Cov yam ntxwv ntawm kev kho mob ntawm dyslipidemia hauv cov neeg mob uas muaj hom 2 mob ntshav qab zib mellitus Cov ntawv ntawm ib tsab xov xwm scientific hauv txoj kev tshwj xeeb - Tshuaj thiab Kev Noj Qab Haus Huv

Ntawm hom 2 mob ntshav qab zib mellitus, yoo mov hyperglycemia thiab tom qab cov zaub mov thauj khoom tsis xav tias qhov kev pheej hmoo ywj pheej rau tus mob plawv, tab sis cov nyhuv ntawm dyslipidemia ntawm kev pheej hmoo ntawm mob plawv mob ntshav hauv cov qauv ntawm kev pheej hmoo tseem ceeb rau tus thawj.

Raws li kev tshawb fawb thib 3 hauv Lub Tebchaws Kev Noj Qab Haus Huv thiab Khoom Noj Hauv Tebchaws Asmeskas, 69% ntawm cov neeg mob ntshav qab zib muaj lipid metabolism tsis txaus (V.

Muaj cov pov thawj ntawm kev nce ntxiv hauv platelet sib sau thaum raug cov glycated LDL.

Cov nyhuv ntawm hyperglycemia ntawm atherogenesis nyob rau hauv lub vascular phab ntsa tau paub los ntawm kev txhim kho kev lag luam dav dav vaus endothelial kev ua haujlwm tsis txaus ntseeg thiab muaj qhov nce ntxiv ntawm oxidative kev nyuaj siab (F Cerielo li al., 1997). Cov tsos ntawm cov nyhuv ntawm kev nplaum ntawm cov ntshav monocytes mus rau vascular endothelium yog ib qho ua rau lub hauv paus loj ntawm kev txhim kho atherosclerotic txhab ntawm lub vascular phab ntsa. Cov laj thawj tseem ceeb rau kev nce hauv monocyte-endothelial kev sib txuam hauv cov ntshav qab zib hom 2 yog oxidative kev nyuaj siab thiab qhov nce ntxiv ntawm qhov kev xav ntawm cov khoom kawg metabcated metabolic. Kev nce qib ntawm lipid peroxidation tej zaum yuav tsis yog qhov ua rau, tab sis ib qho kev xav txog ntawm kev muaj micro- thiab macroangiopathies.

Vim muaj ntau cov txiaj ntsig ntawm dyslipidemia mus rau kev tsim cov micro- thiab macroangiopathies hauv cov ntshav qab zib mellitus, cov kws tshaj lij ntawm European Diabetes Policy Group hauv 1998 tau npaj cov kev pheej hmoo rau kev txhim kho cov hlab plawv hauv cov neeg mob uas muaj hom 2 mob ntshav qab zib nyob ntawm seb muaj ntshav qab zib dyslipidemia (Cov Lus 5).

Cov kev sib raug zoo ntawm qib ntawm dyslipoproteinemia nyob rau hauv cov neeg mob uas muaj ntshav qab zib hom 2 thiab kev pheej hmoo ntawm kev tsim mob plawv.

Lub Koom Haum American Kab Mob Ntshav Qab Zib rau cov neeg mob ntshav qab zib, tab sis tsis muaj kev soj ntsuam kev mob ntshav siab ntawm txoj hlab ntshav atherosclerosis, sib luag rau cov neeg mob mob txhim kho cov hlab ntshav txhaws txog cov kev pheej hmoo ntawm cov mob plawv.

Cov ntawv sau ntawm cov haujlwm scientific hauv lub ntsiab lus "Cov yam ntxwv ntawm kev kho mob ntawm dyslipidemia hauv cov neeg mob uas muaj ntshav qab zib hom 2"

S.A. URAZGILDEEVA 1 3, MD, O.F. MALYGINA 2, Ph.D.

1 Lub Chaw Tshawb Fawb Txog Kev Tshawb Fawb - Kev Tshawb Nrhiav thiab Kev Kawm “Cardiology”, Kws Qhia Txog Tshuaj, Tsev Kawm Hauv Nroog St. Petersburg

2 North-West State Medical University. I.I. Mechnikov, St. Petersburg

3 Lub Chaw Rau Atherosclerosis thiab Lipid Qhov Tsis Zoo ntawm Lub Tsev Kho Mob Tsev Qeb Qib No. 122 muaj npe tom qab L.G. Sokolova, St. Petersburg

FEATURES KEV KHO MOB DYSLIPIDEMIA

HAUV QAIB Nrog 2 HOM DIABETES MELLITUS

Kev soj ntsuam yog mob siab rau cov yam ntxwv ntawm kev kuaj mob thiab kev kho mob ntawm dyslipidemia rau cov neeg mob uas muaj ntshav qab zib hom 2 mob ntshav txhaws txhawm rau tiv thaiv kev mob plawv mob hnyav.

phiaj lipid qib

kev nyab xeeb ntawm kev kho lipid-txo qis

Mob Ntshav Qab Zib mellitus (DM) yog ib qho muaj mob ntsig txog kev noj qab haus huv uas tau coj mus rau xyoo XXI. kev kis tau zoo thoob qhov txhia chaw. Raws li International Diabetes Federation hais li cas, qhov tshwm sim ntawm tus kabmob no hauv ntiaj teb thaum xyoo 2015 tau txog 415 lab tus tib neeg. Thaum xyoo 2040, kev nce ntxiv ntawm cov neeg mob mus rau 682 lab yog qhov kev cia siab, uas yog, tus kabmob no tuaj yeem kuaj sai sai rau txhua tus neeg thib kaum hauv lub ntiaj teb. Yog li, ntshav qab zib tiag ua rau qhov kev txhim kho muaj sia nyob ntev ntawm tib neeg. Qhov teeb meem no hauv Russia rov hais dua thoob ntiaj teb. Yog li, raws li lub Xeev Chaw Tso Npe ntawm Cov Neeg Mob Ntshav Qab Zib, Lub Ib Hlis 2015 muaj kwv yees li ntawm 4.1 lab tus neeg hauv Lavxias thiab ntau dua 90% ntawm lawv muaj mob ntshav qab zib hom 2 - 3.7 lab. Tib lub sijhawm, cov txiaj ntsig ntawm kev tswj hwm thiab kev tshawb fawb kis mob FSBI "Lub Chaw Tshawb Nrhiav Kev Tshawb Nrhiav Endocrinological" ntawm Lub Chaw Haujlwm Saib Xyuas Kev Noj Qab Haus Huv ntawm Lavxias lub sijhawm nyob rau xyoo 2002 txog 2010, tau qhia tias cov naj npawb tseeb ntawm cov neeg mob ntshav qab zib nyob rau hauv Lavxias yog 3-4 zaug ntau dua li sau npe thiab nce mus txog 9-10 lab tus neeg, uas yog kwv yees li 7% ntawm cov pejxeem. Raws li International Diabetes Federation, nyob hauv tebchaws Russia muaj txog 12,1 lab tus neeg mob ntshav qab zib thiab peb lub teb chaw nyob rau theem thib tsib uas hais txog cov kabmob no, uas tau tawm hauv Tuam Tshoj, Is Nrias teb, Tebchaws Asmeskas thiab Brazil uantej. Tus naj npawb ntawm cov vascular muaj teeb meem ntawm cov ntshav qab zib, uas yog ib qho tseem ceeb ua rau kev tsis taus thiab kev tuag ntawm cov neeg mob, tseem nce ntxiv.

KEV SAWV DAWS NTAU YAM DAWB LOS THIAB CARDIOVASCULAR Kev Puas Tsuaj

Chronic hyperglycemia hauv ntshav qab zib yog nrog kev puas tsuaj thiab kev ua haujlwm ntawm ntau yam plab hnyuv siab raum thiab cov ntaub so ntswg (tshwj xeeb tshaj yog lub qhov muag, ob lub raum thiab cov leeg), vim muaj kev hloov pauv dav hauv microvasculature lossis microangiopathy. Cov micro thiab macroangiopathies ua rau cov kab mob hauv lub plawv tuag ntau hauv cov neeg mob ntshav qab zib hom 2, uas yog li 4-5 npaug ntawm cov ntsuas no hauv cov pej xeem. 80% ntawm kev tuag ntawm cov neeg mob uas muaj ntshav qab zib hom 2 cuam tshuam nrog kev mob tshwm sim ntawm atherosclerosis, thiab% ntawm lawv tshwm sim los ntawm kab mob plawv coronary (CHD). Ntau tshaj li 75% ntawm tsev kho mob ntawm cov neeg mob ntshav qab zib kuj tseem cuam tshuam nrog kev ua kom pom tseeb ntawm atherosclerosis ntawm ib lossis lwm qhov chaw hauv zos. Yog li, 50-70% ntawm tag nrho cov tsis muaj mob ntawm cov qis qis yog suav nrog cov neeg mob ntshav qab zib.

Micro thiab macroangiopathies ua rau cov neeg mob ntshav siab tuag rau hauv cov neeg mob ntshav qab zib hom 2 ntau dua, uas yog li 4-5 npaug ntawm cov cim no rau cov pej xeem

Qee tus endocrinologist xav txog atherosclerosis ua rau mob ntshav qab zib vim muaj cov txiaj ntsig tsis zoo ntawm hyperglycemia thiab caj ces ntawm cov vascular system. Los ntawm kev sib piv nrog microvascular cov teeb meem: mob ntshav qab zib retinopathy thiab nephropathy - atherosclerosis tseem hu ua macrovascular tsis meej. Tib lub sijhawm, nws pom tseeb rau cov kws kho plawv hais tias atherosclerosis hauv cov neeg mob ntshav qab zib hom 2 yog tus kab mob ywj siab, thaum ntshav qab zib ua ib qho tseem ceeb txaus ntshai tshaj plaws rau kev txhim kho atherosclerosis. Yog li, kev tshawb fawb loj tshaj plaws, INTRHEART, ua rau xyoo 2000-2004, pom tias ntshav qab zib yog qhov tseem ceeb thib peb rau kev loj hlob ntawm tus mob myocardial infarction (AMI) hauv cov muaj hnub nyoog nruab nrab

tom qab kev ua txhaum ntawm lipid metabolism thiab haus luam yeeb, txawm tias ua ntej ntawm txoj hlab ntshav siab.

