Effect of normalization of fasting glucose by intensified insulin therapy and influence of eNOS polymorphisms on the incidence of restenosis after peripheral angioplasty in patients with type 2 diabetes: a randomized, open-label clinical trial
Primary objective was to evaluate whether an intensified insulin therapy (IIT) incorporating the target of normal fasting glucose and HbA1c levels could halve the incidence of restenosis/amputation/SCA/death at 6 months after peripheral angioplasty compared with standard care (SC) in patients with t...
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creator | Piatti, Pier Marco Marone, Enrico Mantero, Manuela Setola, Emanuela Galluccio, Elena Lucotti, Pietro Shehaj, Ermal Villa, Valentina Perticone, Francesca Venturini, Massimo Palini, Alessio Airoldi, Flavio Faglia, Ezio Del Maschio, Alessandro Colombo, Antonio Chiesa, Roberto Bosi, Emanuele Monti, Lucilla D. |
description | Primary objective was to evaluate whether an intensified insulin therapy (IIT) incorporating the target of normal fasting glucose and HbA1c levels could halve the incidence of restenosis/amputation/SCA/death at 6 months after peripheral angioplasty compared with standard care (SC) in patients with type 2 diabetes (DMT2) affected by critical limb ischemia (CLI). Forty-six consecutive patients with DMT2 and CLI were randomly assigned to a parallel, open-label study with IIT (basal-bolus glulisine + glargine administrations) or SC (glargine administration + oral antidiabetic drugs). A SNP of eNOS (rs753482-A>C) and circulating CD34
+
and CD34
+
KDR
+
progenitor cells were determined. At the end of the study, although HbA1c levels were lower in IIT than in SC (6.9 ± 1.3 % vs. 7.6 ± 1.2 %,
p
|
doi_str_mv | 10.1007/s00592-012-0426-x |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1785236486</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2990740621</sourcerecordid><originalsourceid>FETCH-LOGICAL-c372t-9a795e6c2b5bf36b1d2a8813d506c6bfef76cd95c451b75c78e93fbe3dfd5ebb3</originalsourceid><addsrcrecordid>eNp1ks1u1TAQhSMEopfCA7BBltiwIGA7cZywq6ryI1V0Aawj2xnf68qxje2Ipq_NC-BwW4SQWFi2Zr45c6yZqnpO8BuCMX-bMGYDrTEpp6VdffOg2pG2oTWjTfOw2uGhxTVr6XBSPUnpGheQN_3j6oTSAXPetbvq54XWoDLyGjkfZ2HNrcjGuy2gRcrG7dHeLsonQHJFxmVwyWgDU3mnxRqH8gGiCCsSbotpu4BTsNXD56svKHi7zj6Gg0lzQv43XjBlpnssQiqiPpmEhM4QUYBowiZqi-be-GCLka03CsUbuJzQD5MPKK8BEEWTERIypHdIoFhM-NncwvQa-QCutiVnkSo-jSp6ORphn1aPtLAJnt3dp9W39xdfzz_Wl1cfPp2fXdaq4TTXg-ADg05RyaRuOkkmKvqeNBPDneqkBs07NQ1MtYxIzhTvYWi0hGbSEwMpm9Pq1VE3RP99Kb8cZ5MUWCsc-CWNhPdlUF3bdwV9-Q967ZfoiruRNB3jZVjDUChypFT0KUXQY4hmFnEdCR63jRiPGzGWQY_bRow3pebFnfIiZ5j-VNyvQAHoEUgl5fYQ_2r9X9VfEiPJDg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1365777699</pqid></control><display><type>article</type><title>Effect of normalization of fasting glucose by intensified insulin therapy and influence of eNOS polymorphisms on the incidence of restenosis after peripheral angioplasty in patients with type 2 diabetes: a randomized, open-label clinical trial</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Piatti, Pier Marco ; Marone, Enrico ; Mantero, Manuela ; Setola, Emanuela ; Galluccio, Elena ; Lucotti, Pietro ; Shehaj, Ermal ; Villa, Valentina ; Perticone, Francesca ; Venturini, Massimo ; Palini, Alessio ; Airoldi, Flavio ; Faglia, Ezio ; Del Maschio, Alessandro ; Colombo, Antonio ; Chiesa, Roberto ; Bosi, Emanuele ; Monti, Lucilla D.