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“Giant” colon lipoma: what kind of findings are necessary for the indication of endoscopic resection?
1944
Letters to the Editor
5. Vogt DP, Lederman RJ, Catey WD, et al. Neurologic complications of liver transplantation. Transplantation 1988;45:1057– 61. 6. Russell W, Walker RW, Brochstein JA. Neurologic complications of immunosuppressive agents. Neurol Clin 1988;6:261– 78.
Reprint requests and correspondence: Adrian Reuben, M.B.B.S., F.R.C.P., Division of Gastroenterology and Hepatology, Department of Medicine, Medical University of South Carolina, Clinical Science Building, Room 916, 96 Jonathan Lucas Street, P.O. Box 25063, Charleston, SC 29425. Received June 13, 2000; accepted Jan. 25, 2001.
Detection of Helicobacter pylori With Stool Antigen Test in Children With Gastroesophageal Reflux Disease TO THE EDITOR: Gastroesophageal reflux disease (GERD) is a common problem in childhood and characterized by reflux of acidic gastric contents into the esophagus. Major pathophysiological factors for GERD include transient lower esophageal sphincter relaxation, decreased esophageal clearance, and delayed gastric emptying. Gastric acid hypersecretion has also been found in refractory GERD (1). The relationship between Helicobacter pylori and GERD is not fully understood. It has been shown that there is an inverse correlation and H. pylori may have a protective role against GERD. Ammonia, a powerful neutralizing substance, and hypochlorhydria caused by severe corpus gastritis have been accepted as potential protective mechanisms (2– 4). It has also been reported that GERD incidence increased after eradication of H. pylori infection (5). In this study, we wanted to determine the prevalence of H. pylori infection in patients with GERD. A total of 15 patients with GERD (eight boys, 53.3%), 1– 8 yr of age (mean 3.3 ⫾ 2.5) were included. Diagnosis of GERD was established by 24-h esophageal pH monitoring. The patients had no symptoms of gastritis, and the most common symptoms were vomiting in 13 patients (86.7%), chronic cough in seven (46.7%), and wheezing in two (13.3%). The presence of H. pylori was defined by the H. pylori stool antigen test with a commercial kit (Premier Platinum, Meridian Diagnostics, Cincinnati, OH) using ELISA. The H. pylori stool antigen test is a noninvasive, simple, and fast method, especially in young patients, and has a sensitivity and specificity ranging from 93% to 100% (6, 7). Of the 15 patients, H. pylori was positive in one (6.7%). In our study, the prevalence of H. pylori infection was low, similar to other studies in which the prevalence has been found to be 8 –16% (8, 9). Larger controlled studies need to
AJG – Vol. 96, No. 6, 2001
be performed to examine the possible relationship between H. pylori infection and GERD. Hu¨lya Demir, M.D. Serpil Ercis, M.D. Nurten Koc¸ak, M.D. Gu¨ls¸en Hasc¸elik, M.D. Hasan Ozen, M.D. Aysel Yu¨ce, M.D. Figen Gu¨rakan, M.D. Inci Nur Saltık, M.D. Gastroenterology Unit Department of Pediatrics Hacettepe University Ihsan Dog˘ramacı Children’s Hospital Ankara, Turkey
REFERENCES 1. Metz DC, Kroser JA. Helicobacter pylori and gastroesophageal reflux disease. Gastroenterol Clin North Am 1999;28:971– 85. 2. Werdmuller BF, Loffeld RJ. Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis. Dig Dis Sci 1997;42:103–5. 3. Vicari JJ, Peek RM, Falk GW, et al. The seroprevalence of cagA-positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease. Gastroenterology 1998;115: 50 –7. 4. Wu JC, Sung JJ, Ng EK, et al. Prevalence and distribution of Helicobacter pylori in gastroesophageal reflux disease: A study from the East. Am J Gastroenterol 1999;94:1790 – 4. 5. Fallone CA, Barkun AN, Friedman G, et al. Is Helicobacter pylori eradication associated with gastroesophageal reflux disease. Am J Gastroenterol 2000;95:914 –20. 6. Chang MC, Wu MS, Wang HH, et al. Helicobacter pylori stool antigen (HpSA) test—a simple, accurate and non-invasive test for detection of Helicobacter pylori infection. Hepatogastroenterology 1999;46:299 –302. 7. Fanti L, Mezzi G, Cavallero A, et al. A new simple immunoassay for detecting Helicobacter pylori infection: Antigen in stool specimens. Digestion 1999;60:456 – 60. 8. Cargill G, Atlan P, Tudor D, et al. Association of Helicobacter pylori and reflux esophagitis in symptomatic children. Gastroenterology 1994;106:A59. 9. Rosioru C, Glassman MS, Halata MS, Schwarz SM. Esophagitis and Helicobacter pylori in children: Incidence and therapeutic implications. Am J Gastroenterol 1993;88:510 –3. Reprint requests and correspondence: Hu¨lya Demir, M.D., Hacettepe Ihsan Dog˘ramacı Cocuk Hastanesi, Gastroenteroloji Unitesi, 06100 Ankara, Turkey. Received Jan. 18, 2001; accepted Jan. 30, 2001.
