Allelic polymorphism −491A/T in apo E gene modulates the lipid-lowering response in combined hyperlipidemia treatment
Background Combined hyperlipidemia (CHL) is one of the dyslipidemias more frequently found in clinical practice, and lipid‐lowering drugs are often necessary in its management. Some genetic loci have been associated with CHL expression, and some studies have shown modulation of drugs efficiency in t...
Saved in:
| Published in | European journal of clinical investigation Vol. 32; no. 6; pp. 421 - 428 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
Blackwell Science Ltd
01.06.2002
Blackwell Publishing Ltd |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0014-2972 1365-2362 |
| DOI | 10.1046/j.1365-2362.2002.00996.x |
Cover
| Abstract | Background Combined hyperlipidemia (CHL) is one of the dyslipidemias more frequently found in clinical practice, and lipid‐lowering drugs are often necessary in its management. Some genetic loci have been associated with CHL expression, and some studies have shown modulation of drugs efficiency in the treatment of dyslipidemias by genetic polymorphisms. We have investigated whether common polymorphisms and mutations in the apolipoprotein (apo) E, lipoprotein lipase (LPL), and apo CIII genes influence atorvastatin or bezafibrate responses in patients with CHL.
Design One hundred and sixteen subjects participating in the ATOMIX study (Atorvastatin in Mixed dyslipidemia) were randomized to treatment with either atorvastatin or bezafibrate. Apolipoprotein E genotype and common −491A/T and −219T/G polymorphisms in the apo E gene promoter region, Sst I polymorphism in the apo CIII gene (3238C/G), and D9N and N291S common mutations in the LPL gene were determined by polymerase chain reaction (PCR) and restriction enzyme digestion.
Results Statistical analysis showed the influence of the −491A/T polymorphism in atorvastatin and bezafibrate treatments. Subjects carrying the −491T allele showed an increased LDL‐cholesterol‐lowering effect with atorvastatin compared with −491T allele noncarriers (−35% vs. −27%, P = 0·037). Subjects carrying the −491T allele, when on bezafibrate treatment, showed a lower triglyceride reduction compared with −491T allele noncarriers (−23% vs. −39%, P = 0·05).
Conclusions In our study, the −491A/T polymorphism in the apo E gene promoter region modulated the lipid‐lowering efficiency of atorvastatin and bezafibrate in CHL patients. Such influence might explain some of the interindividual response variabilities observed for the two drugs, and could help in CHL management. |
|---|---|
| AbstractList | Background
Combined hyperlipidemia (CHL) is one of the dyslipidemias more frequently found in clinical practice, and lipid‐lowering drugs are often necessary in its management. Some genetic loci have been associated with CHL expression, and some studies have shown modulation of drugs efficiency in the treatment of dyslipidemias by genetic polymorphisms. We have investigated whether common polymorphisms and mutations in the apolipoprotein (apo) E, lipoprotein lipase (LPL), and apo CIII genes influence atorvastatin or bezafibrate responses in patients with CHL.
Design
One hundred and sixteen subjects participating in the ATOMIX study (Atorvastatin in Mixed dyslipidemia) were randomized to treatment with either atorvastatin or bezafibrate. Apolipoprotein E genotype and common −491A/T and −219T/G polymorphisms in the apo E gene promoter region, Sst I polymorphism in the apo CIII gene (3238C/G), and D9N and N291S common mutations in the LPL gene were determined by polymerase chain reaction (PCR) and restriction enzyme digestion.
Results
Statistical analysis showed the influence of the −491A/T polymorphism in atorvastatin and bezafibrate treatments. Subjects carrying the −491T allele showed an increased LDL‐cholesterol‐lowering effect with atorvastatin compared with −491T allele noncarriers (−35% vs. −27%,
P
= 0·037). Subjects carrying the −491T allele, when on bezafibrate treatment, showed a lower triglyceride reduction compared with −491T allele noncarriers (−23% vs. −39%,
P
= 0·05).
Conclusions
In our study, the −491A/T polymorphism in the apo E gene promoter region modulated the lipid‐lowering efficiency of atorvastatin and bezafibrate in CHL patients. Such influence might explain some of the interindividual response variabilities observed for the two drugs, and could help in CHL management. Combined hyperlipidemia (CHL) is one of the dyslipidemias more frequently found in clinical practice, and lipid-lowering drugs are often necessary in its management. Some genetic loci have been associated with CHL expression, and some studies have shown modulation of drugs efficiency in the treatment of dyslipidemias by genetic polymorphisms. We have investigated whether common polymorphisms and mutations in the apolipoprotein (apo) E, lipoprotein lipase (LPL), and apo CIII genes influence atorvastatin or bezafibrate responses in patients with CHL. One hundred and sixteen subjects participating in the ATOMIX study (Atorvastatin in Mixed dyslipidemia) were randomized to treatment with either atorvastatin or bezafibrate. Apolipoprotein E genotype and common -491A/T and -219T/G polymorphisms in the apo E gene promoter region, Sst I polymorphism in the apo CIII gene (3238C/G), and D9N and N291S common mutations in the LPL gene were determined by polymerase chain reaction (PCR) and restriction enzyme digestion. Statistical analysis showed the influence of the -491A/T polymorphism in atorvastatin and bezafibrate treatments. Subjects carrying the -491T allele showed an increased LDL-cholesterol-lowering effect with atorvastatin compared with -491T allele noncarriers (-35% vs. -27%, P = 0.037). Subjects carrying the -491T allele, when on bezafibrate treatment, showed a lower triglyceride reduction compared with -491T allele noncarriers (-23% vs. -39%, P = 0.05). In our study, the -491A/T polymorphism in the apo E gene promoter region modulated the lipid-lowering efficiency of atorvastatin and bezafibrate in CHL patients. Such influence might explain some of the interindividual response variabilities observed for the two drugs, and could help in CHL management. Background Combined hyperlipidemia (CHL) is one of the dyslipidemias more frequently found in clinical practice, and lipid‐lowering drugs are often necessary in its management. Some genetic loci have been associated with CHL expression, and some studies have shown modulation of drugs efficiency in the treatment of dyslipidemias by genetic polymorphisms. We have investigated whether common polymorphisms and mutations in the apolipoprotein (apo) E, lipoprotein lipase (LPL), and apo CIII genes influence atorvastatin or bezafibrate responses in patients with CHL. Design One hundred and sixteen subjects participating in the ATOMIX