- Email: [email protected]
Response to Drs. Chase et al.
THE AMERICAN JOURNAL OF GASTROENTEROLOGY © 2002 by Am. Coll. of Gastroenterology Published by Elsevier Science Inc.
Vol. 97, No. 6, 2002 ISSN 0002-9270/02/$22.00
LETTERS TO THE EDITOR Implication of Detecting Mucosal Dysplasia in a Patient With Ulcerative Colitis TO THE EDITOR: We read with interest the case report by Mesiya et al. (1) that relates to the endoscopic resection of a large hamartoma of the colon in an adult with ulcerative colitis. The authors found a 50-mm polypoid lesion in the ascending colon of a 50-yr-old patient with underlying idiopathic ulcerative pancolitis. Biopsies of the polypoid lesion initially revealed benign inflammatory tissue. A repeat colonoscopy with complete endoscopic resection of the polypoid lesion was performed 2 wk after these initial biopsies were obtained. Histological examination of the resected polypoid lesion demonstrated it to be a hamartoma. According to the authors’ description of the initial colonoscopic examination, random biopsies from various regions of the colon (not from the polypoid mass) were interpreted to reveal chronic ulcerative colitis with focal low grade dysplasia. Our concern relates to the wisdom of not performing colectomy, or at the least not explicitly recommending vigilant colonoscopic surveillance, in a patient with documented low grade dysplasia in the setting of underlying ulcerative colitis. If the patient under discussion had confirmed low grade dysplasia (agreement that dysplasia is present by two pathologists) associated with ulcerative colitis, one would ordinarily recommend that the patient consider undergoing a total colectomy, because of the risk of developing colon carcinoma in the future. Mucosal dysplasia is a neoplastic (albeit not malignant) change that mandates intervention. Even low grade dysplasia is a strong predictor of future colon cancer in patients with ulcerative colitis. Surveillance data from St. Mark’s Hospital found that the 5-yr predictive value of developing high grade dysplasia or carcinoma from low grade dysplasia was 54% (2). Expert opinions in two recently published reviews on inflammatory bowel disease (ulcerative colitis) and colorectal cancer (3, 4) suggest, in the clinical algorithms presented, that once a diagnosis of dysplasia is confirmed, colectomy is the recommended approach. According to Drs. Eaden and Mayberry: “When low-grade dysplasia is found, the finding should be discussed with the patient and a joint decision made about whether to return to surveillance or to opt for colectomy. The patient must be made aware that first, even if he or she has surgery, a cancer will not necessarily be found; and second, that a repeat colonoscopy will not necessarily confirm the presence of abnormal histology even if present. Any ambiguity in histological biopsy interpretation should be confirmed by a second experienced pathologist” (3). In the case presented by Dr. Mesiya and colleagues, the finding of
low grade dysplasia associated with underlying ulcerative colitis has important clinical implications that should be explicitly addressed, regardless of the interesting finding of a hamartomatous colon lesion, which was able to be resected utilizing expert endoscopic technique. Michael P. Chase, M.D. William M. Bauer, M.D. Joseph C. Yarze, M.D., F.A.C.P., F.A.C.G. Gastroenterology Associates of Northern New York Glens Falls, New York
REFERENCES 1. Mesiya S, Chotiprasidhi P, Kida M, Harty R. Giant hamartoma of the ascending colon in an adult with ulcerative colitis. Am J Gastroenterol 2001;96:3014 –5. 2. Connell WR, Lennard-Jones JE, Wiliams CB, et al. Factors affecting the outcome of endoscopic surveillance for cancer in ulcerative colitis. Gastroenterology 1994;107:934 – 44. 3. Eaden JA, Mayberry JF. Colorectal cancer complicating ulcerative colitis: A review. Am J Gastroenterol 2000;95:2710 –9. 4. Itzkowitz SH. Inflammatory bowel disease and cancer. Gastroenterol Clin North Am 1997;26:129 –39.
