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Splenic artery aneurysm secondary to pancreatic carcinoma
AJG – December, 2000
Letters to the Editor
In conclusion, mutations of the CFTR gene may play a role in the etiology of some patients with TCP. The far lower frequency of CFTR mutations, when compared with chronic idiopathic pancreatitis, suggests that either genetic susceptibility per se has a smaller role in TCP, or that the genetic factors that contribute to each form of chronic pancreatitis are different.
3659
7. Mercier B, Lissens W, Novelli G, et al. Identification of eight novel mutations in a collaborative analysis of a part of the second transmembrane domain of the CFTR gene. Genomics 1993;16:296 –7. Reprint requests and correspondence: Peter Durie, M.D., Department of Pediatrics, University of Toronto, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8. Received May 23, 2000; accepted June 7, 2000.
ACKNOWLEDGMENTS Supported by research grants from the Canadian Cystic Fibrosis Foundation and the National Institutes of Health (NIDDK-49096-05).
Splenic Artery Aneurysm Secondary to Pancreatic Carcinoma
Eesh Bhatia, M.D. Department of Endocrinology Sanjay Gandhi Postgraduate Institute of Medical Sciences Lucknow, India
TO THE EDITOR: The splenic artery is the visceral vessel most likely to develop pseudoaneurysms (1). These lesions occur either due to disruption of the vessel wall as a result of the direct action of elastase and other digestive enzymes released by the inflamed pancreas, or as a result of a penetrating or blunt trauma. White et al. reviewed arteriograms of 72 cases of pancreatitis and 84 cases of carcinoma of the pancreas (2). They found arterial aneurysms in 10% of the patients with pancreatitis, while no aneurysms were found in patients with a pancreatic carcinoma. They concluded that the presence of an aneurysm is a helpful distinguishing feature of pancreatitis. A 72-yr-old man consulted our hospital with back pain and a history of tarry stool. The laboratory tests showed that the serum level of carbohydrate antigen 19-9 was markedly elevated (3463 U/ml), whereas the serum levels of amylase, elastase, and carcinoembryonic antigen were within normal ranges. Computed tomography (CT) demonstrated a 12-mm aneurysm arising from the splenic artery, which was connected to a hypoattenuating area behind the splenic artery (Fig. 1). Celiac arteriography also demonstrated a 15-mm aneurysm and an irregularity on the proximal side of the splenic artery. Embolization of the aneurysm by steel coils and N-butyl cyanoacrylate was serially performed. We could not differentiate whether the aneurysm was induced
Peter Durie, M.D. Julian Zielenski, Ph.D. David Lam, B.Sc. Research Institute The Hospital for Sick Children University of Toronto Toronto, Canada Sadiq S. Sikora, M.B.B.S. Department of Gastrointestinal Surgery Gourdas Choudhuri, M.D. Department of Gastroenterology Sanjay Gandhi Postgraduate Institute of Medical Sciences Lucknow, India Lap-Chee Tsui, Ph.D. Research Institute The Hospital for Sick Children Department of Molecular and Medical Genetics University of Toronto Toronto, Canada
REFERENCES 1. Mohan V, Nagolimath SJ, Yajnik CS, et al. Fibrocalculous pancreatic diabetes. Diabetes Metab Rev 1998;14:153–70. 2. Durie PR. Pancreatitis and mutations in the CF gene (editorial). N Engl J Med 1998;339:687–5. 3. Cohn JA, Friedman KJ, Noone PG, et al. Relation between mutations of the cystic fibrosis gene and idiopathic pancreatitis. N Engl J Med 1998;339:653– 8. 4. Sharer N, Schwarz M, Malone G, et al. Mutations of the cystic fibrosis gene in patients with chronic pancreatitis. N Engl J Med 1998;339:645–52. 5. Chillon M, Casals T, Mercier B, et al. Mutations in the cystic fibrosis gene in patients with congenital absence of the vas deferens. N Engl J Med 1995;332:1475– 80. 6. Aznarez I, Onay T, et al. An efficient protocol for CFTR mutation detection based on multiplex heteroduplex analysis (mHET). Pediatric Pulmonology 1998;(suppl)17:332.
Figure 1. Contrast-enhanced CT showed a splenic artery aneurysm (arrow) with a hypoattenuating mass (arrowheads) behind it.
