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Metabolic bone disease is present at diagnosis in patients with inflammatory bowel disease
Summary Aim : To establish whether bone disease is present at diagnosis in inflammatory bowel disease and to identify contributory metabolic abnormalities. Methods : Newly diagnosed patients with inflammatory bowel disease (19 males, 15 females; mean age, 44 years; range, 17–79 years; 23 ulcerative...
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Published in: | Alimentary pharmacology & therapeutics 2002-11, Vol.16 (11), p.1895-1902 |
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creator | Lamb, E. J. Wong, T. Smith, D. J. Simpson, D. E. Coakley, A. J. Moniz, C. Muller, A. F. |
description | Summary
Aim : To establish whether bone disease is present at diagnosis in inflammatory bowel disease and to identify contributory metabolic abnormalities.
Methods : Newly diagnosed patients with inflammatory bowel disease (19 males, 15 females; mean age, 44 years; range, 17–79 years; 23 ulcerative colitis, 11 Crohn's disease) were compared against standard reference ranges and a control group with irritable bowel syndrome (eight males, 10 females; mean age, 40 years; range, 19–64 years). Bone mineral density (g/cm2, dual‐energy X‐ray absorptiometry: lumbar spine and femoral neck) and biochemical bone markers were measured.
Results : Femoral neck bone mineral density, T‐ and Z‐scores (mean ± s.d., respectively) were lower in inflammatory bowel disease patients than in irritable bowel syndrome controls (0.78 ± 0.12 vs. 0.90 ± 0.16, P = 0.0046; − 0.88 ± 0.92 vs. 0.12 ± 1.17, P = 0.0018; − 0.30 ± 0.89 vs. 0.61 ± 1.10, P = 0.0030). Lumbar spine bone mineral density and T‐scores were also significantly lower in patients than controls (0.98 ± 0.15 vs. 1.08 ± 0.13, P = 0.0342; − 1.05 ± 1.39 vs. − 0.14 ± 1.19, P = 0.0304). Compared with controls, the urinary deoxypyridinoline : creatinine ratio was increased (7.66 vs. 5.70 nmol/mmol, P = 0.0163) and serum 25‐hydroxy vitamin D was decreased (18.7 vs. 28.5 µg/L, P = 0.0016); plasma osteocalcin and serum parathyroid hormone did not differ (P > 0.05).
Conclusions : The bone mineral density is reduced at diagnosis, prior to corticosteroid treatment, in both Crohn's disease and ulcerative colitis. Our data suggest that this is attributable to increased resorption rather than decreased bone formation. |
doi_str_mv | 10.1046/j.1365-2036.2002.01363.x |
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Aim : To establish whether bone disease is present at diagnosis in inflammatory bowel disease and to identify contributory metabolic abnormalities.
Methods : Newly diagnosed patients with inflammatory bowel disease (19 males, 15 females; mean age, 44 years; range, 17–79 years; 23 ulcerative colitis, 11 Crohn's disease) were compared against standard reference ranges and a control group with irritable bowel syndrome (eight males, 10 females; mean age, 40 years; range, 19–64 years). Bone mineral density (g/cm2, dual‐energy X‐ray absorptiometry: lumbar spine and femoral neck) and biochemical bone markers were measured.
Results : Femoral neck bone mineral density, T‐ and Z‐scores (mean ± s.d., respectively) were lower in inflammatory bowel disease patients than in irritable bowel syndrome controls (0.78 ± 0.12 vs. 0.90 ± 0.16, P = 0.0046; − 0.88 ± 0.92 vs. 0.12 ± 1.17, P = 0.0018; − 0.30 ± 0.89 vs. 0.61 ± 1.10, P = 0.0030). Lumbar spine bone mineral density and T‐scores were also significantly lower in patients than controls (0.98 ± 0.15 vs. 1.08 ± 0.13, P = 0.0342; − 1.05 ± 1.39 vs. − 0.14 ± 1.19, P = 0.0304). Compared with controls, the urinary deoxypyridinoline : creatinine ratio was increased (7.66 vs. 5.70 nmol/mmol, P = 0.0163) and serum 25‐hydroxy vitamin D was decreased (18.7 vs. 28.5 µg/L, P = 0.0016); plasma osteocalcin and serum parathyroid hormone did not differ (P > 0.05).
