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Spontaneous bacterial peritonitis and bacteremia in fulminant hepatic failure
2126
Letters to the Editor
REFERENCES 1. Fujisawa T, Kumagai T, Akamatsu, et al. Changes in seroepidemiological pattern of Helicobacter pylori and hepatitis A virus over the last 20 years in Japan. Am J Gastroenterol 1999;94:2094 –9. 2. Furuta T, Kamata T, Takashima M, et al. A study of transmission routes of Helicobacter pylori in relation with seroprevalence of hepatitis A virus. J Clin Microbiol 1997;35:1891–3. 3. Luzza F, Imeneo M, Maletta M, et al. Seroepidemiology of Helicobacter pylori infection and hepatitis A in a rural area: Evidence against a common mode of transmission. Gut 1997; 41:164 – 8. 4. Thomas JE, Gibson GR, Darboe MK, et al. Isolation of Helicobacter pylori from human feces. Lancet 1992;340:1194 –5. 5. Shames B, Krajden S, Fuksa M, et al. Evidence for the occurrence of the same strain of Campylobacter pylori in the stomach and dental placque. J Clin Microbiol 1989;27:2849 –50. 6. Leung W-K, Siu KLK, Kwok CKL, et al. Isolation of Helicobacter pylori from vomitus in children and its implication in gastro-oral transmission. Am J Gastroenterol 1999;94:2881– 4. 7. Nilsson I, Ljungh A, Aleljung P et al. Immunoblot assay for serodiagnosis of Helicobacter pylori infection. J Clin Microbiol 1997;35:427–32. Reprint requests and correspondence: Toru Fujisawa, M.D., The Second Department of Internal Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto City, Nagano Prefecture 390-8621, Japan. Received Mar. 27, 2000; accepted Apr. 4, 2000.
Spontaneous Bacterial Peritonitis and Bacteremia in Fulminant Hepatic Failure TO THE EDITOR: I would like to offer several comments on the discrepancy between the recent work by Dhiman et al. (1) from India and our previous study (2), concerning spontaneous bacterial peritonitis (SBP) in fulminant hepatic failure (FHF). Fourteen (18%) of 79 patients in the Dhiman et al. series were complicated with SBP, which was substantially lower than the 32% (26/82) of our series (p ⫽ 0.05). The authors claimed that this discrepancy might be due to the presence of underlying chronic liver disease in the majority of our patients. All of our patients had no previous history of chronic liver disease, nor evidence of cirrhosis on ultrasound examination of the liver. In all, 68 of them were recognized as HBsAg carriers when presenting these episodes of acute hepatitis because of being HBsAg-positive but were IgM anti-HBc–negative (3). The presence of chronic hepatitis B virus infection in these patients did not usually indicate the presence of significant chronic liver disease. In one study from Taiwan, chronic active hepatitis with or without cirrhosis was recognized in only 15% of asymptomatic HBsAg carriers (4). It should also be pointed out that many of HBsAg-positive patients with FHF were found to be IgM anti-HBc–negative since the availability of
AJG – Vol. 95, No. 8, 2000
this test. For example, in one series from India, 72% of HBsAg-positive patients with FHF were IgM anti-HBc– negative (5). A total of 47% of patients in the Dhiman et al. series were HBsAg-positive, but the results of IgM anti-HBc were not mentioned. On the other hand, nearly one third of patients with SBP in the reported series did not have apparent symptoms and signs of pertionitis. The frequency of SBP in their series should be underestimated without prospective routine surveillance paracentesis. Moreover, 71% (20/28) of SBP patients in our series were ascities culture– positive, compared to 36% (5/14) in the Dhiman et al. series. The fact of this extremely low positive ascities culture rate in their series certainly would reduce the number of patients diagnosed as having bacterascites. Another feature of their series that deserves comment is that the rates of complication and mortality showed no significant difference between patients with SBP and those without. In addition to the high prevalence of SBP, FHF may contribute to increased susceptibility to bacteremia. In our series, SBP and bacteremia were recognized in 26 (32%) and 29 patients (35%), respectively, including 15 (18%) with both SBP and bacteremia. The prevalence of renal failure and gastrointestinal hemorrhage and the mortality rate in patients with SBP (with or without bactermia) were similar to in those with bacteremia (without SBP), which were both significantly higher than in those without SBP and bacteremia. Unfortunately, the significance of bacteremia was not addressed in the Dhiman et al. series. Chia-Ming Chu, M.D. Chang Gung Memorial Hospital Taipei, Taiwan
REFERENCES 1. Dhiman RK, Makharia GK, Jain S, et al. Ascites and spontaneous bacterial peritonitis in fulminant hepatic failure. Am J Gastroenterol 2000;95:233– 8. 2. Chu CM, Chiu KW, Liaw YF. The prevalence and prognostic significance of spontaneous bacterial peritonitis in severe acute hepatitis with ascites. Hepatology 1992;15:799 – 803. 3. Chu CM, Liaw YF, Pao CC, et al. The etiology of acute hepatitis superimposed upon previously unrecognized asymptomatic HBsAg carriers. Hepatology 1989;9:452– 6. 4. Yang PM, Chen DS, Lai MY, et al. Clinicopathologic studies of asymptomatic HBsAg carriers: with special emphasis on carriers older than 40 years. Hepato-Gastroenterology 1987;34: 251– 4. 5. Bal V, Amin SN, Rath S, et al. Virological markers and antibody responses in fulminant viral hepatitis. J Med Virol 1987; 23:75– 82.
Reprint requests and correspondence: Chia-Ming Chu, M.D., Chang Gung Memorial Hospital, Liver Research Unit, 199, Tung Hwa North Road, Taipei 10591, Taiwan. Received Feb. 21, 2000; accepted Apr. 18, 2000.
