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disease and SLE, pANCA was negative after steroid pulse therapy, and the sister and father who had Crohn’s disease were negative for ANCA. These results indicate that pANCA in our patient probably reflected the activity of SLE rather than of Crohn’s disease. In conclusion, the diagnostic criteria for both Crohn’s disease and SLE may overlap, leading to difficulty in the establishment of the correct diagnosis. When pancytopenia and autoimmuno-antibodies, including a positive pANCA, are detected in patients with Crohn’s disease, the coexistence of SLE should be suspected in patients with IBD and complex extraintestinal manifestations. Reprint requests and correspondence: Yoshiyuki Nishida, M.D., The Second Department of Internal Medicine, 7-1 Sakamoto 1-Chome, Nagasaki 852, Japan. REFERENCES 1. Greenstein AJ. Extraintestinal manifestation of Crohn’s disease and ulcerative disease in 700 patients. Medicine 1976;55:401–12. 2. Hauschild S, Schmitt WH, Csernok E, et al. ANCA in systemic vasculitides, collagen vascular diseases, rheumatic disorders and inflammatory bowel diseases. Adv Exp Med Biol 1993;336:245–51. 3. Johnson DA, Diehl AM, Finkelman FD, et al. Crohn’s disease and systemic lupus erythematosus. Am J Gastroenterol 1985;11:869 –70. 4. Constans J, Bernard PH, Bakhach S, et al. Crohn disease and systemic lupus erythematosus, a rare association. Presse Med 1993;22:1193. 5. Nadorra RL, Nakazato Y, Landing BH. Pathologic features of gastrointestinal tract lesions in childhood-onset systemic lupus erythematosus: Study of 26 patients, with review of the literature. Pediatr Pathol 1987;7:245–59. 6. Tan EM, Cohen AS, Fries JF, et al. The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 1982; 25:1271–7. 7. Carr-Locke DL. Sulfasalazine-induced lupus syndrome in a patient with Crohn’s disease. Am J Gastroenterol 1982;77:614 – 6. 8. Brennan P, Hajeer A, Ong KR, et al. Allelic markers close to prolactin are associated with HLA-DRB1 susceptibility alleles among women with rheumatoid arthritis and systemic lupus erythematosus. Arthritis Rheum 1997;40:1383– 6. 9. Nakajima A, Matsuhashi NG, Kodama T, et al. HLA-linked susceptibility and resistance genes in Crohn’s disease. Gastroenterology 1995;109:1462–7. 10. Nishiya K, Chikazawa H, Nishimura S, et al. Anti-neutrophil cytoplasmic antibody in patients with systemic lupus erythematosus is unrelated to clinical features. Clin Rheumatol 1997;16:70 –5.
FIG. 1. Severe colitis after an ammonia solution enema.
the lamina propria, no signs of stenosis were found. (Am J Gastroenterol 1998;93:2601–2602. © 1998 by Am. Coll. of Gastroenterology) INTRODUCTION
Gastroenterologists commonly see acute esophageal lesions caused by caustic substances. Acute colitis caused by drugs or by products used to induce defecation, is also frequent. Otherwise, enemas with caustic substances are rare, although occasionally reported. We describe two cases of proctocolitis caused by caustic products of domestic use and evaluate the acute lesions and their evolution. CASE REPORTS
Case 1
ACUTE COLITIS CAUSED BY CAUSTIC PRODUCTS Jorge da Fonseca, M.D., Maria Jose´ Brito, M.D., Joa˜o Freitas, M.D., and Cunha Leal, M.D. Division of Gastroenterology and Department of Pathology, Hospital Garcia de Orta, Almada, Portugal
We report two cases of acute proctocolitis caused by rectal application of caustic products of domestic use. One 61-yr-old woman applied an ammonia solution enema; the other patient, a 63-yr-old woman, accidentally applied an enema containing lye. Both patients presented with intense anal pain, but the first patient also had abdominal pain with guarding, hematochezia, and leucocytosis. An acute proctocolitis was found at sigmoidoscopy in both patients. Only conservative and symptomatic measures were prescribed in both cases, and a clinical and endoscopic recovery was seen. In spite of persistent fibrosis in Received Apr. 2, 1998; accepted July 22, 1998.
