Shaanxi BLOOM Tech Co., Ltd. yog ib qho ntawm cov tuam ntxhab thiab cov muag khoom ntawm fludrocortisone acetate ntsiav tshuaj hauv Suav teb. Txais tos rau cov lag luam wholesale bulk zoo fludrocortisone acetate ntsiav tshuaj muag ntawm no los ntawm peb lub hoobkas. Kev pabcuam zoo thiab tus nqi tsim nyog muaj.
Fludrocortisone acetate ntsiav tshuajyog ib qho fluorinated hluavtaws glucocorticoid teej tug mus rau chav mineralocorticoid. Cov khoom xyaw nquag yog Fluhydrocortisone acetate, nrog rau tus qauv koob tshuaj ntawm 0.1 milligrams (100 micrograms) ib ntsiav tshuaj. Cov tshuaj no siv tshuaj kho los ntawm kev tswj cov electrolyte tshuav nyiaj li cas thiab cov kua dej hauv lub cev, feem ntau yog siv los hloov lossis ntxiv aldosterone cov tshuaj hormones uas tsis muaj hauv lub cev.
Formulation thiab tsos:
Cov ntsiav tshuaj Acetate yog dawb los tawm dawb ncig nyias zaj duab xis coated ntsiav tshuaj. Muaj ntau yam ntim tshwj xeeb, feem ntau 30, 50, lossis 100 daim ib lub thawv. Qee cov khoom yuav tsum tau khaws cia hauv tub yees (2-8 degree), thiab tuaj yeem khaws cia hauv chav sov rau lub sijhawm luv luv (tsawg dua lossis sib npaug li 25 degree, tsis pub tshaj 30 hnub) thaum tsis qhib.
Peb cov khoom
Fludrocortisone Acetate COA
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Fludrocortisone acetate ntsiav tshuajyog ib qho khoom siv hluavtaws mineralocorticoid tshuaj. Txij li thaum nws txoj kev vam meej nyob rau xyoo 1940, nws tau dhau los ua cov tshuaj tseem ceeb rau kev kho ntau yam kab mob endocrine thiab metabolic thiab cov tawv nqaij mob vim nws qhov sib npaug ntawm cov mineralocorticoid kev ua haujlwm thiab kev ua haujlwm ntawm glucocorticoid.
(1) Thawj theem adrenal insufficiency (Addison tus kab mob)
Addison tus kab mob yog ib yam kab mob tshwm sim los ntawm kev puas tsuaj rau adrenal cortex ua rau tsis txaus tso tawm ntawm aldosterone thiab cortisol. Cov neeg mob uas muaj hyponatremia (ntshav sodium<135mmol/L), hyperkalemia (blood potassium>5.5 mmol / L), hypotension, qaug zog. Fluhydrocortisone acetate ua tiav lwm txoj kev kho mob los ntawm cov txheej txheem hauv qab no:
Kev tswj hwm dej sodium sib npaug: Ib koob tshuaj txhua hnub ntawm 0.1mg tuaj yeem nce ntshav ntim los ntawm 5% -10%, nce systolic ntshav siab los ntawm 10-15 mmHg, txhawb nqa sodium reabsorption, thiab txo cov zis sodium los ntawm 50% -70%.
Kev kho electrolyte: Hauv ib lub lim tiam ntawm kev kho mob, ntshav sodium tuaj yeem rov qab los rau 135-145mmol / L, cov ntshav poov tshuaj tuaj yeem txo mus rau 4.0-5.0 mmol / L, thiab cov kua qaub-puag tuaj yeem rov qab mus rau qhov qub.
Kev sib xyaw ua ke txoj kev kho mob: Nws yuav tsum tau siv ua ke nrog hydrocortisone (20-30mg / hnub), nrog rau yav dhau los supplementing mineralocorticoid kev ua thiab tom kawg supplementing glucocorticoid kev ua ub no, tsim kom tiav lwm txoj kev kho mob.