Nws tseem paub tias tus mob ntshav qab zib ua rau muaj kev phom sij ntau dua ntawm qhov tshwm sim ntawm txoj kev mob plawv thiab ua rau muaj kev pheej hmoo loj thiab tuag ntawm kev txhim kho mob caj dab. IHD hauv cov neeg mob ntshav qab zib muaj cov yam ntxwv ntws uas paub txog ntawm tus kws qhia. Angina pectoris yog ntau lub sijhawm atypical, thiab txawm tias ib qho kev ua txhaum loj ntawm txoj hlab ntshav cov ntshav khiav tsis tuaj yeem nrog mob. Qee qhov xwm txheej, txawm tias AMI tuaj yeem tsis muaj kev mob dab tsi thiab kuaj tau tsuas yog thaum kuaj ECG. Cov chav kawm ntawm AMI tau pom los ntawm kev ua haujlwm qeeb hauv txoj kev kho, uas tuaj yeem ua rau lub pob taws ntawm lub pob zeb laug rov qab ua haujlwm ntau dua li ntawm cov tib neeg uas muaj cov piam thaj hauv lub cev. Ntxiv rau, kev mob plawv dhia tsis xwm yeem thiab cov tsos mob ntawm cov mob plawv tsis zoo tau sau tseg, cov chav kawm uas ua rau mob ntshav qab zib mob microangiopathy mob heev dua.

Raws li kev tshawb nrhiav qhov tseeb ntawm 11 T1MI cov chaw kuaj mob sim ua xyoo 1997 txog 2006 qhia, ntawm 62 txhiab tus neeg mob, 17.1% ntawm cov neeg mob tau mob ntshav qab zib. Rau cov neeg mob no, 30-hnub lub hnub tuag yog 8.5% nrog kev txhim kho ntawm AMI nrog kev nce ntawm BT ntu thiab 2.1% nrog AMI tsis muaj qhov nce ntawm BT ntu, uas yog kwv yees li 2 zaug ntau dua li ntawd hauv cov neeg mob AMI uas tsis muaj ntshav qab zib. Cov kws sau ntawv tshaj tawm xav txog qhov tseeb tseem ceeb hauv kev txiav txim siab kev tswj hwm ntawm cov neeg mob uas xav tau tshaj plaws, txawm tias "kev txhoj puab heev", suav nrog kev txo qis lipid. Coronary angiography feem ntau qhia cov xwm txheej distal ntawm cov hlab ntsha txoj hlab ntshav, uas ua rau nws nyuaj ua rau kev phais mob ntawm myocardium. Cov neeg mob no tseem tau pom los ntawm cov kev mob txhab atherosclerotic ntau ntawm cov leeg vascular, nrog rau cov leeg mob ntshav, nrog cov leeg voos aneurysms thiab lwj ntawm cov quav hniav nrog kev tsim ntawm thrombosis. Nws yuav tsum raug sau tseg tias cov txheej txheem atherosclerotic hauv ntshav qab zib muaj ntau dua li thaum ntxov rau cov tib neeg uas tsis muaj tus kab mob no. Qhov tseeb ntawm qhov muaj ntau cov teeb meem lipid metabolism hauv cov neeg mob ntshav qab zib ua lub luag haujlwm tseem ceeb hauv qhov no.

Cov yam ntxwv ntawm dyslipidemia nyob hauv ntshav qab zib mellitus

Ua raws li lub ntsiab lus txhais ntawm tus kabmob uas tau hais rau hauv kev teeb tsa ntawm kev kho mob tshwj xeeb rau cov neeg mob ntshav qab zib mellitus, ntshav qab zib yog ib pawg ntawm cov kab mob metabolic (metabolic) uas muaj cov kev mob tshwm sim los ntawm kev mob siab, uas yog los ntawm kev ua txhaum ntawm insulin secretion, insulin action, lossis ob yam ntawm cov xwm txheej no. Yog lawm, lub luag haujlwm tseem ceeb ntawm insulin hauv tib neeg lub cev yog los xyuas kom nkag mus ntawm cov piam thaj mus rau hauv lub hlwb thiab nws txoj kev siv los ua lub hauv paus ntawm lub zog ceev. Txawm li cas los xij, cov tshuaj hormone insulin muaj ntau qhov pom dav

kev ua, cuam tshuam rau lwm hom kev sib pauv. Tshaj li cov tshuaj insulin, uas tshwm sim dhau los ntawm kev muaj peev xwm tiv thaiv cov tshuaj insulin hauv cov neeg mob ntshav qab zib hom 2, ua rau muaj kev txhim kho ntawm ntau cov teebmeem uas tuaj yeem xav tias atherogenic. Insulin ntau dhau lawm ua rau cov nplaum muaj peev xwm ntawm monocytes, txhawb kev nthuav dav ntawm HMC cov hlab ntsha, ua rau endothelial kawg thiab kev ua haujlwm hauv platelet thiab platelet loj hlob tau.

Ntau zaus, muaj ntshav qab zib hom 2, mob ntshav qab zib (DLP) muaj, uas yog theem ob hauv qhov. Qee qhov xwm txheej, kev kuaj pom ntawm xws li DLP yuav dhau ua ntej ntawm kev tshawb pom ntawm cov khoom noj carbohydrate metabolism thiab ua lub hauv paus rau kev kuaj ntshav qabzib.

Kev Tshawb Fawb. INTRHEART pom tias cov ntshav qab zib yog qhov tseem ceeb thib peb rau kev loj hlob ntawm tus mob myocardial infarction hauv cov txiv neej nruab nrab tom qab lipid metabolism thiab haus luam yeeb, txawm tias ua ntej nws.

Cov yam ntxwv tseem ceeb ntawm DLP hauv cov ntshav qab zib hom 2 yog qhov nce ntxiv ntawm cov qib triglycerides (TG) nyob rau hauv cov lus sib xyaw ntawm cov lipoproteins tsawg heev (VLDL) thiab qhov txo qis hauv theem ntawm high lipoprotein cholesterol (HDL cholesterol).

Raws li qhov ua rau kev loj hlob ntawm hypertriglyceridemia (GTG) nyob rau hauv hom 2 mob ntshav qab zib, qhov tsis tshua muaj kev cuam tshuam ntawm visceral adipose cov ntaub so ntswg los tiv thaiv cov kab mob ntawm cov tshuaj insulin tuaj yeem raug hu, uas ua rau muaj lipolysis ntau ntxiv, qhov kev nkag ntawm ntau ntawm cov roj ntsha dawb mus rau hauv cov ntshav portal thiab, vim li ntawd, nce cov synthesis ntawm TG thiab VLDL los ntawm daim siab. Tsis tas li ntawd, nrog hyperglycemia, qhov kev ua ntawm endothelial lipoprotein lipase (LPL), uas yog lub luag haujlwm rau catabolism ntawm TG thiab VLDL, raug txo qis, uas ua rau kev ua txhaum ntau dua no. Qhov kev txo qis hauv HDL cov roj (cholesterol) hauv ntshav qab zib hom 2 yog vim muaj qhov ua haujlwm ntawm Hepatic LPL ntau dua thiab muaj HDL catabolism nrawm dua. Qhov kev sib txuam ntawm cov roj (cholesterol) hauv cov lipoproteins tsawg (LDL) hauv cov neeg mob ntshav qab zib feem ntau tsis nce ntxiv, txawm li cas los xij, ntau tus neeg mob tau kuaj nrog kev sib xyaw lossis sib xyaw DLP, tshwj xeeb tshaj yog tias ntshav qab zib tsim tawm tsam ntawm keeb kwm ntawm thawj DLP, tiv thaiv kev ua ntej. Tib lub sijhawm, txawm tias muaj ntshav LDL tsawg, cov neeg mob ntshav qab zib hom 2 yog tus yam ntxwv los ntawm qhov feem tsawg ntawm cov ntshav tsawg LDL nrog atherogenicity vim lawv muaj peev xwm oxidize thiab glycosylate. Nyob rau hauv lem, glycosylation thiab oxidation ntawm HDL ua rau txo qis hauv lawv cov antiatherogenic cov yam ntxwv. Kev loj hlob ntawm cov ntshav qab zib nephropathy nyob rau hauv cov neeg mob ua rau hnyav dua qhov uas twb muaj lawm nce qib TG thiab qhov kev txo qis hauv qib roj HDL. Qhov kev hloov ntawm cov roj lipid muaj peev xwm tshwm sim nyob rau hauv kev cais tawm, tab sis feem ntau lawv tau sib xyaw ua ke thiab hu ua tus mob ntshav qab zib lipid triad 6, 7.

Kev kuaj ntshav kuaj ntshav kuaj ntshav qab zib DLP tuaj yeem yog qhov kev paub tsis txaus yog tias txiav txim siab ncaj qha txog qib ntshav roj LDL tsis ua. Cov tshuaj muaj txiaj ntsig zoo thiab siv Friedwald rau suav cov qib ntshav roj LDL yuav siv tsis tau rau cov neeg mob ntshav qab zib, vim tias qib siab TG thiab cov ntsiab lus tsawg ntawm HDL cov roj cholesterol ua rau muaj qhov cuam tshuam loj heev ntawm qhov tshwm sim. Thaum TG theem ntawm b ntawm 4.5 mmol / L, kev suav ntawm qib theem ntawm LDL cov roj cholesterol siv cov mis no tsis raug. Kev txiav txim siab ncaj qha ntawm cov qib roj cholesterol LDL tuaj yeem ua kom deb ntawm txhua lub chaw soj nstuam. Raws li cov lus pom zoo los ntawm EAB 2011 thiab NOA / RKO 2012, nws raug pom zoo tias cov neeg uas muaj TG qib £ 2.3 mmol / l txiav txim siab txog qib roj (cholesterol) uas tsis cuam tshuam nrog HDL (roj-tsis-HDL). Qhov ntsuas no tau muab xam yooj yim heev - los ntawm cov qib ntawm cov roj (cholesterol) tag nrho, nws yog qhov yuav tsum tau rho cov qib HDL roj 8, 9.