“Giant” Colon Lipoma: What Kind of Findings Are Necessary for the Indication of Endoscopic Resection? TO THE EDITOR: I read with interest the article in the August 2000 issue, “Giant Colon Lipoma—To Attempt Endoscopic Resection or Not?” (1).
AJG – June, 2001
Letters to the Editor
1945
Figure 1. (A) Ordinary endoscopic view showing a large tumor at the rectosigmoid junction. (B) This lesion occupied almost the entire lumen. (C) The magnifying endoscopic view showing a type I pit pattern (original magnification ⫻100). (D) Endoscopic examination in the base of the lesion indicated that this lesion was a subpedunculated type SMT. (E) Endoscopic ultrasonography using a 20-MHz miniprobe demonstrated a hyperechoic mass (one scale mark ⫽ 5 mm). (F) The resected lesion was 45 mm in diameter (one scale mark ⫽ 1 mm). (G) Histological feature of the resected specimen showed lipoma (hematoxylin and eosin, original magnification ⫻15).
Large lipomas may cause symptoms, so resection should be considered for lipomas ⬎20 mm in diameter (2). But the indication of endoscopic resection of colonic lipoma is still a subject of controversy. Recently we encountered a large lipoma of the colon that was judged to be able to be resected endoscopically. A 75-yr-old man was transferred to our hospital for further evaluation of the large colon tumor. He presented with bloody stool. He had no past history of any cancer and no family history of colorectal cancer. Laboratory studies, including complete blood cell counts, serum electrolytes, blood biochemistry, and carcinoembryonic antigen, were within normal limits. Colonoscopy using a magnifying videoscope (CF240ZI, Olympus, Tokyo, Japan) was performed, and a large tumor with slightly reddish mucosa at the rectosigmoid junction of the colon was detected (Fig. 1A). The lesion occupied almost the entire lumen of the colon (Fig. 1B). The magnified view of the lesion under indigo carmine spraying chromoscopy showed a type I pit pattern (Fig. 1C) according to the classification proposed by Kudo et al. (3), indicating that the surface of this lesion was constituted of normal colonic mucosa. Because of the pit pattern this lesion was diagnosed as a submucosal tumor (SMT). Further endoscopic examination in the base of the
lesion indicated that this SMT was soft and subpedunculated, and dangled easily by endoscopic device (Fig. 1D). Endoscopic ultrasonography using a 20-MHz miniprobe demonstrated a hyperechoic mass (Fig. 1E). From these findings, we diagnosed this tumor as a “giant” lipoma and judged that this SMT could be resected endoscopically. Then endoscopic snare polypectomy was performed successfully. The lesion was 45 mm in diameter (Fig. 1F). Histological examination revealed a lipoma (Fig. 1G). Magnifying videoscopy and endoscopic ultrasonography should give good information for the diagnosis of SMT and lipoma. However, detailed endoscopic examination in the base of the lesion is necessary for judgment of the indication of endoscopic resection in the cases of giant lipomas. Satoru Tamura, M.D. Yuichi Yokoyama, M.D. Tomoko Morita, M.D. Takehisa Tadokoro, M.D. Yoshifumi Higashidani, M.D. Saburo Onishi, M.D. First Department of Internal Medicine Kochi Medical School Kochi, Japan
1946
Letters to the Editor
AJG – Vol. 96, No. 6, 2001
REFERENCES 1. Chase MP, Yarze JC, “Giant” colon lipoma—to attempt endoscopic resection or not? Am J Gastroenterol 2000;95:2143– 4. 2. Tammam EK, Fadi HM, Suhayl U. Sigmoid lipoma mimicking carcinoma: Case report with review of diagnosis and management. Gastrointest Endosc 2000;51:495– 6. 3. Kudo S, Tamura S, Nakajima T, et al. Diagnosis of colorectal tumorous lesions by magnifying endoscopy. Gastrointest Endosc 1996;44:8 –14. Reprint requests and correspondence: Satoru Tamura, M.D., First Department of Internal Medicine, Kochi Medical School, Kohasu, Okoh-cho, Nankoku, Kochi 783-8505, Japan. Received Jan. 19, 2001; accepted Jan. 30, 2001.
