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Infrequency of colonization with Oxalobacter formigenes in inflammatory bowel disease: Possible role in renal stone formation
Background and Aim: Calcium oxalate renal stones (RS) and hyperoxaluria are common in patients with inflammatory bowel disease (IBD). The absence of intestinal oxalate degrading bacteria, Oxalobacter formigenes, may cause hyperoxaluria in IBD. The aim of the present study was to examine: (i) the co...
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Published in: | Journal of gastroenterology and hepatology 2004-12, Vol.19 (12), p.1403-1409 |
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description | Background and Aim: Calcium oxalate renal stones (RS) and hyperoxaluria are common in patients with inflammatory bowel disease (IBD). The absence of intestinal oxalate degrading bacteria, Oxalobacter formigenes, may cause hyperoxaluria in IBD. The aim of the present study was to examine: (i) the colonization of O. formigenes in patients with IBD and controls and to correlate its presence with urinary oxalate excretion; and (ii) urinary analytes contributing to RS in IBD.
Methods: Stool samples were studied for O. formigenes using polymerase chain reaction and Southern blotting in patients with IBD (n = 48: ulcerative colitis, 37; Crohn's disease, 11), RS (n = 87) and healthy subjects that were used as controls (n = 48). Levels of urinary oxalate, citrate, calcium, magnesium, creatinine and uric acid were estimated spectrophotometrically in each patient and in 13 controls for 24 h.
Results: Five of the 48 (10.4%) patients with IBD had RS. Five of the 48 (10.4%) patients with IBD, 25 of the 87 (29%) with RS and 27 of the 48 (56%) controls were colonized with O. formigenes (P |
doi_str_mv | 10.1111/j.1440-1746.2004.03510.x |
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Methods: Stool samples were studied for O. formigenes using polymerase chain reaction and Southern blotting in patients with IBD (n = 48: ulcerative colitis, 37; Crohn's disease, 11), RS (n = 87) and healthy subjects that were used as controls (n = 48). Levels of urinary oxalate, citrate, calcium, magnesium, creatinine and uric acid were estimated spectrophotometrically in each patient and in 13 controls for 24 h.
Results: Five of the 48 (10.4%) patients with IBD had RS. Five of the 48 (10.4%) patients with IBD, 25 of the 87 (29%) with RS and 27 of the 48 (56%) controls were colonized with O. formigenes (P < 0.001 for RS vs controls and P = 0.01 for RS vs IBD). Patients without O. formigenes had higher urinary oxalate than those with it (IBD, median 0.48 [range 0.11–2.09]vs 0.43 [range 0.16–1.10] mmol/24 h, P = NS; RS, median 0.59 mmol/24 h, range 0.14–1.90 vs 0.44 mmol/24 h, range 0.23–0.97; P = 0.008, Mann–Whitney U‐test). Median excretion of oxalate was higher in IBD and RS than in controls (0.47 [0.11–2.09], 0.56 [0.14–1.9] and 0.41 [0.21–0.62] mmol/24 h; P < 0.01), respectively. Median calcium was also higher in IBD and RS than in controls (6.50 [1.38–21.00], 6.78 [1.55–20.30] and 4.99 [1.47–9.60] mmol/24 h; P < 0.05, Kruskal–Wallis H‐test), respectively. Median urinary magnesium was higher in IBD than in RS and controls (4.57 [1.50–12.30], 3.60 [0.90–6.35] and 2.49 [0.74–4.80]; P < 0.001, Kruskal–Wallis H‐test), respectively. Urinary citrate excretion was comparable in IBD, RS and controls.
