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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
Main Authors: Lamb, E. J., Wong, T., Smith, D. J., Simpson, D. E., Coakley, A. J., Moniz, C., Muller, A. F.
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container_title Alimentary pharmacology & therapeutics
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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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J. ; Wong, T. ; Smith, D. J. ; Simpson, D. E. ; Coakley, A. J. ; Moniz, C. ; Muller, A. F.</creator><creatorcontrib>Lamb, E. J. ; Wong, T. ; Smith, D. J. ; Simpson, D. E. ; Coakley, A. J. ; Moniz, C. ; Muller, A. F.</creatorcontrib><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 &gt; 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 &amp; 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&amp;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 &amp; 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 &gt; 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. 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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. 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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 &amp; 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 &amp; 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 &gt; 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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source Wiley-Blackwell Read & Publish Collection
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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