A Case of Infectious Enterocolitis with Hyperammonemia
Case reports of hyperammonemia due to urease-producing bacteria are found occasionally, but most of them are associated with urinary tract infections. We experienced a case of infectious enterocolitis with hyperammonemia in which the causative bacteria was speculated to be urease-producing bacteria....
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| Published in | Journal of UOEH Vol. 39; no. 4; pp. 271 - 276 |
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| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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Japan
The University of Occupational and Environmental Health, Japan
2017
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| Online Access | Get full text |
| ISSN | 0387-821X 2187-2864 |
| DOI | 10.7888/juoeh.39.271 |
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| Abstract | Case reports of hyperammonemia due to urease-producing bacteria are found occasionally, but most of them are associated with urinary tract infections. We experienced a case of infectious enterocolitis with hyperammonemia in which the causative bacteria was speculated to be urease-producing bacteria. A Japanese woman in her 70s had been diagnosed with microscopic polyangiitis in a nearby hospital and was transferred to our hospital. Although the microscopic polyangiitis was relatively under control after treatment with steroids and rituximab, frequent diarrhea with hyperammonemia (324 µg/dl) appeared and she became comatose. Her blood ammonia decreased to 47 µg/dl and her consciousness recovered to a normal state after antibiotic treatment for infectious enterocolitis and ammonia detoxification therapy. Liver dysfunction, portosystemic shunt, excessive protein intake and constipation were not observed, and she took no medications that would cause hyperammonemia. Although culture results could not identify urease-producing bacteria, considering the clinical course, acute hyperammonemia was suspected to be due to urease-producing bacteria infection. It is necessary to consider the influence of urease-producing bacteria as a cause of acute hyperammonemia not only in urinary tract infections but also in infective enterocolitis. |
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| AbstractList | Case reports of hyperammonemia due to urease-producing bacteria are found occasionally, but most of them are associated with urinary tract infections. We experienced a case of infectious enterocolitis with hyperammonemia in which the causative bacteria was speculated to be urease-producing bacteria. A Japanese woman in her 70s had been diagnosed with microscopic polyangiitis in a nearby hospital and was transferred to our hospital. Although the microscopic polyangiitis was relatively under control after treatment with steroids and rituximab, frequent diarrhea with hyperammonemia (324 µg/dl) appeared and she became comatose. Her blood ammonia decreased to 47 µg/dl and her consciousness recovered to a normal state after antibiotic treatment for infectious enterocolitis and ammonia detoxification therapy. Liver dysfunction, portosystemic shunt, excessive protein intake and constipation were not observed, and she took no medications that would cause hyperammonemia. Although culture results could not identify urease-producing bacteria, considering the clinical course, acute hyperammonemia was suspected to be due to urease-producing bacteria infection. It is necessary to consider the influence of urease-producing bacteria as a cause of acute hyperammonemia not only in urinary tract infections but also in infective enterocolitis.Case reports of hyperammonemia due to urease-producing bacteria are found occasionally, but most of them are associated with urinary tract infections. We experienced a case of infectious enterocolitis with hyperammonemia in which the causative bacteria was speculated to be urease-producing bacteria. A Japanese woman in her 70s had been diagnosed with microscopic polyangiitis in a nearby hospital and was transferred to our hospital. Although the microscopic polyangiitis was relatively under control after treatment with steroids and rituximab, frequent diarrhea with hyperammonemia (324 µg/dl) appeared and she became comatose. Her blood ammonia decreased to 47 µg/dl and her consciousness recovered to