Cov yam ntxwv tseem ceeb ntawm DLP

mob ntshav qab zib hom 2 yog ib qib nce ntxiv

triglycerides, lipoproteins

tsis tshua muaj neeg ntom ntom thiab txo qib

cov roj lipoprotein ntau heev

Hauv tshwj xeeb lipid lub chaw soj nstuam, nws muaj peev xwm txiav txim siab ntxiv cov yam ntxwv ntawm cov kab mob ntshav qab zib DLP thiab kev pabcuam raws li cov qauv muaj tseeb dua thiab thaum ntxov rau cov ntshav atherogenicity ntawm cov ntshav: cov ntsiab lus ntawm me me ntawm LDL thiab apoV protein. Qee zaum ua cov kev ntsuas no tso cai rau koj los txiav txim siab txog qhov yuav tsum tau kho tshuaj DLP, txawm hais tias cov neeg mob ntshav qab zib hom 2 feem ntau yog cov neeg mob ntshav siab (SS), uas yuav tsum muaj kev kho lipid-txo qis.

HOM 2 DIABETES PATIENTS - PATIENTS A HIGH HUV CARDIOVASCULAR Kev pheej hmoo

Kev ntsuas ntawm qhov kev pheej hmoo ntawm pawg CC yog qhov tseem ceeb tshaj plaws rau kev txhim kho kev tswj hwm tus neeg mob zoo tshaj plaws thiab kev teem sijhawm kho kom tsim nyog uas tuaj yeem tswj hwm qhov qib siab ntawm LDL cov roj (cholesterol) zoo. Raws li cov kev cai ntawm kev pom zoo ESC / EASD pom zoo rau cov ntshav qab zib, ntshav qab zib thiab CVD, tau coj los siv rau xyoo 2014, cov neeg mob ntshav qab zib yuav tsum raug suav hais tias yog ib pawg muaj kev pheej hmoo siab thiab muaj feem yuav muaj mob CC-mob ntau dua: cov neeg mob ntshav qab zib thiab tsawg kawg yog ib qho kev pheej hmoo rau SS cov kab mob lossis kev puas tsuaj rau lub hom phiaj plab hnyuv siab raum yuav tsum raug xam tias yog pawg muaj kev pheej hmoo siab heev, thiab tag nrho lwm cov neeg mob ntshav qab zib ua pawg muaj kev pheej hmoo siab. Cov neeg mob uas muaj mob ntshav qab zib hom 2 lossis hom 1 uas muaj kev puas tsuaj rau lub hom phiaj kabmob thiab microalbuminuria kuj tseem raug cais tias muaj CC-pheej hmoo ntau heev raws li cov lus pom zoo rau kev txhim kho ntawm dyslipidemia NLA / RKO 2012 thiab EAS 2011 ., nrog rau cov neeg mob uas muaj mob rau txoj hlab ntshav liab thiab / lossis mob hlab ntshav hlab plawv atherosclerosis, mob hlab ntsha tawg, nrog rau cov mob raum tsis txaus lossis mob hnyav, nrog rau cov neeg mob uas muaj 10 xyoo muaj CC-kev tuag yog SCORE £ 10% (Cov Lus 1). Nyob rau tib lub sijhawm, txoj kev pheej hmoo ntawm kev tsim kab mob CC-muaj mob rau cov neeg mob ntshav qab zib muaj ntau dua li cov neeg tsis muaj tus kabmob no, thiab cov poj niam nws muaj 5 zaug ntau dua, hauv cov txiv neej 3 zaug 8, 9. Yog li, yog tias qhov kev pheej hmoo ntawm kev tuag yuav raug ntsuas raws li SCORE nplai, , piv txwv, hauv 5%, rau cov poj niam thiab tus txiv neej mob ntshav qab zib nws yog 25 thiab 15%, raws li, i.e., cov neeg mob zoo li no tuaj yeem muab cais ua qhov kev pheej hmoo siab heev ntawm CC-teeb meem.

FEATURES NTAWM HYPOLIPIDEMIC COV TSHUAJ NTAWM COV PATIENTS NROG HOM 2 DIABETES MELLITUS

Cov lus 1. Cov phiaj xwm theem qis ntawm cov roj lipoprotein tsawg (roj cholesterol) rau cov neeg mob ntawm ntau cov hlab plawv (CV) muaj kev pheej hmoo 8, 9

SS-phom sij qeb Cov phom sij ntawm qib LDL cov roj (cholesterol), mmol / l

Kev pheej hmoo siab heev a) cov neeg mob uas muaj IHD thiab / lossis peripheral arterial atherosclerosis, ischemic stroke, paub tseeb los ntawm kev kuaj mob b) cov neeg mob kev txom nyem los ntawm hom 2 lossis hom 1 mob ntshav qab zib nrog kev puas tsuaj rau lub hom phiaj kabmob thiab nrog microalbuminuria c) cov neeg mob uas muaj mob nyhav lossis mob hnyav Kuv nrhiav tsis tau yam koj xav tau? Sim cov ntawv nyeem kev pabcuam xaiv.

Kev pheej hmoo siab a) qhov nce siab hauv ib qho ntawm cov teeb meem pheej hmoo, piv txwv li, HCS hnyav lossis siab AH b) nrog qhov kev pheej hmoo SCORE - ¿5% thiab kuv nrhiav tsis pom qhov koj xav tau? Sim cov ntawv nyeem kev pabcuam xaiv.

ASPEN 505 Atorvastatin 10 mg / placebo 18%

CARE 586 Pravastatin 40 mg / placebo 25% (p = 0.05)

LIPID 1077 Pravastatin 40 mg / placebo 21 °% (p Kuv nrhiav tsis pom dab tsi koj xav tau? Sim cov ntawv xaiv kev pab.

lawv cov txiaj ntsig tseem ceeb yog qhov txo qis hauv qib TG los ntawm 20-50%, cov ntsiab lus ntawm cov roj (cholesterol) tag nrho thiab LDL cov roj (cholesterol) yog txo los ntawm 10-25% raws li kev ua haujlwm ntawm fibrates. Nws yuav tsum raug sau tseg tias raws li kev kho mob nrog fibrates, muaj qhov nce ntxiv ntawm HDL cov cholesterol (los ntawm 10-25%).Ntxiv nrog rau qhov lipid-txo cov nyhuv nws tus kheej, fibrates, hauv fenofibrate tshwj xeeb, muaj cov nyhuv thaiv ntxiv thiab txo qis uric acid hauv cov ntshav. Hauv ib qho ntawm cov kev tshawb fawb thawj zaug ntawm cov tshuaj ntawm cov chav kawm ntawm fibrates, hemphibrozil, HHS, 135 cov neeg mob uas muaj ntshav qab zib hom 2 koom nrog. Hauv cov pawg kho mob nquag, tus naj npawb ntawm SS cov xwm txheej yog 60% tsawg dua ntawm pawg placebo, tab sis vim yog cov qauv me me, qhov sib txawv tsis yog qhov tseem ceeb. Kev tshawb fawb VA-HIT suav nrog cov neeg mob qog roj ntshav LDL ntau, 769 cov neeg mob muaj ntshav qab zib hom 2, uas kwv yees li ib feem peb ntawm tag nrho cov neeg mob (2,531 tus neeg). Hauv cov pab pawg no, qhov sib txawv ntawm tus naj npawb ntawm SS cov sib txawv ntawm cov neeg tau txais gemfibrozil thiab cov placebo yog 24% thiab nws muaj kev xav paub tseeb (p = 0.05).

Kev tshawb nrhiav FIELD thiab ACCORD nrog fenofibrate tau lees paub qhov tseeb tias qhov txo qis ntawm kev pheej hmoo ntawm CC qhov teebmeem tuaj yeem xav tau tsuas yog hauv cov pab pawg ntawm cov neeg uas muaj THG loj thiab cov roj HDL tsawg. Lawv tau pom tias cov ntshav qab zib tsis txaus ua ob qho tib si- thiab kab mob ntshav qab zib. Piv txwv, hauv qhov kev tshawb nrhiav FIELD, muaj qhov tseem ceeb (79%) txo qis ntawm qhov ua tiav ntawm kev rov qab kho qhov muag ntawm retina hauv pab pawg nquag kho mob, thiab qhov kev xav tau rau laser coagulation tsawg dua 37%. Cov kev hloov zoo sib xws tau pom nyob rau hauv cov kab mob ntshav qab zib thiab neuropathy. Txoj kev pheej hmoo ntawm kev mob ntshav qab zib nephropathy poob qis dua 18%, thiab kev nce qib ntawm cov proteinuria los ntawm 14%. Nyob hauv kev cuam tshuam ntawm fenofibrate txoj kev kho, qhov ntau zaus ntawm kev mob siab vim tias tsis mob vim qhov mob ko taw poob qis los ntawm 47%. Nws yuav tsum raug sau tseg tias qhov txo qis ntawm txhua zaus ntawm txhua qhov mob microvascular mob ntshav qab zib tau pom tsis hais txog kev tswj glycemic, ntshav siab lossis qib lipid profile. Lub tshuab ntawm cov nyhuv no tuaj yeem yog vim muaj cov khoom los tiv thaiv thiab antioxidant ntawm fenofibrate thiab xav tau kev kawm ntxiv. Yog li, kev siv cov fibrates, nrog rau kev siv cov tshuaj statins, yog tsim nyog hauv kev kho mob ntawm DLP hauv cov neeg mob ntshav qab zib hom 2.

Nyob rau theem TG tsis tshaj li 4.5 mmol / L, ib qho tshuaj yeeb tshuaj statin yog tshuaj yog thawj qhov kev xaiv tshuaj, thiab thaum tswj hwm THG tshaj (saum toj dua 2.3 mmol / L), tshuaj thib ob, fenofibrate, tau ntxiv rau txoj kev kho. Yog tias theem ntawm TG ntau dua li 4.5 mmol / l, kev tswj hwm tib lub sijhawm ntawm statin thiab fenofibrate 17, 18 tej zaum yuav raug txiav txim siab.Yog li ntawd, kev siv tshuaj lipid-txo qis ua rau cov lus cog tseg rau qee tus kws kho mob hais txog kev saib xyuas tsis tu ncua ntawm kev nyab xeeb ntawm kev kho. Thaum statin thiab fibrate tau siv ua ke, tswj hwm ntawm creatine phosphokinase kev ua si

(CPK) yog ua txhua txhua 3 lub hlis. thawj xyoo ntawm kev kho, tsis hais seb tus neeg mob puas muaj kev tsis txaus siab ntawm cov leeg mob thiab tsis muaj zog. Thiab raws li txhua txhua 6 lub hlis. saib xyuas kev ua haujlwm ntawm alanine aminotransferase (ALT) thiab qib creatinine. Hauv qhov no, kuv xav nco ntsoov tias kev ua haujlwm ntawm ALT thiab CPK yuav tsum raug ntsuas ua ntej pib kev kho lipid-txo qis, uas, txawm li cas los xij, yeej muaj tseeb rau txhua tus neeg mob, tsis yog tsuas yog cov neeg mob ntshav qab zib. Tsis tas li ntawd, nws yuav tsum nco ntsoov tias kev sib xyaw ua ke ntawm gemfibrosil nrog rau cov statins txwv tsis pub vim tias muaj kev pheej hmoo siab ntawm kev phiv tshuaj vim lub peculiarities ntawm pharmacokinetics ntawm cov tshuaj no 8, 9.