Conclusions: Patients with IBD and RS rarely have O. formigenes in their stools as compared with controls; this may contribute to hyperoxaluria in IBD. Hyperoxaluria and hypercalciuria may contribute to RS in patients with IBD. Hypermagnesuria in patients with IBD may protect them from RS.</description><identifier>ISSN: 0815-9319</identifier><identifier>EISSN: 1440-1746</identifier><identifier>DOI: 10.1111/j.1440-1746.2004.03510.x</identifier><identifier>PMID: 15610315</identifier><language>eng</language><publisher>Melbourne, Australia: Blackwell Science Pty</publisher><subject>Adolescent ; Adult ; Biological and medical sciences ; Crohn's disease ; Female ; Follow-Up Studies ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; hyperoxaluria ; Inflammatory Bowel Diseases - complications ; Inflammatory Bowel Diseases - microbiology ; Inflammatory Bowel Diseases - urine ; Kidney Calculi - etiology ; Kidney Calculi - urine ; Male ; Medical sciences ; Middle Aged ; Nephrology. Urinary tract diseases ; Other diseases. Semiology ; Oxalobacter formigenes ; Oxalobacter formigenes - growth & development ; Oxalobacter formigenes - isolation & purification ; renal stone ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; ulcerative colitis ; Urinary lithiasis</subject><ispartof>Journal of gastroenterology and hepatology, 2004-12, Vol.19 (12), p.1403-1409</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4350-6d2dbd60b2e2e018efb330290e6bd6a45cc549167f0985b3f76f94226eb6fa3f3</citedby><cites>FETCH-LOGICAL-c4350-6d2dbd60b2e2e018efb330290e6bd6a45cc549167f0985b3f76f94226eb6fa3f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16364253$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15610315$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KUMAR, RITU</creatorcontrib><creatorcontrib>GHOSHAL, UDAY C</creatorcontrib><creatorcontrib>SINGH, GUNJANA</creatorcontrib><creatorcontrib>MITTAL, RAMA D</creatorcontrib><title>Infrequency of colonization with Oxalobacter formigenes in inflammatory bowel disease: Possible role in renal stone formation</title><title>Journal of gastroenterology and hepatology</title><addtitle>J Gastroenterol Hepatol</addtitle><description>Background and Aim: Calcium oxalate renal stones (RS) and hyperoxaluria are common in patients with inflammatory bowel disease (IBD). The absence of intestinal oxalate degrading bacteria, Oxalobacter formigenes, may cause hyperoxaluria in IBD. The aim of the present study was to examine: (i) the colonization of O. formigenes in patients with IBD and controls and to correlate its presence with urinary oxalate excretion; and (ii) urinary analytes contributing to RS in IBD.
Methods: Stool samples were studied for O. formigenes using polymerase chain reaction and Southern blotting in patients with IBD (n = 48: ulcerative colitis, 37; Crohn's disease, 11), RS (n = 87) and healthy subjects that were used as controls (n = 48). Levels of urinary oxalate, citrate, calcium, magnesium, creatinine and uric acid were estimated spectrophotometrically in each patient and in 13 controls for 24 h.
Results: Five of the 48 (10.4%) patients with IBD had RS. Five of the 48 (10.4%) patients with IBD, 25 of the 87 (29%) with RS and 27 of the 48 (56%) controls were colonized with O. formigenes (P < 0.001 for RS vs controls and P = 0.01 for RS vs IBD). Patients without O. formigenes had higher urinary oxalate than those with it (IBD, median 0.48 [range 0.11–2.09]vs 0.43 [range 0.16–1.10] mmol/24 h, P = NS; RS, median 0.59 mmol/24 h, range 0.14–1.90 vs 0.44 mmol/24 h, range 0.23–0.97; P = 0.008, Mann–Whitney U‐test). Median excretion of oxalate was higher in IBD and RS than in controls (0.47 [0.11–2.09], 0.56 [0.14–1.9] and 0.41 [0.21–0.62] mmol/24 h; P < 0.01), respectively. Median calcium was also higher in IBD and RS than in controls (6.50 [1.38–21.00], 6.78 [1.55–20.30] and 4.99 [1.47–9.60] mmol/24 h; P < 0.05, Kruskal–Wallis H‐test), respectively. Median urinary magnesium was higher in IBD than in RS and controls (4.57 [1.50–12.30], 3.60 [0.90–6.35] and 2.49 [0.74–4.80]; P < 0.001, Kruskal–Wallis H‐test), respectively. Urinary citrate excretion was comparable in IBD, RS and controls.
