Daim Ntawv Qhia Txoj Kev Mus Rau Parathyroidectomy Rau Raum Hloov Cov Neeg Sib Tw

TSAB NTAWV

Mob raum mobmineral thiabmob pob txhatuaj yeem nyob tom qabua tiav raum hloov pauv. Tsis tu ncuahyperparathyroidismtau raug txheeb xyuas txog li 80% ntawm cov neeg mob thoob plaws hauv thawj xyoo tom qabhloov raum. Cov txheej txheem thoob ntiaj teb tsis muaj cov lus pom zoo nruj txog kev tswj hwm ntawmhyperparathyroidism tsis tu ncua. Txawm li cas los xij, nws muaj feem cuam tshuam nrog cov txiaj ntsig tsis zoo thiab cov txiaj ntsig ntawm tus neeg mob, suav nrog kev pheej hmoo ntawm pob txha ntau dua thiab muaj kev pheej hmoo ntau ntxiv ntawm txhua qhov ua rau tuag thiab kev poob tag nrho. Secondary hyperparathyroidism tuaj yeem kho mob (vitamin D, phosphate binders, thiab calcimimetics) lossis phais (parathyroidectomy).

NEW HERB TEA RAUCHRONIC KIDNEY DISEASE PATIENTS

Cov lus qhia cov lus pom zoo qhia txog kev kho mob ua ntej tab sis tsis qhia meej txog qhov pom ntawm cov tshuaj parathyroid hormone lub hom phiaj lossis cov lus qhia thiab lub sijhawm ntawm parathyroidectomy. Tsis muaj cov lus qhia meej lossis kev tshawb fawb ntev txog qhov cuam tshuam ntawm kev kho hyperparathyroidism. Parathyroidectomy muaj txiaj ntsig zoo dua li kev kho mob, txawm hais tias nws cuam tshuam nrog kev pheej hmoo luv luv. Qhov zoo tshaj plaws, parathyroidectomy yuav tsum tau ua ua ntej hloov lub raum kom tiv thaiv hyperparathyroidism tsis tu ncua thiab txhim kho cov txiaj ntsig graft. Tam sim no peb tab tom npaj ib txoj hauv kev rau kev tswj hwm tus mob hyperparathyroidism theem nrab hauv cov neeg mob tsim nyog tau txais kev hloov hauv lub raum uas suav nrog cov cim qhia thiab lub sijhawm (ua ntej lossis tom qab hloov lub raum) ntawm parathyroidectomy, kev ntsuam xyuas ntawm parathyroid gland loj thiab kev koom ua ke ntawm cov qog qog nqaij hlav hauv lub cev. kev txiav txim siab los ntawm ib pab neeg ua haujlwm ntau yam ntawmnephrologists,kws kho mob hluav taws xob, thiabkws phais.

Ntsiab lus:hloov raum, parathyroidectomy, theem nrab hyperparathyroidism

Taw qhia

Lub raum hloov pauv (KT) yog tus qauv kub hloov lub raum kho rau lub raum tsis ua haujlwm. Cov neeg tau txais kev hloov pauv hauv lub raum (KTRs) muaj txoj sia nyob zoo dua, txo qis kev pheej hmoo ntawm cov hlab plawv, txhim kho lub neej zoo, thiab txo cov nqi kev noj qab haus huv ntau dua li cov neeg mob ntshav lim ntshav [1–3]. Txawm li cas los xij, KTRs tau ris lub nra ntev los ntawm lawv cov kab mob raum ntev dhau los (CKD). Txawm hais tias muaj kev vam meej KT raug suav hais tias kho CKD-mineral thiab pob txha tsis zoo (CKD-MBD) mus rau qhov loj, CKD MBD tseem nyob hauv KTRs, txawm hais tias phenotype hloov zuj zus. Tom qab-KT CKD-MBD nyob ntawm cov pob txha yav dhau los, kev pheej hmoo siab thib ob hyperparathyroidism (SHPT), de novo CKD-MBD, thiab kev siv tshuaj tiv thaiv kab mob. Kev koom tes ntawm txhua yam ntawm cov khoom no hloov pauv lub sijhawm [4] (Daim duab 1).

