Investigation of effects of two-different treatment modalities on nerve conduction in patients with ankylosing spondylitis
The objective of this study was to investigate any relationship between peripheral neuropathy and anti-TNF-α therapy used in ankylosing spondylitis (AS). Thirty-nine patients monitored in our clinic with a diagnosis of AS and without neuropathic symptoms were enrolled in the study. Patients were div...
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Veröffentlicht in: | Rheumatology international 2012-02, Vol.32 (2), p.431-434 |
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description | The objective of this study was to investigate any relationship between peripheral neuropathy and anti-TNF-α therapy used in ankylosing spondylitis (AS). Thirty-nine patients monitored in our clinic with a diagnosis of AS and without neuropathic symptoms were enrolled in the study. Patients were divided into two groups. The first consisted of 21 patients using biological agents for more than one year. The control group was made up of 18 patients of similar age and demographic characteristics receiving non-biological therapy. Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) scores were calculated, and sedimentation rate and C-reactive protein (CRP) levels measured. Motor and sensory nerve conduction analysis for the median, tibial, and sural nerves was performed. The nerve conduction results of the biological therapy group were then compared with those of the non-biological therapy group. Thirty-nine patients with a mean age of 37.05 ± 8.1 were enrolled. Patients were divided into two groups, depending on drugs used. The first group (using anti-TNF-α) consisted of 21 patients with a mean age of 42.2 ± 8.8, and the second (the non-biological group) of 18 patients with a mean age of 35.8 ± 7.5. There was no statistically significant difference between the groups in terms of age, sex, drug use, or duration of disease (
p
= 0.052,
p
= 0.55,
p
= 0.33, and
p
= 0.72, respectively). Sedimentation rate, CRP, and BASDAI scores were statistically significantly higher in the second group (
p
= 0.04,
p
= 0.03, and
p
= 0.009, respectively). No statistically significant difference was determined in any parameters at nerve conduction analysis between the two groups (
p
> 0.05). There was a positive correlation between sedimentation rate and median sensory conduction velocity (
p
= 0.02,
r
= 0.48) and tibial conduction velocity (
p
= 0.07,
r
= 0.43). A negative correlation was determined between duration of disease and median distal motor latency (
p
= 0.22,
r
= −0.37) and between length of drug use and median sensory conduction velocity (
p
= 0.02,
r
= −0.38). There was no significant correlation between other clinical and demographic data and nerve conduction parameters. No effect on nerve conduction of biological agents in AS patients without neurological symptoms was determined. Clinicians should be alert for signs and symptoms, suggesting neuropathy in patients given anti-TNF-α. |
doi_str_mv | 10.1007/s00296-010-1677-x |
format | Article |
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p
= 0.052,
p
= 0.55,
p
= 0.33, and
p
= 0.72, respectively). Sedimentation rate, CRP, and BASDAI scores were statistically significantly higher in the second group (
p
= 0.04,
p
= 0.03, and
p
= 0.009, respectively). No statistically significant difference was determined in any parameters at nerve conduction analysis between the two groups (
p
> 0.05). There was a positive correlation between sedimentation rate and median sensory conduction velocity (
p
= 0.02,
r
= 0.48) and tibial conduction velocity (
p
= 0.07,
r
= 0.43). A negative correlation was determined between duration of disease and median distal motor latency (
p
= 0.22,
r
= −0.37) and between length of drug use and median sensory conduction velocity (
p
= 0.02,
r