Prevalence of Irritable Bowel Syndrome and Its Relationship With Helicobacter pylori Infection in a Japanese Population* TO THE EDITOR: The pathogenesis of irritable bowel syndrome (IBS) is still unclear. To investigate the pathogenetic role of Helicobacter pylori infection in the development of IBS, we have examined the prevalence rates of IBS with and without H. pylori infection. Two thousand five hundred people who visited Shimane Institute of Health Science for routine medical checks were prospectively enrolled in our study. After routine medical examination, including an upper GI study and ultrasonographic examination, all subjects were asked standard questions to check for the presence of any symptoms suggesting IBS. H. pylori infection was determined by measurement of serum H. pylori IgG antibody with an ELISA (IMMUNIS antiPYLORI EIA, Institute of Immunology, Tokyo, Japan). Statistical analysis was performed using the 2 test. Differences at p ⬍ 0.05 were considered significant. Of the 2500 persons investigated, 2263 showed no abnormal finding in any medical examination. The presence or absence of symptoms and H. pylori infection was investigated in these 2263 cases. One hundred forty-seven people (6.5%) had symptoms of IBS. The frequency of these symptoms declined with age (p ⬍ 0.05). As shown in Figure 1, the prevalence rate of IBS without H. pylori infection had a tendency to be higher than that of IBS with H. pylori infection. The role of H. pylori infection in the development of IBS is still controversial. Several authors have denied any relationship between H. pylori and IBS, whereas others have suggested a positive relationship (1, 2). Our data rule out any pathogenetic role of H. pylori from two standpoints. The first is the discrepancy between the age-related prevalence of IBS and that of H. pylori infection. Although the prevalence of IBS decreased with age, the H. pylori infection rate * This work was supported in part by grants in aid from Shimane Institute of Health Science.
Figure 1. Age-related prevalence of IBS in cases with (■) and without (䊐) H. pylori infection.
in Japan increases markedly with age (3, 4). The second was the fact that the prevalence of IBS in H. pylori–positive cases was almost equal to and even lower than that in H. pylori–negative cases. Therefore, it is concluded that H. pylori infection dose not play an important role in the prevalence of IBS. Akira Kawamura, M.D. Kyoichi Adachi, M.D. Toshiharu Takashima, M.D. Mika Yuki, M.D. Masahiro Ono, M.D. Yoshikazu Kinoshita, M.D. Department of Internal Medicine II Shimane Medical University Izumo, Japan
REFERENCES 1. Agre´us L, Engstrand L, Sva¨rdsudd K, et al. Helicobacter pylori seropositivity among Swedish adults with and without abdominal symptoms. A population-based epidemiologic study. Scand J Gastroenterol 1995;30:752–7. 2. Locke GR III, Talley NJ, Nelson DK, et al. Helicobacter pylori and dyspepsia: A population-based study of the organism and host. Am J Gastroenterol 2000;95:1906 –13. 3. Asaka M, Kimura T, Kudo M, et al. Relationship of Helicobacter pylori to serum pepsinogens in an asymptomatic Japanese population. Gastroenterology 1992;102:760 – 6. 4. Kawamura A, Adachi K, Takashima T, et al. Prevalence of functional dyspepsia and its relationship with Helicobacter pylori infection in a Japanese population. J Gastroenterol Hepatol (in press). Reprint requests and correspondence: Akira Kawamura, M.D., Department of Internal Medicine II, Shimane Medical University, 89-1 Enya-cho, Izumo-shi, Shimane 693-8501, Japan. Received Jan. 22, 2001; accepted Jan. 30, 2001.