Reprint requests and correspondence: Joseph C. Yarze, M.D., Gastroenterology Associates of Northern New York, P.C., 5 Irongate Center, Glens Falls, NY 12801. Received Nov. 19, 2001; accepted Feb. 18, 2002.
Response to Drs. Chase et al. TO THE EDITOR: We read with interest the comments on our case report. The authors raised the issue of intervention for mucosal low grade dysplasia in patients with chronic ulcerative colitis. Patients with chronic ulcerative colitis with flat mucosal low grade dysplasia possess a significant management challenge. Controversy exists regarding the optimal management of flat mucosal dysplasia in asymptomatic patients with chronic ulcerative colitis. In our case report, focal low grade dysplasia was thought to be reactive, because of the presence of active inflammation, and not neoplastic. These findings were discussed with the patient. Subsequently the anti-inflammatory therapy was intensified, colonoscopy with biopsies was repeated, and dysplasia was not detected. Because of the limited scope of the topic of our case report these details were not mentioned. We agree with the authors regarding the current recommendations for the management of low grade dysplasia in patients with chronic
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ulcerative colitis. We believe this will clarify the question raised by the authors. Sikandar Mesiya, M.D. Richard Harty, M.D. Department of Gastroenterology University Hospital Oklahoma City, Oklahoma Reprint requests and correspondence: Richard Harty, M.D., Professor and Chief, Department of Gastroenterology, University Hospital, 7 North Pavilion, Room 526, P.O. Box 26307, Oklahoma City, OK 73126-0307. Received Feb. 18, 2002; accepted Feb. 18, 2002.
Economic Impact of Hospitalization for End-Stage Liver Disease TO THE EDITOR: The article by Ko et al. (1) examining hospital-based outcomes of end-stage liver disease (ESLD) is of significant interest. Cirrhosis and complications from portal hypertension are recognized as significant causes of mortality and resource utilization in the United States (2). Direct medical costs related to chronic liver disease and cirrhosis are estimated in excess of $1.4 billion, excluding patients with chronic hepatitis C (3). The majority (90%) of these expenses are from hospital or inpatient-based medical care. Among patients with chronic hepatitis C seen in nonfederal institutions, total direct costs of hospital-based care (including liver transplantation) are estimated in excess of $514 million annually (4). Although the authors were able to characterize the medical care of ESLD patients by physician specialty, an overall severity of hepatic disease (such as the Child-Pugh classification) could not be determined from the administrative database studied. The absence of significant differences in adjusted hospital-based mortality for all ESLD patients and a greater length of stay with nonspecialist physician care may be related to variations in hepatic disease severity that remain unknown. The observation of increased variceal bleeding and upper endoscopy use among nonspecialist physicians is also unclear without knowing the severity of hepatic disease in this population. The utilization of outcomes from symptomatic portal hypertension as measures of hepatic disease severity, however, is limited given their inexact correlation (5). Although a number of limitations inherent to administrative databases are described, several other considerations warrant further mention. It is not known whether self-reported conditions were accurately characterized as principal or secondary by diagnosis-related group codes. The importance of this relates to an institution’s reimbursement for inpatient clinical care based on the appropriate identification of a primary diagnosis (6). These inaccuracies may be further compounded by the absence of specific International
AJG – Vol. 97, No. 6, 2002