Conclusions: Patients with IBD and RS rarely have O. formigenes in their stools as compared with controls; this may contribute to hyperoxaluria in IBD. Hyperoxaluria and hypercalciuria may contribute to RS in patients with IBD. Hypermagnesuria in patients with IBD may protect them from RS.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Crohn's disease</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>hyperoxaluria</subject><subject>Inflammatory Bowel Diseases - complications</subject><subject>Inflammatory Bowel Diseases - microbiology</subject><subject>Inflammatory Bowel Diseases - urine</subject><subject>Kidney Calculi - etiology</subject><subject>Kidney Calculi - urine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Other diseases. Semiology</subject><subject>Oxalobacter formigenes</subject><subject>Oxalobacter formigenes - growth & development</subject><subject>Oxalobacter formigenes - isolation & purification</subject><subject>renal stone</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>ulcerative colitis</subject><subject>Urinary lithiasis</subject><issn>0815-9319</issn><issn>1440-1746</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNqNkFFvFCEQx4nR2LP6FQwv-rYnLAu7a-KDNu21tWl90Gj6Qlh2UE4WKuzl7kz87mXvLu2rhDCE-f1nmD9CmJI5zevdck6rihS0rsS8JKSaE8ZzbvMEzR4ST9GMNJQXLaPtEXqR0pJkktT8OTqiXFDCKJ-hfxfeRPizAq-3OBisgwve_lWjDR6v7fgL32yUC53SI0RsQhzsT_CQsPV5G6eGQY0hbnEX1uBwbxOoBO_xl5CS7RzgGPKR4QheOZzG4GFXZtfhJXpmlEvw6hCP0bez068n58XVzeLi5ONVoSvGSSH6su96QboSSiC0AdMxRsqWgMjPquJa86qlojakbXjHTC1MW5WlgE4YxQw7Rm_3de9iyLOmUQ42aXBOeQirJEVNm5ryOoPNHtQxDxDByLtoBxW3khI5WS-XcnJYTg7LyXq5s15usvT1oceqG6B_FB68zsCbA6CSVs5E5bVNj5xgoio5y9yHPbe2Drb__QF5uTifbllf7PU2jbB50Kv4O8_Jai6_Xy_kj8_NddncfpK37B6UVbDR</recordid><startdate>200412</startdate><enddate>200412</enddate><creator>KUMAR, RITU</creator><creator>GHOSHAL, UDAY C</creator><creator>SINGH, GUNJANA</creator><creator>MITTAL, RAMA D</creator><general>Blackwell Science Pty</general><general>Blackwell Science</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200412</creationdate><title>Infrequency of colonization with Oxalobacter formigenes in inflammatory bowel disease: Possible role in renal stone formation</title><author>KUMAR, RITU ; GHOSHAL, UDAY C ; SINGH, GUNJANA ; MITTAL, RAMA D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4350-6d2dbd60b2e2e018efb330290e6bd6a45cc549167f0985b3f76f94226eb6fa3f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Crohn's disease</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>hyperoxaluria</topic><topic>Inflammatory Bowel Diseases - complications</topic><topic>Inflammatory Bowel Diseases - microbiology</topic><topic>Inflammatory Bowel Diseases - urine</topic><topic>Kidney Calculi - etiology</topic><topic>Kidney Calculi - urine</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Other diseases. Semiology</topic><topic>Oxalobacter formigenes</topic><topic>Oxalobacter formigenes - growth & development</topic><topic>Oxalobacter formigenes - isolation & purification</topic><topic>renal stone</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>ulcerative colitis</topic><topic>Urinary lithiasis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KUMAR, RITU</creatorcontrib><creatorcontrib>GHOSHAL, UDAY C</creatorcontrib><creatorcontrib>SINGH, GUNJANA</creatorcontrib><creatorcontrib>MITTAL, RAMA D</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of gastroenterology and hepatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KUMAR, RITU</au><au>GHOSHAL, UDAY C</au><au>SINGH, GUNJANA</au><au>MITTAL, RAMA D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Infrequency of colonization with Oxalobacter formigenes in inflammatory bowel disease: Possible role in renal stone formation</atitle><jtitle>Journal of gastroenterology and hepatology</jtitle><addtitle>J Gastroenterol Hepatol</addtitle><date>2004-12</date><risdate>2004</risdate><volume>19</volume><issue>12</issue><spage>1403</spage><epage>1409</epage><pages>1403-1409</pages><issn>0815-9319</issn><eissn>1440-1746</eissn><abstract>Background and Aim: Calcium oxalate renal stones (RS) and hyperoxaluria are common in patients with inflammatory bowel disease (IBD). The absence of intestinal oxalate degrading bacteria, Oxalobacter formigenes, may cause hyperoxaluria in IBD. The aim of the present study was to examine: (i) the colonization of O. formigenes in patients with IBD and controls and to correlate its presence with urinary oxalate excretion; and (ii) urinary analytes contributing to RS in IBD.
