

A 43-yr-old woman presented with a 1-day history of massiverectal bleeding and a 3-month history of abdominal pain, fever,night sweats, and a 20-lb weight loss. She had received a 6-monthcourse of isoniazid for a positive PPD skin test 20 yr previously.

Physical examination revealed orthostatic hypotension, diffuse ab-dominal tenderness, and bright red blood per rectum. The hemo-globin was 6.8 g/dl on admission. A radio nuclide RBC scansuggested an area of bleeding in the right lower quadrant. Anarteriogram performed a few hours later did not reveal a bleedingsite. The patient received 7 units of blood to maintain her hemo-globin and cardiovascular stability. Upper endoscopy revealedmild antral gastritis and colonoscopy revealed mild pancolitis.Mucosal biopsies showed evidence of focal active colitis. An AFBstain was negative. Rectal bleeding stopped spontaneously after 2days.

A small bowel follow-through examination was unsuccessful asthe patient could not tolerate the procedure. The patient had an-other episode of massive rectal bleeding 5 days later. A repeat RBCscan showed again an area of bleeding in the right lower quadrant.The patient received 7 units of blood and underwent an emergencyexploratory laparotomy, which revealed 600 cc of ascitic fluid,miliary peritoneal implants, multiple adhesions, and enlargedlymph nodes within the mesentery of the ascending colon with anadherent loop of small bowel. A right hemicolectomy with termi-nal ileal and partial small bowel resection was performed. Histol-ogy of the resected specimen revealed focal small bowel and ilealulcerations with caseating granulomas.

Histology of a mesenteric lymph node showed both caseatingand noncaseating granulomas (Fig 1). Stains for AFB were nega-tive. A chest film only showed old calcified granulomas. Bron-choscopy with alveolar lavage revealed no evidence of tuberculo-sis. A PPD skin test was positive with a 20-mm induration. An HIVtest was negative. After an uneventful postoperative course thepatient was discharged on antituberculosis therapy with isoniazid,rifampin, pyrazinamide, and ethambutal. One day after dischargeshe presented with massive hematemesis and a hemoglobin of 7gm/dl. Upper endoscopy revealed a large clot in the stomach withactive bleeding.

An emergent partial gastrectomy was performed for unrelentingbleeding and a small ulcer was noted at the antrum. Histology ofthe resected specimen showed a medium-sized vessel at the base ofthe ulcer with chronic inflammation and caseating granulomas.After 6 wk, a lymph node culture became positive for Mycobac-terium tuberculosis that was sensitive to standard anti-TB treat-ment. She was discharged 4 weeks after her second operation. Thepatient received 9 months of antituberculosis therapy. Quadrupletherapy (isoniazid, rifampin, pyrazinamide, and ethambutal) wasadministered for the first two months. The patient remains symp-tom free.

DISCUSSION

Massive lower GI bleeding resulting from tuberculous ulcer-ation of the colon, cecum, and terminal ileum has been reported (1,2). Less frequently, massive upper GI bleeding has resulted fromtuberculosis infection creating an aortoenteric fistula, as well asboth gastric and duodenal ulcers (3, 4). Simultaneous upper andlower GI bleeding in a patient with two distinct lesions has notbeen described previously. In obliterative endarteritis, there is newintimal connective tissue formation that obliterates the lumen andmakes massive bleeding an uncommon sequela. Tuberculosisshould be considered in the differential diagnosis of massive gas-trointestinal bleeding in the appropriate clinical setting even in animmunocompetent patient. Massive bleeding from tuberculosis hasbeen treated surgically except in one case that was treated withReceived Feb. 10, 1998; accepted Aug. 4, 1998.

270 BRIEF CASE REPORTS AJG – Vol. 94, No. 1, 1999

transcatheter immobilization (5) and in another case that wasmanaged conservatively (6).

The diagnosis of gastrointestinal tuberculosis can be difficult asthe symptoms, signs, and barium studies are nonspecific. Obtain-ing adequate specimens for a tissue diagnosis by endoscopy isdifficult as tuberculosis lesions are located deep to the mucosa. Inour case AFB stain, histology, and culture of the colonic mucosadid not reveal any evidence of tuberculosis. The diagnosis wasstrongly suspected at the time of laparotomy and 6 weeks later aculture of a mesenteric lymph node grew Mycobacterium tuber-culous, confirming the diagnosis. Diagnostic yield of colonoscopicbiopsy for detecting tuberculosis varies from 60% to 80% (7, 18).Diagnostic yield of upper endoscopy is approximately 50% (9).