= −0.38). There was no significant correlation between other clinical and demographic data and nerve conduction parameters. No effect on nerve conduction of biological agents in AS patients without neurological symptoms was determined. Clinicians should be alert for signs and symptoms, suggesting neuropathy in patients given anti-TNF-α.</description><identifier>ISSN: 0172-8172</identifier><identifier>EISSN: 1437-160X</identifier><identifier>DOI: 10.1007/s00296-010-1677-x</identifier><identifier>PMID: 21120488</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject><![CDATA[Adalimumab ; Adult ; Anti-Inflammatory Agents, Non-Steroidal - administration & dosage ; Antibodies, Monoclonal - administration & dosage ; Antibodies, Monoclonal, Humanized - administration & dosage ; Antirheumatic Agents - administration & dosage ; Etanercept ; Female ; Humans ; Immunoglobulin G - administration & dosage ; Infliximab ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Neural Conduction - drug effects ; Original Article ; Receptors, Tumor Necrosis Factor - administration & dosage ; Rheumatology ; Spondylitis, Ankylosing - drug therapy ; Spondylitis, Ankylosing - physiopathology ; Sulfasalazine - administration & dosage ; Treatment Outcome ; Tumor Necrosis Factor-alpha - administration & dosage ; Tumor Necrosis Factor-alpha - antagonists & inhibitors]]></subject><ispartof>Rheumatology international, 2012-02, Vol.32 (2), p.431-434</ispartof><rights>Springer-Verlag 2010</rights><rights>Springer-Verlag 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c370t-78c719699d959453e4b7be9db3624dd47e00f7476f1d85c660b5495082f00c9e3</citedby><cites>FETCH-LOGICAL-c370t-78c719699d959453e4b7be9db3624dd47e00f7476f1d85c660b5495082f00c9e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00296-010-1677-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00296-010-1677-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21120488$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Capkin, Erhan</creatorcontrib><creatorcontrib>Karkucak, Murat</creatorcontrib><creatorcontrib>Kose, Muammer Muslim</creatorcontrib><creatorcontrib>Çakmak, Vildan Altunayoğlu</creatorcontrib><creatorcontrib>Turkyilmaz, Aysegul Kucukali</creatorcontrib><creatorcontrib>Tosun, Mehmet</creatorcontrib><title>Investigation of effects of two-different treatment modalities on nerve conduction in patients with ankylosing spondylitis</title><title>Rheumatology international</title><addtitle>Rheumatol Int</addtitle><addtitle>Rheumatol Int</addtitle><description>The objective of this study was to investigate any relationship between peripheral neuropathy and anti-TNF-α therapy used in ankylosing spondylitis (AS). Thirty-nine patients monitored in our clinic with a diagnosis of AS and without neuropathic symptoms were enrolled in the study. Patients were divided into two groups. The first consisted of 21 patients using biological agents for more than one year. The control group was made up of 18 patients of similar age and demographic characteristics receiving non-biological therapy. Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) scores were calculated, and sedimentation rate and C-reactive protein (CRP) levels measured. Motor and sensory nerve conduction analysis for the median, tibial, and sural nerves was performed. The nerve conduction results of the biological therapy group were then compared with those of the non-biological therapy group. Thirty-nine patients with a mean age of 37.05 ± 8.1 were enrolled. Patients were divided into two groups, depending on drugs used. The first group (using anti-TNF-α) consisted of 21 patients with a mean age of 42.2 ± 8.8, and the second (the non-biological group) of 18 patients with a mean age of 35.8 ± 7.5. There was no statistically significant difference between the groups in terms of age, sex, drug use, or duration of disease (
p
= 0.052,
p
= 0.55,
p
= 0.33, and
p
= 0.72, respectively). Sedimentation rate, CRP, and BASDAI scores were statistically significantly higher in the second group (
p
= 0.04,
p
= 0.03, and
p
= 0.009, respectively). No statistically significant difference was determined in any parameters at nerve conduction analysis between the two groups (
p
> 0.05). There was a positive correlation between sedimentation rate and median sensory conduction velocity (
p
= 0.02,
r
= 0.48) and tibial conduction velocity (
p
= 0.07,
r
= 0.43). A negative correlation was determined between duration of disease and median distal motor latency (
p
= 0.22,
r
= −0.37) and between length of drug use and median sensory conduction velocity (
