Changes in plasma homocyst(e)ine in the acute phase after stroke
Elevated plasma homocyst(e)ine [H(e)] concentration has been associated with an increased risk of stroke. Although the literature suggests that H(e) increases from the acute to the convalescent phase after a stroke, it is not known whether H(e) changes within the acute period. A prospective, multice...
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| Veröffentlicht in: | Stroke (1970) 2002-02, Vol.33 (2), p.473-478 |
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| container_title | Stroke (1970) |
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| creator | HOWARD, Virginia J SIDES, Elizabeth G NEWMAN, George C COHEN, Stanley N HOWARD, George MALINOW, M. Rene TOOLE, James F |
| description | Elevated plasma homocyst(e)ine [H(e)] concentration has been associated with an increased risk of stroke. Although the literature suggests that H(e) increases from the acute to the convalescent phase after a stroke, it is not known whether H(e) changes within the acute period.
A prospective, multicenter study was conducted to examine changes in H(e) during the 2 weeks after an incident stroke. Blood samples were collected at days 1, 3, 5, 7, and between 10 and 14 days after the stroke.
Seventy-six participants (51 men) were enrolled from 9 sites from February 1997 through June 1998. Mean age was 65.6 years, and subjects had at least two H(e) measurements. The estimated mean H(e) level at baseline was 11.3+/-0.5 micromol/L, which increased consistently to a mean of 12.0+/-0.05, 12.4+/-0.5, 13.3+/-0.5, and 13.7+/-0.7 micromol/L at days 3, 5, 7, and 10 to 14, respectively. The magnitude of the change in H(e) was not affected by age, sex, smoking status, alcohol use, history of hypertension or diabetes, or Rankin Scale Score.
; These data suggest that the clinical interpretation of H(e) after stroke and the eligibility for clinical trials assessing treatment for elevated H(e) levels require an adjustment in time since stroke to properly interpret the observed H(e) levels. |
| doi_str_mv | 10.1161/hs0202.103069 |
| format | Article |
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A prospective, multicenter study was conducted to examine changes in H(e) during the 2 weeks after an incident stroke. Blood samples were collected at days 1, 3, 5, 7, and between 10 and 14 days after the stroke.
Seventy-six participants (51 men) were enrolled from 9 sites from February 1997 through June 1998. Mean age was 65.6 years, and subjects had at least two H(e) measurements. The estimated mean H(e) level at baseline was 11.3+/-0.5 micromol/L, which increased consistently to a mean of 12.0+/-0.05, 12.4+/-0.5, 13.3+/-0.5, and 13.7+/-0.7 micromol/L at days 3, 5, 7, and 10 to 14, respectively. The magnitude of the change in H(e) was not affected by age, sex, smoking status, alcohol use, history of hypertension or diabetes, or Rankin Scale Score.
; These data suggest that the clinical interpretation of H(e) after stroke and the eligibility for clinical trials assessing treatment for elevated H(e) levels require an adjustment in time since stroke to properly interpret the observed H(e) levels.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/hs0202.103069</identifier><identifier>PMID: 11823655</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Acute Disease ; Adult ; Aged ; Aged, 80 and over ; Biological and medical sciences ; Demography ; Female ; Homocysteine - blood ; Homocystine - blood ; Humans ; Magnetic Resonance Imaging ; Male ; Medical sciences ; Middle Aged ; Neurology ; Prospective Studies ; Risk Factors ; Sample Size ; Stroke - blood ; Stroke - diagnosis ; Time Factors ; Tomography, X-Ray Computed ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Stroke (1970), 2002-02, Vol.33 (2), p.473-478</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Feb 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c515t-2dde393bdfdaf2d41c1b38241f56da93ae4f2f60c207e1acad5ddcab322cdcca3</citedby><cites>FETCH-LOGICAL-c515t-2dde393bdfdaf2d41c1b38241f56da93ae4f2f60c207e1acad5ddcab322cdcca3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3673,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13467597$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11823655$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HOWARD, Virginia J</creatorcontrib><creatorcontrib>SIDES, Elizabeth G</creatorcontrib><creatorcontrib>NEWMAN, George C</creatorcontrib><creatorcontrib>COHEN, Stanley N</creatorcontrib><creatorcontrib>HOWARD, George</creatorcontrib><creatorcontrib>MALINOW, M. Rene</creatorcontrib><creatorcontrib>TOOLE, James F</creatorcontrib><creatorcontrib>Stability of Plasma Homocyst(e)ine in Acute Stroke Patients (SHASP) Study Investigators</creatorcontrib><title>Changes in plasma homocyst(e)ine in the acute phase after stroke</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>Elevated plasma homocyst(e)ine [H(e)] concentration has been associated with an increased risk of stroke. Although the literature suggests that H(e) increases from the acute to the convalescent phase after a stroke, it is not known whether H(e) changes within the acute period.