Conclusions : The bone mineral density is reduced at diagnosis, prior to corticosteroid treatment, in both Crohn's disease and ulcerative colitis. Our data suggest that this is attributable to increased resorption rather than decreased bone formation.</description><identifier>ISSN: 0269-2813</identifier><identifier>EISSN: 1365-2036</identifier><identifier>DOI: 10.1046/j.1365-2036.2002.01363.x</identifier><identifier>PMID: 12390098</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Adolescent ; Adult ; Aged ; Biological and medical sciences ; Biomarkers - analysis ; Bone Density ; Bone Diseases, Metabolic - etiology ; Bone Diseases, Metabolic - physiopathology ; Case-Control Studies ; Colitis, Ulcerative - complications ; Colitis, Ulcerative - physiopathology ; Colonic Diseases, Functional - complications ; Colonic Diseases, Functional - physiopathology ; Crohn Disease - complications ; Crohn Disease - physiopathology ; Diseases of the osteoarticular system ; Female ; Femur Neck - physiopathology ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Inflammatory Bowel Diseases - complications ; Inflammatory Bowel Diseases - physiopathology ; Lumbar Vertebrae - physiopathology ; Male ; Medical sciences ; Middle Aged ; Osteoporosis. Osteomalacia. Paget disease ; Other diseases. Semiology ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><ispartof>Alimentary pharmacology & therapeutics, 2002-11, Vol.16 (11), p.1895-1902</ispartof><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4743-347cf9752417cb2377b358b2ffe2ec101666975835346e487f1659d747b6227c3</citedby><cites>FETCH-LOGICAL-c4743-347cf9752417cb2377b358b2ffe2ec101666975835346e487f1659d747b6227c3</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=14439598$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12390098$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lamb, E. J.</creatorcontrib><creatorcontrib>Wong, T.</creatorcontrib><creatorcontrib>Smith, D. J.</creatorcontrib><creatorcontrib>Simpson, D. E.</creatorcontrib><creatorcontrib>Coakley, A. J.</creatorcontrib><creatorcontrib>Moniz, C.</creatorcontrib><creatorcontrib>Muller, A. F.</creatorcontrib><title>Metabolic bone disease is present at diagnosis in patients with inflammatory bowel disease</title><title>Alimentary pharmacology & therapeutics</title><addtitle>Aliment Pharmacol Ther</addtitle><description>Summary
Aim : To establish whether bone disease is present at diagnosis in inflammatory bowel disease and to identify contributory metabolic abnormalities.
Methods : Newly diagnosed patients with inflammatory bowel disease (19 males, 15 females; mean age, 44 years; range, 17–79 years; 23 ulcerative colitis, 11 Crohn's disease) were compared against standard reference ranges and a control group with irritable bowel syndrome (eight males, 10 females; mean age, 40 years; range, 19–64 years). Bone mineral density (g/cm2, dual‐energy X‐ray absorptiometry: lumbar spine and femoral neck) and biochemical bone markers were measured.
Results : Femoral neck bone mineral density, T‐ and Z‐scores (mean ± s.d., respectively) were lower in inflammatory bowel disease patients than in irritable bowel syndrome controls (0.78 ± 0.12 vs. 0.90 ± 0.16, P = 0.0046; − 0.88 ± 0.92 vs. 0.12 ± 1.17, P = 0.0018; − 0.30 ± 0.89 vs. 0.61 ± 1.10, P = 0.0030). Lumbar spine bone mineral density and T‐scores were also significantly lower in patients than controls (0.98 ± 0.15 vs. 1.08 ± 0.13, P = 0.0342; − 1.05 ± 1.39 vs. − 0.14 ± 1.19, P = 0.0304). Compared with controls, the urinary deoxypyridinoline : creatinine ratio was increased (7.66 vs. 5.70 nmol/mmol, P = 0.0163) and serum 25‐hydroxy vitamin D was decreased (18.7 vs. 28.5 µg/L, P = 0.0016); plasma osteocalcin and serum parathyroid hormone did not differ (P > 0.05).