3660
Letters to the Editor
by pancreatitis or a pancreatic carcinoma. During surgery, a firm mass was palpated in the region of the pancreatic body that had invaded to the mesocolon and the jejunum. A dorsal pancreatectomy combined with partial resection of the jejunum was performed en bloc. Macroscopically, the resected specimen contained a scirrhous lesion measuring 45 ⫻ 35-mm in the body of the pancreas. The histological diagnosis was a moderately differentiated tubular adenocarcinoma arising in the body of the pancreas. The splenic artery was completely involved with the tumor and communicated with the pseudoaneurysm. There was direct tumor extension into the mucosa of the jejunum. According to the histopathological findings, we believe that the pathogenesis of this pseudoaneurysm was disruption of the splenic artery induced by arterial invasion of the carcinoma. Thus, the presence of an aneurysm does not always exclude the possibility of a pancreatic carcinoma. In this case, an irregularly shaped hypoattenuating area behind the aneurysm on CT indicated the presence of carcinoma. Percutaneous transcatheter embolization of pseudoaneurysms has been reported as both a form of definitive therapy and as a temporary measure until surgery can be performed safely (3, 4). We also performed this technique, and the patient’s condition was stable during surgery.
ACKNOWLEDGMENT This work was supported in part by a Grant-in-Aid for Cancer Research from the Ministry of Health and Welfare of Japan. Hiroyoshi Furukawa, M.D. Department of Diagnostic Radiology National Cancer Center Hospital Tokyo, Japan Noriyoshi Fukushima, M.D. Department of Clinical Laboratory National Cancer Center Hospital Tokyo, Japan Kazuaki Shimada, M.D. Department of Surgery National Cancer Center Hospital Tokyo, Japan
REFERENCES 1. Gadacz TR, Trunkey D, Kieffer RF. Visceral vessel erosion associated with pancreatitis. Case reports and a review of the literature. Arch Surg 1978;113:1438 – 40. 2. White AF, Baum S, Buranasiri S. Aneurysms secondary to pancreatitis. AJR 1976;127:393– 6. 3. Mandel SR, Jaques PF, Mauro MA, et al. Nonoperative management of peripancreatic arterial aneurysms. A 10-year experience. Ann Surg 1987;205:126 – 8. 4. Boudghe´ne F, L’Hermine´ C, Bigot JM. Arterial complications of pancreatitis: Diagnosis and therapeutic aspects in 104 cases. J Vasc Interv Radiol 1993;4:551– 8.
AJG – Vol. 95, No. 12, 2000
Reprint requests and correspondence: Hiroyoshi Furukawa, M.D., Department of Diagnostic Radiology, National Cancer Center Hospital, 5-1-1, Tsukiji, Chuo-ku, Tokyo 104, Japan. Received June 7, 2000; accepted June 19, 2000.
Re: Sharma et al.—Colorectal Cancer Screening by Primary Care Physicians TO THE EDITOR: The article by Sharma et al. in the June 2000 issue on colorectal cancer screening by primary care physicians has many serious flaws that should have been caught and exposed by your reviewers. First, the physicians queried were identified through a “database that was supplied to us by TAP Pharmaceuticals.” Do we know how many of these doctors were board certified and how many were residency trained? What is their association with TAP Pharmaceuticals? Second, and most importantly, this entire study makes broad generalizations based on a survey response rate of 19.5%. This is the most abysmally low response rate I have ever seen in a reputable medical journal. One can’t seriously make believable conclusions about the screening patterns of America’s primary care doctors based on such a limited sample. The authors make the dubious assertion that the respondents probably represented doctors most “interested in colorectal cancer screening (CRCS).” Third, the study used as its “gold standard” the opinions of three “recognized national authorities.” It is not stated whether any of these “authorities” were primary care doctors. This is important since specialists tend to be biased toward their own screening modality (e.g., radiologists sing the praises of a barium enema, gastroenterologists swear by the colonoscopy, etc.). As a primary care doctor myself, I’ve learned to trust the guidelines published by researchers and epidemiologists who don’t have financial incentives in any one screening modality. The most useful guidelines in this regard come from the reports of the U.S. Preventive Services Task Force (USPSTF), which was used as a reference in the article (1). Fourth, the authors’ experts recommend stopping CRCS in otherwise healthy individuals over age 75. Since there will soon be over 800,000 Americans over age 100 this advice may be overly pessimistic. I frequently have very healthy elderly patients visit me who haven’t been to a doctor for screening in many years. Since some in this age range may live 15 or more years, colon cancer screening may arguably be prudent. The authors’ own discussion states “Published guidelines stress that CRCS must be individualized and that the appropriate age to stop is dependent on the judgment of individual patients and their physicians.” They then criticize their physician respondents for screening into advanced age! The USPSTF guidelines available when the survey was done states (1) “There is little
Letters to the Editor
In conclusion, mutations of the CFTR gene may play a role in the etiology of some patients with TCP. The far lower frequency of CFTR mutations, when compared with chronic idiopathic pancreatitis, suggests that either genetic susceptibility per se has a smaller role in TCP, or that the genetic factors that contribute to each form of chronic pancreatitis are different.