p
= 0.02,
r
= −0.38). There was no significant correlation between other clinical and demographic data and nerve conduction parameters. No effect on nerve conduction of biological agents in AS patients without neurological symptoms was determined. Clinicians should be alert for signs and symptoms, suggesting neuropathy in patients given anti-TNF-α.</description><subject>Adalimumab</subject><subject>Adult</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - administration & dosage</subject><subject>Antibodies, Monoclonal - administration & dosage</subject><subject>Antibodies, Monoclonal, Humanized - administration & dosage</subject><subject>Antirheumatic Agents - administration & dosage</subject><subject>Etanercept</subject><subject>Female</subject><subject>Humans</subject><subject>Immunoglobulin G - administration & dosage</subject><subject>Infliximab</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Neural Conduction - drug effects</subject><subject>Original Article</subject><subject>Receptors, Tumor Necrosis Factor - administration & dosage</subject><subject>Rheumatology</subject><subject>Spondylitis, Ankylosing - drug therapy</subject><subject>Spondylitis, Ankylosing - physiopathology</subject><subject>Sulfasalazine - administration & dosage</subject><subject>Treatment Outcome</subject><subject>Tumor Necrosis Factor-alpha - administration & dosage</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><issn>0172-8172</issn><issn>1437-160X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kU9P3DAQxa0KVLbQD9ALsrj0lHacf46PFaKAhNRLkbhFiT3Zmib2YjsL20_fSZeCVKkXe578mzcePcY-CPgkAOTnCJCrOgMBmailzJ7esJUoC0kK7g7YCoTMs4aOI_YuxnsgXdfwlh3lQuRQNs2K_bp2W4zJrrtkveN-4DgMqFNcyvToM2NJB3SJp4BdmpZq8qYbbbJIlOMOwxa59s7M-o-JdXxDdkRG_mjTD965n7vRR-vWPG6I2y3N8YQdDt0Y8f3zfcxuv158P7_Kbr5dXp9_ucl0ISFlstFSqFopoypVVgWWvexRmb6o89KYUiLAIEtZD8I0laYF-6pUFTT5AKAVFsfs4953E_zDTMu2k40ax7Fz6OfYKiGbSoKoiTz7h7z3c3D0uQUq8qaqgCCxh3TwMQYc2k2wUxd2rYB2iaXdx9LCoimW9ol6Tp-N535C89LxNwcC8j0Q6cmtMbxO_r_rbxeJmok</recordid><startdate>20120201</startdate><enddate>20120201</enddate><creator>Capkin, Erhan</creator><creator>Karkucak, Murat</creator><creator>Kose, Muammer Muslim</creator><creator>Çakmak, Vildan Altunayoğlu</creator><creator>Turkyilmaz, Aysegul Kucukali</creator><creator>Tosun, Mehmet</creator><general>Springer-Verlag</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20120201</creationdate><title>Investigation of effects of two-different treatment modalities on nerve conduction in patients with ankylosing spondylitis</title><author>Capkin, Erhan ; Karkucak, Murat ; Kose, Muammer Muslim ; Çakmak, Vildan Altunayoğlu ; Turkyilmaz, Aysegul Kucukali ; Tosun, Mehmet</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c370t-78c719699d959453e4b7be9db3624dd47e00f7476f1d85c660b5495082f00c9e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adalimumab</topic><topic>Adult</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - administration & dosage</topic><topic>Antibodies, Monoclonal - administration & dosage</topic><topic>Antibodies, Monoclonal, Humanized - administration & dosage</topic><topic>Antirheumatic Agents - administration & dosage</topic><topic>Etanercept</topic><topic>Female</topic><topic>Humans</topic><topic>Immunoglobulin G - administration & dosage</topic><topic>Infliximab</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Neural Conduction - drug effects</topic><topic>Original Article</topic><topic>Receptors, Tumor Necrosis Factor - administration & dosage</topic><topic>Rheumatology</topic><topic>Spondylitis, Ankylosing - drug therapy</topic><topic>Spondylitis, Ankylosing - physiopathology</topic><topic>Sulfasalazine - administration & dosage</topic><topic>Treatment Outcome</topic><topic>Tumor Necrosis Factor-alpha - administration & dosage</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Capkin, Erhan</creatorcontrib><creatorcontrib>Karkucak, Murat</creatorcontrib><creatorcontrib>Kose, Muammer Muslim</creatorcontrib><creatorcontrib>Çakmak, Vildan Altunayoğlu</creatorcontrib><creatorcontrib>Turkyilmaz, Aysegul Kucukali</creatorcontrib><creatorcontrib>Tosun, Mehmet</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Rheumatology