A prospective, multicenter study was conducted to examine changes in H(e) during the 2 weeks after an incident stroke. Blood samples were collected at days 1, 3, 5, 7, and between 10 and 14 days after the stroke.
Seventy-six participants (51 men) were enrolled from 9 sites from February 1997 through June 1998. Mean age was 65.6 years, and subjects had at least two H(e) measurements. The estimated mean H(e) level at baseline was 11.3+/-0.5 micromol/L, which increased consistently to a mean of 12.0+/-0.05, 12.4+/-0.5, 13.3+/-0.5, and 13.7+/-0.7 micromol/L at days 3, 5, 7, and 10 to 14, respectively. The magnitude of the change in H(e) was not affected by age, sex, smoking status, alcohol use, history of hypertension or diabetes, or Rankin Scale Score.
; These data suggest that the clinical interpretation of H(e) after stroke and the eligibility for clinical trials assessing treatment for elevated H(e) levels require an adjustment in time since stroke to properly interpret the observed H(e) levels.</description><subject>Acute Disease</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Demography</subject><subject>Female</subject><subject>Homocysteine - blood</subject><subject>Homocystine - blood</subject><subject>Humans</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Prospective Studies</subject><subject>Risk Factors</subject><subject>Sample Size</subject><subject>Stroke - blood</subject><subject>Stroke - diagnosis</subject><subject>Time Factors</subject><subject>Tomography, X-Ray Computed</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0039-2499</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0MtLw0AQBvBFFFurR68SBEUPqTv7SLI3pfiCghc9h8k-TGoedTc59L83pYWCpxmYHx_DR8gl0DlAAg9loIyyOVBOE3VEpiCZiEXCsmMypZSrmAmlJuQshBWllPFMnpIJQMZ4IuWUPC5KbL9tiKo2WtcYGozKrun0JvR39r5q7fbQlzZCPfQ2WpcYxt311keh992PPScnDutgL_ZzRr5enj8Xb_Hy4_V98bSMtQTZx8wYyxUvjDPomBGgoeAZE-BkYlBxtMIxl1DNaGoBNRppjMaCM6aN1shn5HaXu_bd72BDnzdV0LausbXdEPIUBJOQqhFe_4OrbvDt-FsOKs0EAKQjindI-y4Eb12-9lWDfpMDzbe95rte812vo7_ahw5FY81B74scwc0eYNBYO4-trsLBcZGkUqX8D3gMf8Q</recordid><startdate>20020201</startdate><enddate>20020201</enddate><creator>HOWARD, Virginia J</creator><creator>SIDES, Elizabeth G</creator><creator>NEWMAN, George C</creator><creator>COHEN, Stanley N</creator><creator>HOWARD, George</creator><creator>MALINOW, M. Rene</creator><creator>TOOLE, James F</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20020201</creationdate><title>Changes in plasma homocyst(e)ine in the acute phase after stroke</title><author>HOWARD, Virginia J ; SIDES, Elizabeth G ; NEWMAN, George C ; COHEN, Stanley N ; HOWARD, George ; MALINOW, M. Rene ; TOOLE, James F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c515t-2dde393bdfdaf2d41c1b38241f56da93ae4f2f60c207e1acad5ddcab322cdcca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Acute Disease</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>Demography</topic><topic>Female</topic><topic>Homocysteine - blood</topic><topic>Homocystine - blood</topic><topic>Humans</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Prospective Studies</topic><topic>Risk Factors</topic><topic>Sample Size</topic><topic>Stroke - blood</topic><topic>Stroke - diagnosis</topic><topic>Time Factors</topic><topic>Tomography, X-Ray Computed</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HOWARD, Virginia