Letters to the Editor
5. Vogt DP, Lederman RJ, Catey WD, et al. Neurologic complications of liver transplantation. Transplantation 1988;45:1057– 61. 6. Russell W, Walker RW, Brochstein JA. Neurologic complications of immunosuppressive agents. Neurol Clin 1988;6:261– 78.
Reprint requests and correspondence: Adrian Reuben, M.B.B.S., F.R.C.P., Division of Gastroenterology and Hepatology, Department of Medicine, Medical University of South Carolina, Clinical Science Building, Room 916, 96 Jonathan Lucas Street, P.O. Box 25063, Charleston, SC 29425. Received June 13, 2000; accepted Jan. 25, 2001.
Detection of Helicobacter pylori With Stool Antigen Test in Children With Gastroesophageal Reflux Disease TO THE EDITOR: Gastroesophageal reflux disease (GERD) is a common problem in childhood and characterized by reflux of acidic gastric contents into the esophagus. Major pathophysiological factors for GERD include transient lower esophageal sphincter relaxation, decreased esophageal clearance, and delayed gastric emptying. Gastric acid hypersecretion has also been found in refractory GERD (1). The relationship between Helicobacter pylori and GERD is not fully understood. It has been shown that there is an inverse correlation and H. pylori may have a protective role against GERD. Ammonia, a powerful neutralizing substance, and hypochlorhydria caused by severe corpus gastritis have been accepted as potential protective mechanisms (2– 4). It has also been reported that GERD incidence increased after eradication of H. pylori infection (5). In this study, we wanted to determine the prevalence of H. pylori infection in patients with GERD. A total of 15 patients with GERD (eight boys, 53.3%), 1– 8 yr of age (mean 3.3 ⫾ 2.5) were included. Diagnosis of GERD was established by 24-h esophageal pH monitoring. The patients had no symptoms of gastritis, and the most common symptoms were vomiting in 13 patients (86.7%), chronic cough in seven (46.7%), and wheezing in two (13.3%). The presence of H. pylori was defined by the H. pylori stool antigen test with a commercial kit (Premier Platinum, Meridian Diagnostics, Cincinnati, OH) using ELISA. The H. pylori stool antigen test is a noninvasive, simple, and fast method, especially in young patients, and has a sensitivity and specificity ranging from 93% to 100% (6, 7). Of the 15 patients, H. pylori was positive in one (6.7%). In our study, the prevalence of H. pylori infection was low, similar to other studies in which the prevalence has been found to be 8 –16% (8, 9). Larger controlled studies need to
AJG – Vol. 96, No. 6, 2001
be performed to examine the possible relationship between H. pylori infection and GERD. Hu¨lya Demir, M.D. Serpil Ercis, M.D. Nurten Koc¸ak, M.D. Gu¨ls¸en Hasc¸elik, M.D. Hasan Ozen, M.D. Aysel Yu¨ce, M.D. Figen Gu¨rakan, M.D. Inci Nur Saltık, M.D. Gastroenterology Unit Department of Pediatrics Hacettepe University Ihsan Dog˘ramacı Children’s Hospital Ankara, Turkey
REFERENCES 1. Metz DC, Kroser JA. Helicobacter pylori and gastroesophageal reflux disease. Gastroenterol Clin North Am 1999;28:971– 85. 2. Werdmuller BF, Loffeld RJ. Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis. Dig Dis Sci 1997;42:103–5. 3. Vicari JJ, Peek RM, Falk GW, et al. The seroprevalence of cagA-positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease. Gastroenterology 1998;115: 50 –7. 4. Wu JC, Sung JJ, Ng EK, et al. Prevalence and distribution of Helicobacter pylori in gastroesophageal reflux disease: A study from the East. Am J Gastroenterol 1999;94:1790 – 4. 5. Fallone CA, Barkun AN, Friedman G, et al. Is Helicobacter pylori eradication associated with gastroesophageal reflux disease. Am J Gastroenterol 2000;95:914 –20. 6. Chang MC, Wu MS, Wang HH, et al. Helicobacter pylori stool antigen (HpSA) test—a simple, accurate and non-invasive test for detection of Helicobacter pylori infection. Hepatogastroenterology 1999;46:299 –302. 7. Fanti L, Mezzi G, Cavallero A, et al. A new simple immunoassay for detecting Helicobacter pylori infection: Antigen in stool specimens. Digestion 1999;60:456 – 60. 8. Cargill G, Atlan P, Tudor D, et al. Association of Helicobacter pylori and reflux esophagitis in symptomatic children. Gastroenterology 1994;106:A59. 9. Rosioru C, Glassman MS, Halata MS, Schwarz SM. Esophagitis and Helicobacter pylori in children: Incidence and therapeutic implications. Am J Gastroenterol 1993;88:510 –3. Reprint requests and correspondence: Hu¨lya Demir, M.D., Hacettepe Ihsan Dog˘ramacı Cocuk Hastanesi, Gastroenteroloji Unitesi, 06100 Ankara, Turkey. Received Jan. 18, 2001; accepted Jan. 30, 2001.