Classification of Diseases (ninth revision) codes for relevant liver-related conditions including spontaneous bacterial peritonitis. Etiologies such as biliary cirrhosis and sclerosing cholangitis in the International Classification of Diseases (ninth revision) system may also include nonhepatic conditions that bias toward observing increased disease burden and resource utilization (7). Direct medical costs for secondary diagnoses such as diabetes mellitus may also be significant among ESLD patients, yet this was not explicitly reported. The recognition of specific hepatic disease etiologies and complications from portal hypertension by coding and classification systems are required for determining the impact of chronic liver disease at a national level. Subsequent work in this aspect of health services research will allow for appropriate health planning initiatives and resource allocation. Jayant A. Talwalkar, M.D., M.P.H. Outcomes Research Unit Division of Gastroenterology and Hepatology Mayo Clinic and Foundation Rochester, Minnesota
REFERENCES 1. Ko CW, Kelley K, Meyer KE. Physician specialty and the outcomes and cost of admissions for end-stage liver disease. Am J Gastroenterol 2001;96:3411– 8. 2. Saadatmand F, Stinson FS, Grant BF, Dufour MC. Surveillance Report #52: Liver cirrhosis mortality in the United States, 1970-96. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism, Division of Biometry and Epidemiology, 1999. 3. The American Gastroenterological Association. The burden of gastrointestinal diseases. Bethesda, MD: The American Gastroenterological Association, 2001:41–3. 4. Kim WR, Gross JB Jr, Poterucha JJ, et al. Outcome of hospital care of liver disease associated with hepatitis C in the United States. Hepatology 2001;33:201– 6. 5. Boyer TD. Portal hypertension and bleeding esophageal varices. In: Zakim DL, Boyer TD, eds. Hepatology: A textbook of liver diseases, 3rd ed. Philadelphia: Saunders, 1990:572– 615. 6. Jollis JG, Ancukiewicz M, DeLong ER, et al. Discordance of databases designed for claims payment versus clinical information systems. Implications for outcomes research. Ann Intern Med 1993;119:844 –50. 7. Lawthers AG, McCarthy EP, Davis RB, et al. Identification of in-hospital complications from claims data. Is it valid? Med Care 2000;38:785–95. Reprint requests and correspondence: Jayant A. Talwalkar, M.D., M.P.H., Division of Gastroenterology/Hepatology, Mayo Foundation, 200 First Street Southwest, Rochester, MN 55905. Received Dec. 28, 2001; accepted Feb. 18, 2002.
Response to Dr. Talwalkar TO THE EDITOR: We thank Dr. Talwalker for his comments on our article. He correctly noted that we could not determine the overall severity of liver disease from the
Vol. 97, No. 6, 2002 ISSN 0002-9270/02/$22.00
LETTERS TO THE EDITOR Implication of Detecting Mucosal Dysplasia in a Patient With Ulcerative Colitis TO THE EDITOR: We read with interest the case report by Mesiya et al. (1) that relates to the endoscopic resection of a large hamartoma of the colon in an adult with ulcerative colitis. The authors found a 50-mm polypoid lesion in the ascending colon of a 50-yr-old patient with underlying idiopathic ulcerative pancolitis. Biopsies of the polypoid lesion initially revealed benign inflammatory tissue. A repeat colonoscopy with complete endoscopic resection of the polypoid lesion was performed 2 wk after these initial biopsies were obtained. Histological examination of the resected polypoid lesion demonstrated it to be a hamartoma. According to the authors’ description of the initial colonoscopic examination, random biopsies from various regions of the colon (not from the polypoid mass) were interpreted to reveal chronic ulcerative colitis with focal low grade dysplasia. Our concern relates to the wisdom of not performing colectomy, or at the least not explicitly recommending vigilant colonoscopic surveillance, in a patient with documented low grade dysplasia in the setting of underlying ulcerative colitis. If the patient under discussion had confirmed low grade dysplasia (agreement that dysplasia is present by two pathologists) associated with ulcerative colitis, one would ordinarily recommend that the patient consider