a normal state after antibiotic treatment for infectious enterocolitis and ammonia detoxification therapy. Liver dysfunction, portosystemic shunt, excessive protein intake and constipation were not observed, and she took no medications that would cause hyperammonemia. Although culture results could not identify urease-producing bacteria, considering the clinical course, acute hyperammonemia was suspected to be due to urease-producing bacteria infection. It is necessary to consider the influence of urease-producing bacteria as a cause of acute hyperammonemia not only in urinary tract infections but also in infective enterocolitis. Case reports of hyperammonemia due to urease-producing bacteria are found occasionally, but most of them are associated with urinary tract infections. We experienced a case of infectious enterocolitis with hyperammonemia in which the causative bacteria was speculated to be urease-producing bacteria. A Japanese woman in her 70s had been diagnosed with microscopic polyangiitis in a nearby hospital and was transferred to our hospital. Although the microscopic polyangiitis was relatively under control after treatment with steroids and rituximab, frequent diarrhea with hyperammonemia (324 µg/dl) appeared and she became comatose. Her blood ammonia decreased to 47 µg/dl and her consciousness recovered to a normal state after antibiotic treatment for infectious enterocolitis and ammonia detoxification therapy. Liver dysfunction, portosystemic shunt, excessive protein intake and constipation were not observed, and she took no medications that would cause hyperammonemia. Although culture results could not identify urease-producing bacteria, considering the clinical course, acute hyperammonemia was suspected to be due to urease-producing bacteria infection. It is necessary to consider the influence of urease-producing bacteria as a cause of acute hyperammonemia not only in urinary tract infections but also in infective enterocolitis. |
| Author | OTSUJI, Ken HARAYAMA, Nobuya SAITO, Mitsumasa ARAI, Hideaki NIHEI, Shunichi NAGATA, Keiji ENDO, Takeru AIBARA, Keiji KAMOCHI, Masayuki KANAZAWA, Ayako SIMIZU, Satoko |
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| CitedBy_id | crossref_primary_10_1136_bcr_2023_256225 crossref_primary_10_1016_j_ymgmr_2021_100825 crossref_primary_10_1155_2020_3136074 crossref_primary_10_3389_fmed_2020_589825 crossref_primary_10_7759_cureus_20108 |
| Cites_doi | 10.3918/jsicm.22.33 10.1111/j.1528-1157.1992.tb01708.x 10.1136/gut.46.6.849 10.1016/j.jhep.2010.11.031 10.1126/science.1110591 10.1128/MMBR.59.3.451-480.1995 10.1016/S0140-6736(02)11084-1 10.3893/jjaam.23.205 10.1128/JB.52.4.461-466.1946 |
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| References | 3. Samtoy B & DeBeukelaer MM (1980): Ammonia encephalopathy secondary to urinary tract infection with Proteus mirabilis. Pediatrics 65: 294−297 6. Albrecht J & Norenberg MD (2006): Glutamine: A Trojan horse in ammonia neurotoxicity. Hepatology 44: 788−794 2. Tamura N, Shiino Y & Suzuki K (2015): Two case reports of hyperammonemia with urinary tract infection by urease-producing bacteria. J Jpn Soc Intensive Care Med 22: 33−37 (in Japanese) 13. Christensen WB (1946): Urea decomposition as a means of differentiating Proteus and paracolon cultures from each other and from Salmonella and Shigella types. J Bacteriol 52: 461−466 11. Kondo T, Ishida M, Kaneko S et al (1992): Is 2-propyl-4-pentenoic acid, a hepatotoxic metabolite of valproate, responsible for valproate-induced hyperammonemia? Epilepsia 33: 550−554 10. Aires CC, Cruchten AV, Ijlst L, Almeida IT, Duran M, Wanders RJ & Silva MF (2011): New insights on the mechanisms of valproate-induced hyperammonemia: inhibition of hepatic N-acetylglutamate synthase activity by valproyl-CoA. J Hepatol 55: 426−434 12. Mobley HL, Island MD & Hausinger RP (1995): Molecular biology of microbial ureases. Microbiol Rev 59: 451−480 8. Plauth M, Roske AE, Romaniuk P, Roth E, Ziebig R & Lochs H (2000): Post-feeding hyperammonaemia in patients with transjugular intrahepatic portosystemic shunt and liver cirrhosis: role of small intestinal ammonia release and route of nutrient administration. Gut 46: 849−855 5. Kuze N, Nishizaka Y, Okamoto K, Wakayama T, Imanaka M, Kubo Y, Oda Y & Amitani R (2000): Empyema thoracis accompanied by hyperammonemic encephalopathy. Nihon Kokyuki Gakkai