</creator><creatorcontrib>Piatti, Pier Marco ; Marone, Enrico ; Mantero, Manuela ; Setola, Emanuela ; Galluccio, Elena ; Lucotti, Pietro ; Shehaj, Ermal ; Villa, Valentina ; Perticone, Francesca ; Venturini, Massimo ; Palini, Alessio ; Airoldi, Flavio ; Faglia, Ezio ; Del Maschio, Alessandro ; Colombo, Antonio ; Chiesa, Roberto ; Bosi, Emanuele ; Monti, Lucilla D.</creatorcontrib><description>Primary objective was to evaluate whether an intensified insulin therapy (IIT) incorporating the target of normal fasting glucose and HbA1c levels could halve the incidence of restenosis/amputation/SCA/death at 6 months after peripheral angioplasty compared with standard care (SC) in patients with type 2 diabetes (DMT2) affected by critical limb ischemia (CLI). Forty-six consecutive patients with DMT2 and CLI were randomly assigned to a parallel, open-label study with IIT (basal-bolus glulisine + glargine administrations) or SC (glargine administration + oral antidiabetic drugs). A SNP of eNOS (rs753482-A>C) and circulating CD34
+
and CD34
+
KDR
+
progenitor cells were determined. At the end of the study, although HbA1c levels were lower in IIT than in SC (6.9 ± 1.3 % vs. 7.6 ± 1.2 %,
p
< 0.05), IIT did not reduce the cumulative incidence of restenosis/amputation/SCA/death (52 and 65 %, respectively, odd ratio 0.59; CI 95 %: 0.21–1.62,
p
= 0.59). rs753482AC+CC as compared with rs753482AA increased the cumulative incidence of restenosis/amputation/SCA/death (79 and 42 %; odd ratio 5.3; CI 95 %: 1.41–19.5,
p
< 0.02). Baseline CD34
+
KDR
+
were higher in rs753482AA (166.2 ± 154.0 × 10
6
events) than in rs753482AC+CC (63.1 ± 26.9 × 10
6
events,
p
< 0.01). At the end of the study, the highest circulating CD34
+
KDR
+
were found in IIT rs753482AA (246.9 ± 194.0 × 10
6
events) while the lowest levels were found in SC rs753482AC+CC (70.9 ± 45.0 × 10
6
events
).
IIT did not decrease the cumulative incidence of restenosis/amputation/SCA/death in DMT2 and CLI patients. These patients correspond to a class of fragile subjects at high risk of cardiovascular events, and new predictors of restenosis should be contemplated, such as of eNOS polymorphism, (rs753482-A>C SNP) and circulating endothelial progenitor cells.</description><identifier>ISSN: 0940-5429</identifier><identifier>EISSN: 1432-5233</identifier><identifier>DOI: 10.1007/s00592-012-0426-x</identifier><identifier>PMID: 22907764</identifier><identifier>CODEN: ACDAEZ</identifier><language>eng</language><publisher>Milan: Springer Milan</publisher><subject>Aged ; Aged, 80 and over ; Angioplasty ; Blood Glucose - drug effects ; Blood Glucose - metabolism ; Clinical trials ; Diabetes ; Diabetes Mellitus, Type 2 - drug therapy ; Diabetes Mellitus, Type 2 - epidemiology ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - metabolism ; Extremities - blood supply ; Fasting ; Female ; Glucose ; Humans ; Hypoglycemic Agents - administration & dosage ; Incidence ; Insulin - administration & dosage ; Internal Medicine ; Kaplan-Meier Estimate ; Male ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Middle Aged ; Nitric Oxide Synthase Type III - genetics ; Original Article ; Peripheral Arterial Disease - epidemiology ; Peripheral Arterial Disease - genetics ; Peripheral Arterial Disease - metabolism ; Polymorphism ; Polymorphism, Genetic - physiology ; Treatment Outcome</subject><ispartof>Acta diabetologica, 2013-06, Vol.50 (3), p.373-382</ispartof><rights>Springer-Verlag 2012</rights><rights>Springer-Verlag Italia 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-9a795e6c2b5bf36b1d2a8813d506c6bfef76cd95c451b75c78e93fbe3dfd5ebb3</citedby><cites>FETCH-LOGICAL-c372t-9a795e6c2b5bf36b1d2a8813d506c6bfef76cd95c451b75c78e93fbe3dfd5ebb3</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/s00592-012-0426-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00592-012-0426-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22907764$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Piatti, Pier Marco</creatorcontrib><creatorcontrib>Marone, Enrico</creatorcontrib><creatorcontrib>Mantero, Manuela</creatorcontrib><creatorcontrib>Setola, Emanuela</creatorcontrib><creatorcontrib>Galluccio, Elena</creatorcontrib><creatorcontrib>Lucotti, Pietro</creatorcontrib><creatorcontrib>Shehaj, Ermal</creatorcontrib><creatorcontrib>Villa, Valentina</creatorcontrib><creatorcontrib>Perticone, Francesca</creatorcontrib><creatorcontrib>Venturini, Massimo</creatorcontrib><creatorcontrib>Palini, Alessio</creatorcontrib><creatorcontrib>Airoldi, Flavio</creatorcontrib><creatorcontrib>Faglia, Ezio</creatorcontrib><creatorcontrib>Del Maschio, Alessandro</creatorcontrib><creatorcontrib>Colombo, Antonio</creatorcontrib><creatorcontrib>Chiesa, Roberto</creatorcontrib><creatorcontrib>Bosi, Emanuele</creatorcontrib><creatorcontrib>Monti, Lucilla D.</creatorcontrib><title>Effect of normalization of fasting glucose by intensified insulin therapy and influence of eNOS polymorphisms on the incidence of restenosis after peripheral angioplasty in patients with type 2 diabetes: a randomized, open-label clinical trial</title><title>Acta diabetologica</title><addtitle>Acta Diabetol</addtitle><addtitle>Acta Diabetol</addtitle><description>Primary objective was to evaluate whether an intensified insulin therapy (IIT) incorporating the target of normal fasting glucose and HbA1c levels could halve the incidence of restenosis/amputation/SCA/death at 6 months after peripheral angioplasty compared with standard care (SC) in patients with type 2 diabetes (DMT2) affected by critical limb ischemia (CLI). Forty-six consecutive patients with DMT2 and CLI were randomly assigned to a parallel, open-label study with IIT (basal-bolus glulisine + glargine administrations) or SC (glargine administration + oral antidiabetic drugs). A SNP of eNOS (rs753482-A>C) and circulating CD34
+
and CD34
+
KDR
+
progenitor cells were determined. At the end of the study, although HbA1c levels were lower in IIT than in SC (6.9 ± 1.3 % vs. 7.6 ± 1.2 %,
p
< 0.05), IIT did not reduce the cumulative incidence of restenosis/amputation/SCA/death (52 and 65 %, respectively, odd ratio 0.59; CI 95 %: 0.21–1.62,
p
= 0.59). rs753482AC+CC as compared with rs753482AA increased the cumulative incidence of restenosis/amputation/SCA/death (79 and 42 %; odd ratio 5.3; CI 95 %: 1.41–19.5,
p
< 0.02). Baseline CD34
+
KDR
+
were higher in rs753482AA (166.2 ± 154.0 × 10
6
events) than in rs753482AC+CC (63.1 ± 26.9 × 10
6
events,
p
< 0.01). At the end of the study, the highest circulating CD34
+
KDR
+
were found in IIT rs753482AA (246.9 ± 194.0 × 10
6
events) while the lowest levels were found in SC rs753482AC+CC (70.9 ± 45.0 × 10
6
events
).