Methods: Stool samples were studied for O. formigenes using polymerase chain reaction and Southern blotting in patients with IBD (n = 48: ulcerative colitis, 37; Crohn's disease, 11), RS (n = 87) and healthy subjects that were used as controls (n = 48). Levels of urinary oxalate, citrate, calcium, magnesium, creatinine and uric acid were estimated spectrophotometrically in each patient and in 13 controls for 24 h.
Results: Five of the 48 (10.4%) patients with IBD had RS. Five of the 48 (10.4%) patients with IBD, 25 of the 87 (29%) with RS and 27 of the 48 (56%) controls were colonized with O. formigenes (P < 0.001 for RS vs controls and P = 0.01 for RS vs IBD). Patients without O. formigenes had higher urinary oxalate than those with it (IBD, median 0.48 [range 0.11–2.09]vs 0.43 [range 0.16–1.10] mmol/24 h, P = NS; RS, median 0.59 mmol/24 h, range 0.14–1.90 vs 0.44 mmol/24 h, range 0.23–0.97; P = 0.008, Mann–Whitney U‐test). Median excretion of oxalate was higher in IBD and RS than in controls (0.47 [0.11–2.09], 0.56 [0.14–1.9] and 0.41 [0.21–0.62] mmol/24 h; P < 0.01), respectively. Median calcium was also higher in IBD and RS than in controls (6.50 [1.38–21.00], 6.78 [1.55–20.30] and 4.99 [1.47–9.60] mmol/24 h; P < 0.05, Kruskal–Wallis H‐test), respectively. Median urinary magnesium was higher in IBD than in RS and controls (4.57 [1.50–12.30], 3.60 [0.90–6.35] and 2.49 [0.74–4.80]; P < 0.001, Kruskal–Wallis H‐test), respectively. Urinary citrate excretion was comparable in IBD, RS and controls.
Conclusions: Patients with IBD and RS rarely have O. formigenes in their stools as compared with controls; this may contribute to hyperoxaluria in IBD. Hyperoxaluria and hypercalciuria may contribute to RS in patients with IBD. Hypermagnesuria in patients with IBD may protect them from RS.</abstract><cop>Melbourne, Australia</cop><pub>Blackwell Science Pty</pub><pmid>15610315</pmid><doi>10.1111/j.1440-1746.2004.03510.x</doi><tpages>7</tpages></addata></record> |
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subjects | Adolescent Adult Biological and medical sciences Crohn's disease Female Follow-Up Studies Gastroenterology. Liver. Pancreas. Abdomen Humans hyperoxaluria Inflammatory Bowel Diseases - complications Inflammatory Bowel Diseases - microbiology Inflammatory Bowel Diseases - urine Kidney Calculi - etiology Kidney Calculi - urine Male Medical sciences Middle Aged Nephrology. Urinary tract diseases Other diseases. Semiology Oxalobacter formigenes Oxalobacter formigenes - growth & development Oxalobacter formigenes - isolation & purification renal stone Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ulcerative colitis Urinary lithiasis |
title | Infrequency of colonization with Oxalobacter formigenes in inflammatory bowel disease: Possible role in renal stone formation |
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