Yuav ua li cas lub raum raug rhuav tshem ib kauj ruam los ntawm High Uric Acid

Kev puas tsuaj ntawm high uric acid rau lub raum

Hyperuricemia (HUA) ua rau lub raum puas thiab muab faib ua peb hom hauv qab no:

1. Mob uric acid nephropathy yog vim muaj ntau ntawm uric acid crystals nyob rau hauv lub raum interstitium thiab lub raum tubules, thiab lub raum tubules puv thiab thaiv los ntawm uric acid, ua rau oliguric mob raum tsis ua hauj lwm. Nws yog tshwm sim nyob rau hauv theem nrab gouty nephropathy, xws li lytic qog syndrome.

2. Cov kab mob uric acid nephropathy yog tshwm sim los ntawm kev tso tawm ntawm urate crystals nyob rau hauv lub raum medulla, uas yog tshwm sim nyob rau hauv thawj gouty nephropathy, thiab Lao Li belongs rau hom no.

3. Uric acid raum pob zeb tuaj yeem pom nyob rau hauv thawj thiab theem nrab gouty nephropathy.

Nyem rau cistanche cov txiaj ntsig thiab kev mob tshwm sim rau tus kab mob raum

Tam sim no, nws ntseeg tau tias cov txheej txheem ntawm HUA ua rau lub raum puas yog raws li hauv qab no:

Ua kom cov renin-angiotensin system (RAS) thiab cyclooxygenase 2 (COX-2) systems

High uric acid activates RAS, ua rau lub cev kub siab thiab glomerular siab, hyperperfusion, thiab raum fibrosis. Angiotensin Ⅱ (Ang Ⅱ) tuaj yeem tswj cov kev qhia ntawm COX-2 thiab kev tsim cov prostaglandins los ntawm mitogen-activated protein kinase (MAPK) teeb liab txoj kev, thiab tom qab ntawd induce qhov kev loj hlob, hypertrophy, thiab Inflammatory cell infiltration ntawm lub phab ntsa.

Kev ua haujlwm tsis zoo ntawm cov cell endothelial

Uric acid inhibits zus tau tej cov nitric oxide (NO) nyob rau hauv endothelial hlwb thiab txo nws cov hauj lwm los ntawm ib tug series ntawm complex mechanisms. Raws li cov antioxidant ntau tshaj plaws nyob rau hauv lub cev, nws ncaj qha noj ntau ntawm NO thiab tsim 6-aminouracil, ua rau muaj qhov txawv txav endothelial cell ua haujlwm, ua rau cov vasodilation tsis muaj zog, thiab ua rau qeeb ntawm kev loj hlob ntawm endothelial hlwb, yog li ua rau kub siab. thiab kab mob vascular.

Lub luag haujlwm ntawm inflammatory yam

Raws li qhov ua rau muaj kev mob tshwm sim, uric acid tuaj yeem txhawb kev sib txuas ntawm platelet-derived growth factor (PDGF) thiab txhawb cov monocytes los tsim monocyte chemoattractant (MCP-1), interleukin-1 (lL{{4}). }) thiab qog necrosis factor (TNF-ɑ) thiab lwm yam inflammatory yam, thiab cov inflammatory yam yog ncaj qha los yog tsis ncaj qha cuam tshuam rau lub raum puas.

rog rog

Qhov tshwm sim ntawm gout nyob rau hauv cov neeg mob rog rog yog 2 npaug ntau dua li ntawm cov pejxeem. Cov adipocytokines secreted los ntawm cov rog nyob rau hauv tib neeg lub cev tuaj yeem ua rau lub paj hlwb ua rau lub cev tsis muaj zog, ua rau cov zis sodium tsis muaj zog los ntawm RAS thiab lub cev muaj zog ntawm ob lub raum, thiab txhim kho lub raum tubular sodium reweighting. Kev nqus dej ua rau sodium thiab dej tuav ua rau ntshav siab, ua rau lub xeev glomerular hyperfiltration. Tsis tas li ntawd, Leptin, TNF- , thiab IL -6 secreted los ntawm cov ntaub so ntswg adipose ncaj qha txhawb o thiab ua rau lub raum puas.