IIT did not decrease the cumulative incidence of restenosis/amputation/SCA/death in DMT2 and CLI patients. These patients correspond to a class of fragile subjects at high risk of cardiovascular events, and new predictors of restenosis should be contemplated, such as of eNOS polymorphism, (rs753482-A>C SNP) and circulating endothelial progenitor cells.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Angioplasty</subject><subject>Blood Glucose - drug effects</subject><subject>Blood Glucose - metabolism</subject><subject>Clinical trials</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Diabetes Mellitus, Type 2 - epidemiology</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Extremities - blood supply</subject><subject>Fasting</subject><subject>Female</subject><subject>Glucose</subject><subject>Humans</subject><subject>Hypoglycemic Agents - administration & dosage</subject><subject>Incidence</subject><subject>Insulin - administration & dosage</subject><subject>Internal Medicine</subject><subject>Kaplan-Meier Estimate</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Middle Aged</subject><subject>Nitric Oxide Synthase Type III - genetics</subject><subject>Original Article</subject><subject>Peripheral Arterial Disease - epidemiology</subject><subject>Peripheral Arterial Disease - genetics</subject><subject>Peripheral Arterial Disease - metabolism</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic - physiology</subject><subject>Treatment Outcome</subject><issn>0940-5429</issn><issn>1432-5233</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1ks1u1TAQhSMEopfCA7BBltiwIGA7cZywq6ryI1V0Aawj2xnf68qxje2Ipq_NC-BwW4SQWFi2Zr45c6yZqnpO8BuCMX-bMGYDrTEpp6VdffOg2pG2oTWjTfOw2uGhxTVr6XBSPUnpGheQN_3j6oTSAXPetbvq54XWoDLyGjkfZ2HNrcjGuy2gRcrG7dHeLsonQHJFxmVwyWgDU3mnxRqH8gGiCCsSbotpu4BTsNXD56svKHi7zj6Gg0lzQv43XjBlpnssQiqiPpmEhM4QUYBowiZqi-be-GCLka03CsUbuJzQD5MPKK8BEEWTERIypHdIoFhM-NncwvQa-QCutiVnkSo-jSp6ORphn1aPtLAJnt3dp9W39xdfzz_Wl1cfPp2fXdaq4TTXg-ADg05RyaRuOkkmKvqeNBPDneqkBs07NQ1MtYxIzhTvYWi0hGbSEwMpm9Pq1VE3RP99Kb8cZ5MUWCsc-CWNhPdlUF3bdwV9-Q967ZfoiruRNB3jZVjDUChypFT0KUXQY4hmFnEdCR63jRiPGzGWQY_bRow3pebFnfIiZ5j-VNyvQAHoEUgl5fYQ_2r9X9VfEiPJDg</recordid><startdate>20130601</startdate><enddate>20130601</enddate><creator>Piatti, Pier Marco</creator><creator>Marone, Enrico</creator><creator>Mantero, Manuela</creator><creator>Setola, Emanuela</creator><creator>Galluccio, Elena</creator><creator>Lucotti, Pietro</creator><creator>Shehaj, Ermal</creator><creator>Villa, Valentina</creator><creator>Perticone, Francesca</creator><creator>Venturini, Massimo</creator><creator>Palini, Alessio</creator><creator>Airoldi, Flavio</creator><creator>Faglia, Ezio</creator><creator>Del Maschio, Alessandro</creator><creator>Colombo, Antonio</creator><creator>Chiesa, Roberto</creator><creator>Bosi, Emanuele</creator><creator>Monti, Lucilla D.</creator><general>Springer Milan</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>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope></search><sort><creationdate>20130601</creationdate><title>Effect of normalization of fasting glucose by intensified insulin therapy and influence of eNOS polymorphisms on the incidence of restenosis after peripheral angioplasty in patients with type 2 diabetes: a randomized, open-label clinical trial</title><author>Piatti, Pier Marco ; Marone, Enrico ; Mantero, Manuela ; Setola, Emanuela ; Galluccio, Elena ; Lucotti, Pietro ; Shehaj, Ermal ; Villa, Valentina ; Perticone, Francesca ; Venturini, Massimo ; Palini, Alessio ; Airoldi, Flavio ; Faglia, Ezio ; Del Maschio, Alessandro ; Colombo, Antonio ; Chiesa, Roberto ; Bosi, Emanuele ; Monti, Lucilla D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-9a795e6c2b5bf36b1d2a8813d506c6bfef76cd95c451b75c78e93fbe3dfd5ebb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Angioplasty</topic><topic>Blood Glucose - drug effects</topic><topic>Blood Glucose - metabolism</topic><topic>Clinical trials</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 2 - drug therapy</topic><topic>Diabetes Mellitus, Type 2 - epidemiology</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Extremities - blood supply</topic><topic>Fasting</topic><topic>Female</topic><topic>Glucose</topic><topic>Humans</topic><topic>Hypoglycemic Agents - administration & dosage</topic><topic>Incidence</topic><topic>Insulin - administration & dosage</topic><topic>Internal Medicine</topic><topic>Kaplan-Meier Estimate</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Middle Aged</topic><topic>Nitric Oxide Synthase Type III - genetics</topic><topic>Original Article</topic><topic>Peripheral Arterial Disease - epidemiology</topic><topic>Peripheral Arterial Disease - genetics</topic><topic>Peripheral Arterial Disease - metabolism</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic - physiology</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Piatti, Pier Marco</creatorcontrib><creatorcontrib>Marone, Enrico</creatorcontrib><creatorcontrib>Mantero, Manuela</creatorcontrib><creatorcontrib>Setola, Emanuela</creatorcontrib><creatorcontrib>Galluccio, Elena</creatorcontrib><creatorcontrib>Lucotti, Pietro</creatorcontrib><creatorcontrib>Shehaj, Ermal</creatorcontrib><creatorcontrib>Villa, Valentina</creatorcontrib><creatorcontrib>Perticone, Francesca</creatorcontrib><creatorcontrib>Venturini, Massimo</creatorcontrib><creatorcontrib>Palini, Alessio</creatorcontrib><creatorcontrib>Airoldi, Flavio</creatorcontrib><creatorcontrib>Faglia, Ezio</creatorcontrib><creatorcontrib>Del Maschio, Alessandro</creatorcontrib><creatorcontrib>Colombo, Antonio</creatorcontrib><creatorcontrib>Chiesa, Roberto</creatorcontrib><creatorcontrib>Bosi, Emanuele</creatorcontrib><creatorcontrib>Monti, Lucilla D.</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>Immunology Abstracts</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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><jtitle>Acta diabetologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Piatti, Pier Marco</au><au>Marone, Enrico</au><au>Mantero, Manuela</au><au>Setola, Emanuela</au><au>Galluccio, Elena</au><au>Lucotti, Pietro</au><au>Shehaj, Ermal</au><au>Villa, Valentina</au><au>Perticone, Francesca</au><au>Venturini, Massimo</au><au>Palini, Alessio</au><au>Airoldi, Flavio</au><au>Faglia, Ezio</au><au>Del Maschio, Alessandro</au><au>Colombo, Antonio</au><au>Chiesa, Roberto</au><au>Bosi, Emanuele</au><au>Monti, Lucilla D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of normalization of fasting glucose by intensified insulin therapy and influence of eNOS polymorphisms on the incidence of restenosis after peripheral angioplasty in patients with type 2 diabetes: a randomized, open-label clinical trial</atitle><jtitle>Acta diabetologica</jtitle><stitle>Acta Diabetol</stitle><addtitle>Acta