3659
7. Mercier B, Lissens W, Novelli G, et al. Identification of eight novel mutations in a collaborative analysis of a part of the second transmembrane domain of the CFTR gene. Genomics 1993;16:296 –7. Reprint requests and correspondence: Peter Durie, M.D., Department of Pediatrics, University of Toronto, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8. Received May 23, 2000; accepted June 7, 2000.
ACKNOWLEDGMENTS Supported by research grants from the Canadian Cystic Fibrosis Foundation and the National Institutes of Health (NIDDK-49096-05).
Splenic Artery Aneurysm Secondary to Pancreatic Carcinoma
Eesh Bhatia, M.D. Department of Endocrinology Sanjay Gandhi Postgraduate Institute of Medical Sciences Lucknow, India
TO THE EDITOR: The splenic artery is the visceral vessel most likely to develop pseudoaneurysms (1). These lesions occur either due to disruption of the vessel wall as a result of the direct action of elastase and other digestive enzymes released by the inflamed pancreas, or as a result of a penetrating or blunt trauma. White et al. reviewed arteriograms of 72 cases of pancreatitis and 84 cases of carcinoma of the pancreas (2). They found arterial aneurysms in 10% of the patients with pancreatitis, while no aneurysms were found in patients with a pancreatic carcinoma. They concluded that the presence of an aneurysm is a helpful distinguishing feature of pancreatitis. A 72-yr-old man consulted our hospital with back pain and a history of tarry stool. The laboratory tests showed that the serum level of carbohydrate antigen 19-9 was markedly elevated (3463 U/ml), whereas the serum levels of amylase, elastase, and carcinoembryonic antigen were within normal ranges. Computed tomography (CT) demonstrated a 12-mm aneurysm arising from the splenic artery, which was connected to a hypoattenuating area behind the splenic artery (Fig. 1). Celiac arteriography also demonstrated a 15-mm aneurysm and an irregularity on the proximal side of the splenic artery. Embolization of the aneurysm by steel coils and N-butyl cyanoacrylate was serially performed. We could not differentiate whether the aneurysm was induced
Peter Durie, M.D. Julian Zielenski, Ph.D. David Lam, B.Sc. Research Institute The Hospital for Sick Children University of Toronto Toronto, Canada Sadiq S. Sikora, M.B.B.S. Department of Gastrointestinal Surgery Gourdas Choudhuri, M.D. Department of Gastroenterology Sanjay Gandhi Postgraduate Institute of Medical Sciences Lucknow, India Lap-Chee Tsui, Ph.D. Research Institute The Hospital for Sick Children Department of Molecular and Medical Genetics University of Toronto Toronto, Canada
REFERENCES 1. Mohan V, Nagolimath SJ, Yajnik CS, et al. Fibrocalculous pancreatic diabetes. Diabetes Metab Rev 1998;14:153–70. 2. Durie PR. Pancreatitis and mutations in the CF gene (editorial). N Engl J Med 1998;339:687–5. 3. Cohn JA, Friedman KJ, Noone PG, et al. Relation between mutations of the cystic fibrosis gene and idiopathic pancreatitis. N Engl J Med 1998;339:653– 8. 4. Sharer N, Schwarz M, Malone G, et al. Mutations of the cystic fibrosis gene in patients with chronic pancreatitis. N Engl J Med 1998;339:645–52. 5. Chillon M, Casals T, Mercier B, et al. Mutations in the cystic fibrosis gene in patients with congenital absence of the vas deferens. N Engl J Med 1995;332:1475– 80. 6. Aznarez I, Onay T, et al. An efficient protocol for CFTR mutation detection based on multiplex heteroduplex analysis (mHET). Pediatric Pulmonology 1998;(suppl)17:332.
Figure 1. Contrast-enhanced CT showed a splenic artery aneurysm (arrow) with a hypoattenuating mass (arrowheads) behind it.
