Kev txhaj tshuaj Pramlintide

Hom 1 mob ntshav qab zib mellitus yog ib qho kev tiv thaiv kab mob -kev kho mob tsis sib haum xeeb uas tshwm sim los ntawm kev ua tiav ntawm pancreatic beta- kev ua haujlwm ntawm tes, ua rau cov neeg mob tsis tuaj yeem tso cov tshuaj insulin endogenous thiab amylin, yog li yuav tsum tau hloov pauv cov tshuaj insulin mus ntev.

Txawm li cas los xij, insulin monotherapy feem ntau ua tsis tau zoo los tswj cov ntshav qabzib tom qab peaks thiab tuaj yeem ua rau hypoglycemia thiab hnyav nce. Raws li tib txoj kev kho mob tau pom zoo los ntawm US FDA rau hom 1 ntshav qab zib,Kev txhaj tshuaj PramlintideFeem ntau yog siv rau hauv cov neeg mob uas muaj cov lus teb tsis zoo rau cov tshuaj insulin monotherapy, ua kom muaj qhov sib txawv ntawm qhov chaw kho mob hauv kev txo qis hauv cov ntshav qab zib hom 1.

Cov tsos mob uas siv tau: Pom tseeb hom 1 mob ntshav qab zib mellitus ntawm lub sijhawm ntev -lub sij hawm basal- bolus insulin therapy, tseem nrog 2-teev postprandial qabzib tsis tu ncua siab dua 10.0 mmol / L lossis HbA1c Ntau dua lossis sib npaug li 7.5%, yog tias tsis muaj contraindications.Nyob rau hauv cov neeg mob ntxiv, cov tshuaj insulin nce ntxiv. Cov khoom, los ntawm nws cov txheej txheem tshwj xeeb, smooths postprandial qabzib peaks yam tsis tau nce cov tshuaj insulin, txo tag nrho cov tshuaj insulin, thiab txo qis kev pheej hmoo ntawm hypoglycemia.

Kev tshawb nrhiav pom: Hauv cov neeg mob ntshav qab zib hom 1 uas tau txais cov khoom sib txuas nrog insulin, HbA1c raug txo los ntawm 0.1% -0.67%, 1-teev cov piam thaj tom qab 4.4-7 mmol / L, thiab 2-teev cov piam thaj tom qab los ntawm 3.6-4.8 mmol / L, txhim kho glymic acid ntawm lub hom phiaj.

Feem ntau cov neeg mob uas muaj ntshav qab zib hom 2 muaj qhov cuam tshuam rau pancreatic beta -kev ua haujlwm ntawm tes thiab insulin tsis kam. Cov mob hnyav feem ntau xav tau kev kho mob insulin sib xyaw; Txawm li cas los xij, qee cov neeg mob, txawm tias ntawm cov tshuaj insulin ntxiv rau qhov ncauj tshuaj tiv thaiv kab mob hauv qhov ncauj (xws li sulfonylureas, metformin), tsis ua tiav kev tswj hwm glycemic zoo, tshwj xeeb tshaj yog cov cim kev hloov pauv tom qab, yog ib qho kev sib tw loj hauv kev tswj ntshav qab zib. Raws li kev mob siab rau cov tshuaj insulin, cov khoom lag luam hais txog qhov kev xav tau tsis zoo no hauv cov tshuaj insulin tsis zoo - kho mob ntshav qab zib hom 2.

Cov tsos mob tshwm sim: Kev lees paub hom 2 mob ntshav qab zib mellitus ntawm kev kho mob bolus insulin (nrog lossis tsis muaj metformin thiab / lossis sulfonylureas), nrog rau 2- teev tom qab cov piam thaj siab dua 11.1 mmol / L lossis HbA1c Ntau dua lossis sib npaug li 7.0%, thaum tsis muaj cov tshuaj tiv thaiv kab mob ntshav qab zib hom 2. satiety-txhim kho cov nyhuv ntawm cov khoom pab txo cov calorie kom tsawg, txhawb kev tswj qhov hnyav, txhim kho lipid metabolism, thiab txo qis kev pheej hmoo ntawm cov hlab plawv.

Cov ntaub ntawv kho mob: Hauv insulin- kho cov neeg mob ntshav qab zib hom 2 uas tau txais cov khoom siv ntxiv, HbA1c raug txo los ntawm 0.3% -0.62%, 1-teev cov piam thaj tom qab 4.8 mmol / L, thiab 2-teev postprandial qabzib los ntawm 3.4 mmol / L. Nws kuj tseem txo cov kev xav tau ntawm cov tshuaj insulin, txhawb kev poob phaus, thiab txhim kho glycemic tswj thiab kev ua neej zoo.Piv nrog GLP-1 receptor agonists thiab lwm yam adjunctive agents, cov khoom yog tsim nyog rau cov neeg mob uas muaj siab siab siab rau cov kab mob gastrointestinal thiab ib qho tseem ceeb xav tau rau kev noj qab haus huv ncov.

