refractory dyslipedimia

Download Refractory dyslipedimia

Post on 03-Jun-2015

371 views

Category:

Health & Medicine

3 download

Embed Size (px)

DESCRIPTION

Guidelines in refractory dyslipidemia treatment

TRANSCRIPT

  • 1. Refractory dyslipoproteinemia Pr dr M A. BADRALEX FAC OF MEDPr Dr M A BADR

2. Six Aims for Improvement Safe avoiding injuries to patients from the care that is intended tohelp them. Effective providing services based on scientific knowledge to allwho could benefit and refraining from providing services to those notlikely to benefit (avoiding underuse and overuse) Patient-centered providing care that is respectful of andresponsive to individual patient preferences, needs and values andensuring that patients values guide all clinical decisions. Timely reducing waits and sometimes harmful delays for boththose who receive and those who give care. Efficient avoiding waste, including waste of equipment, supplies,ideas and energy. Equitable providing care that does not vary in quality because ofpersonal characteristics such as gender, ethnicity, geographiclocation, and socio-economic status. 3. Persistence of Use of Lipid-LoweringMedications A Cross-National StudyJerry Avorn, MD; Johanne Monette, MD, MSc; AnneLacour, PhD; Rhonda L. Bohn, MPH; Mark Monane,MD, MS; Helen Mogun, MS; Jacques LeLorier, MD,PhDJAMA. 1998;279:1458-1462.Context. Although clinical trials havedemonstrated the benefits of lipid-lowering therapy,little is known about how these drugs are prescribedConclusion. In all populations studied, patients who wereprescribed lipid-lowering drug regimens remained withoutfilled prescriptions for over a third of the study year onaverage. Rates of persistence varied substantially with choiceof agent prescribed, comorbidity, and socioeconomic status,despite universal coverage of prescription drug costs. After 5years, abouthalfof the surviving original cohort in theUnited States had stopped using lipid-lowering therapyaltogether. 4. Types and Fields of adherence: (simple or combinations)I- In Medication- total stop ( of one or more medicines)- diminish or exceed dose - change type - interrupted treatment. 5. II- In Dieting - unrestricted (exceed total intake) - errors in caloric distribution , number of meals snacks, skip meals, irregular timing ,etc.- Type: Over- intake of Fat , Sugar, etc (salt) 6. III- In Exercise:basal working sports .IV- In Other Behaviours: ( smoking--alcohol drugs addictions-- contraindicated medications (eg. B Blockers). 7. Grades of Non adherenceUncompliance :- Minor and major- Continuous or interrupted- Single or multiple aspects 8. Diagnostic Approach to Uncompliance A- Patient Factors :1- Psychological state after recent discovery( at stages of denial , revolt , despair .)2- Having wrong concepts and belief ( health locus , cause of illness , distorted information.)3- Nonspecific totalitarian lovers of opposing stand.4- Slaves of their habits ( e.g. smoking , diet, exercise )5- Transient depression from failing to achieve goals .6- Transient stress : social , economic , inter-current illness. 9. B- Inadequate Education at ManagementI- unclear objectives Knowledge :,unsuitable,wrong priorities. Skills : psychomotor , communication and cognitive . Attitudes and Behaviors.II- Inadequate methods :(a) In providing knowledge : - Too much , or unsuitable content in a presentation. - Poor performance at the one-to-one education ( listen,motivate, encourage, etc. ). - In small group education: ( ignorance of group dynamics ) - In large group presentation: ( Inability to ensure active participation of audience.) - In mass media education: (inducing panic and confusion). - Inadequate use of AV- aids ,and education facilities . 10. ( b)In teaching skills, inadequate description--demonstration and exercise . (c) Neglect of attitudes changes through model inspiration (good & bad) , contacts ,discussions. etc.III- Absence of follow-up evaluation: - pre and post testing - follow up records of control parameters and compliance - check lists of performance of skills - rating scales for attitude changes 11. How to help patients manage their dyslipidemia: A primary care physicianpharmacist team intervention Julie Villeneuve, MSc; Diane Lamarre, MSc; Marie-Claude Vanier, MSc; Marie- Thrse Lussier, MD, MSc; Jacques Genest Jr., MD, FRCP(C); Eveline Hudon, MD, MClSc; Lucie Blais, PhD; Sylvie Perreault, PhD; Lyne Lalonde, PhDC P J / R P C S E P T E M B E R / OCTO B E R 2 0 0 7 VOL 1 4 0 , N O 5 12. Training of all team members: An 8-hourworkshop was developed to familiarizepharmacistswith:1. The Canadian dyslipidemia treatmentrecom -mendations and dyslipidemia pharmacotherapy26,272. The physician-pharmacist teaminterventionand the clinical tools3. The monitoring and interpretation oflaboratorytests4. Adherence intervention strategies Technical tools to facilitate adherence Devices , I phone , reminder. 