Conclusions : The bone mineral density is reduced at diagnosis, prior to corticosteroid treatment, in both Crohn's disease and ulcerative colitis. Our data suggest that this is attributable to increased resorption rather than decreased bone formation.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - analysis</subject><subject>Bone Density</subject><subject>Bone Diseases, Metabolic - etiology</subject><subject>Bone Diseases, Metabolic - physiopathology</subject><subject>Case-Control Studies</subject><subject>Colitis, Ulcerative - complications</subject><subject>Colitis, Ulcerative - physiopathology</subject><subject>Colonic Diseases, Functional - complications</subject><subject>Colonic Diseases, Functional - physiopathology</subject><subject>Crohn Disease - complications</subject><subject>Crohn Disease - physiopathology</subject><subject>Diseases of the osteoarticular system</subject><subject>Female</subject><subject>Femur Neck - physiopathology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Inflammatory Bowel Diseases - complications</subject><subject>Inflammatory Bowel Diseases - physiopathology</subject><subject>Lumbar Vertebrae - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Osteoporosis. Osteomalacia. Paget disease</subject><subject>Other diseases. Semiology</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><issn>0269-2813</issn><issn>1365-2036</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNqNkLtOwzAUhi0EoqXwCigLbAm-xU4GhqriJhXBUBYWy3FPwFVuxKnavj1OG2Blsv2f75xjfQgFBEcEc3GziggTcUgxExHFmEbYv1m0PULj38IxGmMq0pAmhI3QmXMrjLGQmJ6iEaEsxThNxuj9GTqd1YU1QVZXECytA-0gsC5oWnBQdYHufKo_qtr50FZBozvrcxdsbPfpg7zQZam7ut35ERsofmaco5NcFw4uhnOC3u7vFrPHcP7y8DSbzkPDJWch49LkqYwpJ9JklEmZsTjJaJ4DBUMwEUL4csJixgXwROZExOlScpkJSqVhE3R9mNu09dcaXKdK6wwUha6gXjslKUml3-TB5ACatnauhVw1rS11u1MEq96rWqlen-r1qd6r2ntVW996OexYZyUs_xoHkR64GgDtjC7yVlfGuj-Oc5bGe-72wG1sAbt_f0BNXxf9jX0DDMiSnQ</recordid><startdate>200211</startdate><enddate>200211</enddate><creator>Lamb, E. J.</creator><creator>Wong, T.</creator><creator>Smith, D. J.</creator><creator>Simpson, D. E.</creator><creator>Coakley, A. J.</creator><creator>Moniz, C.</creator><creator>Muller, A. F.</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><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>200211</creationdate><title>Metabolic bone disease is present at diagnosis in patients with inflammatory bowel disease</title><author>Lamb, E. J. ; Wong, T. ; Smith, D. J. ; Simpson, D. E. ; Coakley, A. J. ; Moniz, C. ; Muller, A. F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4743-347cf9752417cb2377b358b2ffe2ec101666975835346e487f1659d747b6227c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - analysis</topic><topic>Bone Density</topic><topic>Bone Diseases, Metabolic - etiology</topic><topic>Bone Diseases, Metabolic - physiopathology</topic><topic>Case-Control Studies</topic><topic>Colitis, Ulcerative - complications</topic><topic>Colitis, Ulcerative - physiopathology</topic><topic>Colonic Diseases, Functional - complications</topic><topic>Colonic Diseases, Functional - physiopathology</topic><topic>Crohn Disease - complications</topic><topic>Crohn Disease - physiopathology</topic><topic>Diseases of the osteoarticular system</topic><topic>Female</topic><topic>Femur Neck - physiopathology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>Inflammatory Bowel Diseases - complications</topic><topic>Inflammatory Bowel Diseases - physiopathology</topic><topic>Lumbar Vertebrae - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Osteoporosis. Osteomalacia. Paget disease</topic><topic>Other diseases. Semiology</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lamb, E. J.</creatorcontrib><creatorcontrib>Wong, T.