Polymerase chain reaction technique in the diagnosis of gastro-intestinal tuberculosis in the absence of tissue and culture positivityhas been described by Anandet al. (10), and may prove to beuseful. Any part of the GI tract can be involved with tuberculosis.The most common site of involvement is the ileocecal region. Thisresults from large amounts of lymphoid tissue in the region andphysiologic stasis. Tuberculosis involving the stomach is rare inview of the presence of gastric acid and lack of lymphoid tissue.The incidence of tuberculosis of the stomach is reported to beabout 0.5% in autopsy material and 0.1% in resected material (11).

In our case both the distal ileum and the stomach were involved.Our patient does not have HIV infection or any known impairmentof the immune function, and had no evidence of active pulmonarytuberculosis. Only 10% to 15% of the immunocompetent patientshave extra pulmonary manifestations and only 20% of the cases ofgastrointestinal tuberculosis are associated with active pulmonarytuberculosis. A high index of suspicion is needed in the absence ofactive pulmonary tuberculosis. Concomitant intestinal and perito-neal tuberculosis are rare. Peritoneal TB mainly results from re-

activation of latent foci, but can result from adjacent spread fromthe intestine, lymph node, and ovaries. In this case, peritoneal TBwas probably from spread from mesenteric lymph nodes andintestine. Tuberculosis ulcers are usually circumferential and causecicatrization. However, obliterative endarteritis results in noncir-cumferential small ischemic ulcers as in this case.

Gastrointestinal and peritoneal tuberculosis are treated withquadruple therapy for 2 months followed by a two-drug regimenfor 7 to 10 months. Surgery is reserved for complications such asmassive bleeding, perforation, obstruction, and fistularization.

Reprint requests and correspondence: Owen J. Smith, M.D., Division ofGastroenterology, UMKC School of Medicine, 2411 Holmes, Kansas City,MO 64108.

REFERENCES

1. Pozniak AL, Dalton-Clark HJ, Ralphs DN. Colonic Tuberculosis pre-senting with massive bleeding. Tubercle 1985;66:295–9.

2. Sherman HI, Johnson R, Brook T. Massive gastrointestinal bleedingfrom tuberculosis of the small intestine. Am J Gastroenterol 1978;70:314–6.

3. Chase RA, Haber MN, Pottage JC, et al. Tuberculous esophagitis witherosion into aortic aneurysm. Arch Pathol Lab Med 1986;110:965–6.

4. Weissman D, Gumaste W, Dave PB, et al. Bleeding from a tuberculousgastric ulcer. Am J Gastroenterol 1990;85:742–3.

5. Ramakantan R, Shah P. Control of life-threatening hemorrhage incecal tuberculosis by transcatheter immobilization. Indian J Gastroen-terol 1990;9:149–50.

6. Hiran S, Pande TK, Kumar S, et al. Massive rectal bleeding due toileocecal tuberculosis (conservative approach) (letter). PostgraduateMed J 1994;12:55–6.

7. Bhargave DK, Kushwaha AK, Dasarathy S, et al. Endoscopic diagno-sis of segmental colonic tuberculosis. Gastrointest Endosc 1992;38:571–4.

8. Shah S, Thomas V, Mathan M, et al. Colonoscopic study of 50 patientswith colonic tuberculosis. Gut 1992;33:347–51.

FIG. 1. Mesenteric lymph node with both caseating (large arrow) and noncaseating granulomas. Note the giant cell formation (small arrow) (H & E,34).

AJG – January 1999 BRIEF CASE REPORTS 271

9. Al Kavawi MA, Mohamed AE, Yasawy MI, et al. Protean manifesta-tion of gastrointestinal tuberculosis: Report on 130 patients. J ClinGastroenterol 1995;20:225–32.

10. Anand BS, Schneider FE, El-Zaatari FA, et al. Diagnosis of intestinaltuberculosis by polymerase chain reaction on endoscopic biopsy spec-imens. Am J Gastroenterol 1994;89:2248–9.