Cov txheej txheem los kho cov kev kho mob tshwj xeeb rau cov neeg mob ntshav qab zib tso tshuaj statins rau cov neeg mob ntshav qab zib hom 1 thiab ntshav qab zib hom 2 nyob rau qhov muaj kev pheej hmoo siab heev lossis yog tias cov hom phiaj ntawm LDL thiab TG cov cholesterol tsis ua tiav.

Xav txog qhov tsis tseem ceeb ntawm kev kho lipid-txo qis kev kho mob txhawm rau txo qhov kev pheej hmoo ntawm SS cov xwm txheej hauv cov neeg mob ntshav qab zib hom 2, Kuv xav nco ntsoov qhov tseeb tias kev sim ntau ntawm cov kev sim tau pom qhov tseem ceeb ntawm

glycemic tswj hauv kev txo qis kev pheej hmoo ntawm kev mob vascular hloov mus rau hauv pawg no ntawm cov neeg mob 19, 20, 21.

Cov neeg mob uas muaj hom 2 mob ntshav qab zib mellitus feem ntau yuav tsum tau cais raws li cov kab mob plawv heev.

Kev mob ntshav siab (Dyslipidemia) hauv cov neeg mob ntshav qab zib muaj nws tus yam ntxwv: qib triglycerides ntau ntawm cov roj HDL cholesterol, ntxiv rau cov ntsiab lus ntawm cov roj ntshav tsawg LDL.

Raws li lub hom phiaj hauv kev kho mob ntawm dyslipidemia nyob rau hauv cov neeg mob uas muaj hom 2 mob ntshav qab zib mellitus, ntxiv rau theem ntawm LDL cov cholesterol, cov zaub mov tsis yog HDL-C yuav siv tau.

Lub chav kawm tseem ceeb ntawm cov tshuaj pom zoo rau siv rau cov neeg mob hom 2 mob ntshav qab zib mellitus yog statins, feem ntau yog atorvastatin thiab sawv-vastatin.

Ntxiv rau cov statins, ib qho ezetimibe cholesterol absorption inhibitor tuaj yeem siv, thiab fenofibrate kuj yuav siv los txo qis triglycerides thiab tiv thaiv microvascular cov teeb meem hauv cov neeg mob uas muaj ntshav qab zib hom 2. f

1. IDF Ntshav Qab Zib Atlas, 7 zaug, 2015. http // www. ntshav qab zibatlas.org/resources/2015-atlas.html.

2. Cov lus pom zoo hauv chaw kho mob: “Cov txheej txheem rau kev kho mob tshwj xeeb rau cov neeg mob ntshav qab zib mellitus”, 7th tsab, 2015, kho los ntawm II. Dedova, M.V. 6-kovoy.

3. Yusuf S, Hawken S, Ounpuu S li al. INTERHEART Kev Soj Ntsuam Tub Tshawb Fawb. Kev cuam tshuam ntawm cov kev hloov pauv uas muaj feem cuam tshuam nrog myocardial infarction nyob rau hauv 52 coutries (Txoj Kev Kawm INTERHEART): kev kawm tshawb xyuas cov ntaub ntawv. Lancet, 2004, 364 (9438): 937-952.

4. Donahoe SM, Atewart GC, McCabe CY li al. Mob ntshav qab zib thiab lub neej tuag tom qab mob ntshav sib luag. LAMA, 2007, 298 (7): 765-775.

5. Krasilnikova E.I., Pav Siab Y. V., Shlyakhto E.V. Lub luag haujlwm ntawm cov tshuaj insulin hauv kev txhim kho atherosclerosis. Hauv phau ntawv. Atherosclerosis Cov teeb meem ntawm pathogenesis thiab kev kho mob. SPb. Xyoo 2006: 137-163.

6. Glinkina I.V. Kev kho mob lipid metabolism hauv cov ntshav qab zib hom 2. Tus kws kho mob tuaj koom, 2002, 6: 6-8.

7. Sniderman AD, Lamarche B, Tilley J et al. Hypertriglyceridemic hyperapoB hauv ntshav qab zib hom 2. Cov Kab Mob Ntshav Qab Zib, 2002, 25 (3): 579-582.

8. ESC / EAS Cov Lus Qhia rau kev tswj hwm ntawm dyslipidemias. Pab Pawg Ua Haujlwm rau kev tswj hwm ntawm dyslipidemias ntawm European Society of Cardiology (ESC) thiab European

Atherosclerosis Society (EAS). Atherosclerosis. 2011, 217: S1-S44.

9. Kev kuaj mob thiab kho cov lipid metabolism tsis haum rau kev tiv thaiv thiab kho atherosclerosis Cov lus pom zoo los ntawm Lavxias (V kho dua). Atherosclerosis thiab dyslipidemia, 2012, 4.

10. Pom zoo rau cov ntshav qab zib, mob ntshav qab zib thiab mob plawv. Cov European Society of Cardiology (ESC) Kev Ntshav Qab Zib, Kab Mob Ntshav Qab Zib thiab Cov Kab Mob Ntshav Qab Zib Ua Haujlwm Pab Pawg koom tes nrog European Lub Koom Haum rau Kev Tshawb Fawb Ntshav Qab Zib (EASD). Lavxias Phau Ntawv Journal of Cardiology, 2014, 3 (107): 7-61.

11. Kwiterovich PO. Dyslipidemia hauv Cov Pab Pawg Tshwj Xeeb. Dyslipidemia, 2010: 124.

12.2013 ACC / AHA cov lus qhia txog kev kho mob ntshav siab txhawm rau txo kev mob plawv atherosclerotic rau cov neeg mob ntshav siab: cov lus ceeb toom ntawm American College of Cardiology / American Heart Association Task Force ntawm Cov Qauv Qhia. Kev ncig ncig, 2014, 129, 25 (Cov Khoom Siv 2): 1-45.

13. Jones PH, Davidson MH, Stein EA li al. Kev sib piv ntawm kev ua tau zoo thiab kev nyab xeeb ntawm rosuv-astatin tiv thaiv atorvastatin, simvastin thiab pravastatin hla cov koob tshuaj (sim STELLAR). Amer. J. Cardiol., 2003, 92 (2): 152-160.

14. Urazgildeeva S.A. Kev kho mob hypolipidemic hauv kev xyaum ntawm tus kws kho mob dav dav rau tus neeg mob sab nrauv. Cov lus qhia kho mob hauv tsev kho mob. 2013, 6: 56-64.

15. Warraich HL, Wong ND, Rana JS. Lub luag haujlwm rau kev sib txuam ua ke hauv kev kho mob ntshav qab zib dyslipidemia. Cib. Cardiol. Rep, 2015, 17 (5): 32.

16. Keech A, Simes RJ, Pauv P et al. Qhov muaj txiaj ntsig ntawm kev kho fenofibrate mus sij hawm ntev rau cov kev mob plawv hauv 9795 cov neeg uas muaj hom ntshav qab zib hom mellitus 2 (txoj kev tshawb no FIELD): kev sim mus tshuaj. Lancet, 2005, 366 (9500): 1849-1861.

17. Lub Tsev P, Mant, Diaz J, Turner C. Pawg Neeg Qhia Kev Txhim Kho. Kev tswj cov ntshav qab zib hom 2: cov ntsiab lus ntawm NICE cov lus qhia tshiab. BMJ, 2008, 336 (7656): 1306-1308.

18. Hom 2 mob ntshav qab zib rau cov laus: kev tswj hwm. NICE cov lus qhia luam tawm: 2 Hlis ntuj nqeg 2015. zoo. org.uk/guidance/ng28.

19. UK Qhov Yuav Tsim Muaj Kev Mob Ntshav Qab Zib (UKPDS) Pawg. Kev tswj ntshav khov-tso ntshav qab zib ntau nrog sulphonylure-as lossis insulin piv nrog kev kho mob niaj hnub thiab muaj kev pheej hmoo rau cov neeg mob ntshav qab zib 2 (UKPDS). Lancet, 1998, 352 (9178): 837-853.

20. Khaw KT, Wareham N li al. Koom Haum Hemoglobin A1C nrog cov kab mob plawv thiab kev tuag hauv cov neeg laus: European Kev Tuaj Saib Xyuas Kev Nyab Xeeb mus rau Cancer hauv Norfolk. Ann. Cuv. Med, 2004, 141 (6): 413-420.

21. Hardy DS, Hoelscher DM, Aragaki C et al., Koom Tes ntawm glycemic Performance index thiab glycemic load nrog kev pheej hmoo ntawm incidentcoronary mob plawv ntawm Cov Neeg Dawb thiab African Asmeskas nrog thiab tsis muaj mob ntshav qab zib hom 2: Atherosclerosis Risk hauv zej zog Kev Tshawb Fawb. Ann. Epidemiol., 2010, 20 (8): 610-616.

