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decrease in the size of the fluid collection to 2.0 cm ⫻ 2.1 cm, and his symptoms had improved; 12 wk after that he was asymptomatic and a CT scan showed complete resolution of the peripancreatic fluid collection. Drug-induced pancreatitis has been associated with sulfonamide derivatives. Case reports of pancreatitis have been associated with celecoxib (1, 2), which also has a sulfa moiety, as well as traditional nonsteroidal anti-inflammatory drugs without sulfa moieties (3, 4). In this case, other likely causes of acute pancreatitis (alcohol ingestion, cholelithiasis) were excluded. To our knowledge there have been no reports of acute pancreatitis associated with cyclobenzaprine, diazepam, or drugs similar to them. Thus, given the temporal relationship, we suspect that this case of acute pancreatitis was associated with the ingestion of rofecoxib. Although rofecoxib does contain a sulfur atom in its structure, it does not have a sulfonamide moiety, excluding a sulfonamide allergic reaction. The role of prostaglandins in acute pancreatitis is still controversial (5). In one animal model of sodium toracholate– induced acute pancreatitis, indomethecin decreased levels of local prostaglandins and increased mortality (6). Although not conclusive, these and other data support the notion that selective and nonselective nonsteroidal anti-inflammatory drug– induced pancreatitis may be a physiological consequence of the mechanism of action of this drug class. The rarity of this complication of a widely used medication suggests that host genetic factors play an important role. Nevertheless, this case report, put into context of the medical literature, suggests rofecoxib should be added to a growing list of selective and nonselective cyclooxygenase inhibitors that have been associated with acute pancreatitis. Ravi K. Amaravadi, M.D. Brian C. Jacobson, M.D., M.P.H. Daniel H. Solomon, M.D., M.P.H. Michael A. Fischer, M.D. Divisions of Gastroenterology, Rheumatology, and Pharmacoepidemiology and Pharmacoeconomics Department of Medicine Brigham and Women’s Hospital Harvard Medical School Boston, Massachusetts
REFERENCES 1. Baciewicz AM, Sokos DR, King TJ. Acute pancreatitis associated with celecoxib. Ann Intern Med 2000;132:680. 2. Carrillo-Jiminez, R, Nurnberger M. Celecoxib-induced acute pancreatitis and hepatatis: A case report. Arch Intern Med 2000;160:553–5. 3. Castiella A, Lopez P, Bujanda L, Arenas JI. Possible association of acute pancreatitis with naproxen. J Clin Gastroenterol 1995;21:258. 4. Wilmink T, Frick TW. Drug-induced pancreatitis. Drug Saf 1996;14:406 –23.
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5. Rao KN. Pathophysiology of pancreatitis: The role of prostaglandins. Prostaglandins 1993;45:309 –13. 6. Closa D, Hotter G, Rosello-Catafau J, et al. Prostanoids and oxygen free radicals in early stages of experimental acute pancreatitis. Dig Dis Sci 1994;39:1537– 43.
Reprint requests and correspondence: Michael A. Fischer, M.D., Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women’s Hospital, BLI/341, 221 Longwood Avenue, Boston, MA 02115. Received Sep. 27, 2001; accepted Nov. 15, 2001.
Physician Compliance With Colon Cancer Screening TO THE EDITOR: The American Cancer Society has established specific screening guidelines for colorectal cancer and recommends, for individuals 50 yr or older, fecal occult blood testing (FOBT) every year and sigmoidoscopy every 3–5 yr; if either is positive, a colonoscopy is recommended (1). Surveys indicate that 18 – 82% and 11–53% of respondents comply with FOBT and sigmoidoscopy recommendations, respectively (2), whereas 38% of gastroenterologists follow these guidelines (3). We wished to explore compliance with screening guidelines for colon cancer by a cohort of various physicians. Study candidates were members of the local county medical society who graduated from medical school before 1976 (i.e, aged 50 or older). Each was mailed a one-page survey that explained the purpose of the study and explored demographic variables as well as compliance history with FOBT, sigmoidoscopy, and colonoscopy guidelines. Informed consent was implied with the return of the survey. Of 363 mailed surveys, 168 were returned, for a onetime-mailing response rate of 46.3%. Three were excluded from analysis because participants were younger than 50. For statistical analysis, several variables had to be modified because of insufficient sample sizes. Race was dichotomized into white/non-Hispanic versus other, and medical specialty was divided into family/internal medicine versus other. Among this sample, 108 participants (65.5%) were ages 50 –59, 42 (25.5%) were 60 – 69, and 15 (9.1%) were 70 –79. The majority were male (147 [90.2%], n ⫽ 163). Most were white/non-Hispanic (122 [74.0%]). Although 51 (30.7%) were in either family practice or internal medicine, the remainder (112 [67.5%]) were in other specialties (data were missing for two respondents). In analyzing the data, we developed a general risk variable and determined compliance. The general risk variable was created according to the following: if one or more of the risk categories was checked, a value of 1 was credited; if
