Dyslipidemia a cikin ciwon sukari shine yanayin lokacin da jinin mai haƙuri ya ƙunshi babban abun ciki na lipoproteins da lipids.
Excessarfin waɗannan abubuwan masu haɗari yana da haɗari saboda yana ƙara haɗarin mummunan aiki a cikin aikin jijiyoyin zuciya, galibi yana haifar da bayyanar atherosclerosis. Babban taro na cholesterol yana taimakawa bayyanar cututtukan cututtukan cututtukan fata.
Hyperlipidemia yawanci yana hade da ciwon sukari. Hoton asibiti na wannan yanayin yana kama da alamun cututtukan zuciya da atherosclerosis. Kuna iya gano shi bayan gwajin gwaji.
Dyslipidemia: menene, abubuwan haɓakawa don ciwon sukari
Lipoproteins sune macromolecular, mahaukatan mahaifa wadanda ke dauke da sifofin protein da lipids daban-daban a cikin jini. Hydrophobic triglycerides tare da ƙwayoyin cholesterol ester sun zama ainihin abubuwan lipoproteins, wanda ke kewaye da sunadarai na amphipathic da phospholipids.
Babban sinadarin lipoproteins yana dauke da 100-5000 cholesterol esters da kwayoyin triglyceride. Abubuwan kariya na farfajiya na lipoproteins sune alo-lipoproteins. Ba wai kawai za su saki lipids daga tsakiya ba ne, har ma suna shiga cikin safarar abubuwan lipoproteins da kuma ƙididdigar yawan ƙwayar lila.
Ana buƙatar Apolipoprotein B100 don samar da lipoproteins na hepatic na ƙwararru daban-daban (low, matsakaici, mai yawa). Apo B 48 yana da alhakin shigarwar chylomicrons daga hanji. Kuma ApoA-1 shine babban tsarin furotin na HDL.
Dyslipidemia a cikin nau'in ciwon sukari na 2 ana haifar dashi ta hanyar abubuwa da yawa:
- Balagaggen metabolism.
- Obese.
- Wani mummunan sakamako bayan ɗaukar babban adadin wasu kwayoyi (beta-blockers, diuretics, androgens, systemic corticosteroids, progestins, immunosuppressants, AIPs).
- Maganin gado.
- Cututtukan haɗin gwiwa (mafi yawan lokuta tare da ciwon sukari - wannan hypothyroidism).
Me yasa ciwon sukari ya katse lipoprotein da metabolism na chylomicron? Bayan cin abinci, ƙwayoyin triglycerides (fats na abinci) tare da cholesterol suna ɗaukar ƙananan hanji kuma an shigar da su cikin tsakiya na ƙirƙirar chylomicrons wanda ke shiga cikin ƙwayar lymphatic, kuma bayan an haɗa su cikin wurare ta cikin maɗaukakiyar vena cava.
A cikin gado mai kyau, chylomicron da adipose nama tsotsar nama suna ɗaure enzymes lipoprotein. A sakamakon haka, ana fitar da kitse mai mai kyauta.
FFAs ana kama su da adipocytes, inda suke sake bayyana a cikin tsarin triglycerides. Idan ƙwayar FFA ta kama ƙwayar tsoka, to, yana amfani da su azaman tushen makamashi, yana haɗuwa da metabolism na ciki.
Ragowar (ragowar chylomicron) samfurori ne na aikin lipolytic wanda ya ɓace kusan 75% na triglycerides, wanda yake hanzari yana lalata hanta.
PL - maganin hepatic lipase (triglyceride), hydrolyzing triglycerides na chylomicron remnants, har yanzu yana shiga cikin kawar da ragowar. A cikin nau'in 2 na ciwon sukari mellitus, rashin aiki a cikin metabolism na ragowar holomicron da chylomicrons yakan faru. Haka kuma, tare da wannan nau'in cututtukan ƙwayar cuta na yau da kullum, an rage yawan ayyukan LPL.