study (Atorvastatin in Mixed dyslipidemia) were randomized to treatment with either atorvastatin or bezafibrate. Apolipoprotein E genotype and common −491A/T and −219T/G polymorphisms in the apo E gene promoter region, Sst I polymorphism in the apo CIII gene (3238C/G), and D9N and N291S common mutations in the LPL gene were determined by polymerase chain reaction (PCR) and restriction enzyme digestion. Results Statistical analysis showed the influence of the −491A/T polymorphism in atorvastatin and bezafibrate treatments. Subjects carrying the −491T allele showed an increased LDL‐cholesterol‐lowering effect with atorvastatin compared with −491T allele noncarriers (−35% vs. −27%, P = 0·037). Subjects carrying the −491T allele, when on bezafibrate treatment, showed a lower triglyceride reduction compared with −491T allele noncarriers (−23% vs. −39%, P = 0·05). Conclusions In our study, the −491A/T polymorphism in the apo E gene promoter region modulated the lipid‐lowering efficiency of atorvastatin and bezafibrate in CHL patients. Such influence might explain some of the interindividual response variabilities observed for the two drugs, and could help in CHL management. Combined hyperlipidemia (CHL) is one of the dyslipidemias more frequently found in clinical practice, and lipid-lowering drugs are often necessary in its management. Some genetic loci have been associated with CHL expression, and some studies have shown modulation of drugs efficiency in the treatment of dyslipidemias by genetic polymorphisms. We have investigated whether common polymorphisms and mutations in the apolipoprotein (apo) E, lipoprotein lipase (LPL), and apo CIII genes influence atorvastatin or bezafibrate responses in patients with CHL.BACKGROUNDCombined hyperlipidemia (CHL) is one of the dyslipidemias more frequently found in clinical practice, and lipid-lowering drugs are often necessary in its management. Some genetic loci have been associated with CHL expression, and some studies have shown modulation of drugs efficiency in the treatment of dyslipidemias by genetic polymorphisms. We have investigated whether common polymorphisms and mutations in the apolipoprotein (apo) E, lipoprotein lipase (LPL), and apo CIII genes influence atorvastatin or bezafibrate responses in patients with CHL.One hundred and sixteen subjects participating in the ATOMIX study (Atorvastatin in Mixed dyslipidemia) were randomized to treatment with either atorvastatin or bezafibrate. Apolipoprotein E genotype and common -491A/T and -219T/G polymorphisms in the apo E gene promoter region, Sst I polymorphism in the apo CIII gene (3238C/G), and D9N and N291S common mutations in the LPL gene were determined by polymerase chain reaction (PCR) and restriction enzyme digestion.DESIGNOne hundred and sixteen subjects participating in the ATOMIX study (Atorvastatin in Mixed dyslipidemia) were randomized to treatment with either atorvastatin or bezafibrate. Apolipoprotein E genotype and common -491A/T and -219T/G polymorphisms in the apo E gene promoter region, Sst I polymorphism in the apo CIII gene (3238C/G), and D9N and N291S common mutations in the LPL gene were determined by polymerase chain reaction (PCR) and restriction enzyme digestion.Statistical analysis showed the influence of the -491A/T polymorphism in atorvastatin and bezafibrate treatments. Subjects carrying the -491T allele showed an increased LDL-cholesterol-lowering effect with atorvastatin compared with -491T allele noncarriers (-35% vs. -27%, P = 0.037). Subjects carrying the -491T allele, when on bezafibrate treatment, showed a lower triglyceride reduction compared with -491T allele noncarriers (-23% vs. -39%, P = 0.05).RESULTSStatistical analysis showed the influence of the -491A/T polymorphism in atorvastatin and bezafibrate treatments. Subjects carrying the -491T allele showed an increased LDL-cholesterol-lowering effect with atorvastatin compared with -491T allele noncarriers (-35% vs. -27%, P = 0.037). Subjects carrying the -491T allele, when on bezafibrate treatment, showed a lower triglyceride reduction compared with -491T allele noncarriers (-23% vs. -39%, P = 0.05).In our study, the -491A/T polymorphism in the apo E gene promoter region modulated the lipid-lowering efficiency of atorvastatin and bezafibrate in CHL patients. Such influence might explain some of the interindividual response variabilities observed for the two drugs, and could help in CHL management.CONCLUSIONSIn our study, the -491A/T polymorphism in the apo E gene promoter region modulated the lipid-lowering efficiency of atorvastatin and bezafibrate in CHL patients. Such influence might explain some of the interindividual response variabilities observed for the two drugs, and could help in CHL management. |
| Author | Civeira, F. Pocoví, M. Aristegui, R. Díaz, C. Recalde, D. García-Otín, A.-L. Sol, J. M. Masramon, X. Hernández, G. |
| Author_xml | – sequence: 1 givenname: A.-L. surname: García-Otín fullname: García-Otín, A.-L. organization: Departamento de Bioquímica y Biología Molecular y Celular, Universidad de Zaragoza – sequence: 2 givenname: F. surname: Civeira fullname: Civeira, F. organization: Servicio de Medicina Interna, Hospital Universitario Miguel Servet, Zaragoza – sequence: 3 givenname: R. surname: Aristegui fullname: Aristegui, R. organization: Departamento de I + D de Pfizer, Barcelona, Spain – sequence: 4 givenname: C. surname: Díaz fullname: Díaz, C. organization: Departamento de I + D de Pfizer, Barcelona, Spain – sequence: 5 givenname: D. surname: Recalde fullname: Recalde, D. organization: Departamento de Bioquímica y Biología Molecular y Celular, Universidad de Zaragoza – sequence: 6 givenname: J. M. surname: Sol fullname: Sol, J. M. organization: Departamento de I + D de Pfizer, Barcelona, Spain – sequence: 7 givenname: X. surname: Masramon fullname: Masramon, X. organization: Departamento de I + D de Pfizer, Barcelona, Spain – sequence: 8 givenname: G. surname: Hernández fullname: Hernández, G. organization: Departamento de I + D de Pfizer, Barcelona, Spain – sequence: 9 givenname: M. surname: Pocoví fullname: Pocoví, M. email: mpocovi@posta.unizar.es organization: Departamento de Bioquímica y Biología Molecular y Celular, Universidad de Zaragoza |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/12059987$$D View this record in MEDLINE/PubMed |
| BookMark | eNqNkd1u0zAYhi00xLrBLSCLA87S-SdOHAkhVVUZkwYIUcSh5cZfVhfHzuxUbe-AYy6RKyFZx5B2tCNb8vO8_uz3DJ344AEhTMmUkry42EwpL0TGeMGmjBA2JaSqiun-GZo8HJygCSE0z1hVslN0ltKGECIpZy_QKWVEVJUsJ2g3cw6crXEX3KENsVvb1OI_v37nFZ1dLLH1WHcBL_ANeMBtMFune0i4XwN2trMmc2EH0fobHCF1wScYnTq0K-vB4PWhg3gHQms17iPovgXfv0TPG-0SvLpfz9H3D4vl_GN2_eXyaj67zmqe50XGTNOU-fAkkQMXdVMQDYZzYKbMpZHGMFlTXQqjBRWGNIyRGlZ8JbTWK0Y0P0dvj7ldDLdbSL1qbarBOe0hbJMqqaSMiWoA3zwCN2Eb_TCbolVFaSUrPkCv76HtqgWjumhbHQ_q338OgDwCdQwpRWj-I0SN1amNGhtSY0NqrE7dVaf2g_r-kVrbXvc2-D5q654S8O4YsLMODk--WC3mV8Nm0LOjblMP-wddx5-qKHkp1I_Pl2opvn76JudSSf4XjIvDBg |