Letters to the Editor
REFERENCES 1. Fujisawa T, Kumagai T, Akamatsu, et al. Changes in seroepidemiological pattern of Helicobacter pylori and hepatitis A virus over the last 20 years in Japan. Am J Gastroenterol 1999;94:2094 –9. 2. Furuta T, Kamata T, Takashima M, et al. A study of transmission routes of Helicobacter pylori in relation with seroprevalence of hepatitis A virus. J Clin Microbiol 1997;35:1891–3. 3. Luzza F, Imeneo M, Maletta M, et al. Seroepidemiology of Helicobacter pylori infection and hepatitis A in a rural area: Evidence against a common mode of transmission. Gut 1997; 41:164 – 8. 4. Thomas JE, Gibson GR, Darboe MK, et al. Isolation of Helicobacter pylori from human feces. Lancet 1992;340:1194 –5. 5. Shames B, Krajden S, Fuksa M, et al. Evidence for the occurrence of the same strain of Campylobacter pylori in the stomach and dental placque. J Clin Microbiol 1989;27:2849 –50. 6. Leung W-K, Siu KLK, Kwok CKL, et al. Isolation of Helicobacter pylori from vomitus in children and its implication in gastro-oral transmission. Am J Gastroenterol 1999;94:2881– 4. 7. Nilsson I, Ljungh A, Aleljung P et al. Immunoblot assay for serodiagnosis of Helicobacter pylori infection. J Clin Microbiol 1997;35:427–32. Reprint requests and correspondence: Toru Fujisawa, M.D., The Second Department of Internal Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto City, Nagano Prefecture 390-8621, Japan. Received Mar. 27, 2000; accepted Apr. 4, 2000.
Spontaneous Bacterial Peritonitis and Bacteremia in Fulminant Hepatic Failure TO THE EDITOR: I would like to offer several comments on the discrepancy between the recent work by Dhiman et al. (1) from India and our previous study (2), concerning spontaneous bacterial peritonitis (SBP) in fulminant hepatic failure (FHF). Fourteen (18%) of 79 patients in the Dhiman et al. series were complicated with SBP, which was substantially lower than the 32% (26/82) of our series (p ⫽ 0.05). The authors claimed that this discrepancy might be due to the presence of underlying chronic liver disease in the majority of our patients. All of our patients had no previous history of chronic liver disease, nor evidence of cirrhosis on ultrasound examination of the liver. In all, 68 of them were recognized as HBsAg carriers when presenting these episodes of acute hepatitis because of being HBsAg-positive but were IgM anti-HBc–negative (3). The presence of chronic hepatitis B virus infection in these patients did not usually indicate the presence of significant chronic liver disease. In one study from Taiwan, chronic active hepatitis with or without cirrhosis was recognized in only 15% of asymptomatic HBsAg carriers (4). It should also be pointed out that many of HBsAg-positive patients with FHF were found to be IgM anti-HBc–negative since the availability of
AJG – Vol. 95, No. 8, 2000
this test. For example, in one series from India, 72% of HBsAg-positive patients with FHF were IgM anti-HBc– negative (5). A total of 47% of patients in the Dhiman et al. series were HBsAg-positive, but the results of IgM anti-HBc were not mentioned. On the other hand, nearly one third of patients with SBP in the reported series did not have apparent symptoms and signs of pertionitis. The frequency of SBP in their series should be underestimated without prospective routine surveillance paracentesis. Moreover, 71% (20/28) of SBP patients in our series were ascities culture– positive, compared to 36% (5/14) in the Dhiman et al. series. The fact of this extremely low positive ascities culture rate in their series certainly would reduce the number of patients diagnosed as having bacterascites. Another feature of their series that deserves comment is that the rates of complication and mortality showed no significant difference between patients with SBP and those without. In addition to the high prevalence of SBP, FHF may contribute to increased susceptibility to bacteremia. In our series, SBP and bacteremia were recognized in 26 (32%) and 29 patients (35%), respectively, including 15 (18%) with both SBP and bacteremia. The prevalence of renal failure and gastrointestinal hemorrhage and the mortality rate in patients with SBP (with or without bactermia) were similar to in those with bacteremia (without SBP), which were both significantly higher than in those without SBP and bacteremia. Unfortunately, the significance of bacteremia was not addressed in the Dhiman et al. series. Chia-Ming Chu, M.D. Chang Gung Memorial Hospital Taipei, Taiwan
REFERENCES 1. Dhiman RK, Makharia GK, Jain S, et al. Ascites and spontaneous bacterial peritonitis in fulminant hepatic failure. Am J Gastroenterol 2000;95:233– 8. 2. Chu CM, Chiu KW, Liaw YF. The prevalence and prognostic significance of spontaneous bacterial peritonitis in severe acute hepatitis with ascites. Hepatology 1992;15:799 – 803. 3. Chu CM, Liaw YF, Pao CC, et al. The etiology of acute hepatitis superimposed upon previously unrecognized asymptomatic HBsAg carriers. Hepatology 1989;9:452– 6. 4. Yang PM, Chen DS, Lai MY, et al. Clinicopathologic studies of asymptomatic HBsAg carriers: with special emphasis on carriers older than 40 years. Hepato-Gastroenterology 1987;34: 251– 4. 5. Bal V, Amin SN, Rath S, et al. Virological markers and antibody responses in fulminant viral hepatitis. J Med Virol 1987; 23:75– 82.
Reprint requests and correspondence: Chia-Ming Chu, M.D., Chang Gung Memorial Hospital, Liver Research Unit, 199, Tung Hwa North Road, Taipei 10591, Taiwan. Received Feb. 21, 2000; accepted Apr. 18, 2000.