HMG-COA reductase inhibitors (statins)

Hauv chav kawm, cov tshuaj no feem ntau ua siab ntev thiab ua tau zoo tshaj plaws hauv kev txo qis ntawm LDL cov roj cholesterol, thiab yog li niaj hnub no lawv tau nrov tshaj plaws hauv kev kho mob hyperlipidemia.
Lovastatin, simvastatin thiab pravastatin yog cov tshuaj tiv thaiv ntawm cov hu ua fungi lossis derivatives ntawm cov metabolites no. Thaum fluvastatin, atorvastatin thiab rosuvastatin muaj cov tshuaj yeeb yam zoo tag nrho. Lovastatin thiab simvastatin yog "cov tshuaj", vim tias lawv pib muaj cov tshuaj yeeb tshuaj tsuas yog tom qab muaj hydrolysis nyob hauv lub siab. Cov tshuaj uas tseem nyob ntawd twb raug tswj fwm nyob hauv daim foos lawm.
Mechanism ntawm kev ua. HMG-CoA reductase inhibitors, txwv tsis pub cov enzyme tseem ceeb ntawm cov roj (synthesis), HMG-CoA reductase, kuj ua rau txo qis ntawm Apo B100 uas muaj lipoproteins thiab txhawb nqa LDL receptors. Raws li qhov tshwm sim, cov ntsiab lus ntshav ntawm LDL cov roj cholesterol thiab VLDL triglycerides poob qis, tshwj xeeb tshaj yog rau cov neeg mob ntshav qab zib hom 2.
Cov Tshuaj Pharmacokinetics Txoj hnyuv nqus ntawm cov tshuaj no txawv ntawm 30% (atorvastatin) txog rau 90% (fluvastatin). Txhua yam statins yog metabolized hauv daim siab hauv 50% (pravastatin) - 79% (simvastatin). Statins yog cov muaj feem ntau hauv cov protein khi daim ntawv (> 80%), tshwj tsis yog pravastatin, uas cov protein khi yog tsawg dua 50%. Lovastatin, simvastatin thiab atorvastatin yog metabolized hauv cytochrome P450 system los ntawm CYP3A4 enzyme, thiab fluvastatin thiab rosuvastatin yog cov substrates rau CYP2C29 enzyme, txawm hais tias rosuvastatin raug cais tawm feem ntau tsis hloov. Pravastatin tshem tawm tau tshwm sim los ntawm sulfonation thiab dhau los ntawm daim siab-tso ntshav organic anionic protein, uas yog lub luag haujlwm rau kev ntes cov statins los ntawm cov ncig ncig. Daim nplooj siab yog lub vev xaib tseem ceeb rau kev tshem tawm statins. Qhov tsis pom qhov zoo los ntawm lub raum yog yam ntxwv tsuas yog siv rau pravastatin, tab sis nrog lub raum tsis ua haujlwm, qib ntawm pravastatin hauv cov ntshav tsis nce ntxiv, vim nws muaj qib siab ntawm kev tshem tawm hauv lub siab. Qib ntawm lovastatin thiab rosuvastatin nce ntxiv hauv cov neeg mob uremic. Txij li qhov qis qis qis tshaj tawm yog qhov pom ntawm atorvastatin (70 mg%.

Qhov phiv loj ntawm statins yog myositis, uas tsis tshua muaj kev txhim kho.

1 kis / 2000 tus neeg mob. Txawm hais tias statins tsis yog rau cov tshuaj hepatotoxic, qhov kev kuaj mob hepatic nce tuaj yeem tiv thaiv lawv cov keeb kwm yav dhau los, thiab yog li, daim siab kev ua haujlwm yuav tsum tau kuaj ua ntej los kho cov statins. Statins tsis cuam tshuam rau cov metabolism hauv carbohydrate.
Statins yog contraindicated thaum cev xeeb tub thiab pub niam mis. Hauv cov neeg laus, kev kho mob yuav tsum tau nqa tawm pib nrog cov koob tshuaj tsawg kawg nkaus, txij li nws ua tau kom muaj kev nkag siab ntau ntxiv rau lawv.
Sab sij huam. Cov kev mob tshwm sim feem ntau suav nrog arthralgia, dyspepsia, cem quav, thiab mob plab. Cov neeg mob tsis tshua muaj mob myopathy thiab rhabdomyolysis, uas tau nrog cov mob leeg loj heev tau piav qhia. Tsis tshua muaj, kab mob hepatotoxicity pom thaum kho statin.

Sequestrants ntawm cov kua tsib kua qaub

Cov kab uas muaj cov kua tsib hauv cov hnyuv cov kua tsib kua qaub, uas yog hu ua cov kab mob kua tsib kua qaub (SCFA), ua rau muaj qhov LDL-C tsawg dua 15-30% thiab tib lub sijhawm ua rau muaj kev cuam tshuam ntawm HDL. SCFAs tuaj yeem ntxiv cov triglycerides. Lub American Diabetes Association tau lees paub SCFA ua kev kho mob tseem ceeb rau dyslipidemia hauv cov neeg mob ntshav qab zib mellitus, thiab lawv cov txiaj ntsig HDL-txo qis yog synergistic nrog HMG-CoA reductase inhibitors (statins) thaum siv ua ke. Cov tshuaj ntawm no series Colesevelam tseem ua tau zoo txo ​​qib HbAlc hauv T2DM - 0.5% ntau dua cov placebo. Hauv qhov no, Lub Ib Hlis 2008, lub log tau lees paub los ntawm FDA raws li lwm cov tshuaj tiv thaiv kab mob ntshav.
Mechanism ntawm kev ua. SKHK khi cov kua tsib kua tsib hauv cov hnyuv, thaiv lawv qhov kev nqus. Kev txo qis hauv kev ua kom tiav ntawm cov kua tsib yog cov txhawb cov kab mob hepatic enzyme 7-alpha-hydroxylase, uas yog lub luag haujlwm rau kev hloov pauv ntawm cov roj cholesterol mus rau cov kua tsib. Kev nce ntxiv hauv kev hloov pauv cov roj cholesterol mus rau hauv cov kua tsib yog cov tshuaj tua kab mob, cuam tshuam, LDL receptors, uas ua rau kom qhov kev tshem ntawm LDL ntau los ntawm cov ntshav. Raws li qhov tshwm sim, SCFA txo tag nrho cov roj cholesterol, LDL, apolipoprotein B thiab nce qhov nce siab ntawm HDL-C. Cov kev ua haujlwm uas ua rau kev txo qis glycemia nyob rau hauv kev cuam tshuam ntawm SCFA tseem tsis tau paub.
Cov Tshuaj Pharmacokinetics SKHK tau nqus mus rau qhov tsawg kawg nkaus thiab qhia lawv cov nyhuv ntawm theem hnyuv. Cov nyhuv ua kom zoo li nyob ntawm cov neeg cov roj (cholesterol) txo qis thiab tshwm sim tom qab ob peb lub lis piam.
Kev sib cuam tshuam txog yeeb tshuaj. SKHK cuam tshuam rau kev nqus thiab qhov kev nqus ntawm kev nqus ntawm ntau cov tshuaj, suav nrog sulfonamides, anticonvulsants, antiarrhythmic thiab tshuaj tiv thaiv qhov ncauj. Txawm li cas los xij, yog tias cov tshuaj muaj "nqaim kev kho mob", nws yuav tsum tau noj 4 teev ua ntej noj SCFA lossis 4 teev tom qab noj SCFA.
Kho cov kev ua tau zoo, qhov muaj yeej thiab tshwm sim. SKHK yog siv los tshem tawm hypercholesterolemia, tab sis txij li lawv tuaj yeem ua rau nce triglycerides, qhov ntsuas no ntawm cov rog metabolism yuav tsum tau soj ntsuam ntxiv. Rau tib qho laj thawj, SCLC yuav tsum tsis txhob raug rau cov neeg mob uas muaj hyper-triglyceridemia uas twb muaj lawm. Vim tias qhov tshwm sim ntawm kev quav tawv ntawm cov neeg mob uas tau txais SCFA, qhov tshwm sim no tuaj yeem yog qhov teeb meem tshwj xeeb rau cov neeg mob ntshav qab zib. Vim yog cov txiaj ntsig cov txiaj ntsig hypoglycemic, nws zoo dua rau Wheelworms sau cia hom ntshav qab zib 2. Lub sijhawm tsis dhau sijhawm - zam kev noj nrog sulfonamides thiab lwm yam tshuaj, saib lub sijhawm ib nrab ua ntej thiab 6 teev tomqab noj tshuaj SCFA, tuaj yeem muaj teebmeem rau ntau.
Cov kev phiv loj ntawm SCFA yog cem quav thiab dyspepsia. Kuj pom muaj tus mob myalgia, pancreatitis, mob ntshav siab los ntawm hemorrhoids, tsam plab thiab ua rau lub siab enzymes nce siab.
Cov sib txuam thiab cov kev txwv. SKHK yog contraindicated nyob rau hauv cov neeg mob nrog pob zeb hauv lub zais plab, nrog txoj kev ua kom tiav biliary lossis lub plab zom mov, thiab tshwj xeeb yuav tsum tau noj rau cov neeg mob uas nce triglycerides hauv cov ntshav.

Fibric acid derivatives (fenofibrate thiab heme-fibrosyl) yog PPAR alpha agonists thiab muaj lub suab tshaj tawm rau lipid metabolism, txo kev pheej hmoo ntawm cov xwm txheej plawv. Lawv raug pom zoo rau kev kho mob ntawm dyslipidemia hauv cov neeg mob ntshav qab zib mellitus. Feem ntau, hauv cov neeg mob ntshav qab zib, fibrates txo cov roj triglycerides los ntawm 35-50%, LDL-C los ntawm 5-20% thiab nce HDL-C los ntawm 10-20%. Fenofibrate suav hais tias yog ib qho kev xaiv tseem ceeb rau kev kho ntshav siab LDL-C hauv cov neeg mob ntshav qab zib nyob rau hauv cov neeg mob ntshav qab zib tsis muaj peev xwm muab lub hom phiaj lipid thiab muaj cov teebmeem synergistic thaum siv nrog statins.


Mechanism ntawm kev ua. Los ntawm kev ua kom tiav PPAR-a, fibrates hloov lipid metabolism raws li hauv qab no:

  • nce lipoprotein lipase synthesis,
  • nce cov synthesis ntawm apo A-I thiab apo A-P, uas yog cov protein HDL tseem ceeb,
  • nce cov synthesis ntawm ABC-A1, uas pab txhawb cov khiav ntawm cov roj cholesterol kom apo A-1 hauv cov txheej txheem ntawm HDL biogenesis,
  • txo apo A-C, tshuaj tiv thaiv lipoprotein lipase thiab nce apo A-V, cov synthesis uas txo cov qib lipoproteins nplua nuj hauv TG,
  • txo cov kev qhia txog qhov tseem ceeb muaj feem ua rau cov roj cholesterol (Nieman-Xaiv C1-nyiam 1).