undergoing a total colectomy, because of the risk of developing colon carcinoma in the future. Mucosal dysplasia is a neoplastic (albeit not malignant) change that mandates intervention. Even low grade dysplasia is a strong predictor of future colon cancer in patients with ulcerative colitis. Surveillance data from St. Mark’s Hospital found that the 5-yr predictive value of developing high grade dysplasia or carcinoma from low grade dysplasia was 54% (2). Expert opinions in two recently published reviews on inflammatory bowel disease (ulcerative colitis) and colorectal cancer (3, 4) suggest, in the clinical algorithms presented, that once a diagnosis of dysplasia is confirmed, colectomy is the recommended approach. According to Drs. Eaden and Mayberry: “When low-grade dysplasia is found, the finding should be discussed with the patient and a joint decision made about whether to return to surveillance or to opt for colectomy. The patient must be made aware that first, even if he or she has surgery, a cancer will not necessarily be found; and second, that a repeat colonoscopy will not necessarily confirm the presence of abnormal histology even if present. Any ambiguity in histological biopsy interpretation should be confirmed by a second experienced pathologist” (3). In the case presented by Dr. Mesiya and colleagues, the finding of
low grade dysplasia associated with underlying ulcerative colitis has important clinical implications that should be explicitly addressed, regardless of the interesting finding of a hamartomatous colon lesion, which was able to be resected utilizing expert endoscopic technique. Michael P. Chase, M.D. William M. Bauer, M.D. Joseph C. Yarze, M.D., F.A.C.P., F.A.C.G. Gastroenterology Associates of Northern New York Glens Falls, New York
REFERENCES 1. Mesiya S, Chotiprasidhi P, Kida M, Harty R. Giant hamartoma of the ascending colon in an adult with ulcerative colitis. Am J Gastroenterol 2001;96:3014 –5. 2. Connell WR, Lennard-Jones JE, Wiliams CB, et al. Factors affecting the outcome of endoscopic surveillance for cancer in ulcerative colitis. Gastroenterology 1994;107:934 – 44. 3. Eaden JA, Mayberry JF. Colorectal cancer complicating ulcerative colitis: A review. Am J Gastroenterol 2000;95:2710 –9. 4. Itzkowitz SH. Inflammatory bowel disease and cancer. Gastroenterol Clin North Am 1997;26:129 –39.
Reprint requests and correspondence: Joseph C. Yarze, M.D., Gastroenterology Associates of Northern New York, P.C., 5 Irongate Center, Glens Falls, NY 12801. Received Nov. 19, 2001; accepted Feb. 18, 2002.
Response to Drs. Chase et al. TO THE EDITOR: We read with interest the comments on our case report. The authors raised the issue of intervention for mucosal low grade dysplasia in patients with chronic ulcerative colitis. Patients with chronic ulcerative colitis with flat mucosal low grade dysplasia possess a significant management challenge. Controversy exists regarding the optimal management of flat mucosal dysplasia in asymptomatic patients with chronic ulcerative colitis. In our case report, focal low grade dysplasia was thought to be reactive, because of the presence of active inflammation, and not neoplastic. These findings were discussed with the patient. Subsequently the anti-inflammatory therapy was intensified, colonoscopy with biopsies was repeated, and dysplasia was not detected. Because of the limited scope of the topic of our case report these details were not mentioned. We agree with the authors regarding the current recommendations for the management of low grade dysplasia in patients with chronic
1562
Letters to the Editor
ulcerative colitis. We believe this will clarify the question raised by the authors. Sikandar Mesiya, M.D. Richard Harty, M.D. Department of Gastroenterology University Hospital Oklahoma City, Oklahoma Reprint requests and correspondence: Richard Harty, M.D., Professor and Chief, Department of Gastroenterology, University Hospital, 7 North Pavilion, Room 526, P.O. Box 26307, Oklahoma City, OK 73126-0307. Received Feb. 18, 2002; accepted Feb. 18, 2002.