Koyaya, juriyawar insulin yana ƙarfafa samuwar chylomicrons a cikin hanji. Game da ciwon sukari irin na 1, toshewar jijiyoyin jiki na faruwa ne kawai da lalata cuta. An bayyana wannan ta hanyar raguwa mai yawa a cikin ayyukan Ll, wanda ke tattare da babban ƙaruwa mai yawa a cikin adadin triglycerides bayan cin abinci.
Hyperlipidemia kuma na iya faruwa sakamakon lahani irin na asali. VLDLP an samar da shi ta hanta, cholesterol da estal triglycerides suna cikin zuciyar, kuma phospholipids da kwayoyin Apo 100 suna kan farfajiya.
Samun VLDL a cikin hanta yana motsawa ta hanyar yawan FFA na kyallen takaddun adipose. Amma haɓaka aikin haɓaka a cikin hanta na cholesterol da FFA a cikin cututtukan da ba su da insulin kuma ana iya yiwuwa, wannan shine dalilin da yasa samarwa VLDL shima ya ƙaru.
Triglycerides a cikin VLDL a cikin plasma suna da ruwa sosai a cikin LPL, suna jujjuya su zuwa ƙaramin LSPP da VLDL. Abin lura ne cewa LPPs suna kama da ragowar chylomicron, amma sun bambanta a cikin wannan ban da amfani a cikin hanta, ana kama su cikin jini zuwa LDL. Don haka, ayyukan LPL yana ba da aikin al'ada na rayuwa wanda ya fara daga VLDL, wucewa STD, kuma ya ƙare tare da LDL.
ApoVUO shine kawai furotin da ke zaune akan saman LDL wanda yake shine ligand ga masu karɓar LDL. Saboda haka, abubuwan LDL a cikin jini ya dogara da dalilai biyu:
- kasancewar masu karɓar LDL;
- LDL kayayyakin.
A cikin nau'in ciwon sukari na 2, ƙwayoyin cuta ta VLDL sau da yawa suna hauhawa. Increasedara yawan taro na cholesterol ta hanyar LDL a cikin ƙwayar cuta mai narkewa ana bayyana shi ta haɓaka abun ciki a cikin kowace ƙwayar lipoprotein.
Peroxidation ko glycation na LDL yana haifar da lalacewa ta al'ada ta kawar da barbashi na lipoprotein, yana haifar da gaskiyar cewa sun fara tattarawa akan bangon jijiyoyin bugun gini. Bugu da kari, insulin yana karfafa magana ta hanyar LDL mai karɓar kwayoyin, kuma, a sakamakon haka, juriya insulin ko rashi na hormone shima yana iya tasiri metabolism na LDL.
HDL tsari ne mai rikitarwa. Ana kiran barbashi mai farawa prebeta-HDL. Waɗannan su ne masu karɓar ƙwayoyin sel na kyauta, don haka HDL shine matakin farko na jigilar cholesterol zuwa hanta da kyallen takarda, inda suke fita daga jiki.
Cholesterol esters kuma zasu iya zama bangare na barbashi na VLDL da chylomicrons a gaban sinadarin sufuri na cholesteryl ester. A cikin nau'in ciwon sukari na 2 na sukari, yawanci ana amfani da ƙididdigar HDL-C saboda karuwar jigilar cholesterol ester daga HDL zuwa HDL.
Koyaya, tare da nau'in ciwon sukari na 1, HDL-C ya kasance al'ada ko ɗan ƙara damuwa.
Babban ka'idodin magani
Hanyar kulawa da cututtukan cututtukan cututtukan cututtukan mahaifa ta samo asali ne daga ka'idodi uku. Wannan shine kula da sukari na jini, asarar nauyi da abinci.
A cikin nau'in na biyu na ciwon sukari, yawan cin abinci mai sauƙi na carbohydrates, cholesterol da kitsen mai ya kamata a iyakance. A cikin menu na yau da kullun, yana da kyawawa don haɗa samfuran da ke ɗauke da ƙwayoyin kitse na monounsaturated da fiber na abin da ake ci, don haka inganta bayanin martaba.