Ntxiv rau cov txiaj ntsig saum toj no, fi-kwv tij esters txo qis mob hepatic lipogenesis los ntawm khi rau hepatic X receptor (PCR), inhibiting PCR-mediated lipogenesis. Ntxiv mus, ntxiv rau kev cuam tshuam cov lipid metabolism, fibrates tuaj yeem muaj cov nyhuv antiatherogenic los ntawm cov haujlwm hauv qab no:

  • fenofibrate txo qib C-reactive protein, interleukin 6 thiab lipoprotein cuam tshuam phospholipase A2, peb qhov cim ntawm o,
  • fenofibrate txo qis kev ua haujlwm ntawm matrix hlau protease thiab tuaj yeem txhim kho platelet stability,
  • fenofibrate, tab sis tej zaum tsis yog lwm yam kev tsim nyog ntawm phibric acid, txhawb cov synthesis ntawm vascular endothelial N0 synthetase,
  • fibrinic acid derivatives txwv tsis pub nce ntxiv ntawm hom 1 plasminogen activator inhibitor uas muaj kev cuam tshuam los ntawm insulin, uas txhim kho kev ua haujlwm fibrinolytic hauv T2DM, uas yog pom los ntawm hyperinsulinemia.

Fenofibrate ua tau zoo dua li gemfibrozil, txo cov ntshav ntawm LDL-C hauv cov neeg mob uas muaj qhov pib nce qib ntawm LDL thiab txo cov ntshav uas muaj roj cholesterol tsis suav nrog HDL-C hauv cov neeg mob hypertriglyceridemia. Fenofibrate tej zaum yuav muaj txiaj ntsig zoo hauv kev txo qis LDL ntau ntau hauv cov neeg mob uas tsis tshua muaj TG thaum statins, nicotinic acid, thiab SCFA tau pom tias tsis muaj txiaj ntsig. Fenofibrate txo qis qib uric acid, nce ntxiv kev nthuav dav ntawm ura-tov.
Kev cuam tshuam nrog lwm yam tshuaj. Feem ntau, fibrates yuav tsum tau siv nrog ceev faj nrog statins, vim qhov no ua rau muaj kev pheej hmoo ntawm myopathy thiab rhabdo-myolysis. Txij li cov fibrates tau khi zoo rau albumin, lawv txhim kho cov nyhuv ntawm warfarin.
Kho cov kev ua tau zoo, qhov muaj yeej thiab tshwm sim. Kev soj ntsuam kev ua tau zoo ntawm cov fibrates tau kawm txog ntau qhov kev tshawb fawb. Raws li cov ntaub ntawv tau hauv lawv, cov lus pom hauv qab no tuaj yeem kos tau:

  • kev txheeb xyuas yav dhau los ntawm NNT cov ntaub ntawv (Helsinky Lub Siab Rov Sib Ntsib, gemfibrozil) tau pom tias qhov zoo tshaj plaws rau gemfibrozil yog nyob rau hauv cov pab pawg muaj kev pheej hmoo siab: leej twg muaj tib lub sij hawm coefficient siab heev ntawm cov cholesterol-LDL / cholesterol-HDL (> 5) thiab TG qib> 200 mg%. Hauv pab pawg no ua rau muaj 71% txo rau qhov kev pheej hmoo ntawm PRS,
  • hauv VA-HIT txoj kev tshawb (Veteran Affears HDL Intertin Trial), tib lub sijhawm, cov txiaj ntsig zoo ntawm gemfibrozil tau qhia rau cov qib sib txawv ntawm cov tsis hnov ​​lus carbohydrate metabolism - los ntawm qhov tsis hnov ​​qab lub siab mus rau mob ntshav qab zib,
  • nyob rau hauv kev kawm txog DIAS (Kev Ntshav Qab Zib Aterosclerosis Kev Kawm Txog Kev Mob Ntshav Qab Zib) fenofibrate rau cov neeg mob uas muaj ntshav qab zib hom 2 ua rau muaj kev loj hlob qeeb ntawm atherosclerosis, uas tau pom tias ua li angiographically,

Raws li cov ntaub ntawv tau txais, kev muaj peev xwm ntawm kev kho cov neeg mob ntshav qab zib hom 2 nrog cov fibrates yog suav tias yog cov khoom pov thawj. Niaj hnub no, ntshav qab zib ntshav qab zib yog thawj txoj kev xaiv. Fibrates yuav tsum yog kws kho rau cov neeg mob uas tsis zam kev noj haus statins, lossis ib feem ntawm kev sib koom tes kho mob hauv cov neeg mob uas muaj kev sib xyaw nrog hyperlipidemia nrog rau LDL-C kom ntau. Ntxiv mus, hauv kev sib xyaw, qhov zoo dua ntawm cov fibrates yog muab rau fenofibrate.
Fibrates (tshwj xeeb tshaj yog fenofibrate) kuj tseem siv tau los txo qis LDL hauv cov neeg mob uas muaj TG qib qis heev, tab sis rau lub hom phiaj no, kev nyiam yog muab rau cov tshuaj ntawm lwm cov chav kawm - statins, nicotinic acid thiab SCFA.
Yuav kom ua tiav cov txiaj ntsig siab, kev kho mob nrog fibrates txog li 3-6 lub hlis yog xav tau.
Txij li thaum fibrates nce qhov kev pheej hmoo ntawm kev tsim cholelithiasis, lawv yuav tsum tsis txhob raug rau cov neeg mob ntshav qab zib nrog lub cev tsis muaj peev xwm ntawm lub plab me vim tias mob ntshav qab zib autonomic neuropathy.
Fibrates raug tshem tawm feem ntau los ntawm lub raum, thiab yog li ntawd tshwj xeeb yuav tsum tau them rau qib ntawm kev muaj mob hauv cov neeg mob ntshav qab zib nephropathy, zoo li hauv cov neeg laus laus. Fibrates tsis yog tshuaj rau cov poj niam cev xeeb tub thiab thaum lactation.
Kev mob plab zom mov yog cov kev mob tshwm sim ntau tshaj plaws ntawm kev kho mob fibrate thiab suav nrog dyspepsia, xeev siab, ntuav, cem quav lossis zawv plab, mob plab thiab nce roj. Hauv 2-3% ntawm cov neeg mob, qhov tawv nqaij tshwm sim. Cov kev mob tshwm sim los ntawm cov leeg hlwb, xws li kiv taub hau, tsaug zog, tsis pom kev, npau taws rau lub cev, kev nyuaj siab, mob libido, thiab mob erectile kawg, txhim kho nrog kev kho nrog gemfibrozil.


NICOTIC ACID (Niacin)

Niacin (niacin, nicotinamide) yog tshuaj vitamin (B3, PP) thiab tau siv coj los kho hyperlipidemia rau 50 xyoo dhau los. Hauv kev txhaj tshuaj loj, ua kom ntau tshaj qhov kev xav tau nyob rau txhua hnub, niacin txo qis ntshav ntshav ntawm VLDL thiab LDL, ntawm ib sab tes, thiab nce qib HDL, ntawm lwm qhov. Qhov no tsuas yog cov tshuaj gi-polypidemic uas txo qis qib ntawm lipoprotein (a). Txawm li cas los xij, ntau cov kev mob tshwm sim ua rau siv tsis yooj yim.
Niacin raug pom zoo ua thawj kab kev kho mob rau hypertriglyceridemia thiab / lossis LDL-C uas muaj qib HDL-C tsawg. Hauv qhov no, niacin tuaj yeem ua ke nrog statins, SCFA lossis ezetimibe.
Mechanism ntawm kev ua. Niacin cuam tshuam cov metabolism hauv apo-lipoprotein B (apo B-muaj lipoproteins), ib yam li HDL. Los ntawm kev ua GPR109A receptor hauv adipocyte, niacin ua rau txo qis hauv cAMP, uas rov ua rau txo qis qib ntawm cov tshuaj hormones-rhiab lipase hauv adipose nqaij. Raws li qhov tshwm sim, qhov hydrolysis ntawm TG thiab kev ua kom rog ntawm fatty acids los ntawm adipose nqaij raug txo. Qhov no txo ​​qhov kev nqus ntawm cov roj ntsha dawb (FFAs) rau hauv lub siab, uas yog qhov chaw tseem ceeb rau kev tsim TG hauv LDL. Tsis tas li ntawd, niacin txo qis qib TG los ntawm kev txwv cov kev ua ntawm digricerol acyl transferase 2, qhov tseem ceeb enzyme hauv triglyceride synthesis.
Nco ntsoov tias beta-hydroxybutyrate yog lub ntuj tso rau hauv GPR109A, thiab yog li ua haujlwm ntawm GPR109A tsub kom lub cev tiv thaiv kab mob rau kev txhim kho ketoacidosis.
Cov nyhuv ntawm apo B-muaj lipoproteins yog kho kom haum xeeb los ntawm qhov kev nqis tes ntawm nicotinic acid ntawm qhov sib txuas ntawm VLDL hluavtaws. Niacin txo lub siab ua haujlwm ntawm VLDL, uas cuam tshuam nrog kev txo qis ntawm cov dej ntws ntawm FFA los ntawm cov nqaij mos adipose mus rau lub siab. Tsis tas li ntawd, niacin inhibits kev coj ua ke ntawm TG thiab ua rau kev cuam tshuam ntawm intracellular apo B hauv hepatocytes. Hauv cov kev tshawb fawb soj ntsuam, qhov kev txo VLDL ntau dua tau raug pom tsuas yog thaum yoo mov TG txo. Vim tias LDL yog qhov sib xyaw ua ke ntawm VLDL, yog li ntawd, qhov txo qis hauv VLDL ntxiv nrog kev txo qis hauv LDL hauv cov ntshav.
Tsis tas li ntawd, dhau ntawm prostaglandin-mediated mechanism, nicotinic acid ua rau kom muaj zog ntawm cov nplaim macrophage receptor CD36, uas koom nrog hauv oxidation ntawm LDL.
Niacin nce qib HDL-C kom ntau dua li lwm cov tshuaj lipid-hloov kho, thiab qhov no yog vim qhov txo qis hauv HDL tshem tawm, uas, nyeg, yuav yog qhov tshwm sim ntawm kev txo qis hauv TG hauv cov ntshav.
Niacin txhawb kev ua ke ntawm ABC-A1, qhov kev hloov pauv tseem ceeb ntawm cov theem thaum ntxov ntawm kev thim rov qab cov roj tsheb thauj khoom.
Yog li niacin:

  • inhibits kev tso tawm ntawm FFA los ntawm cov nqaij mos adipose,
  • nce kev ua si ntawm lipoprotein lipase,
  • txo triglyceride synthesis,
  • txo cov thauj ntawm triglycerides ntawm VLDL,
  • inhibits lipolysis.