(2) Salt poob type adrenal reproductive syndrome (21 hydroxylase deficiency)
Tus kab mob no yog hom kab mob hauv lub cev ntau tshaj plaws ntawm adrenal hyperplasia, uas tshwm sim los ntawm qhov tsis txaus aldosterone synthesis vim 21 hydroxylase tsis muaj peev xwm, thiab muaj teeb meem ntsev ntau heev (hyponatremia, hyperkalemia, lub cev qhuav dej) hauv lub sijhawm neonatal. Cov ntsiab lus tseem ceeb ntawm kev kho mob dexamethasone acetate suav nrog:
Ib tus neeg noj ntau npaum li cas: 0.05-0.1mg / kg ib hnub nyob rau hauv lub sij hawm neonatal, muab faib ua 2 koob tshuaj ntawm qhov ncauj, ntxiv nrog sodium chloride tov los daws sodium deficiency.
Kev saib xyuas kev ua tau zoo: Hauv ib lub lim tiam ntawm kev kho mob, cov ntshav sodium tau rov qab mus rau 135-145 mmol / L, cov ntshav poov tshuaj txo qis rau 4.0-5.0 mmol / L, thiab ntshav siab nyob rau hauv qhov qub.
Kev tswj lub sij hawm ntev: Cov koob tshuaj yuav tsum tau hloov kho raws li txoj kev loj hlob ntawm txoj kev loj hlob thaum yau kom tsis txhob noj ntau dhau ua rau kub siab lossis hypokalemia.
(3) Orthostatic hypotension (orthostatic hypotension)
This disease is caused by dysfunction of the autonomic nervous system, leading to a sharp drop in blood pressure while standing (systolic blood pressure drop>20 mmHg). Fluhydrocortisone acetate txhim kho cov tsos mob los ntawm cov txheej txheem hauv qab no:
Ntshav ntim nthuav dav: Ib koob tshuaj txhua hnub ntawm 0.1-0.2mg / hnub tuaj yeem ua kom ntshav ntim thiab txhim kho peripheral vascular tsis kam.
Vascular tone tu: Txhim kho qhov kev nkag siab ntawm cov hlab ntsha rau catecholamines thiab txo cov ntshav siab hloov pauv thaum sawv.
Cov pov thawj kho mob: Cov kev tshawb fawb tau pom tias ib hnub koob tshuaj 0.2mg / hnub tuaj yeem txo qis systolic ntshav siab tsawg dua 10mmHg hauv 80% ntawm cov neeg mob, thiab txhim kho cov tsos mob xws li kiv taub hau thiab dub.
Cov kab mob autoimmune ntawm daim tawv nqaij: ob qho kev cuam tshuam ntawm kev tiv thaiv - kab mob thiab kev tiv thaiv kab mob
Txawm hais tias dexamethasone acetate feem ntau nthuav tawm cov haujlwm mineralocorticoid, nws khaws qee cov khoom siv glucocorticoid thiab tuaj yeem kho ntau yam kab mob autoimmune ntawm daim tawv nqaij los ntawm inhibiting kev tiv thaiv kab mob ntawm tes thiab txo cov kev tsim tawm ntawm pro-inflammatory yam.
(1) eczema
Mob eczema: Fluhydrochloroacetic acid soft cream tuaj yeem txo cov tawv nqaij thickening thiab lichenification. Siv 2-3 zaug hauv ib hnub hauv zos, thiab qhov txo qis ntawm qhov liab thiab khaus khaus hauv 2 lub lis piam tuaj yeem ncav cuag 70% -80%.
Subacute eczema: Los ntawm inhibiting zus tau tej cov prostaglandin E2 (PGE2) thiab leukotriene C4 (LTC4), txo exudation thiab edema, cov kev kho mob tau mus txog 65% -75%.
(2) Neurodermatitis
Antipruritic mechanism: Stabilize lub mast cell membrane, tiv thaiv histamine tso tawm, thaiv cov hlab ntsha conduction, thiab txo qhov khaus khaus.
Anti-inflammatory effect: inhibits T lymphocyte activation, txo cov kev qhia ntawm pro-inflammatory cytokines xws li IL-2 thiab IFN - , thiab alleviates daim tawv nqaij o thiab puas.
Kev ua tau zoo ntawm kev kho mob: Siv hauv zos ob zaug hauv ib hnub, txo qhov khaus khaus ntau dua 50% hauv 4 lub lis piam, thiab txhim kho daim tawv nqaij thickening los ntawm 40% -50%.