Tsis tu ncua HPT muaj nyob rau hauv txog li 80% ntawm cov neeg mob thoob plaws hauv thawj xyoo tom qab KT thiab nws cov kev soj ntsuam thiab biochemical tshwm sim yuav nyob mus ib txhis yog tias tsis kho kom tsim nyog [5–7]. Cov txheej txheem thoob ntiaj teb tsis muaj cov lus pom zoo nruj heev txog kev tswj hwm qib siab pretransplant PTH, tab sis qhov cuam tshuam tsis zoo ntawm HPT tsis tu ncua ntawm kev cog qoob loo thiab cov txiaj ntsig ntawm tus neeg mob ua rau nws tsim nyog los txheeb xyuas cov phiaj xwm hauv kev tswj hwm ntawm SHPT hauv cov neeg mob tsim nyog rau KT los ntawm kev txheeb xyuas cov pov thawj qub thiab tshiab. .

SHPT thiab tertiary HPT (THPT): pathophysiology

HPT is very common in CKD patients. It is present in ∼50% of patients with stage 3 or 4 CKD and in >90% ntawm cov neeg mob raum tsis ua haujlwm [8]. Kev paub txog pathophysiology ntawm SHPT tau nthuav dav heev nyob rau xyoo tsis ntev los no. Ob leeg parathyroid hormone (PTH) thiab fibroblast kev loj hlob zoo tshaj 23 (FGF-23) yog cov tseem ceeb contributors rau SHPT uas qhia tib lub raum cuam tshuam rau calcium (txhim kho reabsorption) thiab nyob rau hauv phosphate (nce excretion) tab sis muaj ib tug opposite nyhuv ntawm lub raum. metabolism ntawm vitamin D [9] PTH. PTH ua lub luag haujlwm tseem ceeb hauv kev tuav cov calcium: thaum cov qib calcium hauv cov ntshav poob qis dua li cov ntsiab lus ib txwm muaj, calcium-sensing receptor (CaSR) tau qhib los txhawb kev tso tawm PTH los ntawm cov qog parathyroid. PTH nce pob txha resorption, tso calcium nyob rau hauv cov ntshav; activates lub hloov dua siab tshiab nyob rau hauv tubular hlwb ntawm 25-hydroxyvitamin D rau nws active daim ntawv 1,25-dihydroxy vitamin D [1,25(OH)2D] thiab reabsorption ntawm calcium; thiab txhim kho FGF-23 ntau lawm los ntawm upregulation ntawm nuclear receptor-txog 1 nyob rau hauv osteocytes (Daim duab 2). Nyob rau hauv cov tubules ze ze, PTH ua rau lub internalization ntawm sodium-phosphate cotransporters NPTIIa thiab NPTIIC, nce phosphaturia thiab txo cov ntshav phosphate [10, 11]. Kev rov qab los ntawm cov calcium hauv cov ntshav mus rau cov txiaj ntsig zoo silences CaSRs, normalizing PTH qhov tseem ceeb [12, 13]. Txoj kev them nyiaj no tsis ua haujlwm zoo hauv CKD yuav ua rau muaj ntau yam tseem ceeb los ntawm kev nce qib ntawm SHPT thiab CKD: hypocalcemia, hyperphosphatemia, qis qis ntawm cov vitamin D, thiab siab FGF-23 qib. Cov pob txha teb rau PTH yog qhov tsis txaus ntseeg hauv CKD siab heev, qhov tshwm sim hu ua hyporesponsiveness lossis PTH tsis kam (Daim duab 3). Cov ntsiab lus tseem ceeb ntawm PTH tsis kam yog phosphate loading, calcitriol deficiency, oxidative stress, parathyroid hormone 1 receptor (PTH1R) downregulation, thiab dysfunction, tsub zuj zuj ntawm PTH fragments, antagonists ntawm Wnt / -catenin pathway, thiab uremic toxins. Lub xub ntiag ntawm PTH fragments nyob rau hauv kev koom tes nrog desensitization ntawm PTH1R yuav piav qhia txog qhov muaj feem ntau ntawm cov pob txha pob txha qis thaum lub sij hawm SHPT thiab qhov tshwm sim tsis tu ncua hypocalcemia [14].