| CitedBy_id | crossref_primary_10_1177_1089253206294368 crossref_primary_10_1038_sj_tpj_6500384 crossref_primary_10_2165_11584380_000000000_00000 crossref_primary_10_1517_14796678_1_2_191 crossref_primary_10_1517_14656566_7_11_1417 crossref_primary_10_1177_1074248406293732 crossref_primary_10_2165_00129784_200808030_00003 crossref_primary_10_1002_phar_1981 crossref_primary_10_1016_j_ahj_2005_02_006 crossref_primary_10_1016_S0939_4753_03_80024_8 crossref_primary_10_1007_s00109_004_0631_3 crossref_primary_10_1016_j_vph_2005_07_012 crossref_primary_10_1111_jdi_13651 crossref_primary_10_2217_pgs_15_158 crossref_primary_10_1002_14651858_CD003697_pub2 crossref_primary_10_1515_dmdi_2011_107 crossref_primary_10_2217_14622416_9_10_1475 crossref_primary_10_3390_ijms21082884 crossref_primary_10_1186_1479_7364_1_2_111 |
| Cites_doi | 10.1093/nar/16.3.1215 10.1161/01.ATV.13.7.1110 10.1161/01.ATV.9.3.326 10.1016/S0002-9149(98)00036-8 10.1161/01.ATV.15.4.468 10.1038/ng0198-69 10.1016/0021-9150(91)90234-T 10.1161/01.CIR.103.9.1198 10.1016/S0002-9343(99)00148-5 10.1161/01.CIR.96.3.733 10.1016/S0022-2275(20)43176-1 10.1097/00041433-199904000-00005 10.1016/S0002-9149(98)00035-6 10.1016/S0022-2275(20)39943-0 10.1056/NEJM196702022760507 10.1016/0026-0495(93)90066-W 10.1161/01.ATV.17.11.2729 10.1016/S0014-5793(97)01543-3 10.1038/ng0595-28 10.1161/01.CIR.98.19.2088 10.1016/S0002-9149(98)00437-8 10.1016/0021-9150(90)90134-5 10.1093/ajcn/68.6.1215 10.1093/hmg/9.1.57 10.1161/01.CIR.85.6.2025 10.1016/0021-9150(94)05439-P 10.1016/0026-0495(90)90068-N 10.1161/01.CIR.85.1.37 10.1126/science.3283935 10.1046/j.1469-1809.2000.6440269.x 10.1016/S0021-9150(96)06031-5 10.1001/jama.1994.03520210050031 10.1111/j.1399-0004.1997.tb02488.x 10.1097/00041433-199806000-00002 10.1016/S0026-0495(98)90240-2 10.1046/j.1365-2362.2001.00859.x |
| ContentType | Journal Article |
| Copyright | Copyright Blackwell Scientific Publications Ltd. Jun 2002 |
| Copyright_xml | – notice: Copyright Blackwell Scientific Publications Ltd. Jun 2002 |
| CorporateAuthor | the ATOMIX Study Group ATOMIX Study Group. Atorvastatin in Mixed dyslipidemia |
| CorporateAuthor_xml | – name: the ATOMIX Study Group – name: ATOMIX Study Group. Atorvastatin in Mixed dyslipidemia |
| DBID | BSCLL AAYXX CITATION CGR CUY CVF ECM EIF NPM 7QO 7U7 7U9 8FD C1K FR3 H94 K9. NAPCQ P64 7X8 |
| DOI | 10.1046/j.1365-2362.2002.00996.x |
| DatabaseName | Istex CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Biotechnology Research Abstracts Toxicology Abstracts Virology and AIDS Abstracts Technology Research Database Environmental Sciences and Pollution Management Engineering Research Database AIDS and Cancer Research Abstracts ProQuest Health & Medical Complete (Alumni) Nursing & Allied Health Premium Biotechnology and BioEngineering Abstracts MEDLINE - Academic |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Nursing & Allied Health Premium Virology and AIDS Abstracts Biotechnology Research Abstracts Technology Research Database Toxicology Abstracts AIDS and Cancer Research Abstracts ProQuest Health & Medical Complete (Alumni) Engineering Research Database Biotechnology and BioEngineering Abstracts Environmental Sciences and Pollution Management MEDLINE - Academic |
| DatabaseTitleList | CrossRef MEDLINE MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1365-2362 |
| EndPage | 428 |
| ExternalDocumentID | 138412111 12059987 10_1046_j_1365_2362_2002_00996_x ECI996 ark_67375_WNG_T5QMS8C8_8 |
| Genre | article Multicenter Study Clinical Trial Randomized Controlled Trial Research Support, Non-U.S. Gov't Journal Article |
| GroupedDBID | --- -~X .3N .55 .GA .GJ .Y3 05W 0R~ 10A 1OB 1OC 29G 31~ 33P 36B 3SF 4.4 50Y 50Z 51W 51X 52M 52N 52O 52P 52R 52S 52T 52U 52V 52W 52X 53G 5GY 5HH 5LA 5RE 5VS 66C 702 7PT 8-0 8-1 8-3 8-4 8-5 8UM 930 A01 A03 AAESR AAEVG AAHQN AAIPD AAMMB AAMNL AANHP AANLZ AAONW AASGY AAXRX AAYCA AAZKR ABCQN ABCUV ABDBF ABEML ABLJU ABPVW ABQWH ABXGK ACAHQ ACBWZ ACCZN ACGFS ACGOF ACIWK ACMXC ACPOU ACPRK ACRPL ACSCC ACUHS ACXBN ACXQS ACYXJ ADBBV ADBTR ADEOM ADIZJ ADKYN ADMGS ADNMO ADOZA ADXAS ADZMN AEFGJ AEIGN AEIMD AENEX AEUYR AEYWJ AFBPY AFEBI AFFNX AFFPM AFGKR AFRAH AFWVQ AFZJQ AGHNM AGQPQ AGXDD AGYGG AHBTC AHEFC AIACR AIDQK AIDYY AIQQE AITYG AIURR ALAGY ALMA_UNASSIGNED_HOLDINGS ALUQN ALVPJ AMBMR AMYDB ASPBG ATUGU AVWKF AZBYB AZFZN AZVAB BAFTC BDRZF BFHJK BHBCM BMXJE BROTX BRXPI BSCLL BY8 C45 CAG COF CS3 D-6 D-7 D-E D-F DCZOG DPXWK DR2 DRFUL DRMAN DRSTM DU5 DUUFO EAD EAP EAS EBB EBC EBD EBS EBX EJD EMB EMK EMOBN EPT ESX EX3 F00 F01 F04 F5P FEDTE FUBAC FZ0 G-S G.N GODZA H.X HF~ HGLYW HVGLF HZI HZ~ IHE IX1 J0M K48 KBYEO LATKE LC2 LC3 LEEKS LH4 LITHE LOXES LP6 LP7 LUTES LW6 LYRES MEWTI MK0 MK4 MRFUL MRMAN MRSTM MSFUL MSMAN MSSTM MXFUL MXMAN MXSTM N04 N05 N9A NF~ O66 O9- OIG OVD P2P P2W P2X P2Z P4B P4D PALCI Q.N Q11 QB0 Q~Q R.K RIWAO RJQFR ROL RX1 SAMSI SUPJJ SV3 TEORI TUS UB1 W8V W99 WBKPD WH7 WHWMO WIH WIJ WIK WOHZO WOW WQJ WVDHM WXI WXSBR X7M XG1 YFH ZGI ZXP ZZTAW ~IA ~WT AAHHS ACCFJ ADZOD AEEZP AEQDE AEUQT AFPWT AIWBW AJBDE WRC WUP AAYXX CITATION CGR CUY CVF ECM EIF NPM 7QO 7U7 7U9 8FD C1K FR3 H94 K9. NAPCQ P64 7X8 |
| ID | FETCH-LOGICAL-c3446-2dff7436554e35cf60aed33e2d748d8dd28c1a75da515d0f220ceb3b5aaab20a3 |
| IEDL.DBID | DR2 |
| ISSN | 0014-2972 |
| IngestDate | Fri Sep 05 00:43:18 EDT 2025 Wed Aug 13 07:45:28 EDT 2025 Wed Feb 19 02:36:42 EST 2025 Wed Oct 01 01:35:11 EDT 2025 Thu Apr 24 23:10:58 EDT 2025 Wed Jan 22 16:57:02 EST 2025 Sun Sep 21 06:19:36 EDT 2025 |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 6 |
| Language | English |
| License | http://onlinelibrary.wiley.com/termsAndConditions#vor |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c3446-2dff7436554e35cf60aed33e2d748d8dd28c1a75da515d0f220ceb3b5aaab20a3 |
| Notes | istex:35C9DF807FAE743E43EABBA4911969385B91177D ark:/67375/WNG-T5QMS8C8-8 ArticleID:ECI996 Departamento de Bioquímica y Biología Molecular y Celular, Universidad de Zaragoza, Zaragoza, Spain (A.‐L. García‐Otín, D. Recalde, M. Pocoví); Servicio de Medicina Interna, Hospital Universitario Miguel Servet, Zaragoza, Spain (F. Civeira); Departamento de I + D de Pfizer, Barcelona, Spain (R. Aristegui, C. Díaz, J. M. Sol, X. Masramon, G. Hernández). ObjectType-Article-1 SourceType-Scholarly Journals-1 content type line 14 ObjectType-Article-2 ObjectType-Feature-1 content type line 23 ObjectType-Undefined-3 |
| PMID | 12059987 |
| PQID | 199119893 |
| PQPubID | 36545 |
| PageCount | 8 |
| ParticipantIDs | proquest_miscellaneous_71812259 proquest_journals_199119893 pubmed_primary_12059987 crossref_primary_10_1046_j_1365_2362_2002_00996_x crossref_citationtrail_10_1046_j_1365_2362_2002_00996_x wiley_primary_10_1046_j_1365_2362_2002_00996_x_ECI996 istex_primary_ark_67375_WNG_T5QMS8C8_8 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | June 2002 |