</creatorcontrib><creatorcontrib>Smith, D. J.</creatorcontrib><creatorcontrib>Simpson, D. E.</creatorcontrib><creatorcontrib>Coakley, A. J.</creatorcontrib><creatorcontrib>Moniz, C.</creatorcontrib><creatorcontrib>Muller, A. F.</creatorcontrib><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>Alimentary pharmacology & therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lamb, E. J.</au><au>Wong, T.</au><au>Smith, D. J.</au><au>Simpson, D. E.</au><au>Coakley, A. J.</au><au>Moniz, C.</au><au>Muller, A. F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Metabolic bone disease is present at diagnosis in patients with inflammatory bowel disease</atitle><jtitle>Alimentary pharmacology & therapeutics</jtitle><addtitle>Aliment Pharmacol Ther</addtitle><date>2002-11</date><risdate>2002</risdate><volume>16</volume><issue>11</issue><spage>1895</spage><epage>1902</epage><pages>1895-1902</pages><issn>0269-2813</issn><eissn>1365-2036</eissn><abstract>Summary
Aim : To establish whether bone disease is present at diagnosis in inflammatory bowel disease and to identify contributory metabolic abnormalities.
Methods : Newly diagnosed patients with inflammatory bowel disease (19 males, 15 females; mean age, 44 years; range, 17–79 years; 23 ulcerative colitis, 11 Crohn's disease) were compared against standard reference ranges and a control group with irritable bowel syndrome (eight males, 10 females; mean age, 40 years; range, 19–64 years). Bone mineral density (g/cm2, dual‐energy X‐ray absorptiometry: lumbar spine and femoral neck) and biochemical bone markers were measured.
Results : Femoral neck bone mineral density, T‐ and Z‐scores (mean ± s.d., respectively) were lower in inflammatory bowel disease patients than in irritable bowel syndrome controls (0.78 ± 0.12 vs. 0.90 ± 0.16, P = 0.0046; − 0.88 ± 0.92 vs. 0.12 ± 1.17, P = 0.0018; − 0.30 ± 0.89 vs. 0.61 ± 1.10, P = 0.0030). Lumbar spine bone mineral density and T‐scores were also significantly lower in patients than controls (0.98 ± 0.15 vs. 1.08 ± 0.13, P = 0.0342; − 1.05 ± 1.39 vs. − 0.14 ± 1.19, P = 0.0304). Compared with controls, the urinary deoxypyridinoline : creatinine ratio was increased (7.66 vs. 5.70 nmol/mmol, P = 0.0163) and serum 25‐hydroxy vitamin D was decreased (18.7 vs. 28.5 µg/L, P = 0.0016); plasma osteocalcin and serum parathyroid hormone did not differ (P > 0.05).
Conclusions : The bone mineral density is reduced at diagnosis, prior to corticosteroid treatment, in both Crohn's disease and ulcerative colitis. Our data suggest that this is attributable to increased resorption rather than decreased bone formation.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>12390098</pmid><doi>10.1046/j.1365-2036.2002.01363.x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adolescent Adult Aged Biological and medical sciences Biomarkers - analysis Bone Density Bone Diseases, Metabolic - etiology Bone Diseases, Metabolic - physiopathology Case-Control Studies Colitis, Ulcerative - complications Colitis, Ulcerative - physiopathology Colonic Diseases, Functional - complications Colonic Diseases, Functional - physiopathology Crohn Disease - complications Crohn Disease - physiopathology Diseases of the osteoarticular system Female Femur Neck - physiopathology Gastroenterology. Liver. Pancreas. Abdomen Humans Inflammatory Bowel Diseases - complications Inflammatory Bowel Diseases - physiopathology Lumbar Vertebrae - physiopathology Male Medical sciences Middle Aged Osteoporosis. Osteomalacia. Paget disease Other diseases. Semiology Stomach. Duodenum. Small intestine. Colon. Rectum. Anus |
title | Metabolic bone disease is present at diagnosis in patients with inflammatory bowel disease |
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