CASE REPORT

A 74-yr-old white man with a past history of coronary arterybypass grafting 1 month before presentation was seen in theemergency department for sudden onset of massive hematochezia.After initial resuscitation, he underwent a colonoscopy and biop-sies were taken from the abnormal area of the sigmoid colon (Fig.1). The pathology was described as a sarcomatoid stromal tumor.On initial workup, a CT scan of the abdomen demonstrated a largemass in the left retroperitoneum arising from the upper pole of thekidney and invading the left sigmoid colon, and bilateral pulmo-nary nodules (Fig. 2). Laboratory results were significant for ahemoglobin level of 7.8 g/dl. The patient underwent a left hemi-colectomy and a left radical nephrectomy, with an uneventfulpostoperative period. The final pathology revealed a renal cellcarcinoma with clear cell and sarcomatoid-type components.

DISCUSSION

Most gastrointestinal bleeding associated with renal cell carci-noma is due to metastatic disease, which is present in approxi-mately 25% of patients at the time of diagnosis (5, 6). Commonsites of metastasis include the lungs, lymph nodes, skeletal system,liver, and brain (5). Renal cell carcinoma metastasizing to thegastrointestinal tract is a rare event, accounting for 7.1% of allsmall bowel metastases, and most often occurring in the patientwith disseminated disease (5). Bleeding is usually limited to theupper gastrointestinal tract and can be massive or occult, mainlyassociated with metastases or local recurrence with duodenal in-volvement (7). Although colonic involvement has been described,most cases were due to metastases causing late symptoms after thediagnosis of renal cell carcinoma was made, with only one casedescribing rectal bleeding as the presenting symptom (2).

In conclusion, the clinical manifestations of renal cell carcinomaare almost endless. In the case of rectal bleeding with a localizedabnormality at colonoscopy, we need to be aware of the possibilityof an infiltrating renal tumor as the primary cause of bleeding and

realize the usefulness of the endoscopic biopsy and ancillary ra-diographic studies to obtain the diagnosis.

Reprint requests and correspondence: Danny Chung, M.D., c/o TheDepartment of Research, Western Reserve Care System, 500 Gypsy Lane,Youngstown, OH 44501.

REFERENCES

1. Melicow MM, Uson AC. Nonurologic symptoms in patients with renalcancer. JAMA 1960;172:146–51.

2. Roumen RMH, Corten RLFM, Meijer JWR. Rectal bleeding as the firstclinical symptom of renal cell carcinoma. Netherland J Surg 1989;41:117.

3. Weigensberg IJ. Metastatic renal carcinoma: Unusual and deceptivepresenting features. South Med J 1972;65:611–6.

4. Short TP, Thomas E, Joshi PN, et al. Occult gastrointestinal bleeding inrenal cell carcinoma: Value of endoscopic evaluation. Am J Gastroen-terol 1993;88:300–2.

5. Thomason PA, Peterson LS, Staniunas RJ. Solitary colonic metastasisfrom renal-cell carcinoma 17 years after nephrectomy. Report of a case.Dis Colon Rectum 1991;34:709–12.

6. Wahner-Roedler DL, Sebo TJ. Renal cell carcinoma: Diagnosis basedon metastatic manifestations. Mayo Clin Proc 1997;72:935–41.

7. Lynch-Nyhan A, Fishman EK, Kadir S. Diagnosis and management ofmassive gastrointestinal bleeding owing to duodenal metastasis fromrenal cell carcinoma. J Urol 1987;138:611–3.

8. Black JAR, Mendelson RM. Duodenal haemorrhage resulting fromrenal cell carcinoma metastases. Australasian Radiology 1995;39:396–8.

TUBERCULOUS COLITIS MIMICKINGCROHN’S DISEASE

Christian Arnold, M.D., Darius Moradpour, M.D., andHubert E. Blum, M.D.

Department of Medicine II, University of Freiburg,Freiburg, Germany

Intestinal tuberculosis is a rare disease in western countriesand may mimic a variety of gastrointestinal disorders. Here,Received June 26, 1998; accepted June 30, 1998.