| PublicationDateYYYYMMDD | 2002-06-01 |
| PublicationDate_xml | – month: 06 year: 2002 text: June 2002 |
| PublicationDecade | 2000 |
| PublicationPlace | Oxford, UK |
| PublicationPlace_xml | – name: Oxford, UK – name: England – name: Oxford |
| PublicationTitle | European journal of clinical investigation |
| PublicationTitleAlternate | Eur J Clin Invest |
| PublicationYear | 2002 |
| Publisher | Blackwell Science Ltd Blackwell Publishing Ltd |
| Publisher_xml | – name: Blackwell Science Ltd – name: Blackwell Publishing Ltd |
| References | International Task Force of Coronary Heart Disease. Prevention of coronary heart disease: scientific background and new clinical guidelines. Recommendations of the European Atherosclerosis Society. Nutr Metab Cardiovasc Dis 1992; 2:113-56. Venkatesan S, Cullen P, Pacy P, Halliday D, Scott. J. Stable isotopes show a direct relation between VLDL apoB overproduction and serum triglyceride levels and indicate a metabolically and biochemically coherent basis for familial combined hyperlipidemia. Arterioscler Thromb 1993; 13:1110-8. Reymer PWA, Gagné E, Groenemeyer BE, Zhang H, Forsyth I, Jansen H et al. A lipoprotein lipase mutation (Asn291Ser) is associated with reduced HDL cholesterol levels in premature atherosclerosis. Nat Genet 1995; 10:28-34. Fredrickson DS, Levy RI, Lees RS. Fat transport in lipoprotein. An integrated approach to mechanisms and disorders. N Engl J Med 1967; 276:32-44. Sanllehy C, Casals E, Rodriguez-Villar C, Zambon D, Ojuel J, Ballesta AM et al. Lack of interaction of apolipoprotein E phenotype with the lipoprotein response to lovastatin or gemfibrozil in patients with primary hypercholesterolemia. Metabolism 1998; 47:560-5. Mahley RW. Apolipoprotein E. cholesterol transport protein with expanding role in cell biology. Science 1988; 240:622-30. Ordovas JM, Lopez-Miranda J, Pérez-Jiménez F, Rodriguez C, Park JS, Cole T et al. Effect of apolipoprotein E and A-IV phenotypes on the low density lipoprotein response to HMG CoA reductase inhibitor therapy. Atherosclerosis 1995; 113:157-66. Ordovas JM, Civeira F, Genest JJ Jr, Craig S, Robbins AH, Meade T et al. Restriction fragment length polymorphisms of the apolipoprotein A-I, C-III, A-IV gene locus. Relationships with lipids, apolipoproteins, and premature coronary artery disease. Atherosclerosis 1991; 87:75-86. Ginsberg HN. Effects of statins on triglyceride metabolism. Am J Cardiol 1998; 81:32B-35B. Hixson JE, Vernier DT. Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with Hha I. J Lipid Res 1990; 31:545-8. Mailly F, Tugrul Y, Reymer PWA, Bruin T, Seed M, Groenemeyer BF et al. A common variant in the gene for lipoprotein lipase (Asp9 - >Asn). Functional implications and prevalence in normal and hyperlipidemic subjects. Arterioscler Thromb Vasc Biol 1995; 15:468-78. Juo SH, Beaty TH, Kwiterovich PO Jr. Etiologic heterogeneity of hyperapobetalipoproteinemia (hyperapoB). Results from segregation analysis in families with premature coronary artery disease. Arterioscler Thromb Vasc Biol 1997; 17:2729-36. Sarkkinen E, Korhonen M, Erkkila A, Ebeling T, Uusitupa M. Effect of apolipoprotein E polymorphism on serum lipid response to the separate modification of dietary fat and dietary cholesterol. Am J Clin Nutr 1998; 68:1215-22. Miller SA, Dykes DD, Polesky HF. A simple salting out procedure for extracting DNA from human nucleated cells. Nucleic Acids Res 1988; 16:1215. Nestel P, Simons L, Barter P, Clifton P, Colquhoun D, Hamilton-Craig I et al. A comparative study of simvastatin and gemfibrozil in combined hyperlipoproteinemia: prediction response by baseline lipids, apo E genotype, lipoprotein (a) and insulin. Atherosclerosis 1997; 129:231-9. Vega GL, Grundy SM. Effect of statins on metabolism of apo-B-containing lipoproteins in hypertriglyceridemic men. Am J Cardiol 1998; 81:36B-42B. Lopez-Miranda J, Ordovas JM, Mata P, Lichtenstein AH, Clevidence B, Judd JT et al. Effect of apolipoprotein E phenotype on diet-induced lowering of plasma low density lipoprotein cholesterol. J Lipid Res 1994; 35:1965-75. O'Malley JP, Illingwoth DR. The influence of apolipoprotein E phenotype on the response to lovastatin therapy in patients with heterozygous familial hypercholesterolemia. Metabolism 1990; 39:150-4. Manninen V, Tenkanen L, Koskinen P, Huttunen JK, Manttari M, Heinonen OP et al. Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study Implications for Treatment. Circulation 1992; 85:37-45. Clee SM, Zwinderman AH, Engert JC, Zwarts KY, Molhuizen HOF, Roomp K et al. Common genetic variation in ABCA1 is associated with altered lipoprotein levels and a modified risk for coronary artery disease. Circulation 2001; 103:1198-205. Aouizerat BE, Allayee H, Bodnar J, Kras KL, Peltonen L, De Bruin TW et al. Novel genes for familial combined hyperlipidemia. Curr Opin Lipidol 1999; 10:113-22. Babirak SP, Iverius PH, Fujimoto WY, Brunzell JD. Detection and characterization of the heterozygote state for lipoprotein lipase deficiency. Arteriosclerosis 1989; 9:326-34. De Graaf J, Stalenhoef AFH. Defects of the lipoprotein metabolism in familial combined hyperlipidemia. Curr Opin Lipidol 1998; 9:189-96. Genest JJ Jr, Martin-Munley SS, McNamara JR, Ordovas JM, Jenner J, Myers RH et al. Familial lipoprotein disorders in patients with premature coronary artery disease. Circulation 1992; 85:2025-33. Wilson PW, Myers RH, Larson MG, Ordovas JM, Wolf PA, Schaefer EJ. Apolipoprotein E alleles, dyslipidemia, and coronary heart disease. JAMA 1994; 272:1666-71. Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994; 344:1383-9. Talmud PJ, Palmen J, Miller G, Humphries SE. Effect of microsomal triglyceride transfer protein gene variants (-493G> T, Q95H and H297Q) on plasma lipid levels in healthy middle-aged UK men. Ann Hum Genet 2000; 64:269-76. Valveny N, Esteban E, Kandil M, Moral P. APO E polymorphism in Spanish and Moroccan populations. Clin Genet 1997; 51:354-6. Gerdes C, Fisher RM, Nicaud V, Boer J, Humphries SE, Talmud PJ et al. Lipoprotein lipase variants D9N and N291S are associated with increased plasma triglyceride and lower high-density lipoprotein cholesterol concentrations: studies in the fasting and postprandial states: the European Atherosclerosis Research Studies. Circulation 1997; 96:733-40. Carmena R, Roederer G, Mailloux H, Lussier-Cacan S, Davignon. J. The response to lovastatin treatment in patients with heterozygous familial hypercholesterolemia is modulated by apolipoprotein E polymorphism. Metabolism 1993; 42:895-901. De Knijff P, Stalenhoef AF, Mol MJ, Gevers Leuven JA, Smit J, Erkelens DW et al. Influence of apo E polymorphism on the response to simvastatin treatment in patients with heterozygous familial hypercholesterolemia. Atherosclerosis 1990; 