Economic Impact of Hospitalization for End-Stage Liver Disease TO THE EDITOR: The article by Ko et al. (1) examining hospital-based outcomes of end-stage liver disease (ESLD) is of significant interest. Cirrhosis and complications from portal hypertension are recognized as significant causes of mortality and resource utilization in the United States (2). Direct medical costs related to chronic liver disease and cirrhosis are estimated in excess of $1.4 billion, excluding patients with chronic hepatitis C (3). The majority (90%) of these expenses are from hospital or inpatient-based medical care. Among patients with chronic hepatitis C seen in nonfederal institutions, total direct costs of hospital-based care (including liver transplantation) are estimated in excess of $514 million annually (4). Although the authors were able to characterize the medical care of ESLD patients by physician specialty, an overall severity of hepatic disease (such as the Child-Pugh classification) could not be determined from the administrative database studied. The absence of significant differences in adjusted hospital-based mortality for all ESLD patients and a greater length of stay with nonspecialist physician care may be related to variations in hepatic disease severity that remain unknown. The observation of increased variceal bleeding and upper endoscopy use among nonspecialist physicians is also unclear without knowing the severity of hepatic disease in this population. The utilization of outcomes from symptomatic portal hypertension as measures of hepatic disease severity, however, is limited given their inexact correlation (5). Although a number of limitations inherent to administrative databases are described, several other considerations warrant further mention. It is not known whether self-reported conditions were accurately characterized as principal or secondary by diagnosis-related group codes. The importance of this relates to an institution’s reimbursement for inpatient clinical care based on the appropriate identification of a primary diagnosis (6). These inaccuracies may be further compounded by the absence of specific International
AJG – Vol. 97, No. 6, 2002
Classification of Diseases (ninth revision) codes for relevant liver-related conditions including spontaneous bacterial peritonitis. Etiologies such as biliary cirrhosis and sclerosing cholangitis in the International Classification of Diseases (ninth revision) system may also include nonhepatic conditions that bias toward observing increased disease burden and resource utilization (7). Direct medical costs for secondary diagnoses such as diabetes mellitus may also be significant among ESLD patients, yet this was not explicitly reported. The recognition of specific hepatic disease etiologies and complications from portal hypertension by coding and classification systems are required for determining the impact of chronic liver disease at a national level. Subsequent work in this aspect of health services research will allow for appropriate health planning initiatives and resource allocation. Jayant A. Talwalkar, M.D., M.P.H. Outcomes Research Unit Division of Gastroenterology and Hepatology Mayo Clinic and Foundation Rochester, Minnesota
REFERENCES 1. Ko CW, Kelley K, Meyer KE. Physician specialty and the outcomes and cost of admissions for end-stage liver disease. Am J Gastroenterol 2001;96:3411– 8. 2. Saadatmand F, Stinson FS, Grant BF, Dufour MC. Surveillance Report #52: Liver cirrhosis mortality in the United States, 1970-96. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism, Division of Biometry and Epidemiology, 1999. 3. The American Gastroenterological Association. The burden of gastrointestinal diseases. Bethesda, MD: The American Gastroenterological Association, 2001:41–3. 4. Kim WR, Gross JB Jr, Poterucha JJ, et al. Outcome of hospital care of liver disease associated with hepatitis C in the United States. Hepatology 2001;33:201– 6. 5. Boyer TD. Portal hypertension and bleeding esophageal varices. In: Zakim DL, Boyer TD, eds. Hepatology: A textbook of liver diseases, 3rd ed. Philadelphia: Saunders, 1990:572– 615. 6. Jollis JG, Ancukiewicz M, DeLong ER, et al. Discordance of databases designed for claims payment versus clinical information systems. Implications for outcomes research. Ann Intern Med 1993;119:844 –50. 7. Lawthers AG, McCarthy EP, Davis RB, et al. Identification of in-hospital complications from claims data. Is it valid? Med Care 2000;38:785–95. Reprint requests and correspondence: Jayant A. Talwalkar, M.D., M.P.H., Division of Gastroenterology/Hepatology, Mayo Foundation, 200 First Street Southwest, Rochester, MN 55905. Received Dec. 28, 2001; accepted Feb. 18, 2002.
Response to Dr. Talwalkar TO THE EDITOR: We thank Dr. Talwalker for his comments on our article. He correctly noted that we could not determine the overall severity of liver disease from the