11. Palmer ED, Tuberculosis of the stomach and the stomach in tubercu-losis. Am Rev Tuberc 1950;61:116–30.

REMISSION OF M ENETRIER’S DISEASE AFTER APROLONGED PERIOD WITH THERAPEUTICERADICATION OF HELICOBACTER PYLORI

Taimei Kaneko, M.D., Taiji Akamatsu, M.D.,Akira Gotoh, M.D., Kazuhisa Shimodaira, M.D.,Toshiki Shimizu, M.D., Kendo Kiyosawa, M.D.,

Tsutomu Katsuyama, M.D., and Atsushi Momose, M.D.

2nd Department of Internal Medicine, Department ofEndoscopy, Department of Laboratory Medicine, Shinshu

University School of Medicine, Matsumoto; and the Departmentof Internal Medicine, Kamijo Memorial Hospital,

Matsumoto, Japan

We report here a case of Me´netrier’s disease (MD) thatrequired a prolonged period for remission after eradicationtherapy of Helicobacter pylori (HP). The appropriate timeneeded to judge the efficacy of the eradication therapy for HPinfection in an MD case is discussed. (Am J Gastroenterol1999;94:272–273. © 1999 by Am. Coll. of Gastroenterology)

INTRODUCTION

Menetrier’s disease (MD) is a rare condition that was firstreported by Me´netrier in 1888 (1). It is characterized by remarkablehypertrophy of the gastric mucosa accompanied by hypoproteine-mia from protein loss from the gastric mucosa. Recently, there arereports describing the improvement of MD after eradication ther-apy for HP infection (2–5). This report shows an unusual case ofMD that required a prolonged period of over 6 months for remis-sion after eradication therapy.

CASE REPORT

A 34-yr-old man was admitted to Kamijo Memorial Hospital inearly January 1995 complaining of upper abdominal discomfort.Gastrointestinal endoscopy (GIE) showed enlarged gastric foldslocated at the greater curvature of the body (Fig 1a). Forty mg/dayof histamine H2 receptor antagonist (famotidine) was given to treatsymptoms for 3 months in response to the diagnosis of hypertro-phic gastritis. The abdominal discomfort disappeared quickly, butthe pretibial pitting edema gradually progressed. Laboratory in-vestigations showed hypoproteinemia, and serum total protein (TP)was reduced to 4.7 g/l. Serum albumin (Alb) was also reduced to3.0 g/l. The result ofa1-antitrypsin clearance test (67.2 mg/day,normal,13 mg/day) suggest the existence of protein-losing gas-tropathy. Follow-up GIE performed in April 1995 showed thecontinued presence of enlarged gastric folds.Helicobacter pyloriwere seen in the gastric biopsy specimen. A course of 14 days ofantibacterial treatment with 1500 mg/day of amoxicillin combinedwith 30 mg/day of proton pump inhibitor (lansoprazole) wasstarted in May 1995.

The patient was referred to Shinshu University Hospital in July1995. Laboratory findings showed worsening of the hypoproteine-mia (TP 4.3 g/l and Alb 2.8 g/l), but no other abnormalities. GIEperformed in our hospital 2 months after eradication therapyshowed the continued presence of enlarged gastric folds (Fig 1b).Histologic findings were compatible with MD, which consist offoveolar hyperplasia, glandular atrophy, and mild infiltration ofmononuclear cells. The eradication therapy was judged to besuccessful. In spite of successful eradication, TP and Alb increasedvery slowly until August 1996, reaching 7.2 g/l and 4.9 g/l,respectively. GIE performed in September 1996 showed disappear-ance of the enlarged gastric folds and erosions (Fig 1c). Histologicfindings of the biopsy specimen showed reduction of hyperplasiaof the foveolar epithelium. There was no recurrence of the enlargedfolds and hypoproteinemia for two years after eradication therapy.

DISCUSSION

The topic is the period required for the remission of enlargedgastric folds or hypoproteinemia. According to other reports, theaverage period is about 4–7 wk (2–5). This case required a pro-longed period of more than 6 months for the endoscopic and bloodchemical improvement. The same situation was reported by Rog-geroet al. with 15 cases of lymphoma of the mucosa-associatedReceived Jan. 28, 1998; accepted Aug. 4, 1998.

FIG. 1. a. Endoscopic appearance before the eradication therapy shows enlarged gastric folds and erosions located at the greater curvature of the gastricbody. b. Endoscopic appearance 2 months after the eradication therapy shows the continued presence of enlarged gastric folds. c. Endoscopic appearance morethan one year after the eradication therapy shows disappearance of enlarged gastric folds and erosions.

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