83:89-97. Farnier M and the Cerivastatin Study Group. Cerivastatin in the treatment of mixed hyperlipidemia: the Right Study. Am J Cardiol 1998; 82:47J-51J. Talmud P, Humphries SE. Apolipoprotein C-III gene variation and dyslipidaemia. J Lipid Res 1997; 8:154-8. Staels B, Dallongeville J, Auwerx J, Schoonjans K, Leitersdorf E, Fruchart JC. Mechanism of fibrates on lipid and lipoprotein metabolism. Circulation 1998; 98:2088-93. Lambert J-C, Brousseau T, Defosse V, Evans A, Arveiler D, Ruidavets J-B et al. Independent association of an apo E gene promoter polymorphism with increased risk of myocardial infarction and decreased apo E plasma concentrations-the ECTIM Study. Hum Mol Genet 2000; 9:57-61. East C. Combined hyperlipidemia as a risk factor for premature atherosclerosis disease. Am J Med 1999; 107:46S-47S. Artiga MJ, Bullido MJ, Sastre I, Recuero M, Garcia MA, Aldudo J et al. Allelic polymorphisms in the transcriptional regulatory region of the apolipoprotein E gene. FEBS Lett 1998; 421:105-8. Bullido MJ, Artiga MJ, Recuero M, Sastre I, García MA, Aldudo J et al. A polymorphism in the regulatory region of apoE associated with risk for Alzheimer's dementia. Nat Genet 1998; 18:69-71. Kakko S, Tamminen M, Paivansalo M, Kauma H, Rantala AO, Lilja M et al. Variation at the cholesterol ester transfer protein gene in relation to plasma high density lipoproteins cholesterol levels and carotid intima-media thickness. Eur J Clin Invest 2001; 31:593-602. 1990; 31 1995; 15 1990; 39 2000; 9 1988; 16 1993; 42 1989; 9 1995; 10 1994; 272 2000; 64 1995; 113 1998; 81 1967; 276 1988; 240 1998; 82 1999; 107 2001; 103 1998; 47 1997; 8 1998; 68 1990; 83 1994; 344 1993; 13 1998; 18 1997; 51 1997; 129 1991; 87 1997; 96 1997; 17 1999; 10 1994; 35 1998; 421 1998; 98 1992; 2 1998; 9 2001; 31 1992; 85 e_1_2_6_31_2 e_1_2_6_30_2 Talmud P (e_1_2_6_25_2) 1997; 8 e_1_2_6_18_2 e_1_2_6_19_2 e_1_2_6_12_2 e_1_2_6_35_2 e_1_2_6_13_2 e_1_2_6_34_2 e_1_2_6_10_2 e_1_2_6_33_2 Scandinavian Simvastatin Survival Study Group. (e_1_2_6_9_2) 1994; 344 e_1_2_6_32_2 e_1_2_6_16_2 e_1_2_6_39_2 e_1_2_6_17_2 e_1_2_6_38_2 e_1_2_6_14_2 e_1_2_6_37_2 e_1_2_6_15_2 e_1_2_6_36_2 e_1_2_6_20_2 International Task Force of Coronary Heart Disease. (e_1_2_6_11_2) 1992; 2 e_1_2_6_40_2 e_1_2_6_8_2 e_1_2_6_7_2 e_1_2_6_29_2 e_1_2_6_4_2 e_1_2_6_3_2 e_1_2_6_6_2 e_1_2_6_5_2 e_1_2_6_23_2 e_1_2_6_22_2 e_1_2_6_21_2 East C (e_1_2_6_2_2) 1999; 107 e_1_2_6_28_2 e_1_2_6_27_2 Wilson PW (e_1_2_6_24_2) 1994; 272 e_1_2_6_26_2 |
| References_xml | – reference: Juo SH, Beaty TH, Kwiterovich PO Jr. Etiologic heterogeneity of hyperapobetalipoproteinemia (hyperapoB). Results from segregation analysis in families with premature coronary artery disease. Arterioscler Thromb Vasc Biol 1997; 17:2729-36. – reference: Babirak SP, Iverius PH, Fujimoto WY, Brunzell JD. Detection and characterization of the heterozygote state for lipoprotein lipase deficiency. Arteriosclerosis 1989; 9:326-34. – reference: Talmud PJ, Palmen J, Miller G, Humphries SE. Effect of microsomal triglyceride transfer protein gene variants (-493G> T, Q95H and H297Q) on plasma lipid levels in healthy middle-aged UK men. Ann Hum Genet 2000; 64:269-76. – reference: Hixson JE, Vernier DT. Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with Hha I. J Lipid Res 1990; 31:545-8. – reference: De Graaf J, Stalenhoef AFH. Defects of the lipoprotein metabolism in familial combined hyperlipidemia. Curr Opin Lipidol 1998; 9:189-96. – reference: Venkatesan S, Cullen P, Pacy P, Halliday D, Scott. J. Stable isotopes show a direct relation between VLDL apoB overproduction and serum triglyceride levels and indicate a metabolically and biochemically coherent basis for familial combined hyperlipidemia. Arterioscler Thromb 1993; 13:1110-8. – reference: Ordovas JM, Lopez-Miranda J, Pérez-Jiménez F, Rodriguez C, Park JS, Cole T et al. Effect of apolipoprotein E and A-IV phenotypes on the low density lipoprotein response to HMG CoA reductase inhibitor therapy. Atherosclerosis 1995; 113:157-66. – reference: Genest JJ Jr, Martin-Munley SS, McNamara JR, Ordovas JM, Jenner J, Myers RH et al. Familial lipoprotein disorders in patients with premature coronary artery disease. Circulation 1992; 85:2025-33. – reference: Lambert J-C, Brousseau T, Defosse V, Evans A, Arveiler D, Ruidavets J-B et al. Independent association of an apo E gene promoter polymorphism with increased risk of myocardial infarction and decreased apo E plasma concentrations-the ECTIM Study. Hum Mol Genet 2000; 9:57-61. – reference: Wilson PW, Myers RH, Larson MG, Ordovas JM, Wolf PA, Schaefer EJ. Apolipoprotein E alleles, dyslipidemia, and coronary heart disease. JAMA 1994; 272:1666-71. – reference: Farnier M and the Cerivastatin Study Group. Cerivastatin in the treatment of mixed hyperlipidemia: the Right Study. Am J Cardiol 1998; 82:47J-51J. – reference: Artiga MJ, Bullido MJ, Sastre I, Recuero M, Garcia MA, Aldudo J et al. Allelic polymorphisms in the transcriptional regulatory region of the apolipoprotein E gene. FEBS Lett 1998; 421:105-8. – reference: Ginsberg HN. Effects of statins on triglyceride metabolism. Am J Cardiol 1998; 81:32B-35B. – reference: Carmena R, Roederer G, Mailloux H, Lussier-Cacan S, Davignon. J. The response to lovastatin treatment in patients with heterozygous familial hypercholesterolemia is modulated by apolipoprotein E polymorphism. Metabolism 1993; 42:895-901. – reference: Bullido MJ, Artiga MJ, Recuero M, Sastre I, García MA, Aldudo J et al. A polymorphism in the regulatory region of apoE associated with risk for Alzheimer's dementia. Nat Genet 1998; 18:69-71. – reference: Kakko S, Tamminen M, Paivansalo M, Kauma H, Rantala AO, Lilja M et al. Variation at the cholesterol ester transfer protein gene in relation to plasma high density lipoproteins cholesterol levels and carotid intima-media thickness. Eur J Clin Invest 2001; 31:593-602. – reference: Fredrickson DS, Levy RI, Lees RS. Fat transport in lipoprotein. An integrated approach to mechanisms and disorders. N Engl J Med 1967; 276:32-44. – reference: Nestel P, Simons L, Barter P, Clifton P, Colquhoun D, Hamilton-Craig I et al. A comparative study of simvastatin and gemfibrozil in combined hyperlipoproteinemia: prediction response by baseline lipids, apo E genotype, lipoprotein (a) and insulin. Atherosclerosis 1997; 129:231-9. – reference: Talmud P, Humphries SE. Apolipoprotein C-III gene variation and dyslipidaemia. J Lipid Res 1997; 8:154-8. – reference: Staels B, Dallongeville J, Auwerx J, Schoonjans K, Leitersdorf E, Fruchart JC. Mechanism of fibrates on lipid and lipoprotein metabolism. Circulation 1998; 98:2088-93. – reference: Miller SA, Dykes DD, Polesky HF. A simple salting out procedure for extracting DNA from human nucleated cells. Nucleic Acids Res 1988; 16:1215. – reference: Clee SM, Zwinderman AH, Engert JC, Zwarts