Idan mai ciwon suga yana kokawa game da nauyin kiba, to yawan kumburin triglycerides a cikin jininsa zai ragu da kashi 18%, kuma ƙwayoyin cholesterol-suna rage ƙwayoyin cuta za su ragu da kashi 8%.
Yana da mahimmanci a lura cewa tare da cututtukan da ba su da insulin-insulin, shan magunguna masu rage sukari, gami da ƙarin insulin, kawai wani ɓangaren dawo da matakan al'ada na mai mai.
Don haka, Metformin kawai zai iya rage ƙwayar plasma triglycerides zuwa 10%, Pioglitazone - har zuwa 20%, kuma Rosiglitazone ba shi da wani tasiri akan metabolism na lipid. Game da LDL-C, magunguna masu rage sukari suna shafar wannan tsari kamar haka:
- Metformin yana raguwa da 5-10%;
- Pioglitazone yana ƙaruwa da 5-15%;
- Rosiglitazone yana ƙaruwa da 15% ko fiye.
Harkokin insulin yana ba da gudummawa ga rage raguwa a cikin LDL-C. Kuma sulfonamides basu da tasiri mai mahimmanci akan metabolism na lipid.
A cikin nau'in 1 na ciwon sukari, maganin kwantar da hankali a cikin jiki na iya rage LDL-C plasma da triglycerides. Koyaya, matakin diyya don maganin ƙwaƙwalwar ƙwayar ƙwayar ƙwayar cuta ba ya tasiri HDL-C a cikin nau'i na biyu na ciwon sukari.
Sulfanilamides cewa ƙananan sukari na jini ba su shafar maida hankali kan HDL-C. Koyaya, Metformin, saboda raguwa a cikin triglycerides, yana ƙaruwa HDL-C, amma ba da yawa ba.
Pioglitazone da Rosiglitazone suna haɓaka HDL-C a cikin marasa lafiya da ke fama da ciwon sukari na 2. Don haka, don daidaita tsarin mai mai a cikin masu fama da ciwon sukari da ke fama da rashin insulin, maganin rage rage kiba ya zama dole. Kuma a cikin yanayin nau'in ciwon sukari na farko, ya zama dole don biyan diyya don metabolism metabolism.
Hypolipidemia a cikin ciwon sukari ana bi da shi tare da statins da wasu kwayoyi, waɗanda suka haɗa da Niacin, SCF, Fenofibrate, Ezetimibe. Irin waɗannan kwayoyi suna rage ƙwayar LDL.
Don haɓaka HDL-C, ana amfani da fibrates da nicotinic acid, wanda ke ba da damar rage ƙimar triglycerides. Gemfibrozil, Fenofibrate, da Niacin ya kamata a kasafta su daga rukuni na biyu. Idan matakin LDL-C ya yi yawa sosai, to an sanya allurai masu girman jiki zuwa ga masu ciwon suga.
Cutar cututtukan cututtukan ƙwayar cuta ana kawar da ita ta hanyoyi uku:
- doara yawan sashi na statins;
- haɗuwa da satin tare da fibrates;
- hade da satins tare da niacin.
Dalilan da yakamata a aiwatar da cikakkiyar kulawa da rage kiɗa mai yalwa. Na farko, wannan hanyar ta rage karfin LDL-C da LDL-C.
Abu na biyu, maganin haɗin gwiwa yana rage haɗarin halayen masu illa kuma yana rage cholesterol-LDL da ke haɗuwa da shan fibrates.
Abu na uku, wannan hanyar tana ba da damar yin amfani da SCLC a cikin marasa lafiya da ke fama da cutar sikila da kuma wani nuna alamun damuwa na LDL-C.
Rukunin kwayoyi da aka yi amfani da su don maganin dyslipidemia
Akwai nau'ikan magunguna guda uku waɗanda ke shafar maganin lipoproteins na plasma. Waɗannan su ne Hgor-COA reductase inhibitors, masu biye da bile acid, fibrates.