FIG. 1. Colonoscopy showing area of mucosal abnormality in the trans-verse colon, biopsy demonstrated sarcomatoid tumor.

FIG. 2. CT scan showing tumor originating from left kidney invading thecolonic wall.

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we report the case of a 63-yr-old patient who presented withprofuse bleeding from a deep rectal ulcer. Similar lesions werefound in different parts of the colon. Multilocular colorectalcarcinoma was suspected based on the macroscopic appear-ance. Histology, however, suggested Crohn’s disease. Intestinaltuberculosis was initially ruled out by negative staining foracid-fast bacilli, mycobacterial culture, and polymerase chainreaction analysis. A treatment for Crohn’s disease was started.Endoscopic reexamination revealed progressive disease withextensive ulcerations of the terminal ileum. Histopathologicalexamination then revealed acid-fast bacilli in the colonic mu-cosa typical for mycobacterium tuberculosis infection. Thiscase emphasizes the need to include intestinal tuberculosis inthe initial differential diagnosis of ulcerative colorectal lesionsalso in the western population. (Am J Gastroenterol 1998;93:2294–2296. © 1998 by Am. Coll. of Gastroenterology)

INTRODUCTION

The incidence of tuberculosis in Western countries has in-creased considerably in recent years, mostly due to the AIDSepidemic and immigrants from developing countries (1). In mostcases, tuberculosis involves the lungs and lymph nodes. Gastroin-testinal tuberculosis, however, has to be considered, especiallyamong immunocompromised patients and individuals from devel-oping countries. Frequently, clinical findings are difficult to inter-pret, especially if tuberculosis exists without pulmonary symp-toms. In different studies, the lung is involved in about 20% ofprimary gastrointestinal infections (2). In primary pulmonary tu-berculosis the gastrointestinal tract is involved in about 25% ofcases (3). The spectrum of gastrointestinal involvement in patientswith tuberculosis is broad, ranging from rare infections of theesophagus or tuberculous peritonitis to the more frequent involve-ment of the terminal ileum, colon, and rectum. Differential diag-nosis of gastrointestinal tuberculosis includes Crohn’s disease (4),colorectal carcinoma (5), and a variety of infectious diseases (2).

CASE REPORT

A 63-yr-old woman of Caucasian origin presented with malaise,low grade fever, and diarrhea of 6 months duration. She had lost 7kg of body weight and occasionally observed bloody stools. Herpast medical history revealed no significant diseases. She was notimmunocompromised and had not traveled abroad during the last2 yr. She had a balanced nutritional intake, was a nonsmoker, andlived under normal social conditions.

Physical examination revealed a deep ulcerous lesion of the rec-tum, highly suspicious for rectal carcinoma. Physical examinationotherwise was normal. Laboratory findings showed a mild hypochro-mic anemia. White cell and platelet counts were normal, as were liverenzymes, blood urea nitrogen, and electrolytes. Erythrocyte sedimen-tation rate was 72 mm in the first hour and C-reactive protein levelwas 8.9 mg/dl. Blood and stool cultures were negative for all bacterialpathogens, including mycobacteria. Tuberculin test was negative. Achest x-ray examination performed before admission was unremark-able. Sonography revealed a mass adjacent to the ascending colon andanother in the sigmoid colon. Colonoscopy showed a deep ulcerouslesions in the rectum and sigmoid colon. Furthermore, a tumorouslesion in the ascending colon near the cecum was found that could not

be passed with the endoscope. Barium enema revealed a filiformstenosis of the ascending colon.

Based on the endoscopic appearance, the findings were consid-ered highly suspicious for multilocular colorectal carcinoma. His-tology, however, revealed a marked chronic infection in all biopsies.A part from lympho-plasmacellular infiltrates and microabscesses,noncaseating granulomas and epitheloid cells were seen in the mucosaand partially submucosa, consistent withCrohn’s disease. Acid-fastbacilli were not detected. In view of these results, Crohn’s diseasewas diagnosed and treatment with corticosteroids was initiated.