Cov Tshuaj Pharmacokinetics Niacin tau nrawm thiab nrawm rau hauv lub plab thiab txoj hnyuv me. Qhov siab tshaj plaws nyob rau hauv cov ntshav yog pom 45 feeb tom qab kev tswj hwm, thiab lub sijhawm ntev - 4-5 teev tom qab kev tswj hwm. Vasodilation tshwm sim li 20 feeb tom qab noj cov tsis muaj qhov niacin thiab ntev txog li ib teev. Txog 12% ntawm niacin raug nthuav tawm tsis hloov pauv ntawm cov zis, tab sis yog tias cov koob tshuaj ntau dua 1000 mg / hnub, cov txheej txheem metabolic ntawm niacin nyob rau hauv lub cev yog saturated thiab nws tau tawm hauv cov zis hauv qhov loj dua. Niacin sau ntau nyob rau hauv daim siab, tus po thiab adipose nqaij.
Kev sib cuam tshuam txog yeeb tshuaj. Rhabdo-myolysis tsis tshua muaj kev loj hlob thaum niacin raug coj nrog statins. Txij li thaum niacin cuam tshuam nrog SCFA, lub sijhawm nruab nrab ntawm niacin thiab SCFA yuav tsum 1 teev ua ntej thiab 4-6 teev tom qab noj SCFA. Txij li thaum niacin dilates cov hlab ntsha, nws tuaj yeem ua rau muaj qhov muaj txiaj ntsig hypotensive ntawm cov tshuaj uas nthuav cov hlab ntsha - nitrates thiab calcium channel blockers.

Tshuaj, koob tshuaj thiab kho mob tshaj
NICOTINAMIDE (NICOTINAMIDE) - qhov koob tshuaj thawj zaug yog 100 mg 2 zaug ib hnub, nrog rau txhua lub lim piam nce ntawm 100 mg, kom txog rau thaum cov koob tau nce mus txog 500 mg 2 zaug hauv ib hnub. Tom ntej no, cov koob tshuaj yog titrated rau 500 mg kom tau txais txiaj ntsig kho hom phiaj. Cov koob tshuaj tuaj yeem ncav 4 g / hnub, tab sis feem ntau 1500 mg / hnub txaus. kom tshem tawm cov hypertriglyceridemia. Yog tias muaj qhov tshaj tawm txog daim tawv nqaij, tom qab 1 teev ua ntej noj niacin, tshuaj aspirin raug txhaj tshuaj tsawg kawg.
Kev ua haujlwm ntev niacin muaj nyob hauv ntsiav tshuaj ntawm 500, 750 thiab 1000 mg. Thawj koob tshuaj yog 500 mg, uas nce 500 mg rau txhua 4 asthiv. Cov tshuaj txij nkawm yog 1-2 g nyob rau ib hnub. Qhov ntau yog 2 g / hnub.

Cov chaw kho mob ua tau. Hauv koob tshuaj 3-4 g ib hnub, nicotinic acid cuam tshuam rau theem ntawm lipoproteins raws li hauv qab no:

  • txo cov theem ntawm LDL-C los ntawm 20-30%,
  • txo cov theem ntawm TG los ntawm 20-50%,
  • nce qib ntawm HDL-C los ntawm 25-50%,
  • txo qis lipoprotein (a) los ntawm 30%.

Hais txog kev soj ntsuam kev ua tau zoo, txiav txim siab los ntawm qhov thiaj li xaus kev pom zoo coj los ntsuam xyuas atherosclerosis, nicotinic acid txo:

  • tag nrho cov neeg tuag
  • hlab plawv thaum tuag,
  • qhov ntau zaus ntawm nonfatal myocardial infarction.

Sab sij huam, contraindications. Txog li 30% ntawm cov neeg mob tsis tuaj yeem thev niacin vim nws cov kev mob tshwm sim: liab liab, dryness, ichthyosis thiab khaus ntawm daim tawv nqaij, dub acanthosis, mob plab, mob plab peptic, kab mob siab, mob plab, nce uric acid, gout, insulin tsis kam, hyperglycemia, hypotension thiab tsis nco qab (tsis yog feem ntau), atrial arrhythmia (tsis paub txog), thiab lom amblyopia (tsis tshua muaj).
Cov tawv nqaij liab yuav txo tau los ntawm kev noj cov tshuaj me me ntawm cov tshuaj aspirin lossis lwm yam tshuaj tiv thaiv prostaglandin (ibuprofen 200 mg), uas tau sau ntawv 30 feeb ua ntej niacin. Cov kev mob tshwm sim tuaj yeem txo qis yog tias kev kho mob pib nrog kev txhaj tshuaj tsawg kawg, cov tshuaj no tau noj nrog zaub mov, tab sis tsis nrog haus dej. Tsis tas li ntawd, nws raug nquahu kom pib kho nrog cov tsis muaj tshuaj ntev thiab hloov mus rau qhov ntev ntev tsuas yog tias qhov liab liab ua tsis tau thiab tsis tuaj yeem tshem tawm los ntawm kev noj tshuaj prostaglandin inhibitor. Tawm tsam keeb kwm ntawm kev kho mob nrog lub sijhawm ntev ntawm nicotinic acid, qhov pib ntawm liab yog qhov tsis paub tseeb, ntau zaus muaj mob plab lossis mob siab.
Cov neeg mob uas muaj cov kab mob ua rau lub cev tsis mob carbohydrate thaum ntxov (yoo mov hyperglycemia, NTG) tej zaum yuav muaj ntshav qab zib mellitus thaum kho mob niacin, thiab cov neeg mob ntshav qab zib muaj peev xwm xav tau ntau dua ntawm cov tshuaj muaj suab thaj, txawm hais tias HbAlc tsis nce ntxiv. Ntxiv mus, kev nce ntxiv hauv glycemia tsis cuam tshuam rau qhov txo qis hauv zaus ntawm kev mob plawv hauv qab ntawm niacin.
Niacin yog contraindicated rau hauv cov neeg mob uas tseem ceeb lossis tsis tau hais txog kev ua haujlwm ntawm lub siab ua haujlwm, mob plab peptic, thaum cev xeeb tub thiab lactation, mus txog 16 xyoo thiab nrog lub raum tsis ua haujlwm.


OMEGA-3 TSEEB ACIDS

Cov tshuaj ntawm cov chav kawm no muaj cov saw ntev omega-3 fatty acids (EFAs) - eicosopentaenoic acid (EPA) thiab docosahexaenoic acid (DHA) - thiab yog siv los txo hypertriglyceridemia. Txawm li cas los xij, lawv cov txiaj ntsig zoo tsis txwv rau qhov tshwm sim nyob rau theem ntawm triglycerides, thiab nws tau tsim tau hais tias lawv muaj cov nyhuv los tiv thaiv atherogenic thiab txo cov kev pheej hmoo ntawm kev txhim kho mob plawv thiab tsis txaus ntseeg txog kev tuag arrhythmogenic. Raws li qhov tshwm sim, American Association of Cardiology pom zoo kom cov neeg mob plawv noj 1 g ib hnub ntawm EPA ntxiv rau DHA. Nws kuj tau pom tias cov kua qaub no tiv thaiv cov hnub nyoog ntsig txog cov leeg mob, dementia, thiab tseem muaj cov txiaj ntsig zoo hauv qee qhov kev nyuaj siab.
Hauv cov kab mob ntshav qab zib mellitus, lawv raug pom zoo rau kev kho mob tiv thaiv hypertriglyceridemia thiab siv dav ua kev kho mob ntxiv rau statins, vim lawv txo qis triglycerides thiab insulin kuj nyob rau hauv T2DM.
Lub mechanism ntawm kev txiav txim thiab chaw soj ntsuam ua tau zoo. Nws ntseeg tias WFAs cuam tshuam cov synthesis ntawm VLDL thiab triglycerides hauv lub siab. Ntxiv mus, lawv cuam tshuam triglycerides rau qhov loj tshaj, thiab tawm tsam keeb kwm ntawm ib koob ntawm 3-6 g ib hnub, qib ntawm TG txo los ntawm 25-50%. Zoo li gemfibrozil, WFA tuaj yeem nce LDL thiab cov roj (cholesterol) tag nrho los ntawm 10%, tshwj xeeb yog cov neeg mob ntshav sib xyaw ua ke. HDL OZHK tsis cuam tshuam. Cov txiaj ntsig zoo ntawm WFA ntawm kev cuam tshuam systolic siab rau kev kho cov tib neeg uas muaj kev mob ntshav siab tau piav qhia.
Nrog T2DM, muaj qhov nce qis hauv LDL thiab cov roj (cholesterol) tag nrho. Hauv T2DM, OZHK feem ntau yog siv los ua tshuaj txuas rau kev kho statin nyob rau hauv cov ntaub ntawv ntawm kev tiv thaiv hypertriglyceridemia thiab kom txo tau cov tshuaj insulin.
Cov Tshuaj Pharmacokinetics OZHK nrawm nrawm tom qab kev tswj hwm thiab tau faib tawm hauv lub cev. Lub cev rog yog tshem tawm thaum lub zog ua kom cov pa oxygen rau CO2 thiab dej.
Kev cuam tshuam nrog lwm yam tshuaj. Txij li WFAs txwv cov platelet sib sau ua ke, yuav tsum tau saib xyuas tshwj xeeb thaum sau tshuaj anticoagulants, thrombolytics, thiab platelet inhibitors. Cov tseem ceeb hauv tsev kho mob ntawm qhov kev cuam tshuam nrog no tsis paub txog.
Npaj npaj, koob tshuaj thiab kho mob ntxig. Cov koob tshuaj ib txwm ntawm WFA muaj nyob hauv tsiav tshuaj yog 4 g ib hnub, uas noj ib zaug lossis 2 zaug hauv ib hnub. Cov tshuaj tuaj yeem raug tshem tawm yog tias qhov txiaj ntsig xav tau tsis tiav hauv ob lub hlis.
Sab nraud thiab contraindications. Feem ntau, halitosis, hloov pauv ntawm saj, mob plab tsis xis nyob, mob nraub qaum, mob khaub thuas-zoo li cov tsos mob, muaj kev cuam tshuam ntau ntxiv rau kev kis tus kab mob, thiab kev nce siab ntawm cov mob angina tshwm sim thaum kho nrog WFA. Muaj kev nce qib ntawm kev kuaj mob siab - ALT thiab ACT, uas yuav tsum tau saib xyuas hauv kev kho mob OZHK.
OZHK cov tshuaj yuav tsum tsis txhob raug rau cov poj niam cev xeeb tub thiab lactating, nrog rau cov muaj hnub nyoog qis dua 18 xyoo. Nws tsis paub meej tias WFA cuam tshuam rau daim siab thiab lub raum ua haujlwm.