Yawancin lokaci ana amfani da Statins don rage yawan LDL-C, saboda haka an sanya su don maganin hyperlipidemia. Pravastatin, Simvastatin, Lovastatin sune metabolites na fungi ko abubuwan asalin metabolites. Kuma Rosuvastatin, Atorvastatin, Fluvastatin magungunan roba ne.
Ana daukar Simvastatin da Lovastatin a matsayin "masu ba da tallafi", saboda suna da tasirin warkewa kawai bayan hydrolysis a cikin hanta. Kuma wasu siffofin an kebe su da tsari mai aiki.
Ka'idojin aiki na HMG-COA reductase Inhibitors shine su murƙushe wani mahimmin kwaro na cholesterol. Bugu da ƙari, waɗannan wakilai suna ƙaddamar da aikin samar da Apo B100, wanda ke kunna masu karɓar LDL kuma sun haɗa lipoproteins. Wannan yana haifar da gaskiyar cewa tattarawar triglycerides na VLDL, cholesterol LDL, ba zato ba tsammani ya ragu cikin jini.
Pharmacokinetics na statins:
- sha daga 30 zuwa 90%;
- metabolized da hanta daga 50 zuwa 79%;
- more kodan da kodan.
Tare da hulɗa da statins tare da FFA, yawan shan su yana raguwa. Hakanan, an lura da irin wannan sakamako tare da haɗakar magunguna waɗanda ke haifar da tasirin tasirin cutar ta Lovastatin.
Bugu da kari, alamomin Lovastatin, atorvastatin da Simvastatin zasu karu bayan sun sha ruwan innabi. Tare da gabatarwar Warfarin da Rosuvastatin, haɓaka aikin prothrombin yana faruwa.
A cikin adadin yau da kullun na 10-40 mg, HMG-COA reductase inhibitors ƙananan LDL cholesterol maida hankali ne zuwa 50% kuma ƙara HDL-C ta 5-10%.
Ana nuna Statins ga masu ciwon sukari tare da ƙara yawan TG kuma tare da cholesterol mai ƙarfi na LDL. Sun kuma hana samuwar sinadarin gallstones, wanda yake da matukar mahimmanci ga masu ciwon suga.
Myositis shine mafi muni mara wahala bayan an dauki statins, amma da wuya ya sami ci gaba. Abubuwan cutarwa irin su:
- maƙarƙashiya
- arthralgia;
- ciwon ciki
- dyspepsia da cutar gudawa;
- tsokoki na jijiyoyin jiki.
Masu bin Bile acid sune resins waɗanda suke ɗaure acid bile a cikin hanjin. Irin waɗannan kwayoyi suna rage LDL-C zuwa 30% ta hanyar canza abubuwan HDL. Wataƙila, SCFAs na iya ƙaruwa triglycerides.
A cikin lura da dyslipidemia tare da ciwon sukari na mellitus, tasirin bile acid masu bin tafarkin sun yi kama da aikin statins, amma tare da haɗin gwiwar waɗannan magungunan. Ana amfani da SCFA kaɗan a cikin hanji. An ƙaddamar da tasirin warkewa ta matakin rage ƙwaƙanin cholesterol, wanda ke bayyana kanta a cikin makonni 2-3.
SCFAs suna shafar shan kwayoyi da yawa, gami da hana maganin hana haihuwa, antiarrhythmic da anticonvulsants. Don haka, sauran kudaden ya kamata a ɗauka ne kawai bayan 4 hours sun wuce bayan ɗaukar SCFA.
Ana amfani da jerin hanyoyin Bile acid don kawar da hypercholesterolemia. Amma tunda wannan rukuni na kwayoyi na iya haifar da karuwa a cikin triglyceride maida hankali, yana da mahimmanci don sarrafa wannan alamar a yayin jiyya. Sabili da haka, bai kamata a dauki SCFA a cikin masu haƙuri da hyper-triglyceridemia ba.