Six weeks later, the patient presented in good physical condi-tion. Fever had resolved. Colonoscopy showed unchanged lesionsin the rectum, sigmoid, and ascending colon. Biopsies showed thesame histological pattern as before; acid-fast stains were negative.Corticosteroid treatment was continued.

In the ensuing month, the patient lost 3 kg of body weight, devel-oped a fever of 39°C, and had severe watery diarrhea. She appearedmalnourished and acutely ill on physical examination. On rectalexamination, the deep ulcerous lesion was found to have increased insize. Laboratory tests showed a hematocrit of 29.8%; the hemoglobinlevel had fallen to 9.2 g/dl; the white cell count was normal.C-reactive protein was 13.2 mg/dl; erythrocyte sedimentation ratewas 120 mm in the first hour. AST was 80 U/L, ALT 84 U/L.

Colonoscopy revealed the initially described ulcerous lesions ofthe rectum and the sigmoid colon. In addition, the ileocecal valvewas totally destroyed with ulcer and pseudopolyp formation (Fig.1). A chest x-ray showed bilateral micronodular lesions, distributedpredominantly in the peri- and infrahilar areas. Active pulmonarytuberculosis was suspected, but acid-fast bacilli were not detectedin the sputum and bronchoalveolar lavage. Because miliary tuber-culosis was nevertheless suspected, a percutaneous liver biopsywas performed, which revealed granuloma formation with epithe-loid cells, central caseating necrosis, and acid-fast bacilli in Ziehl-Neelsen staining. At the same time, the biopsy of the colon showedReceived Jan. 15, 1998; accepted July 1, 1998.

FIG. 1. Endoscopic view of the terminal ileum showing chronic inflam-mation with flattened mucosa, destroyed ileocecal valve, and pseudopolypformation.

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a high number of acid-fast bacilli upon auramin-rhodamin stainingand granulomatous ulceration. Polymerase chain reaction (PCR)analysis of the bronchoalveolar fluid was positive forMycobacte-rium tuberculosis.

The patient was started on a tuberculostatic therapy with isoniazid,rifampicin, pyrazinamid, and ethambutol. She improved gradually andher fever resolved within a few days. She continued to have waterydiarrhea due to the multiple ulcerous lesions and the destroyed analsphincter. A temporary ileostomy was therefore performed. The pa-tient subsequently gained weight but needed parenteral nutritionalsupport for the next weeks. Currently, the patient is free of symptomsand is continuing the tuberculostatic treatment.

DISCUSSION

The incidence of tuberculosis has decreased substantially overthe last decades. In most cases, tuberculosis involves the lungs butevery other organ may be affected. In the gastrointestinal tract, thececum is the most common site of involvement, followed by thejejuno-ileum, colon, and rectum. Active pulmonary disease is notalways the source of infection, as only 25% of patients with gastro-intestinal tuberculosis have primary infection of the lungs (3).

The manifestation of gastrointestinal tuberculosis is variable.Symptoms are nonspecific and include fever, night sweats, weightloss, abdominal pain, and diarrhea. Complications include severediarrhea with malabsorption and protein-losing enteropathy, hem-orrhage, and obstruction. Formation of fistulas and perforationoccur rarely (2, 6).

Our case illustrates a typical manifestation of gastrointestinaltuberculosis. Furthermore, it demonstrates the diagnostic difficul-ties. Gastrointestinal tuberculosis can mimic Crohn’s disease orcolorectal carcinoma. Further differential diagnosis includes Yer-sinia infection, ameboma, histoplasmosis, and various fungal in-fections (2). Infectious diseases have to be ruled out by culture,serological tests, and histology. Endoscopic differences are notspecific for each of the differential diagnosis. Usually, the ileocecalregion is involved as a unit in gastrointestinal tuberculosis. Ab-dominal CT scan is not specific for tuberculosis but can detectmasses or segmental bowel involvement (7). The diagnostic pro-cedure of choice is colonoscopy and biopsy (8). Deep biopsyshould be taken preferably from the margins of ulcerations, be-cause tuberculous granulomas are often submucosal as comparedwith the mucosal granulomas in Crohn’s disease. Staining foracid-fast bacilli must be performed. However, only 50–80% ofcases can be diagnosed by histological examination. Sensitivityand specificity for acid-fast bacilli staining is even lower, as only30–60% of cases may be diagnosed by this technique (2).