lipid metabolism tsis meej

Lipid deposition nyob rau hauv epithelial hlwb nkoos zus tau tej cov cytokines, ncaj qha nkoos epithelial hlwb los tsim extracellular matrix, thiab koom nyob rau hauv kev puas tsuaj ntawm lub raum tubular epithelium los ntawm oxidation, prompting epithelial hlwb los tsim ntau yam cytokines ntsig txog o thiab fibrosis, los yog Indirect kev koom tes nyob rau hauv cov mob loj zuj zus ntawm lub raum tubules thiab interstitium.

Tsis tas li ntawd, txoj kev tshawb no kuj pom tau hais tias cov hlau lead raug nyob rau hauv ib puag ncig, kev hloov hauv urate transporter kev ua, thiab caj ces tseem muaj feem xyuam rau txoj kev loj hlob ntawm gouty nephropathy.

HUA tuaj yeem tsis tsuas yog ua rau lub raum puas los ntawm cov txheej txheem saum toj no, tab sis kuj yog ib qho kev ua haujlwm ywj pheej ntawm IgA nephropathy, ntshav qab zib nephropathy, kab mob raum, mob raum raug mob, thiab lwm yam, uas yuav ua rau lub raum puas tsuaj hauv cov kab mob saum toj no. [3].

Kev kho mob ntawm gouty nephropathy

txoj kev ua neej

Txo qhov hnyav, txwv cov nqaij purine-nplua nuj, thiab cov nqaij nruab deg, txwv cov khoom noj uas muaj fructose, tsis txhob noj cov khoom noj uas tsis muaj rog lossis tsis muaj rog, thiab txwv tsis pub haus cawv los tswj HUA. Cov kev tshawb fawb soj ntsuam tau pom tias tsuas yog kev hloov pauv hauv kev ua neej tuaj yeem txo qis SUA qib los ntawm 10 feem pua ​​​​rau 18 feem pua ​​[3,4].

kev kho mob

Cov tshuaj uas inhibits uric acid synthesis

Allopurinol

Tam sim no, nws tseem yog thawj kab tshuaj rau kev kho mob ntawm hyperuricemia, muaj zog uric acid-txo cov nyhuv, kev ua siab ntev, thiab kev ua haujlwm siab. Nws cov metabolite oscypurine yog qhov tseem ceeb ntawm kev txo cov uric acid, thiab nws tsuas yog tawm los ntawm ob lub raum. Thaum lub raum ua haujlwm poob qis, cov koob tshuaj yuav tsum raug txo kom tsim nyog kom tsis txhob muaj kev phiv loj los ntawm kev txuam nrog hauv lub cev. Nyob rau hauv xyoo tas los no, allopurinol tau tshaj tawm cov ntaub ntawv ntawm cov tshuaj tua kab mob tuag taus. Cov kev tshawb fawb tau pom tias qhov tshwm sim ntawm qhov tshwm sim tsis zoo no cuam tshuam rau cov neeg uas muaj HLA-B * 5801 alleles zoo. Nws raug nquahu kom ua cov tshuaj ntsuam genetic test rau cov neeg mob ua ntej noj tshuaj, uas feem ntau txwv nws daim ntawv thov.

febuxostat

Kuj hu ua febuxostat, nws tuaj yeem txo cov ntshav uric acid los ntawm inhibiting cov haujlwm ntawm xanthine oxidase, tiv thaiv thiab txo cov synthesis ntawm uric acid los ntawm hypoxanthine thiab xanthine. Tsis zoo li allopurinol, febuxostat feem ntau yog metabolized nyob rau hauv daim siab, thiab ib feem me me yog tawm los ntawm ob lub raum. Rau me me mus rau nruab nrab lub raum tsis txaus, tsis tas yuav kho cov tshuaj. Nws yog qhov tsim nyog rau cov neeg uas tsis haum rau allopurinol lossis leej twg tsis tuaj yeem zam tau lossis tsis muaj txiaj ntsig hauv kev kho mob. Pom zoo rau kev kho mob ntev hyperuricemia nrog keeb kwm ntawm gout.