13. Major drugs ineffective for manyHypertension Drugs 10-30%ACE InhibitorsHeart Failure Drugs 15-25%Beta BlockersAnti Depressants 20-50%SSRIs Cholesterol Drugs 30-70% Statins Asthma Drugs 40-70% Beta-2-agonistsSource: Amy Miller, Personalized Medicine Coalition 14. Quantitative medicine is the key to reducing healthcare costs and improvinghealthcare outcomesNon-responders,toxic respondersPatients with same diagnosis Non-toxic responders Misdiagnosed 15. PharmacogenomicsThe study of genome-derived data to predict abodys response to a drug or susceptibility to adisease: Human genetic variation in DNA Single nucleotide polymorphisms (SNPs) Copy number differences Insertions Deletions Duplications Rearrangements RNA and protein expression differences 16. Affymetrix Microarrays 1.28cm50um ~107 oligonucleotides, half Perfectly Match mRNA (PM), half have one Mismatch (MM) Gene expression computed from PM and MM 17. Affymetrix Microarray Raw ImageGene ValueD26528_at193D26561_cds1_at-70D26561_cds2_at 144D26561_cds3_at 33D26579_at318D26598_at1764D26599_at1537D26600_at1204D28114_at707Scannerraw dataenlarged section of raw image 18. SNPs Occur when a single nucleotide (A,T,C,or G) in thegenome sequence is altered, e.g., AAGGCTAA toATGGCTAA Comprise 90% of all human genetic variation Exist every 100 to 300 bases along the 3-billion-basehuman genome Found in both coding (i.e., gene) and noncoding regionsof the genome. Usually have no effect on cell function, but some couldpredispose people to disease or influence their responseto a drug 19. The influence of SLCO1B1 (OATP1B1)genepolymorphisms on response to statintherapySPR Romaine1, KM Bailey1,AS Hall2 and AJ Balmforth11Division of Cardiovascular and DiabetesResearch, Leeds Institute of Genetics, Health andTherapeutics, University of Leeds, Leeds, UK and2Multidisciplinary Cardiovascular ResearchCentre (MCRC), Leeds Institute of Genetics,Health and Therapeutics, University of Leeds,Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) arewell established in the treatment of hypercholesterolaemia and theprevention of coronary artery disease. 20. SNPhepatocytes and recent interest has focused on genetic variation in hepaticinflux and efflux transporters for their potential to explain these differences.In this review we explore current literature regarding the pharmacokineticand pharmacodynamic influence of the common c.388A4G and c.521T4Csingle-nucleotide polymorphisms (SNPs) within the solute carrier organicanion transporter 1B1 (SLCO1B1) gene, encoding the organic aniontransporter polypeptide 1B1 (OATP1B1) influx transporter. We discuss theirpotential to predict the efficacy of statin therapy and the likelihood thatpatients will experience adverse effects.The Pharmacogenomics Journal (2010) 21. An association study of 43SNPs in 16 candidategenes with atorvastatinresponse ABSTRACT Variation in individual response to statin therapy has been widely studied for a potential genetic component. Multiple genes have been identified as potential modulators of statin response, but few study findings have replicated.The Pharmacogenomics Journal (2005) 5,352358& 2005 Nature Publishing Group All rightsreserved 1470-269X/05 $30.00www.nature.com/tpj 22. Pharmacogenomics blames thepatient, NOT the drugs Treatment failure Toxicity Adverse events 23. Dont blame my genes!!! Make a good drug New paradigm of research should focuson molecular targets Drug structure Focus on lifestyle changes Therapeutic drug monitoring Patient counseling, error reporting Increase healthcare availability first 24. What are effective medication combinations for dyslipidemia?JosephSaseen,PharmD,FCCP;ElizabethTweed ,BSN,MLIS University of Colorado at Denver and Health Sciences 25. LDL - HYPERCHOLEST TARGET VALUES NOT STATIN ACHIEVED NOTCOMBINATION WITHTOLERATEDEZETIMIBE TARGETACHIEVED AND TOLERATEDEZETEMIBEADDITITIONALBILE ACID BINDINGBILE ACID BINDING RESINLDL-APHERESIS FIBRATE/ CADNIACIN 26. HYPERTRIGLICEREDEMIALIFE STYLE MODIFICATION SECONDARY CAUSES; ALCOHOL,DIABETES,OBESITY FIBRATE TARGET VALUES NOT ACHIEVEDTARGETVALUESNOT ACHIEVEDTOLERATED AND WELLTOLERATED CONSIDER STATIN COMBINATIONWITH NIACINNIACIN 27. COMBINED HYPERLIPOPROT LIFE STYLE MODIFICATION STATIN POSIBLE COMBINATIONSTATIN WITH NICOTINIC TARGET NOT ACHIEVED FIBRATE WITHG NICOTINIC FIBRATEFIBRATE WITH EZETIMIBEANDSTATIN WITH FIBRATE 28. Lp(a) hyperlipoproteinemiaOPTIMIZE CARDIOVASCULAR RISK FACTORS ATHEROSCLEROSISNOATHEROSCLEROSIS STATIN COMBINATION STATINWITH NIACIN CAD WORSEN CONSIDERAPHERESIS 29. DIABETIC DYSLIPOPROTEINEMIAGLUCOSE CONTROL ISOLATEDCOMBINED HLPHYPERTRIGLYCERIDEMIA LDL-HYPERCHOLEST STATIN FIBRATE TARGET NOT ACHIEVEDINCREASESTATIN + STATIN + STATIN+STATIN EZETEMIBENIACIN fibrate 30. Apheresis What can transfusion medicine offer topatients with hypercholesterolemia?Recent advances in affinity columntechnology now enable the efficientremoval of LDL-cholesterol directly fromthe bloodstream by apheresis. This newtherapeutic tool may reduce the risk ofprogressive atherosclerotic disease inhypercholesterolemic patients who areresistant to diet and drugs 31. Non-HDL Cholesterol(Non-HDL Chol =