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Letters to the Editor
none were checked, a value of 0 was assigned. Compliance was determined by comparing the reported testing with the recommended testing based upon age. Because we used age groupings in the demographic inquiry rather than a single specific age, we made an assumption that the respondent was in the midpoint of the age category. According to the results, the majority of the sample (149 [90.3%]) reported no risk factors for colon cancer. Fifty-two percent of the sample followed the recommended guidelines for screening. The presence of one or more risk factors for colon cancer was significantly associated with screening compliance (p ⫽ 0.0098). Specifically, the odds of complying with screening recommendations were 5.7 times higher for those with one or more risk factors versus no risk factors. It appears that physicians, particularly those with risk factors for colon cancer, have a higher compliance with screening guidelines for colon cancer than other physicians and the general population [about 40% of the latter comply (4)]. The rationales for those physicians who are noncompliant warrant further empirical investigation. The potential limitations of this study include the small sample size, use of age groupings rather than specific ages, response rate, and the self-report nature of the data, which entailed recollection. The authors acknowledge Harry Khamis, Ph.D., Professor and Director of the Statistical Consulting Center at Wright State University in Dayton, OH, for his assistance in the preparation of this letter. Junaid Malik, M.D. Randy A. Sansone, M.D. Departments of Internal Medicine and Psychiatry Education Kettering Medical Center Kettering, Ohio Departments of Psychiatry and Internal Medicine Wright State University Dayton, Ohio
REFERENCES 1. Byers T, Levin B, Rothenberger D, et al. American Cancer Society Guidelines for screening and surveillance for early detection of colorectal polyps and cancer: Update 1997. CA Cancer J Clin 1997;47:154 – 60. 2. Vernon SW. Adherence of colorectal cancer screening: A brief overview. Ann N Y Acad Sci 1995;168:292–5. 3. Afridi SA, Jafri SF, Marshall JB. Do gastroenterologists themselves follow the American Cancer Society recommendations for colorectal cancer screening? Am J Gastroenterol 1994;89: 2184 –7. 4. Burt RW. Colon cancer screening. Gastroenterology 2000;119: 837–53.
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Reprint requests and correspondence: Randy A. Sansone, M.D., Sycamore Primary Care Center, 2115 Leiter Road, Miamisburg, OH 45342. Received Nov. 16, 2001; accepted Dec. 3, 2001.
Gallbladder Carcinoma Secondary to Repetitive Hepatic Arterial Chemoembolization TO THE EDITOR: A 67-yr-old man presented in 1995 with a 2-month history of anorexia. In 1992 he had a biopsyproven alcohol-related cirrhosis. Abdominal CT demonstrated a spreading type of hepatocellular carcinoma in the right lobe of the liver with an atrophy of the left lobe. The ␣-fetoprotein level was elevated, at 780 ng/ml (normal ⬍ 10). A biopsy proved the hepatocellular carcinoma nature of the tumor. Because of the left lobe atrophy, hepatic arterial chemoembolization (HACE) was performed. During the next 3 yr he had nine courses of HACE. In 1998 he presented with a 15-day history of progressive jaundice and fever. The value of ␣-fetoprotein was within the normal range. A cholangiogram showed lesions of secondary sclerosing cholangitis. Endoscopic stent placement was partially effective. A surgical procedure was then performed, consisting of hepaticojejunal anastomosis with cholecystectomy. Pathologically, there was transmural fibrosis of the gallbladder wall with thickening of the wall (12 mm), and replacement of it with granulation tissue. An adenocarcinoma infiltrating the serosa was found in the gallbladder. No gallstones were identified. The patient died a few days later during a septic schock. Risk factors for gallbladder cancer include gallstones, female sex, obesity, polyps, and, in some countries, chronic infection with Salmonella typhi (1). Longstanding chronic cholecystitis with calcification of the gallbladder wall (porcelain gallbladder) is another predisposing factor of cancer. Our case report provides evidence for a direct link between chronic acalculous cholecystitis and cancer. The mechanism by which chemoembolization may cause cholecystitis is well known. An endarteritis may be produced in the territory supplied by the cystic artery, resulting in ischemia of the gallbladder with subsequent acute and chronic cholecystitis (2). The decreased vascularity may help to progress to fibrosis of the wall. The progression to cancer is speculative. Usually, patients with hepatocellular carcinoma treated with HACE die before the potential emergence of such a complication. But other malignancies with a better prognosis (3) (islet cell carcinoma, carcinoid tumor) treated with HACE could develop this kind of tumor. Physicians will be aware of this complication. Cholecystectomy has