(1) Ntshav Qab Zib nrog rau lub raum tsis ua haujlwm

Mob ntshav qab zib raum tsis zoo yog ib qho teeb meem tshwm sim. Kev txo cov tshuaj tshem tawm ua rau muaj kev nce ntxiv thiab qhov tsis zoo - qhov kev pheej hmoo tshwm sim, yuav tsum tau ua tib zoo xaiv cov tshuaj tiv thaiv kab mob. Cov khoom yog feem ntau lub raum excreted; Txawm li cas los xij, cov kev tshawb fawb pharmacokinetic qhia pom qhov kev tshem tawm zoo sib xws hauv cov neeg mob uas muaj lub raum tsis zoo rau lub raum tsis zoo (Ccr 20–50 mL / min) piv nrog cov neeg noj qab haus huv, tso cai rau kev noj tshuaj tas li.

Cov tsos mob tshwm sim: Hom 1 lossis hom 2 mob ntshav qab zib mellitus nrog rau lub raum tsis ua haujlwm (Ccr 20–50 mL / min) thiab cov tshuaj insulin tsis txaus, yam tsis muaj kev txwv. Pramlintide yuav tsum tau txiav tawm yog tias lub raum ua haujlwm tsis zoo (Ccr<20 mL/min) or dialysis is initiated.

(2) Mob ntshav qab zib mellitus

Kev rog rog yog qhov tseem ceeb ntawm kev pheej hmoo thiab cuam tshuam rau kev tswj glycemic, feem ntau nrog cov tshuaj insulin tsis kam. Insulin monotherapy tuaj yeem ua rau qhov hnyav nce, ua rau lub voj voog tsis zoo. Los ntawm kev txhim kho lub hauv paus satiety thiab txo cov khoom noj kom tsawg, cov khoom pab kom poob phaus, txhim kho cov tshuaj insulin, thiab ua kom muaj kev tswj hwm ntawm cov piam thaj thiab lub cev hnyav.

Cov tsos mob uas siv tau: Hom 1 lossis hom 2 mob ntshav qab zib mellitus nrog kev rog rog (BMI Ntau dua lossis sib npaug li 28 kg / m²), tswj cov tshuaj insulin tsis txaus, thiab cov hom phiaj tswj qhov hnyav.Dose titration, saib xyuas cov piam thaj, noj zaub mov, thiab tawm dag zog. Kev noj zaub mov zoo yuav tsum tau saib xyuas kom tsis txhob muaj kev noj zaub mov tsis txaus los ntawm kev txo qis qab los noj mov.

(3) Cov neeg mob uas muaj cim Postprandial Glycemic Variability

Qee cov neeg mob ntshav qab zib mellitus (hom 1 lossis 2) tau txais cov piam thaj sai sai (4.4-7.0 mmol / L) tab sis qhov kev hloov pauv loj heev: tom qab 1-2 teev nce siab tom qab poob sai, ua rau postprandial hyperglycemia thiab preprandial hypoglycemia. Kev kho mob insulin monotherapy tsis tuaj yeem ua raws li cov kev hloov pauv no. Cov khoom, los ntawm kev ncua lub plab khoob thiab suppressing postprandial glucagon, stabilizes postprandial peaks thiab txo cov excursion.

Cov tsos mob tshwm sim: Hom 1 lossis hom 2 mob ntshav qab zib mellitus nrog ceev ceev cov piam thaj 4.4-7.0 mmol / L tab sis 2-teev cov piam thaj tom qab noj mov ntau dua lossis sib npaug 5.0 mmol / L, lossis nquag postprandial hyperglycemia (Ntau dua lossis sib npaug rau 11.1 mmol / L)<3.9 mmol/L).Postprandial glucose should be closely monitored, with titration of Pramlintide and insulin doses to achieve stable control.

Ntxiv nrog rau cov ntsiab lus tseem ceeb,Kev txhaj tshuaj PramlintideNws muaj lub luag haujlwm ntxiv hauv kev txhim kho glycemic kev tswj hwm thiab daws cov teeb meem nyuaj hauv kev kho mob.