FGF-23. FGF-23 nce thaum ntxov hauv CKD los tiv thaiv phosphate tsub zuj zuj [13] los ntawm kev them nyiaj rau qhov txo qis phos phate glomerular pom. FGFs teeb liab los ntawm plaub qhov sib txawv FGF receptors (FGFR1-4), uas yog tag nrho cov tyrosine kinase receptors. FGFR1c yog tej zaum qhov tseem ceeb tshaj plaws FGFR rau FGF-23 signaling, tsawg kawg nyob rau hauv lub cev nqaij daim tawv, thiab yuav tsum muaj lub xub ntiag ntawm coreceptor -Klotho [15]. Hauv cov kab mob sib thooj, FGF-23 khi rau FGFR1-Klotho complex txhawb phosphaturia los ntawm kev txo qis ntawm cov phosphate transporters NPTIIA thiab NPTIIC thiab kuj txo cov plab nqus ntawm phosphate los ntawm kev txo qis CYP27B1 (ie 122D) tiam] [9, 10]. FGF-23 kuj tseem suppresses 1- - hydroxylase ob qho tib si hauv Klotho-dependent zam (FGFR1) thiab los ntawm FGFR3 thiab FGFR4 hauv Klotho- ywj pheej [16]. Txo 1,25 (OH) 2D muaj, nyob rau hauv lem, txhim khu PTH synthesis [17]. Tsis tas li ntawd, o, albuminuria [18], thiab lwm yam tseem ceeb kuj txo lub raum Klotho qhia thaum ntxov hauv CKD, ua rau tsis kam mus rau FGF-23 [19]. Hauv CKD qib siab, cov teebmeem phosphaturic ntawm PTH thiab FGF-23 tsis muaj pov thawj ntxiv lawm, thiab cov qib ntshav phosphate siab kuj nce PTH qib [20, 21].

FGF-23 activates FGFRs los ntawm ob txoj hauv kev tseem ceeb: Klotho-dependent activation ntawm mitogen-activated protein kinase (MAPK) cascade thiab Klotho-ywj siab cascade uas ua los ntawm kev ua kom muaj calcineurin-nuclear yam ntawm activated T-cells (NFAT ) (Daim duab 2). Tshwj xeeb, hauv cov qog parathyroid, FGF-23 downregulates PTH secretion principally los ntawm classic Klotho-dependent activation los yog thib ob los ntawm Klotho- ywj siab cascade [22]. Hauv SHPT hnyav, cov nyhuv inhibitory no tsis muaj vim qhov txo qis FGF-23–Klotho-dependent receptors hauv cov qog parathyroid [23, 24].

Cov theem ua ntu zus hauv kev txhim kho SHPT.

Kev txhim kho HPT yog tus cwj pwm los ntawm plaub tus qauv sib txuas ntawm parathyroid hyperplasia. Thawj theem polyclonal proliferation yog tus cwj pwm los ntawm diffuse hyperplasia lossis thaum ntxov nodularity hauv diffuse hyperplasia. Yog hais tias tsis tsim nyog thiab aggressively tswj, parathy roid glands tsim kev loj hlob monoclonal expansion nrog nodular hyperplasia los yog ib tug nodular caj pas [23, 25]. Ntev mus ntev thiab tswj tsis tau HPT ua rau muaj kev hloov pauv ntawm diffuse mus rau nodular hyperplasia (Daim duab 4). Cov nodules feem ntau tshwm sim ua haujlwm ntawm autonomous adenomas xws li hauv thawj HPT. Nodular hyperplasia yog tus cwj pwm los ntawm kev txo qis ntawm cov vitamin D receptor, CaSR, FGFR1, thiab nws cov co-receptor Klotho, ua rau SPHT refractory rau kev kho mob xws li vitamin D agents thiab calcimimetics. Qhov no yog lub ntsiab lus ntawm tsis muaj rov qab, hu ua THPT [25]. THPT feem ntau pom muaj tom qab KT, txawm hais tias nws yuav raug soj ntsuam hauv cov neeg mob ntawm kev lim ntshav. Hauv cov neeg mob dialysis, THPT yuav tsum txawv ntawm SHPT nrog iatrogenic hypercalcemia thiab / lossis hyperphosphatemia ntsig txog kev kho mob ntau dhau, xws li vitamin D [23]