A 61-yr-old woman, suffering from well documented psychiatric illness manifested by psychogenic itching, washed herself with an ammonia solution, to eradicate imaginary parasites. Believing that she had an intestinal reservoir of parasites, she applied an ammonia solution enema. This provoked anal pain, diffuse abdominal colic, tenesmus, and bright red hematochezia. She presented to the emergency room lucid and cooperative. Her vital signs were normal. Palpation of the lower abdomen revealed tenderness and guarding, but there were no clinical or radiological signs of bowel perforation. Laboratory analyses on admission revealed a normal hematocrit and an elevated WBC (13.800/mm3) with 76% neutrophils. An urgent sigmoidoscopy showed diffuse erythematous friable mucosa, with large ulcerations covered by yellowish exudate (Fig. 1). Acetaminophen was sufficient to relieve the pain, and no steroids or antibiotics were prescribed. Gradually, the bowel movements became less frequent, and the pain and the hematochezia subsided. At day 6 the WBC count was 6.300/mm3, and hemoglobin was normal. A sigmoidoscopy showed an erythematous colon with some sparse ulcerations, but without the wide ulcers of the first examination. Biopsies revealed ulcers penetrating up to the submucosa, atrophic glands, and fibrosis of the lamina propria.
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Three months later, follow-up barium enema was normal, as well as the endoscopic appearance of the colonic mucosa, but biopsies taken from the rectum and sigmoid colon showed chronic inflammation and fibrosis. At present, the patient has no symptoms of colonic disease. Case 2 A 63-yr-old woman used laxatives on a daily basis, as well as frequent applications of water enemas to induce defecation. The patient applied a lye enema, reportedly by accident, on one occasion. She presented to the emergency room with burning anal pain. Her vital signs and abdominal examination were normal. Digital rectal examination did not reveal blood. Emergency laboratory evaluation was normal. A sigmoidoscopy was performed and, with the endoscope inverted in the rectal ampulla, disclosed several ulcerations radiating from the anal canal. She was followed as an outpatient, with rapid improvement of her symptoms. Three months later, a sigmoidoscopy showed no lesions, but biopsies from the area where ulcerations had previously been seen, demonstrated chronic inflammation and fibrosis. The annual follow-up revealed no change of bowel habits. DISCUSSION
Acute lesions caused by enemas are occasionally reported in the medical literature. In some cases they are traumatic (1). In others, there may be a thermal injury, e.g., with very hot water enemas. In most cases there is a chemical lesion induced by drugs (2– 4) or by radiological contrast material (5). These cases are well documented. Sometimes the chemical injury is induced by caustics. There are several cases of soap (6), glutaraldehyde (7), and detergent or hydrogen peroxide enemas (8), as well as other products (3, 4). Acute colitis by the caustic agent is induced by direct mucosal damage (2, 3). The severity of the lesions is dependent on the nature and concentration of the products, the number and the duration of the enemas, and the existence of previous damage. After the acute destruction, a regenerative phase begins. Later, some cases show a severe fibrotic evolution with colonic stenosis (9). To prevent stenoses, some authors suggest the use of steroids (10). To the best of our knowledge, there are no previous reports of acute colitis by lye or ammonia enemas. In our cases, the severe lesions provoked by short duration enemas, suggest high concentrations of very aggressive products. No steroid therapy was used, as this remains a controversial issue, and the clinical signs of perforation may be subsequently concealed. The follow-up endoscopic biopsies showed fibrosis, but there were no clinical, endoscopic, or radiological signs of stenosis. Perhaps only a small proportion of these patients with microscopic fibrosis go on to develop colonic stenosis. Reprint requests and correspondence: Jorge da Fonseca, M.D., Hospital Garcia de Orta, Pragal-2800 Almada, Portugal. REFERENCES 1. Large PG, Mukheiber WJ. Injury to rectum and anal canal by enema syringes. Lancet 1956;ii:596 –9. 2. Fortson WC, Tedesco FJ. Drug-induced colitis: A review. Am J Gastroenterol 1984;79:878 –93. 3. de Parades V, Sultan S, Bauer P. Complications ano-rectales et coliques des suppositoires et des lavements. Gastroenterol Clin Biol 1996;20:446 –52.