3660
Letters to the Editor
by pancreatitis or a pancreatic carcinoma. During surgery, a firm mass was palpated in the region of the pancreatic body that had invaded to the mesocolon and the jejunum. A dorsal pancreatectomy combined with partial resection of the jejunum was performed en bloc. Macroscopically, the resected specimen contained a scirrhous lesion measuring 45 ⫻ 35-mm in the body of the pancreas. The histological diagnosis was a moderately differentiated tubular adenocarcinoma arising in the body of the pancreas. The splenic artery was completely involved with the tumor and communicated with the pseudoaneurysm. There was direct tumor extension into the mucosa of the jejunum. According to the histopathological findings, we believe that the pathogenesis of this pseudoaneurysm was disruption of the splenic artery induced by arterial invasion of the carcinoma. Thus, the presence of an aneurysm does not always exclude the possibility of a pancreatic carcinoma. In this case, an irregularly shaped hypoattenuating area behind the aneurysm on CT indicated the presence of carcinoma. Percutaneous transcatheter embolization of pseudoaneurysms has been reported as both a form of definitive therapy and as a temporary measure until surgery can be performed safely (3, 4). We also performed this technique, and the patient’s condition was stable during surgery.
ACKNOWLEDGMENT This work was supported in part by a Grant-in-Aid for Cancer Research from the Ministry of Health and Welfare of Japan. Hiroyoshi Furukawa, M.D. Department of Diagnostic Radiology National Cancer Center Hospital Tokyo, Japan Noriyoshi Fukushima, M.D. Department of Clinical Laboratory National Cancer Center Hospital Tokyo, Japan Kazuaki Shimada, M.D. Department of Surgery National Cancer Center Hospital Tokyo, Japan
REFERENCES 1. Gadacz TR, Trunkey D, Kieffer RF. Visceral vessel erosion associated with pancreatitis. Case reports and a review of the literature. Arch Surg 1978;113:1438 – 40. 2. White AF, Baum S, Buranasiri S. Aneurysms secondary to pancreatitis. AJR 1976;127:393– 6. 3. Mandel SR, Jaques PF, Mauro MA, et al. Nonoperative management of peripancreatic arterial aneurysms. A 10-year experience. Ann Surg 1987;205:126 – 8. 4. Boudghe´ne F, L’Hermine´ C, Bigot JM. Arterial complications of pancreatitis: Diagnosis and therapeutic aspects in 104 cases. J Vasc Interv Radiol 1993;4:551– 8.
AJG – Vol. 95, No. 12, 2000
Reprint requests and correspondence: Hiroyoshi Furukawa, M.D., Department of Diagnostic Radiology, National Cancer Center Hospital, 5-1-1, Tsukiji, Chuo-ku, Tokyo 104, Japan. Received June 7, 2000; accepted June 19, 2000.
Re: Sharma et al.—Colorectal Cancer Screening by Primary Care Physicians TO THE EDITOR: The article by Sharma et al. in the June 2000 issue on colorectal cancer screening by primary care physicians has many serious flaws that should have been caught and exposed by your reviewers. First, the physicians queried were identified through a “database that was supplied to us by TAP Pharmaceuticals.” Do we know how many of these doctors were board certified and how many were residency trained? What is their association with TAP Pharmaceuticals? Second, and most importantly, this entire study makes broad generalizations based on a survey response rate of 19.5%. This is the most abysmally low response rate I have ever seen in a reputable medical journal. One can’t seriously make believable conclusions about the screening patterns of America’s primary care doctors based on such a limited sample. The authors make the dubious assertion that the respondents probably represented doctors most “interested in colorectal cancer screening (CRCS).” Third, the study used as its “gold standard” the opinions of three “recognized national authorities.” It is not stated whether any of these “authorities” were primary care doctors. This is important since specialists tend to be biased toward their own screening modality (e.g., radiologists sing the praises of a barium enema, gastroenterologists swear by the colonoscopy, etc.). As a primary care doctor myself, I’ve learned to trust the guidelines published by researchers and epidemiologists who don’t have financial incentives in any one screening modality. The most useful guidelines in this regard come from the reports of the U.S. Preventive Services Task Force (USPSTF), which was used as a reference in the article (1). Fourth, the authors’ experts recommend stopping CRCS in otherwise healthy individuals over age 75. Since there will soon be over 800,000 Americans over age 100 this advice may be overly pessimistic. I frequently have very healthy elderly patients visit me who haven’t been to a doctor for screening in many years. Since some in this age range may live 15 or more years, colon cancer screening may arguably be prudent. The authors’ own discussion states “Published guidelines stress that CRCS must be individualized and that the appropriate age to stop is dependent on the judgment of individual patients and their physicians.” They then criticize their physician respondents for screening into advanced age! The USPSTF guidelines available when the survey was done states (1) “There is little