KY, Molhuizen HOF, Roomp K et al. Common genetic variation in ABCA1 is associated with altered lipoprotein levels and a modified risk for coronary artery disease. Circulation 2001; 103:1198-205. – reference: Aouizerat BE, Allayee H, Bodnar J, Kras KL, Peltonen L, De Bruin TW et al. Novel genes for familial combined hyperlipidemia. Curr Opin Lipidol 1999; 10:113-22. – reference: International Task Force of Coronary Heart Disease. Prevention of coronary heart disease: scientific background and new clinical guidelines. Recommendations of the European Atherosclerosis Society. Nutr Metab Cardiovasc Dis 1992; 2:113-56. – reference: Ordovas JM, Civeira F, Genest JJ Jr, Craig S, Robbins AH, Meade T et al. Restriction fragment length polymorphisms of the apolipoprotein A-I, C-III, A-IV gene locus. Relationships with lipids, apolipoproteins, and premature coronary artery disease. Atherosclerosis 1991; 87:75-86. – reference: Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994; 344:1383-9. – reference: Valveny N, Esteban E, Kandil M, Moral P. APO E polymorphism in Spanish and Moroccan populations. Clin Genet 1997; 51:354-6. – reference: East C. Combined hyperlipidemia as a risk factor for premature atherosclerosis disease. Am J Med 1999; 107:46S-47S. – reference: Mailly F, Tugrul Y, Reymer PWA, Bruin T, Seed M, Groenemeyer BF et al. A common variant in the gene for lipoprotein lipase (Asp9 - >Asn). Functional implications and prevalence in normal and hyperlipidemic subjects. Arterioscler Thromb Vasc Biol 1995; 15:468-78. – reference: Sarkkinen E, Korhonen M, Erkkila A, Ebeling T, Uusitupa M. Effect of apolipoprotein E polymorphism on serum lipid response to the separate modification of dietary fat and dietary cholesterol. Am J Clin Nutr 1998; 68:1215-22. – reference: Reymer PWA, Gagné E, Groenemeyer BE, Zhang H, Forsyth I, Jansen H et al. A lipoprotein lipase mutation (Asn291Ser) is associated with reduced HDL cholesterol levels in premature atherosclerosis. Nat Genet 1995; 10:28-34. – reference: O'Malley JP, Illingwoth DR. The influence of apolipoprotein E phenotype on the response to lovastatin therapy in patients with heterozygous familial hypercholesterolemia. Metabolism 1990; 39:150-4. – reference: Mahley RW. Apolipoprotein E. cholesterol transport protein with expanding role in cell biology. Science 1988; 240:622-30. – reference: Manninen V, Tenkanen L, Koskinen P, Huttunen JK, Manttari M, Heinonen OP et al. Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study Implications for Treatment. Circulation 1992; 85:37-45. – reference: Gerdes C, Fisher RM, Nicaud V, Boer J, Humphries SE, Talmud PJ et al. Lipoprotein lipase variants D9N and N291S are associated with increased plasma triglyceride and lower high-density lipoprotein cholesterol concentrations: studies in the fasting and postprandial states: the European Atherosclerosis Research Studies. Circulation 1997; 96:733-40. – reference: Lopez-Miranda J, Ordovas JM, Mata P, Lichtenstein AH, Clevidence B, Judd JT et al. Effect of apolipoprotein E phenotype on diet-induced lowering of plasma low density lipoprotein cholesterol. J Lipid Res 1994; 35:1965-75. – reference: Sanllehy C, Casals E, Rodriguez-Villar C, Zambon D, Ojuel J, Ballesta AM et al. Lack of interaction of apolipoprotein E phenotype with the lipoprotein response to lovastatin or gemfibrozil in patients with primary hypercholesterolemia. Metabolism 1998; 47:560-5. – reference: Vega GL, Grundy SM. Effect of statins on metabolism of apo-B-containing lipoproteins in hypertriglyceridemic men. Am J Cardiol 1998; 81:36B-42B. – reference: De Knijff P, Stalenhoef AF, Mol MJ, Gevers Leuven JA, Smit J, Erkelens DW et al. Influence of apo E polymorphism on the response to simvastatin treatment in patients with heterozygous familial hypercholesterolemia. Atherosclerosis 1990; 83:89-97. – volume: 39 start-page: 150 year: 1990 end-page: 4 article-title: The influence of apolipoprotein E phenotype on the response to lovastatin therapy in patients with heterozygous familial hypercholesterolemia publication-title: Metabolism – volume: 31 start-page: 593 year: 2001 end-page: 602 article-title: Variation at the cholesterol ester transfer protein gene in relation to plasma high density lipoproteins cholesterol levels and carotid intima‐media thickness publication-title: Eur J Clin Invest – volume: 272 start-page: 1666 year: 1994 end-page: 71 article-title: Apolipoprotein E alleles, dyslipidemia, and coronary heart disease publication-title: JAMA – volume: 113 start-page: 157 year: 1995 end-page: 66 article-title: Effect of apolipoprotein E and A‐IV phenotypes on the low density lipoprotein response to HMG CoA reductase inhibitor therapy publication-title: Atherosclerosis – volume: 8 start-page: 154 year: 1997 end-page: 8 article-title: Apolipoprotein C‐III gene variation and dyslipidaemia publication-title: J Lipid Res – volume: 10 start-page: 113 year: 1999 end-page: 22 article-title: Novel genes for familial combined hyperlipidemia publication-title: Curr Opin Lipidol – volume: 81 start-page: 32B year: 1998 end-page: 35B article-title: Effects of statins on triglyceride metabolism publication-title: Am J Cardiol – volume: 421 start-page: 105 year: 1998 end-page: 8 article-title: Allelic polymorphisms in the transcriptional regulatory region of the apolipoprotein E gene publication-title: FEBS Lett – volume: 68 start-page: 1215 year: 1998 end-page: 22 article-title: Effect of apolipoprotein E polymorphism on serum lipid response to the separate modification of dietary fat and dietary cholesterol publication-title: Am J Clin Nutr – volume: 9 start-page: 57 year: 2000 end-page: 61 article-title: Independent association of an apo E gene promoter polymorphism with increased risk of myocardial infarction and decreased apo E plasma concentrations‐the ECTIM Study publication-title: Hum Mol Genet – volume: 16 start-page: 1215 year: 1988 article-title: A simple salting out procedure for extracting DNA from human nucleated cells publication-title: Nucleic Acids Res – volume: 81 start-page: 36B year: 1998 end-page: 42B article-title: Effect of statins on metabolism of apo‐B‐containing lipoproteins in hypertriglyceridemic men publication-title: Am J Cardiol – volume: 276 start-page: 32 year: 1967 end-page: 44 article-title: Fat transport in lipoprotein. An integrated approach to mechanisms and disorders publication-title: N Engl J Med – volume: 35 start-page: 1965 year: 1994 end-page: 75 article-title: Effect of apolipoprotein E phenotype on diet‐induced lowering of plasma low density lipoprotein cholesterol publication-title: J Lipid Res – volume: 51 start-page: 354 year: 1997 end-page: 6 article-title: APO E polymorphism in Spanish and Moroccan populations publication-title: Clin Genet – volume: 87 start-page: 75 year: 1991 end-page: 86 article-title: Restriction fragment length polymorphisms of the apolipoprotein A‐I, C‐III, A‐IV gene locus. Relationships with lipids, apolipoproteins, and premature coronary artery disease publication-title: Atherosclerosis – volume: 98 start-page: 2088 year: 1998 end-page: 93 article-title: Mechanism of fibrates on lipid and lipoprotein metabolism publication-title: Circulation – volume: 42 start-page: 895 year: 1993 end-page: 901 article-title: The response to lovastatin treatment in patients with heterozygous familial hypercholesterolemia is modulated by apolipoprotein E polymorphism publication-title: Metabolism – volume: 107 start-page: 46S year: 1999 end-page: 47S article-title: Combined hyperlipidemia as a risk factor for premature atherosclerosis disease publication-title: Am J Med – volume: 85 start-page: 2025 year: 1992 end-page: 33 article-title: Familial lipoprotein disorders in patients with premature coronary artery disease publication-title: Circulation – volume: 9 start-page: 326 year: 1989 end-page: 34 article-title: Detection and characterization of the heterozygote state for lipoprotein lipase deficiency publication-title: Arteriosclerosis – volume: 344 start-page: 1383 year: 1994 end-page: 9 article-title: Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S) publication-title: Lancet – volume: 17 start-page: 2729 year: 1997 end-page: 36 article-title: Etiologic heterogeneity of hyperapobetalipoproteinemia (hyperapoB). Results from segregation analysis in families with premature coronary artery disease publication-title: Arterioscler Thromb Vasc Biol – volume: 9 start-page: 189 year: 1998 end-page: 96 article-title: Defects of the lipoprotein metabolism in familial combined hyperlipidemia publication-title: Curr Opin Lipidol – volume: 15 start-page: 468 year: 1995 end-page: 78 article-title: A common variant in the gene for lipoprotein lipase (Asp9 – >Asn). Functional implications and prevalence in normal and hyperlipidemic subjects publication-title: Arterioscler Thromb Vasc Biol – volume: 83 start-page: 89 year: 1990 end-page: 97 article-title: Influence of apo E polymorphism on the response to simvastatin treatment in patients with heterozygous familial hypercholesterolemia publication-title: Atherosclerosis – volume: 103 start-page: 1198 year: 2001 end-page: 205 article-title: Common genetic variation in ABCA1 is associated with altered lipoprotein levels and a modified risk for coronary artery disease publication-title: Circulation – volume: 85 start-page: 37 year: 1992 end-page: 45 article-title: Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study Implications for Treatment publication-title: Circulation – volume: 64 start-page: 269 year: 2000 end-page: 76 article-title: Effect of microsomal triglyceride transfer protein gene variants (‐493G> T, Q95H and H297Q) on plasma lipid levels in healthy middle–aged UK men publication-title: Ann Hum Genet – volume: 129 start-page: 231 year: 1997 end-page: 9 article-title: A comparative study of simvastatin and gemfibrozil in combined hyperlipoproteinemia: prediction response by baseline lipids, apo E genotype, lipoprotein (a) and insulin publication-title: Atherosclerosis – volume: 18 start-page: 69 year: 1998 end-page: 71 article-title: A polymorphism in the regulatory region of apoE associated with risk for Alzheimer’s dementia publication-title: Nat Genet – volume: 31 start-page: 545 year: 1990 end-page: 8 article-title: Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with Hha I publication-title: J Lipid Res – volume: 2 start-page: 113 year: 1992 end-page: 56 article-title: Prevention of coronary heart disease: scientific background and new clinical guidelines. Recommendations of the European Atherosclerosis Society publication-title: Nutr Metab Cardiovasc Dis – volume: 82 start-page: 47J year: 1998 end-page: 51J article-title: Cerivastatin in the treatment of mixed hyperlipidemia: the Right Study publication-title: Am J Cardiol – volume: 10 start-page: 28 year: 1995 end-page: 34 article-title: A lipoprotein lipase mutation (Asn291Ser) is associated with reduced HDL cholesterol levels in premature atherosclerosis publication-title: Nat Genet – volume: 240 start-page: 622 year: 1988 end-page: 30 article-title: Apolipoprotein E. cholesterol transport protein with expanding role in cell biology publication-title: Science – volume: 13 start-page: 1110 year: 1993 end-page: 8 article-title: Stable isotopes show a direct relation between VLDL apoB overproduction and serum triglyceride levels and indicate a metabolically and biochemically coherent basis for familial combined hyperlipidemia publication-title: Arterioscler Thromb – volume: 96 start-page: 733 year: 1997 end-page: 40 article-title: Lipoprotein lipase variants D9N and N291S are associated with increased plasma triglyceride and lower high‐density lipoprotein cholesterol concentrations: studies in the fasting and postprandial states: the European Atherosclerosis Research Studies publication-title: Circulation – volume: 47 start-page: 560 year: 1998 end-page: 5 article-title: Lack of interaction of apolipoprotein E phenotype with the lipoprotein response to lovastatin or gemfibrozil in patients with primary hypercholesterolemia publication-title: Metabolism – ident: e_1_2_6_13_2 doi: 10.1093/nar/16.3.1215 – ident: e_1_2_6_5_2 doi: 10.1161/01.ATV.13.7.1110 – ident: e_1_2_6_26_2 doi: 10.1161/01.ATV.9.3.326 – ident: e_1_2_6_35_2 doi: 10.1016/S0002-9149(98)00036-8 – ident: e_1_2_6_16_2 doi: 10.1161/01.ATV.15.4.468 – ident: e_1_2_6_36_2 doi: 10.1038/ng0198-69 – ident: e_1_2_6_19_2 doi: 10.1016/0021-9150(91)90234-T – ident: e_1_2_6_40_2 doi: 10.1161/01.CIR.103.9.1198 – volume: 107 start-page: 46S year: 1999 ident: e_1_2_6_2_2 article-title: Combined hyperlipidemia as a risk factor for premature atherosclerosis disease publication-title: Am J Med doi: 10.1016/S0002-9343(99)00148-5 – ident: e_1_2_6_20_2 doi: 10.1161/01.CIR.96.3.733 – volume: 8 start-page: 154 year: 1997 ident: e_1_2_6_25_2 article-title: Apolipoprotein C‐III gene variation and dyslipidaemia publication-title: J Lipid Res – ident: e_1_2_6_14_2 doi: 10.1016/S0022-2275(20)43176-1 – ident: e_1_2_6_6_2 doi: 10.1097/00041433-199904000-00005 – ident: e_1_2_6_34_2 doi: 10.1016/S0002-9149(98)00035-6 – ident: e_1_2_6_27_2 doi: 10.1016/S0022-2275(20)39943-0 – ident: e_1_2_6_3_2 doi: 10.1056/NEJM196702022760507 – ident: e_1_2_6_23_2 doi: 10.1016/0026-0495(93)90066-W – ident: e_1_2_6_7_2 doi: 10.1161/01.ATV.17.11.2729 – ident: e_1_2_6_15_2 doi: 10.1016/S0014-5793(97)01543-3 – ident: e_1_2_6_17_2 doi: 10.1038/ng0595-28 – ident: e_1_2_6_32_2 doi: 10.1161/01.CIR.98.19.2088 – ident: e_1_2_6_12_2 doi: 10.1016/S0002-9149(98)00437-8 – ident: e_1_2_6_29_2 doi: 10.1016/0021-9150(90)90134-5 – ident: e_1_2_6_28_2 doi: 10.1093/ajcn/68.6.1215 – ident: e_1_2_6_37_2 doi: 10.1093/hmg/9.1.57 – volume: 344 start-page: 1383 year: 1994 ident: e_1_2_6_9_2 article-title: Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S) publication-title: Lancet – ident: e_1_2_6_8_2 doi: 10.1161/01.CIR.85.6.2025 – ident: e_1_2_6_22_2 doi: 10.1016/0021-9150(94)05439-P – ident: e_1_2_6_30_2 doi: 10.1016/0026-0495(90)90068-N – ident: e_1_2_6_10_2 doi: 10.1161/01.CIR.85.1.37 – ident: e_1_2_6_33_2 doi: 10.1126/science.3283935 – ident: e_1_2_6_38_2 doi: 10.1046/j.1469-1809.2000.6440269.x – volume: 2 start-page: 113 year: 1992 ident: e_1_2_6_11_2 article-title: Prevention of coronary heart disease: scientific background and new clinical guidelines. Recommendations of the European Atherosclerosis Society publication-title: Nutr Metab Cardiovasc Dis – ident: e_1_2_6_21_2 doi: 10.1016/S0021-9150(96)06031-5 – volume: 272 start-page: 1666 year: 1994 ident: e_1_2_6_24_2 article-title: Apolipoprotein E alleles, dyslipidemia, and coronary heart disease publication-title: JAMA doi: 10.1001/jama.1994.03520210050031 – ident: e_1_2_6_18_2 doi: 10.1111/j.1399-0004.1997.tb02488.x – ident: e_1_2_6_4_2 doi: 10.1097/00041433-199806000-00002 – ident: e_1_2_6_31_2 doi: 10.1016/S0026-0495(98)90240-2 – ident: e_1_2_6_39_2 doi: 10.1046/j.1365-2362.2001.00859.x |
| SSID | ssj0008132 |
| Score | 1.7488484 |
| Snippet | Background Combined hyperlipidemia (CHL) is one of the dyslipidemias more frequently found in clinical practice, and lipid‐lowering drugs are often necessary... Background Combined hyperlipidemia (CHL) is one of the dyslipidemias more frequently found in clinical practice, and lipid‐lowering drugs are often necessary... Combined hyperlipidemia (CHL) is one of the dyslipidemias more frequently found in clinical practice, and lipid-lowering drugs are often necessary in its... |
| SourceID | proquest pubmed crossref wiley istex |
| SourceType | Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 421 |
| SubjectTerms | Adult Anticholesteremic Agents - therapeutic use ApoE Apolipoproteins E - genetics Apolipoproteins E - metabolism Atorvastatin bezafibrate Bezafibrate - therapeutic use Cholesterol - blood DNA - analysis Double-Blind Method Female Heptanoic Acids - therapeutic use Humans Hyperlipidemia, Familial Combined - drug therapy Hyperlipidemia, Familial Combined - genetics Hypolipidemic Agents - therapeutic use lipid-lowering drugs Male Middle Aged Polymorphism, Genetic promoter Promoter Regions, Genetic Pyrroles - therapeutic use transcription Triglycerides - blood |
| Title | Allelic polymorphism −491A/T in apo E gene modulates the lipid-lowering response in combined hyperlipidemia treatment |
| URI | https://api.istex.fr/ark:/67375/WNG-T5QMS8C8-8/fulltext.pdf https://onlinelibrary.wiley.com/doi/abs/10.1046%2Fj.1365-2362.2002.00996.x https://www.ncbi.nlm.nih.gov/pubmed/12059987 https://www.proquest.com/docview/199119893 https://www.proquest.com/docview/71812259 |
| Volume | 32 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| journalDatabaseRights | – providerCode: PRVEBS databaseName: Academic Search Ultimate customDbUrl: https://search.ebscohost.com/login.aspx?authtype=ip,shib&custid=s3936755&profile=ehost&defaultdb=asn eissn: 1365-2362 dateEnd: 20241003 omitProxy: true ssIdentifier: ssj0008132 issn: 0014-2972 databaseCode: ABDBF dateStart: 19980101 isFulltext: true titleUrlDefault: https://search.ebscohost.com/direct.asp?db=asn providerName: EBSCOhost – providerCode: PRVWIB databaseName: Wiley Online Library - Core collection (SURFmarket) issn: 0014-2972 databaseCode: DR2 dateStart: 19970101 customDbUrl: isFulltext: true eissn: 1365-2362 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0008132 providerName: Wiley-Blackwell |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZQkRAX3o9QHj4gblmS2I6T42q1pSBtJWArerOc2FGjzSarfUgtJ44cET-xv4QZ51EV9VAhbivtTtZxZuxvMp-_IeQtF0meotBtzGEJ5JKlEFIm82UuuMyEhRwCDwrPjuLDY_7pRJx0_Cc8C9PqQwwv3DAy3HqNAa6ztgtJ4NRte4YWrMCOaTBCsBOPEE-GTLiK7ZdLJakkZK1weMj9KJU9qacrcF57oSs71W2c9LPrYOhVVOu2pYP7ZNHfUMtGWYx222yUf_9L6_H_3PEDcq9Dr3TcuttDcsvWj8idWVeff0zOx1UFf5LTVVOdLxt4huVmSS9-_uZpOH4_p2VN9aqhUwpua-myMdg8zG4ooFBalavSXPz4VWHfNthQ6bql71q0gqFCCm8NPYW8ee1-apelpgNP_gk5PpjOJ4d-19zBzxmkoH5kigLQSwxwxjKRF3GgrWHMRkbyxCTGREkeaimMBsRlgiKKghwS_0xorbMo0Owp2aub2j4nNDBSpwD04lhbLkSmUyEzZmSRs6DgPPCI7B-kyjvlc2zAUSlXged4Wg1nVuHMYl_OSLmZVWceCQfLVav-cQObd85XBgO9XiB7Tgr17eiDmovPs6_JJFGJR_Z7Z1LdwrFRyERDGhvzyJvhW4h4LOPo2ja7jZIIyiBr9ciz1gMvhxah2k4iPSKcH914zGo6-QgfXvyj3T6565rkuJdTL8nedr2zrwCrbbPXLgr_AACEL6g |
| linkProvider | Wiley-Blackwell |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZQKwEXypu0QH1A3LLNw46T42rZsoXuSsBW9GY5sSOiZpPVPqSWE0eOiJ_YX8KMk01V1EOFuEVKJrGdGfsbz-cZQt4wHmcJJrqNGEyBTIQJmJROXZFxJlJuwIfAg8LjSTQ6YR9O-WlbDgjPwjT5IboNN7QMO1-jgeOG9EEblmys3FK0YAq2VIMeop2oB4ByG8N1aKXvPl_lkor9sEkd7jM3SMSG1tOGOG9807W1ahuH_fwmIHod19qF6XCHlJsuNXyUs956lfay739le_xPfX5IHrQAlvYbjXtE7pjqMbk7bkP0T8hFvyzhKxmd1-XFrIbfWCxn9PLnb5b4_YMpLSqq5jUdUtBcQ2e1xvphZkkBiNKymBf68sevEku3wZpKFw2D16AUtBW8eKPpN3CdF_ZRMysU7ajyT8nJ4XA6GLltfQc3C8ELdQOd5wBgIkA0JuRZHnnK6DA0gRYs1rHWQZz5SnCtAHRpLw8CLwPfP-VKqTTwVPiMbFV1ZV4Q6mmhEsB6UaQM4zxVCRdpqEWehV7OmOcQsfmTMmuTn2MNjlLaIDzDA2s4shJHFktzBtKOrDx3iN9JzpsEILeQeWuVpRNQizMk0Akuv07eyyn_NP4SD2IZO2Rvo02ynTuWEsloyGQLHbLf3QWjx0iOqky9XkqBuAwcV4c8b1TwqmkBJtyJhUO4VaRbt1kOB0dwsfuPcvvk3mg6PpbHR5OPe-S-rZlj96pekq3VYm1eAXRbpa-tSf4B90UzxA |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZQK1VceD9CgfqAuGWbTew4Oa6WXVpgVzy2ojfLiR0RbTaJ9iG1nDhyRPzE_hJmnGyqoh4qxC1SMontzNjfeD7PEPKK8SiNMdFtyGAKZCKIwaR04oqUM5FwAz4EHhSeTMOjE_bulJ-2_Cc8C9Pkh-g23NAy7HyNBl7r7LCNSjZGbhlaMANbpkEPwU7YAzy5y0JwthAgfb5MJRX1gyZzeJ-5fiy2rJ42wnntm64sVbs46mfX4dCrsNauS-O7ZL7tUUNHmfc266SXfv8r2eP_6fI9cqeFr3TQ6Nt9csuUD8jepA3QPyTng6KAj6S0rorzRQU_MV8t6MXP3yzuDw5nNC-pqis6oqC3hi4qjdXDzIoCDKVFXuf64sevAgu3wYpKlw1_16AUNBV8eKPpN3Ccl_ZRs8gV7Yjyj8jJeDQbHrltdQc3DcAHdX2dZQBfQsAzJuBpFnrK6CAwvhYs0pHWfpT2leBaAeTSXub7Xgqef8KVUonvqeAx2Smr0jwl1NNCxYD0wlAZxnmiYi6SQIssDbyMMc8hYvsjZdqmPscKHIW0IXiGx9VwZCWOLBbm9KUdWXnmkH4nWTfpP24g89rqSieglnOkzwkuv07fyhn_NPkSDSMZOWR_q0yynTlWEqloyGMLHHLQ3QWTxziOKk21WUmBqAzcVoc8aTTwsmk-ptuJhEO41aMbt1mOhsdw8ewf5Q7I3sc3Y_nhePp-n9y2BXPsRtVzsrNebswLwG3r5KU1yD8iZDJz |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Allelic+polymorphism+-491A%2FT+in+apo+E+gene+modulates+the+lipid-lowering+response+in+combined+hyperlipidemia+treatment&rft.jtitle=European+journal+of+clinical+investigation&rft.au=Garc%C3%ADa-Ot%C3%ADn%2C+A-L&rft.au=Civeira%2C+F&rft.au=Aristegui%2C+R&rft.au=D%C3%ADaz%2C+C&rft.date=2002-06-01&rft.issn=0014-2972&rft.volume=32&rft.issue=6&rft.spage=421&rft_id=info:doi/10.1046%2Fj.1365-2362.2002.00996.x&rft_id=info%3Apmid%2F12059987&rft.externalDocID=12059987 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0014-2972&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0014-2972&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0014-2972&client=summon |