international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Capkin, Erhan</au><au>Karkucak, Murat</au><au>Kose, Muammer Muslim</au><au>Çakmak, Vildan Altunayoğlu</au><au>Turkyilmaz, Aysegul Kucukali</au><au>Tosun, Mehmet</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Investigation of effects of two-different treatment modalities on nerve conduction in patients with ankylosing spondylitis</atitle><jtitle>Rheumatology international</jtitle><stitle>Rheumatol Int</stitle><addtitle>Rheumatol Int</addtitle><date>2012-02-01</date><risdate>2012</risdate><volume>32</volume><issue>2</issue><spage>431</spage><epage>434</epage><pages>431-434</pages><issn>0172-8172</issn><eissn>1437-160X</eissn><abstract>The objective of this study was to investigate any relationship between peripheral neuropathy and anti-TNF-α therapy used in ankylosing spondylitis (AS). Thirty-nine patients monitored in our clinic with a diagnosis of AS and without neuropathic symptoms were enrolled in the study. Patients were divided into two groups. The first consisted of 21 patients using biological agents for more than one year. The control group was made up of 18 patients of similar age and demographic characteristics receiving non-biological therapy. Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) scores were calculated, and sedimentation rate and C-reactive protein (CRP) levels measured. Motor and sensory nerve conduction analysis for the median, tibial, and sural nerves was performed. The nerve conduction results of the biological therapy group were then compared with those of the non-biological therapy group. Thirty-nine patients with a mean age of 37.05 ± 8.1 were enrolled. Patients were divided into two groups, depending on drugs used. The first group (using anti-TNF-α) consisted of 21 patients with a mean age of 42.2 ± 8.8, and the second (the non-biological group) of 18 patients with a mean age of 35.8 ± 7.5. There was no statistically significant difference between the groups in terms of age, sex, drug use, or duration of disease (
p
= 0.052,
p
= 0.55,
p
= 0.33, and
p
= 0.72, respectively). Sedimentation rate, CRP, and BASDAI scores were statistically significantly higher in the second group (
p
= 0.04,
p
= 0.03, and
p
= 0.009, respectively). No statistically significant difference was determined in any parameters at nerve conduction analysis between the two groups (
p
> 0.05). There was a positive correlation between sedimentation rate and median sensory conduction velocity (
p
= 0.02,
r
= 0.48) and tibial conduction velocity (
p
= 0.07,
r
= 0.43). A negative correlation was determined between duration of disease and median distal motor latency (
p
= 0.22,
r
= −0.37) and between length of drug use and median sensory conduction velocity (
p
= 0.02,
r
= −0.38). There was no significant correlation between other clinical and demographic data and nerve conduction parameters. No effect on nerve conduction of biological agents in AS patients without neurological symptoms was determined. Clinicians should be alert for signs and symptoms, suggesting neuropathy in patients given anti-TNF-α.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>21120488</pmid><doi>10.1007/s00296-010-1677-x</doi><tpages>4</tpages></addata></record> |
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subjects | Adalimumab Adult Anti-Inflammatory Agents, Non-Steroidal - administration & dosage Antibodies, Monoclonal - administration & dosage Antibodies, Monoclonal, Humanized - administration & dosage Antirheumatic Agents - administration & dosage Etanercept Female Humans Immunoglobulin G - administration & dosage Infliximab Male Medicine Medicine & Public Health Middle Aged Neural Conduction - drug effects Original Article Receptors, Tumor Necrosis Factor - administration & dosage Rheumatology Spondylitis, Ankylosing - drug therapy Spondylitis, Ankylosing - physiopathology Sulfasalazine - administration & dosage Treatment Outcome Tumor Necrosis Factor-alpha - administration & dosage Tumor Necrosis Factor-alpha - antagonists & inhibitors |
title | Investigation of effects of two-different treatment modalities on nerve conduction in patients with ankylosing spondylitis |
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