of didanosine accumulate in the liver and have been shown, in laboratory animal studies, to alter calcium homeostasis (9). Acetaminophen leads to impaired mitochondrial oxida- tive metabolism and alters mitchondrial ATPase activity (10). We speculate that having both acetaminophen and didanosine affects mitochondrial metabolism. This may lend support to the interaction between these two drugs, resulting in hepatoxicity. The incidence of hepatocellular damage due to didanosine when it is used without other hepatotoxic medications is low, but when it is used in combination with potential hepatotoxic medications the in- cidence may increase. We suggest that extreme caution should be exercised when patients use potentially hepato- toxic drugs such as acetaminophen in combination with didanosine. Jeffrey C. Lederman, D.O. Haq Nawaz, M.D., M.P.H. Department of Internal and Preventive Medicine Griffin Hospital Derby Yale University School of Medicine New Haven, Connecticut REFERENCES 1. Lankisch P, Droge M, Gottesleben F. Drug induced acute pancreatitis: Incidence and severity. Gut 1995;37:565–7. 2. Dutta S, Ting F, Lai L. Study of prevalence, severity, and etiological factors associated with acute pancreatitis in patients infected with human immunodeficiency virus. Am J Gastro- enterol 1997;92:2044 – 8. 3. Bissuel F, Bruneel F, Habersetzer F, et al. Fulminant hepatitis with severe lactate acidosis in HIV-infected patients on di- danosine therapy. J Intern Med 1994;235:367–71. 4. Ware A, Berggren R, Taylor W. Didanosine-induced hepatitis. Am J Gastroenterol 2000;95:2141–3. 5. Lacaille F, Ortigao MB, Debre M, et al. Hepatic toxicity associated with 2'-3' dideoxyinosine in children with AIDS. J Pediatr Gastroenterol Nutr 1995;20:287–90. 6. Moyle G, Nelson MR, Hawkins D, Gazzard BS. The use and toxicity of didanosine (ddI) in HIV antibody-positive individ- uals intolerant to zidovudine. Q J Med 1993;86:155– 63. 7. Sulkowski M, Thomas DL, Chaisson RE, Moore RD. Hepa- totoxicity associated with antiretroviral therapy in adults in- fected with human immunodeficiency virus and the role of hepatitis C or B virus infection. JAMA 2000;283:74 – 80. 8. Youssef J, Badr M. Disruption of mitochondrial energetics and DNA synthesis by the anti-AIDS drug dideoxyinosine. Toxi- col Lett 1992;60:197–202. 9. Badr M. Effects of anti-AIDS drug dideoxyinosine on hepatic glycolysis in the perfused rat liver: Role of intracellular cal- cium stores. Biochem Pharmacol 1991;41:146 – 8. 10. Katyare S, Satay J. Impaired mitochondrial oxidative energy metabolism following paracetamol-induced hepatotoxicity in the rat. Br J Pharmacol 1989;96:51– 8. Reprint requests and correspondence: Haq Nawaz, M.D., M.P.H., Department of Internal and Preventive Medicine, Griffin Hospital, 130 Division Street, Derby, CT 06418. Received May 7, 2001; accepted July 19, 2001. Previously Undiagnosed Infiltrating Lobular Carcinoma of the Breast Presenting as a Gastric Outlet Obstruction TO THE EDITOR: Before the advent of histamine-2 blocker usage in the late 1970s, duodenal ulceration ac- counted for 60% of gastric outlet obstructions (GOOs) (1). Since that time, the incidence of GOOs has declined dra- matically, and malignancy now accounts for as many as 61% of obstructions (2). Primary gastric adenocarcinoma is the most common malignant cause of GOOs, followed by carcinoma of the pancreas and gallbladder (2, 3). Although several cases of GOOs due to metastatic breast cancer have been reported in the past (4 –7), we believe that we report the first case in which a woman with no prior diagnosis of breast cancer and a history of normal, routine, yearly mam- mograms has presented with GOO due to metastatic infil- trating lobular carcinoma. A 52-yr-old woman presented to our hospital’s emer- gency department after a near-syncopal episode. She com- plained of progressively worsening nausea, vomiting, dys- pepsia, and early satiety during the previous month, and an unexplained 20-lb weight loss in the past year. Her medical history was significant for gastroesophageal reflux disease and recent nonsteroidal anti-inflammatory drug (NSAID) use. She had no history of breast cancer, and had a normal mammogram 6 months earlier. Her Hb was 6.0; Hct, 18.4; and stool, guaiac positive. She was admitted and transfused with 2 U of packed red blood cells. A gastroenterology consultation was obtained, and esophagogastroduodenos- copy was performed. The latter showed no active bleeding, a 1.0-cm duodenal ulcer, and an edematous pylorus. A Campylobacter-like organism test was negative for Helico- bacter pylori. NSAID-induced duodenal ulceration with edema extending to the pylorus was diagnosed. The patient was prescribed omeprazole, advised to discontinue NSAID use, and discharged the next day. One week later, she presented to her primary care phy- sician complaining of nausea, vomiting, dyspepsia, and early satiety, which had been getting progressively worse despite medical therapy. A second esophagogastroduode- noscopy was performed to rule out GOO secondary to scarring. Biopsies were taken. Histological examination showed rows of diffusely infiltrative, poorly differentiated malignant cells with signet ring vacuoles, focally positive for mucin on DPAS and Alcian blue stains (Fig. 1). There was infiltration of the muscularis mucosae, and no evidence of H. pylori infiltration. An initial diagnosis of infiltrating poorly differentiated gastric carcinoma of the diffuse type with signet ring cells was made. The patient was referred to general surgery for abdominal exploration and possible gas- trectomy. Upon presentation to the surgical service, a complete physical exam was performed. Breast examination revealed 3475 AJG – December, 2001 Letters to the Editor