Zasshi 38: 117−121 (in Japanese) 1. De Jonghe B, Janier V, Abderrahim N, Hillion D, Lacherade JC & Outin H (2002): Urinary tract infection and coma. Lancet 360: 996 7. Mora D & Arioli S (2014): Microbial urease in health and disease. PLoS Pathog 10: e1004472 4. Saito N, Yagi T, Hayashida K, Hara Y, Matsumoto H, Mashiko K & Yokota H (2012): Hyperammonemic in urinary tract infection with Staphylococcus intermedius: a case report. JJAAM 23: 205−210 (in Japanese) 9. Elwir S & Rahimi RS (2017): Hepatic encephalopathy: an update on the pathophysiology and therapeutic options. Clinical and Translational Hepatology 5: 142−151 14. Eckburg PB, Bik EM, Bernstein CM, Purdom E, Dethlefsen L, Sargent M, Gill SR, Nelson KE & Relman DA (2005): Diversity of the human intestinal microbial flora. Sciece 308: 1635−1638 11 12 13 14 1 2 3 4 5 6 7 8 9 10 |
| References_xml | – reference: 11. Kondo T, Ishida M, Kaneko S et al (1992): Is 2-propyl-4-pentenoic acid, a hepatotoxic metabolite of valproate, responsible for valproate-induced hyperammonemia? Epilepsia 33: 550−554 – reference: 6. Albrecht J & Norenberg MD (2006): Glutamine: A Trojan horse in ammonia neurotoxicity. Hepatology 44: 788−794 – reference: 8. Plauth M, Roske AE, Romaniuk P, Roth E, Ziebig R & Lochs H (2000): Post-feeding hyperammonaemia in patients with transjugular intrahepatic portosystemic shunt and liver cirrhosis: role of small intestinal ammonia release and route of nutrient administration. Gut 46: 849−855 – reference: 1. De Jonghe B, Janier V, Abderrahim N, Hillion D, Lacherade JC & Outin H (2002): Urinary tract infection and coma. Lancet 360: 996 – reference: 4. Saito N, Yagi T, Hayashida K, Hara Y, Matsumoto H, Mashiko K & Yokota H (2012): Hyperammonemic in urinary tract infection with Staphylococcus intermedius: a case report. JJAAM 23: 205−210 (in Japanese) – reference: 5. Kuze N, Nishizaka Y, Okamoto K, Wakayama T, Imanaka M, Kubo Y, Oda Y & Amitani R (2000): Empyema thoracis accompanied by hyperammonemic encephalopathy. Nihon Kokyuki Gakkai Zasshi 38: 117−121 (in Japanese) – reference: 2. Tamura N, Shiino Y & Suzuki K (2015): Two case reports of hyperammonemia with urinary tract infection by urease-producing bacteria. J Jpn Soc Intensive Care Med 22: 33−37 (in Japanese) – reference: 9. Elwir S & Rahimi RS (2017): Hepatic encephalopathy: an update on the pathophysiology and therapeutic options. Clinical and Translational Hepatology 5: 142−151 – reference: 13. Christensen WB (1946): Urea decomposition as a means of differentiating Proteus and paracolon cultures from each other and from Salmonella and Shigella types. J Bacteriol 52: 461−466 – reference: 7. Mora D & Arioli S (2014): Microbial urease in health and disease. PLoS Pathog 10: e1004472 – reference: 3. Samtoy B & DeBeukelaer MM (1980): Ammonia encephalopathy secondary to urinary tract infection with Proteus mirabilis. Pediatrics 65: 294−297 – reference: 14. Eckburg PB, Bik EM, Bernstein CM, Purdom E, Dethlefsen L, Sargent M, Gill SR, Nelson KE & Relman DA (2005): Diversity of the human intestinal microbial flora. Sciece 308: 1635−1638 – reference: 12. Mobley HL, Island MD & Hausinger RP (1995): Molecular biology of microbial ureases. Microbiol Rev 59: 451−480 – reference: 10. Aires CC, Cruchten AV, Ijlst L, Almeida IT, Duran M, Wanders RJ & Silva MF (2011): New insights on the mechanisms of valproate-induced hyperammonemia: inhibition of hepatic N-acetylglutamate synthase activity by valproyl-CoA. J Hepatol 55: 426−434 – ident: 2 doi: 10.3918/jsicm.22.33 – ident: 3 – ident: 11 doi: 10.1111/j.1528-1157.1992.tb01708.x – ident: 5 – ident: 8 doi: 10.1136/gut.46.6.849 – ident: 10 doi: 10.1016/j.jhep.2010.11.031 – ident: 14 doi: 10.1126/science.1110591 – ident: 6 – ident: 9 – ident: 7 – ident: 12 doi: 10.1128/MMBR.59.3.451-480.1995 – ident: 1 doi: 10.1016/S0140-6736(02)11084-1 – ident: 4 doi: 10.3893/jjaam.23.205 – ident: 13 doi: 10.1128/JB.52.4.461-466.1946 |
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| SubjectTerms | Abdominal Pain - etiology Aged Critical Care Enterococcus faecium Enterocolitis - complications Enterocolitis - drug therapy Female Humans hyperammonemia Hyperammonemia - etiology Hyperammonemia - therapy infectious enterocolitis Pelvic Pain - etiology urease |
| Title | A Case of Infectious Enterocolitis with Hyperammonemia |
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