Diabetol</addtitle><date>2013-06-01</date><risdate>2013</risdate><volume>50</volume><issue>3</issue><spage>373</spage><epage>382</epage><pages>373-382</pages><issn>0940-5429</issn><eissn>1432-5233</eissn><coden>ACDAEZ</coden><abstract>Primary objective was to evaluate whether an intensified insulin therapy (IIT) incorporating the target of normal fasting glucose and HbA1c levels could halve the incidence of restenosis/amputation/SCA/death at 6 months after peripheral angioplasty compared with standard care (SC) in patients with type 2 diabetes (DMT2) affected by critical limb ischemia (CLI). Forty-six consecutive patients with DMT2 and CLI were randomly assigned to a parallel, open-label study with IIT (basal-bolus glulisine + glargine administrations) or SC (glargine administration + oral antidiabetic drugs). A SNP of eNOS (rs753482-A>C) and circulating CD34
+
and CD34
+
KDR
+
progenitor cells were determined. At the end of the study, although HbA1c levels were lower in IIT than in SC (6.9 ± 1.3 % vs. 7.6 ± 1.2 %,
p
< 0.05), IIT did not reduce the cumulative incidence of restenosis/amputation/SCA/death (52 and 65 %, respectively, odd ratio 0.59; CI 95 %: 0.21–1.62,
p
= 0.59). rs753482AC+CC as compared with rs753482AA increased the cumulative incidence of restenosis/amputation/SCA/death (79 and 42 %; odd ratio 5.3; CI 95 %: 1.41–19.5,
p
< 0.02). Baseline CD34
+
KDR
+
were higher in rs753482AA (166.2 ± 154.0 × 10
6
events) than in rs753482AC+CC (63.1 ± 26.9 × 10
6
events,
p
< 0.01). At the end of the study, the highest circulating CD34
+
KDR
+
were found in IIT rs753482AA (246.9 ± 194.0 × 10
6
events) while the lowest levels were found in SC rs753482AC+CC (70.9 ± 45.0 × 10
6
events
).
IIT did not decrease the cumulative incidence of restenosis/amputation/SCA/death in DMT2 and CLI patients. These patients correspond to a class of fragile subjects at high risk of cardiovascular events, and new predictors of restenosis should be contemplated, such as of eNOS polymorphism, (rs753482-A>C SNP) and circulating endothelial progenitor cells.</abstract><cop>Milan</cop><pub>Springer Milan</pub><pmid>22907764</pmid><doi>10.1007/s00592-012-0426-x</doi><tpages>10</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0940-5429 |
ispartof | Acta diabetologica, 2013-06, Vol.50 (3), p.373-382 |
issn | 0940-5429 1432-5233 |
language | eng |
recordid | cdi_proquest_miscellaneous_1785236486 |
source | MEDLINE; SpringerLink Journals |
subjects | Aged Aged, 80 and over Angioplasty Blood Glucose - drug effects Blood Glucose - metabolism Clinical trials Diabetes Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - epidemiology Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - metabolism Extremities - blood supply Fasting Female Glucose Humans Hypoglycemic Agents - administration & dosage Incidence Insulin - administration & dosage Internal Medicine Kaplan-Meier Estimate Male Medicine Medicine & Public Health Metabolic Diseases Middle Aged Nitric Oxide Synthase Type III - genetics Original Article Peripheral Arterial Disease - epidemiology Peripheral Arterial Disease - genetics Peripheral Arterial Disease - metabolism Polymorphism Polymorphism, Genetic - physiology Treatment Outcome |
title | Effect of normalization of fasting glucose by intensified insulin therapy and influence of eNOS polymorphisms on the incidence of restenosis after peripheral angioplasty in patients with type 2 diabetes: a randomized, open-label clinical trial |
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