Diagnosis of intestinal tuberculosis is based on the demonstra-tion of acid-fast bacilli in tissue or stool. However, culture resultsare obtained only after a period of 4–6 wk, resulting in delayeddiagnosis and institution of therapy. Moreover, a positive culturefrom biopsies is rarely obtained. Recently, PCR of biopsy speci-mens obtained endoscopically has been shown to be more sensitiveand reliable than culture and acid-fast stains in diagnosing intes-tinal tuberculosis (9). Sensitivity of this technique is 75–80%,whereas specificity reaches 85–95%, depending on the type ofspecimen (10, 11).

Treatment of intestinal tuberculosis is primarily medical. De-pending on the severity of disease and the immune status of thepatient, a triple or quadruple therapy should be instituted over aperiod of 6–9 months. Complications such as the formation offistulas, perforation, hemorrhage, or involvement of sphincter

structures remain the domain of surgery. Frequently, diagnosis ofintestinal tuberculosis cannot be established until complicationsoccur, as in our case. A preventive treatment with tuberculostaticdrugs must be considered, especially if an immunosuppressivetreatment for Crohn’s disease is initiated. The difficulty of when tostart prophylactic treatment has been pointed out in this case report,as diagnosis of tuberculosis was initially considered to be ruled outby negative results of histology, PCR, and cultures. Althoughinfrequent in immunoncompetent individuals, gastrointestinal tu-berculosis must be kept in mind in the differential diagnosis ofchronic intestinal disease.

ACKNOWLEDGMENT

We gratefully thank Mrs. S. Schmitt-Graeff, M.D., for perform-ing the pathological examinations and H. Schwacha, M.D., forperforming the endoscopy.

Reprint requests and correspondence: Hubert E. Blum, M.D., Depart-ment of Medicine II, University of Freiburg, Hugstetter Strasse 55,D-79106 Freiburg, Germany.

REFERENCES

1. Snider DE, Roper WL. The new tuberculosis. N Engl J Med 1992;326:703–5.

2. Marschall JB. Tuberculosis of the gastrointestinal tract and the peri-toneum. Am J Gastroenterol 1993;88:989–99.

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

4. Jayanthi V, Robinson RJ, Malathi S, et al. Does Crohn’s disease needdifferentiation from tuberculosis? J Gastroenterol Hepatol 1996;11:183–6.

5. Hoss-Schewietzek S, Alles JU, Muhrer KH. Tuberculosis of the largeintestine—a differential diagnosis of inflammatory and neoplastic co-lon tumors. Chirurg 1995;66:731–4.

6. Dobbins WO, Klipstein FA. Chronic infections of the small intestine.In: Yamada T, Alpers DH, Owyang C, et al., eds. Textbook of gas-troenterology, vol 2. Philadelphia: J. B. Lippincott, 1991:1472–858.

7. Bathazar EJ, Massion J. Ileocoecal tuberculosis: CT and radiologicevaluation. Am J Radiol 1990;154:499–503.

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

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

10. Tan MF, Ng WC, Chan SH, et al. Comparative usefulness of PCR inthe detection of Mycobacterium tuberculosis in different clinical spec-imens. J Med Microbiol 1997;46:164–9.

11. Condos R, McClune A, Rom WN, et al. Peripheral-blood-based PCRassays to identify patients with active pulmonary tuberculosis. Lancet1996;347:1082–5.

RIGHT-SIDED SCIATALGIA COMPLICATINGCROHN’S DISEASE

J. F. Demarquay, M.D., F. X. Caroli-Bosc, M.D.,M. Buckley, M.D., E. P. Peten, M.D., P. Chevallier, M.D.,

X. Hebuterne, M.D., and J. P. Delmont, M.D.

Department of Gastroenterology and Radiology, Archet IIHospital, C.H.U. Nice, France

Neurological complications of Crohn’s disease due to in-volvement of the extradural space are extremely rare. A 40-

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