“Giant” Colon Lipoma: What Kind of Findings Are Necessary for the Indication of Endoscopic Resection? TO THE EDITOR: I read with interest the article in the August 2000 issue, “Giant Colon Lipoma—To Attempt Endoscopic Resection or Not?” (1).
AJG – June, 2001
Letters to the Editor
1945
Figure 1. (A) Ordinary endoscopic view showing a large tumor at the rectosigmoid junction. (B) This lesion occupied almost the entire lumen. (C) The magnifying endoscopic view showing a type I pit pattern (original magnification ⫻100). (D) Endoscopic examination in the base of the lesion indicated that this lesion was a subpedunculated type SMT. (E) Endoscopic ultrasonography using a 20-MHz miniprobe demonstrated a hyperechoic mass (one scale mark ⫽ 5 mm). (F) The resected lesion was 45 mm in diameter (one scale mark ⫽ 1 mm). (G) Histological feature of the resected specimen showed lipoma (hematoxylin and eosin, original magnification ⫻15).
Large lipomas may cause symptoms, so resection should be considered for lipomas ⬎20 mm in diameter (2). But the indication of endoscopic resection of colonic lipoma is still a subject of controversy. Recently we encountered a large lipoma of the colon that was judged to be able to be resected endoscopically. A 75-yr-old man was transferred to our hospital for further evaluation of the large colon tumor. He presented with bloody stool. He had no past history of any cancer and no family history of colorectal cancer. Laboratory studies, including complete blood cell counts, serum electrolytes, blood biochemistry, and carcinoembryonic antigen, were within normal limits. Colonoscopy using a magnifying videoscope (CF240ZI, Olympus, Tokyo, Japan) was performed, and a large tumor with slightly reddish mucosa at the rectosigmoid junction of the colon was detected (Fig. 1A). The lesion occupied almost the entire lumen of the colon (Fig. 1B). The magnified view of the lesion under indigo carmine spraying chromoscopy showed a type I pit pattern (Fig. 1C) according to the classification proposed by Kudo et al. (3), indicating that the surface of this lesion was constituted of normal colonic mucosa. Because of the pit pattern this lesion was diagnosed as a submucosal tumor (SMT). Further endoscopic examination in the base of the
lesion indicated that this SMT was soft and subpedunculated, and dangled easily by endoscopic device (Fig. 1D). Endoscopic ultrasonography using a 20-MHz miniprobe demonstrated a hyperechoic mass (Fig. 1E). From these findings, we diagnosed this tumor as a “giant” lipoma and judged that this SMT could be resected endoscopically. Then endoscopic snare polypectomy was performed successfully. The lesion was 45 mm in diameter (Fig. 1F). Histological examination revealed a lipoma (Fig. 1G). Magnifying videoscopy and endoscopic ultrasonography should give good information for the diagnosis of SMT and lipoma. However, detailed endoscopic examination in the base of the lesion is necessary for judgment of the indication of endoscopic resection in the cases of giant lipomas. Satoru Tamura, M.D. Yuichi Yokoyama, M.D. Tomoko Morita, M.D. Takehisa Tadokoro, M.D. Yoshifumi Higashidani, M.D. Saburo Onishi, M.D. First Department of Internal Medicine Kochi Medical School Kochi, Japan
1946
Letters to the Editor
AJG – Vol. 96, No. 6, 2001
REFERENCES 1. Chase MP, Yarze JC, “Giant” colon lipoma—to attempt endoscopic resection or not? Am J Gastroenterol 2000;95:2143– 4. 2. Tammam EK, Fadi HM, Suhayl U. Sigmoid lipoma mimicking carcinoma: Case report with review of diagnosis and management. Gastrointest Endosc 2000;51:495– 6. 3. Kudo S, Tamura S, Nakajima T, et al. Diagnosis of colorectal tumorous lesions by magnifying endoscopy. Gastrointest Endosc 1996;44:8 –14. Reprint requests and correspondence: Satoru Tamura, M.D., First Department of Internal Medicine, Kochi Medical School, Kohasu, Okoh-cho, Nankoku, Kochi 783-8505, Japan. Received Jan. 19, 2001; accepted Jan. 30, 2001.