J</creatorcontrib><creatorcontrib>SIDES, Elizabeth G</creatorcontrib><creatorcontrib>NEWMAN, George C</creatorcontrib><creatorcontrib>COHEN, Stanley N</creatorcontrib><creatorcontrib>HOWARD, George</creatorcontrib><creatorcontrib>MALINOW, M. Rene</creatorcontrib><creatorcontrib>TOOLE, James F</creatorcontrib><creatorcontrib>Stability of Plasma Homocyst(e)ine in Acute Stroke Patients (SHASP) Study Investigators</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HOWARD, Virginia J</au><au>SIDES, Elizabeth G</au><au>NEWMAN, George C</au><au>COHEN, Stanley N</au><au>HOWARD, George</au><au>MALINOW, M. Rene</au><au>TOOLE, James F</au><aucorp>Stability of Plasma Homocyst(e)ine in Acute Stroke Patients (SHASP) Study Investigators</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Changes in plasma homocyst(e)ine in the acute phase after stroke</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>2002-02-01</date><risdate>2002</risdate><volume>33</volume><issue>2</issue><spage>473</spage><epage>478</epage><pages>473-478</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>Elevated plasma homocyst(e)ine [H(e)] concentration has been associated with an increased risk of stroke. Although the literature suggests that H(e) increases from the acute to the convalescent phase after a stroke, it is not known whether H(e) changes within the acute period.
A prospective, multicenter study was conducted to examine changes in H(e) during the 2 weeks after an incident stroke. Blood samples were collected at days 1, 3, 5, 7, and between 10 and 14 days after the stroke.
Seventy-six participants (51 men) were enrolled from 9 sites from February 1997 through June 1998. Mean age was 65.6 years, and subjects had at least two H(e) measurements. The estimated mean H(e) level at baseline was 11.3+/-0.5 micromol/L, which increased consistently to a mean of 12.0+/-0.05, 12.4+/-0.5, 13.3+/-0.5, and 13.7+/-0.7 micromol/L at days 3, 5, 7, and 10 to 14, respectively. The magnitude of the change in H(e) was not affected by age, sex, smoking status, alcohol use, history of hypertension or diabetes, or Rankin Scale Score.
; These data suggest that the clinical interpretation of H(e) after stroke and the eligibility for clinical trials assessing treatment for elevated H(e) levels require an adjustment in time since stroke to properly interpret the observed H(e) levels.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>11823655</pmid><doi>10.1161/hs0202.103069</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Stroke (1970), 2002-02, Vol.33 (2), p.473-478 |
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| source | MEDLINE; Alma/SFX Local Collection; EZB Electronic Journals Library; American Heart Association; Journals@Ovid Complete |
| subjects | Acute Disease Adult Aged Aged, 80 and over Biological and medical sciences Demography Female Homocysteine - blood Homocystine - blood Humans Magnetic Resonance Imaging Male Medical sciences Middle Aged Neurology Prospective Studies Risk Factors Sample Size Stroke - blood Stroke - diagnosis Time Factors Tomography, X-Ray Computed Vascular diseases and vascular malformations of the nervous system |
| title | Changes in plasma homocyst(e)ine in the acute phase after stroke |
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