AJG – Vol. 93, No. 12, 1998 4. Cappell MS, Simon T. Colonic toxicity of administered medications and chemicals. Am J Gastroenterol 1993;88:1684 –99. 5. Creteur V, Douglas D, Galante M, et al. Inflammatory colonic changes produced by contrast material. Radiology 1983;147:77– 8. 6. Pike BF, Phillipi PJ, Lawson EH. Soap colitis. N Engl J Med 1971; 285:217– 8. 7. West AB, Kuan S, Bennick M, et al. Gluteraldehyde colitis following endoscopy: Clinical and pathological features and investigation of an outbreak. Gastroenterology 1995;108:1250 –5. 8. Pumphrey RE. Hydrogen peroxide proctitis. Am J Surg 1951;81: 60 –2. 9. Kim SK, Cho C, Levinsohn EM. Caustic colitis due to detergent enema. AJR 1980;134:397– 8. 10. Mun˜oz-Navas M, Garcia-Villarreal L. Caustic colitis due to formalin enema. Gastrointest Endosc 1992;38:521–2.
SUCCESSFUL USE OF AN HMG-CoA REDUCTASE INHIBITOR AS ADJUNCTIVE THERAPY IN THE MANAGEMENT OF REFRACTORY BILE LEAK COMPLICATING LAPAROSCOPIC CHOLECYSTECTOMY John Rabine, M.D., and Michael P. Jones, M.D., F.A.C.P. Division of Gastroenterology, University of Cincinnati, Cincinnati, and Wright-Patterson Medical Center, Dayton, Ohio
INTRODUCTION
Bile leaks persist because resistance to flow through the damaged portion of the duct is less than resistance to flow through the distal biliary tree and papilla. Endoscopic management focuses on identification and treatment of distal obstruction and minimization of transpapillary resistance (1). An alternative or adjunctive approach, analogous to that used in pancreatic ductal disruption, would be to directly decrease bile flow. Two logical candidates as effective anticholeretic agents are the HMG-CoA reductase inhibitors and somatostatin or its analog, octreotide (2, 3). HMG-CoA reductase inhibitors are potentially useful in decreasing bile acid dependent bile flow, whereas somatostatin or octreotide may effect either bile acid– dependent or –independent flow. We present a case of a refractory bile leak that was managed using combined endoscopic and anticholeretic therapy. Following a suboptimal response to endoscopic therapy, lovastatin was administered. The leak resolved shortly thereafter. This case highlights the potential usefulness of anticholeretic agents in the management of hepatobiliary disorders. CASE REPORT
A 32-yr-old woman was admitted with nausea, right upper quadrant abdominal pain, fever, and leukocytosis 4 days after uncomplicated laparoscopic cholecystectomy for symptomatic cholelithiasis. Laboratory evaluation was remarkable for a white blood cell count of 20.4 3 103 with 81% segmented neutrophils and 12% bands. Liver chemistries were normal. CT scan of the abdomen revealed a fluid collection in the subhepatic space. At laparoscopy a 200-ml biloma was drained and Jackson-Pratt drain left in the gallbladder bed. ERCP was performed 12 h later. Cannulation was difficult and papillotomy was performed. Cholangiography revealed an anomalous communication between a Received Feb. 10, 1998; accepted July 22, 1998.