Ntxiv rau cov tshuaj insulin twj tso kua mis hauv cov neeg mob ntshav qab zib mellitus (feem ntau hom 1) ntawm cov tshuaj insulin nrog kev tsis txaus siab tom qab kev tsis txaus ntseeg, cov khoom siv tau muab tshuaj subcutaneously ua ntej noj mov smooths qabzib tom qab noj mov, txo cov kev xav tau ntawm cov zaub mov noj, txo qis kev pheej hmoo ntawm hypoglycemia, thiab txhim kho kev ruaj ntseg. Tsau- qhov piv ntawm 24-teev kev sib koom ua ke ua rau muaj txiaj ntsig zoo dua tom qab hyperglycemia yam tsis muaj qhov hnyav hnyav.

Perioperative glucose tswj muaj zog cuam tshuam rau kev phais. Hauv cov neeg mob uas muaj cov tshuaj insulin tsis zoo thiab cov viav vias loj tom qab, luv luv -Pramlintide siv ceev ceev tswj kom ua tau raws li lub hom phiaj ntawm kev phais thiab txo qhov kev pheej hmoo. Glucose yuav tsum tau saib xyuas zoo; Kev noj tshuaj yog hloov kho los ntawm hom txheej txheem, thiab kev txuas ntxiv tom qab ua haujlwm yog nyob ntawm kev noj qhov ncauj thiab tswj glycemic.

Kev sib xyaw ua ke hauv cov ntshav qab zib refractory Hauv cov ntshav qab zib refractory tsis tswj los ntawm ntau tus neeg sawv cev (insulin + tshuaj hauv qhov ncauj) nrog cov cim hloov pauv, cov khoom yuav raug ntxiv rau kev txo qis hauv cov piam thaj los ntawm nws cov txheej txheem sib txawv. Dose titration thiab adverse -kev soj ntsuam qhov xwm txheej yog qhov yuav tsum tau zam kom tsis txhob muaj kev cuam tshuam.

Hypoglycemia yog ib qho teeb meem tshwm sim feem ntau ntawm cov khoom. Nws feem ntau tshwm sim thaum pib kho mob, lub sijhawm tshuaj titration, lossis ua ke nrog insulin, sulfonylureas thiab lwm yam qabzib- txo cov tshuaj. Kev tiv thaiv kaw yuav tsum tau zam kom tsis txhob muaj qhov hnyav hnyav (xws li coma, tsis nco qab).

Thaum kho nrog cov khoom no, cov ntshav qabzib yuav tsum tau saib xyuas zoo, tshwj xeeb tshaj yog ua ntej noj mov, 1-2 teev tom qab noj mov, thiab thaum mus pw. Yog tias cov tsos mob hypoglycemic tshwm sim (xws li palpitations, tshee, tawm hws, kiv taub hau, tshaib plab, tsis meej pem, thiab lwm yam), carbohydrates (xws li, cov ntsiav tshuaj qabzib, khoom qab zib, dej qab zib) yuav tsum tau noj tam sim ntawd. Hauv qhov xwm txheej ntawm hypoglycemia hnyav, yuav tsum tau txhaj cov piam thaj hauv cov ntshav.

Kev saib xyuas tshwj xeeb yuav tsum tau them: thaum cov khoom no siv nrog insulin, qhov kev pheej hmoo ntawm hypoglycemia nce ntau. Yog li ntawd, kev kho tshuaj insulin yog qhov tseem ceeb tshwj xeeb. Kev noj zaub mov ua ntej- koob tshuaj insulin yuav tsum raug txo los ntawm 50% thaum pib, thiab tom qab ntawd maj mam hloov kho raws li cov ntshav qabzib; koob tshuaj insulin yuav tsum tsis txhob nce ntxiv yam tsis muaj lus qhia kho mob. Rau cov neeg mob tseem noj sulfonylurea qhov ncauj tshuaj tiv thaiv kab mob ntshav qab zib, koob tshuaj sulfonylurea yuav tsum raug txo kom tsim nyog kom txo qis kev pheej hmoo ntawm hypoglycemia.

Tsis tas li ntawd, cov neeg mob thiab lawv tsev neeg yuav tsum paub txog kev txheeb xyuas cov tshuaj hypoglycemia thiab kev kho mob xwm txheej ceev, nqa cov khoom noj carbohydrate txhua lub sijhawm, thiab tsis txhob tsav tsheb ib leeg lossis ua haujlwm cov cuab yeej ntsuas kom tsis txhob muaj xwm txheej thaum lub sijhawm hypoglycemic. Yog tias hypoglycemia tshwm sim ntau zaus, kev kho mob yuav tsum tau nrhiav kom sai los kho cov koob tshuaj ntawm cov khoom no thiab cov tshuaj sib xyaw ua ke.