Cov tshuaj uas txhawb nqa uric acid excretion

Cov tshuaj no ua rau kom cov uric acid nce ntxiv los ntawm inhibiting reabsorption ntawm urate ions los ntawm lub raum raum tubule, yog li txo qhov concentration ntawm urate nyob rau hauv cov ntshav, alleviating los yog tiv thaiv kev tsim ntawm urate crystals, txo kev sib koom ua ke puas tsuaj, thiab txhawb lub dissolution ntawm urate. crystals uas tau tsim.

Representative drugs are benzbromarone and probenecid. These drugs increase the risk of urinary tract stones. When using these drugs, pay attention to drinking more water and using drugs that alkalize urine. Before using such drugs, the excretion of urinary uric acid should be measured. If the patient's 24-hour urinary uric acid excretion is >3.54 mmol lossis muaj cov zis calculi, cov tshuaj no yuav tsum tau txwv tsis pub siv, thiab yuav tsum tau siv ceev faj rau cov neeg mob uas muaj kab mob rwj lossis lub raum tsis ua haujlwm. Tsis tas li ntawd, benzbromarone muaj lub siab toxicity, thiab yuav tsum tau them nyiaj mloog mus rau kev saib xyuas tus neeg mob lub siab ua haujlwm thaum siv.

Uricase tshuaj

Uricase tuaj yeem oxidize thiab degrade uric acid rau hauv allantoin, uas tuaj yeem txo cov ntshav uric acid thiab ua tiav lub hom phiaj ntawm kev kho mob hyperuricemia. Tam sim no, recombinant uricase tau maj mam txhim kho nyob rau hauv cov nqe lus ntawm antigenicity thiab ib nrab-lub neej, thiab nws yuav dhau los ua ib txoj hauv kev tshiab los txo cov uric acid. Cov biosynthetic uric acid oxidase feem ntau suav nrog:

Recombinant Aspergillus flavus urate oxidase (rasburicase)

Rau kev kho mob thiab tiv thaiv tus mob hyperuricemia hauv cov neeg mob uas muaj hematological malignancies nrog kev pheej hmoo siab mob qog lysis syndrome, tshwj xeeb tshaj yog rau cov neeg mob uas muaj tshuaj tua kab mob hyperuricemia. Qib ntawm cov ntshav uric acid hauv cov neeg mob kho nrog cov tshuaj no tau txo qis thiab tseem nyob rau theem qis thoob plaws lub sijhawm induction chemotherapy.

Pegylated recombinant urate oxidase (PEG-uricase)

Kev txhaj tshuaj txhaj tshuaj tuaj yeem txo cov ntshav uric acid sai sai. Nws yog tsuas yog siv rau HUA hnyav, thiab refractory gout, tshwj xeeb tshaj yog rau cov neeg mob qog lysis syndrome. Cov tshuaj sawv cev yog pegloticase, uas yog pegylated uric acid tshwj xeeb enzyme. Uricase yog khi rau polyethylene glycol los ntawm monomethyl ether covalent daim ntawv cog lus thiab feem ntau yog tawm los ntawm ob lub raum.

lwm yam

Tsis tas li ntawd, cov tshuaj xws li colchicine, losartan, fenofibrate, thiab cilnidipine kuj muaj peev xwm txo qis uric acid.

Kev nce hauv cov ntshav creatinine kuj ua rau Lao Li paub txog qhov tseem ceeb ntawm kev tswj hwm kev noj haus thiab koom tes nrog cov kws kho mob hauv kev kho mob gouty nephropathy. Txij thaum ntawd los, nws qhov kev tawm tsam ntawm gout tau txo qis, thiab nws lub raum ua haujlwm kuj tau zoo thiab tau ruaj khov ntawm thaj tsam 160 μmol / L.

Yog xav paub ntxiv:ali.ma@wecistanche.com