Prevalence of Irritable Bowel Syndrome and Its Relationship With Helicobacter pylori Infection in a Japanese Population* TO THE EDITOR: The pathogenesis of irritable bowel syndrome (IBS) is still unclear. To investigate the pathogenetic role of Helicobacter pylori infection in the development of IBS, we have examined the prevalence rates of IBS with and without H. pylori infection. Two thousand five hundred people who visited Shimane Institute of Health Science for routine medical checks were prospectively enrolled in our study. After routine medical examination, including an upper GI study and ultrasonographic examination, all subjects were asked standard questions to check for the presence of any symptoms suggesting IBS. H. pylori infection was determined by measurement of serum H. pylori IgG antibody with an ELISA (IMMUNIS antiPYLORI EIA, Institute of Immunology, Tokyo, Japan). Statistical analysis was performed using the 2 test. Differences at p ⬍ 0.05 were considered significant. Of the 2500 persons investigated, 2263 showed no abnormal finding in any medical examination. The presence or absence of symptoms and H. pylori infection was investigated in these 2263 cases. One hundred forty-seven people (6.5%) had symptoms of IBS. The frequency of these symptoms declined with age (p ⬍ 0.05). As shown in Figure 1, the prevalence rate of IBS without H. pylori infection had a tendency to be higher than that of IBS with H. pylori infection. The role of H. pylori infection in the development of IBS is still controversial. Several authors have denied any relationship between H. pylori and IBS, whereas others have suggested a positive relationship (1, 2). Our data rule out any pathogenetic role of H. pylori from two standpoints. The first is the discrepancy between the age-related prevalence of IBS and that of H. pylori infection. Although the prevalence of IBS decreased with age, the H. pylori infection rate * This work was supported in part by grants in aid from Shimane Institute of Health Science.
Figure 1. Age-related prevalence of IBS in cases with (■) and without (䊐) H. pylori infection.
in Japan increases markedly with age (3, 4). The second was the fact that the prevalence of IBS in H. pylori–positive cases was almost equal to and even lower than that in H. pylori–negative cases. Therefore, it is concluded that H. pylori infection dose not play an important role in the prevalence of IBS. Akira Kawamura, M.D. Kyoichi Adachi, M.D. Toshiharu Takashima, M.D. Mika Yuki, M.D. Masahiro Ono, M.D. Yoshikazu Kinoshita, M.D. Department of Internal Medicine II Shimane Medical University Izumo, Japan
REFERENCES 1. Agre´us L, Engstrand L, Sva¨rdsudd K, et al. Helicobacter pylori seropositivity among Swedish adults with and without abdominal symptoms. A population-based epidemiologic study. Scand J Gastroenterol 1995;30:752–7. 2. Locke GR III, Talley NJ, Nelson DK, et al. Helicobacter pylori and dyspepsia: A population-based study of the organism and host. Am J Gastroenterol 2000;95:1906 –13. 3. Asaka M, Kimura T, Kudo M, et al. Relationship of Helicobacter pylori to serum pepsinogens in an asymptomatic Japanese population. Gastroenterology 1992;102:760 – 6. 4. Kawamura A, Adachi K, Takashima T, et al. Prevalence of functional dyspepsia and its relationship with Helicobacter pylori infection in a Japanese population. J Gastroenterol Hepatol (in press). Reprint requests and correspondence: Akira Kawamura, M.D., Department of Internal Medicine II, Shimane Medical University, 89-1 Enya-cho, Izumo-shi, Shimane 693-8501, Japan. Received Jan. 22, 2001; accepted Jan. 30, 2001.