Tactics ntawm lipid-txo cov tshuaj kho mob ntshav qab zib


Txo qis LDL-C:

  • dua li cov statins
  • lwm cov tshuaj suav nrog SCFA, ezetimibe, fenofibrate, lossis niacin.


Txhawm rau kom nce HDL-C:

  • nicotinic acid los yog fibrates. Kom qis triglycerides:
  • fibrates (fenofibrate, gemfibrozil), niacin, cov koob tshuaj siab ntau (rau cov neeg mob uas tau nce LDL-C).

Nrog rau kev ua ke hyperlipidemia:

  • kev xaiv thawj: siab ntawm statins,
  • kev xaiv thib ob: statins nyob rau hauv ua ke nrog nrog fibrates,
  • kev xaiv thib peb: statins hauv kev sib xyaw nrog niacin.

Muaj 5 lub laj thawj uas yog vim li cas nws thiaj yuav tsum tau los mus muab kev kho mob sib xyaw kom zoo lipid:

  • ua kom qhov kev txo qis ntawm LDL-C,
  • ua kom qhov siab cov roj-VLDL txo qis,
  • txo cov kev mob tshwm sim ntawm cov tshuaj los ntawm kev siv tshuaj kom tsawg dua ntawm txhua qhov sib xyaw ua ke rau kev kho,
  • lub peev xwm siv SCFA rau hauv cov neeg mob hypertriglyceridemia thiab kev txhawb nqa LDL-C,
  • txhawm rau tshem tawm qhov nce qib ntawm LDL-C uas tau tsim los ntawm kev kho mob ntawm hypertriglyceridemia nrog fibrates

Cov hom phiaj tswj kev mob hnyav - kho mob ntawm dyslipidemia nyob rau hauv hom 2 mob ntshav qab zib

Txo qib theem LDL - Lub hom phiaj tseem ceeb, thiab feem ntau lawv qib tseem nyob tsa txawm tias muaj kev tswj xyuas ntshav qabzib ntau. ADA pom zoo kom pib kho kev noj haus thiab kho tshuaj rau cov neeg mob ntshav qab zib hom 2 uas muaj qhov LDL pib zoo.

Cov Lus Pom Zoo NCEP (AT III) kuj tseem kaw. Hauv ob qho xwm txheej, hom phiaj qib ntawm LDL Cov tshuaj uas cuam tshuam rau lipoprotein metabolism hauv

Yog tuav kev tshawb nrhiav nrog cov statins tshiab, uas muaj cov txiaj ntsig ua tau zoo ntawm lipids thiab lipoproteins, thiab yog li ntawd qhov kev xaiv dav yog xav kom muaj nyob rau hauv lub xyoo tom ntej.

Statins tej zaum yuav muaj txiaj ntsig zoo nyhuv thiab rau theem ntawm TG thiab HDL ntshav. Hauv kev hais txog qhov no, lawv qhov kev siv nyob rau hauv metabolic syndrome thiab hom 2 mob ntshav qab zib yog qhov tseeb, thaum cov qib TG feem ntau tau nce ntxiv thiab qib HDL qis dua. Pom tseeb cov pov thawj uas txhawb zog TG thiab tsawg dua HDL yog cov kev pheej hmoo ntawm cov hlab plawv txhaws qhov yuav tsum tau ua kom tiav cov qib ntsuas ntawm cov ntsuas no.

Ntxiv rau, qhov teeb meem ntawm daim ntawv thov fibrate Txhawm rau txo qis kev mob plawv hauv cov neeg mob uas muaj ntshav qab zib hom 2 nrog dyslipidemia, nyob ib puag ncig cov kev sib tham tau muaj ua ntej lawm, qhov kev daws teebmeem tau zoo tam sim no tau txais raws li ntau cov kev tshawb fawb soj ntsuam. Raws li nrog LDL, kev tswj hwm glycemic tuaj yeem txhim kho TG thiab / lossis HDL, tab sis lawv tsis tshua muaj txog qib hom, txawm tias muaj kev hloov pauv tseem ceeb hauv kev ua neej thiab kev kho hypoglycemic.

Txog phiaj TG qhov tseem ceeb Muaj qee qhov tsis sib xws ntawm ADA thiab NCEP (ATP III). NCEP (ATP III) cais cov qib TG raws li hauv qab no:
500mg% ib txwm

ADA Kuv pom zoo rau thawj ob pawg thiab qib ntawm TG Cov chaw npaj tshuaj rau kho cov teeb meem lipid / lipoprotein ntau ntau

NCEP (APR III) qhia tau tias VLDLP cov khoom lag luam - "tawg faib" - "seem" - yog atherogenic. Hauv kev siv tshuaj, VLDL raug soj ntsuam los ntawm theem ntawm cov lipoproteins uas tseem tshuav. Hauv cov tib neeg muaj TG siab (> 200 mg%), qhov sib txawv ntawm tag nrho cov roj (cholesterol) thiab HDL (tsis yog HDL) yog lub hom phiaj thib ob ntawm kev kho. Qhov ntsuas no rau cov ntshav qab zib hom 2 yuav tsum tsawg dua 130 mg%.

Cov tshuaj tiv thaiv ntawm Intensive Lipid / Lipoprotein Tswj hauv Hom Ntshav Qab Zib 2

1. Cov ntsuas ntshav txhawm rau txiav txim siab seb cov qib roj cholesterol, TG, HDL, LDL yog noj hauv lub plab tas, tom qab 8 teev yoo mov.
2. Qhov siab tshaj plaws glycemic tswj tau tiv thaiv keeb kwm yav dhau los ntawm kev noj haus, poob phaus thiab tshuaj noj yog qhov tsim nyog kom ua tiav HbAlc ruaj khov ntawm 45 mg% rau cov txiv neej thiab> 55 mg% rau cov poj niam.

4. Yog tias lub hom phiaj tseem ceeb ntawm cov roj (cholesterol) thiab LDL tsis tiav, nws yog qhov yuav tsum tau muab tshuaj kho cov tshuaj statin thiab nce ntxiv rau lawv ib hlis twg ib zaug kom ua tiav lub hom phiaj ntawm kev kho mob.
5. Yog tias TG tsis ncav cuag lub hom phiaj theem tiv thaiv keeb kwm ntawm LDL Qhov pib muaj nuj nqis ntawm lipid spectrum rau kev pib kho kev noj haus thiab kev kho tshuaj hauv cov neeg laus mob ntshav qab zib

Cov ntsiab lus tseem ceeb: cov ntaub ntawv los ntawm kev sim kev pheej hmoo ntawm kev tswj hwm ntawm dyslipidemia rau cov neeg mob ntshav qab zib hom 2

- Kev tswj Glycemic kho txhim kho cov lipid profile hauv cov neeg mob ntshav qab zib hom 2 uas muaj dyslipidemia, tab sis tsis tshua rov qab los txog lawv qib kom rov zoo li qub.
- Peb qhov kev tshawb fawb txog kev tiv thaiv thawj tau qhia tias 25-30% txo nyob rau hauv LDL nrog kev kho mob statin rau cov neeg mob ntshav qab zib hom 2 txo cov kev pheej hmoo ntawm cov hlab ntshav li 34-37%.
- Ob txoj kev tshawb fawb txog kev tiv thaiv theem nrab tseem qhia txog kev txo qis ntawm txoj hlab ntaws-hlab ntshav thaum lub sijhawm kev kho mob statin rau cov neeg mob ntshav qab zib hom 2 uas muaj mob ua mob rau cov hlab ntshav txhaws.

- Peb txoj kev tshawb nrhiav yav tom ntej, feem ntau ntawm cov theem nrab prophylaxis, qhia tau tias qhov txo qis ntawm TG qib ntawm 27-31% thiab nce qib HDL los ntawm 5-6% thaum kho nrog fibrates txo txoj kev pheej hmoo ntawm kev mob ntshav siab los yog kev txhim kho ntawm cov hlab ntshav txha caj qaum raws li cov neeg mob hlwb rau cov neeg mob ntshav qab zib hom 2 hom.
- Txhawm rau tswj cov lipid spectrum, chav kawm 4 tshuaj tau siv: statins, kev sib txuas ntawm cov kua tsib kua qaub, nicotinic acid, fibrates.
- Cov cuab yeej siv ntawm kev tswj hwm ntawm lipids / lipoproteins hauv ntshav qab zib hom 2 tau txhais.
- Txhim kho kev cog lus yog tus yuam sij tseem ceeb rau kev ua tiav qhov kev pab cuam zoo.

Cov ntaub ntawv rau cov kws tshaj lij

  • Kws tshuaj -
  • Cov ntawv tshaj tawm -
  • Endocrinology -
  • Kev paub kho qhov dyslipidemia nyob hauv ntshav qab zib hom 2

Cov ntaub ntawv yog npaj rau cov kws kho mob thiab tsis tuaj yeem siv los ntawm lwm tus neeg, suav nrog los hloov kev sib tham nrog tus kws kho mob thiab txiav txim siab txog kev siv cov tshuaj no!

Cia Koj Saib