Mafi sau da yawa, bayan ɗaukar SCFA, maƙarƙashiya da rikicewar dyspeptik na faruwa .. Ba za ku iya haɗuwa da abincinsu ba tare da maganin sulfonamides da sauran kwayoyi ba, lura da hutun sa'o'i shida. SKHK suna contraindicated a gaban duwatsu a cikin mafitsara, gastrointestinal da cikakken biliary buguary da kuma ƙara yawan taro na triglycerides.
Abubuwan Fibric acid irin su Hem fibrosyl da Fenofibrate sune Pon alpha agonists. Irin waɗannan magunguna don ciwon sukari suna da tasiri mai ƙarfi akan metabolism na lipid, rage yiwuwar haɓaka rikitar cututtukan zuciya. Don haka, fibrates ƙananan cholesterol-LDL zuwa 20%, triglycerides - har zuwa 50%, kuma matakin cholesterol-HDL yana ƙaruwa da 10-20%.
Abin lura ne cewa fenofibrate shine madadin mai kyau a cikin lura da babban taro na LDL-C a cikin masu ciwon sukari na ɗaukar statins waɗanda basu da tasirin da ake so.
Fibrates yana tasiri metabolism a cikin ciwon sukari, yana haɓaka kira:
- lipoprotein lipase;
- ABC-A1;
- Apo A-P da apo A-1 (manyan abubuwan kariya na HDL).
Fibrates yana rage bayyanar mahimmancin furotin na daukar cholesterol da rage apo C-III. Hakanan, kwayoyi suna ƙaruwa da A-V na apo, wanda ke haifar da rage yawan haɗarin lipoproteins, tare da babban adadin TG.
Bugu da ƙari, estar fibrate esters yana hana lipogenesis a cikin hanta. Suna hulɗa tare da mai karɓar hepatic X, yana hana PCR-lipogenesis matsakaici. Abubuwan da aka samo daga fibric acid suma suna da tasirin antiatherogenic.
Koyaya, manyan jami'ai na dyslipidemia sune mutum-mutumi, kuma an sanya allurar rigakafi don kamuwa da ciwon sukari na insulin, kawai ga wadanda basu iya jure wa wadannan magungunan ba. Don haɗewar maganin fibrates, ana bada shawarar yin amfani da fenofibrate.
Zai dace a lura cewa irin waɗannan magunguna za'a iya tsara su don rage LDL tare da ƙara yawan taro na TG. Amma a wannan yanayin, ana amfani da kwayoyi daga wasu kungiyoyi sau da yawa, kamar SCFA, nicotinic acid da statins.
Matsakaicin tsawon lokacin maganin fibrate shine watanni 3-6. Tunda waɗannan kwayoyi suna ƙara haɗarin cholelithis, bai kamata masu amfani da cutar sukari suyi amfani da su tare da neuropathy na autonomic ba.
Masu ciwon sukari da ke fama da cututtukan ƙwaƙwalwar ƙwaƙwalwa da marasa lafiya ya kamata su yi amfani da fibrates sosai, tun da ƙoshinsu sun fi cire su. A lokacin shayarwa da lokacin daukar ciki, an hana yin jiyya tare da wadannan jami'ai.
Abubuwan da suka fi dacewa da tasirin tasirin maganin fibrates sune:
- rashin tsoro;
- tashin zuciya
- erectile tabarbarewa;
- ciwon ciki
- fata fatar jiki;
- amai
- zawo
- Dizziness
- maƙarƙashiya da kaya.
Baya ga statins, SCFAs da fibrates, don hyperlipidemia wanda ke tasowa a cikin masu ciwon sukari bayan shekaru 50, ana iya ba da maganin nicotinic acid. Wannan shine kawai wakilin rage rage yawan lipid wanda yake rage yawan yawan lipoprotein, amma yana da yawan sakamako masu illa.
Hakanan, likita na iya yin wasiƙar omega-3 mai kitse don rage hypertriglyceridemia. Bugu da ƙari, OZHK yana rage haɗarin matsalolin zuciya kuma yana da sakamako na rigakafi. Bidiyo a cikin wannan labarin zai gaya maka yadda ake bi da raunin ƙwayar cuta ta hanta.