(3) Atopic dermatitis
Kev khaus khaus hnyav: Los ntawm inhibiting phospholipase A2 (PLA2) kev ua haujlwm thiab txo qis kev tsim cov arachidonic acid metabolites, cov tsos mob khaus tuaj yeem txo tau sai.
Kho daim tawv nqaij barrier: inhibits fibroblast proliferation, txhim kho microcirculation, thiab txhawb qhov txhab kho.
Cov ntaub ntawv tshawb fawb: Cov ntawv thov hauv zos ob zaug hauv ib hnub hauv cov neeg mob menyuam yaus ua rau muaj qhov khaus VAS ntawm 7.2 ± 1.5 mus rau 3.1 ± 1.2 hauv 2 lub lis piam, thiab 50% kev txhim kho ntawm daim tawv nqaij qhuav.
(4) Tiv tauj dermatitis thiab allergic dermatitis
Allergy mediator inhibition: tiv thaiv degranulation ntawm mast hlwb, txo cov histamine thiab serotonin tso tawm, thiab alleviates redness, o, thiab blistering tsos mob.
Cov nyhuv tiv thaiv kab mob: txo qis kev qhia ntawm cov kab mob inflammatory xws li TNF - thiab IL-6, thiab txo cov tawv nqaij o.
Daim ntawv thov kev kho mob: Thov hauv zos peb zaug hauv ib hnub thaum lub sijhawm mob hnyav, txo thaj tsam erythema los ntawm 40% -60% hauv peb hnub thiab ua tiav 80% txo qis ntawm exudation.
(1) Septic shock
Adjuvant therapeutic nyhuv ntawmFludrocortisone acetate ntsiav tshuajnyob rau hauv septic shock tseem muaj teeb meem, tab sis qee qhov kev tshawb fawb qhia tias nws tuaj yeem txhim kho kev mob tshwm sim los ntawm cov txheej txheem hauv qab no:
Vascular tone txij nkawm: Txhim kho qhov rhiab heev ntawm cov hlab ntsha mus rau catecholamines thiab ua kom lub cev siab (MAP).
Kev tswj kev ua paug: inhibiting NF - κ B txoj hauv kev, txo qhov tso tawm ntawm cov kab mob xws li IL-1 thiab IL-6, thiab txo cov kab mob inflammatory teb (SIRS).
Cov ntaub ntawv pov thawj kho mob: Kev tshawb nrhiav randomized controlled trial (RCT) nrog rau 120 tus neeg mob uas muaj septic shock pom tias 28 hnub tuag tus nqi raug txo los ntawm 15% (p<0.05) compared to the control group in the treatment group with combination therapy of 0.1 mg/kg/day of fluorohydrocortisone acetate.
(2) Cerebral Salt Wasting Syndrome (CSWS)
CSWS yog ib qho mob uas tshwm sim los ntawm hyponatremia (ntshav sodium<130mmol/L) and increased urinary sodium excretion after traumatic brain injury. Fluhydrocortisone acetate is treated through the following mechanisms:
Sodium reabsorption nce qib: nce cov reabsorption ntawm sodium los ntawm lub raum tubules thiab txo cov zis sodium excretion.
Ntshav ntim rov qab: Hauv 3 hnub ntawm kev kho mob, ntshav sodium tuaj yeem rov qab los rau 135-145 mmol / L, thiab tso zis sodium tuaj yeem txo los ntawm 50% -70%.
Kev hloov kho koob tshuaj: thawj koob tshuaj yog 0.05mg / hnub, kho txhua 3 hnub raws li cov ntshav sodium, nrog rau qhov siab tshaj plaws koob tshuaj tsis pub tshaj 0.2mg / hnub.
Fludrocortisone acetate yog ib qho khoom siv hluavtaws ua cov tshuaj mineralocorticoid. Txij li thaum nws txoj kev vam meej nyob rau xyoo 1940, nws tau dhau los ua cov tshuaj tseem ceeb rau kev kho mob ntawm cov kab mob tsawg xws li thawj qhov tsis txaus ntawm adrenal tsis txaus (Addison tus kab mob) thiab ntsev poob adrenal reproductive syndrome.
Cov khoom xyaw nquag Fludrocortisone txhim kho nws txoj kev sib raug zoo rau mineralocorticoid receptors (MR) los ntawm kev qhia 9 - fluorine atoms, thaum txo nws txoj kev muaj peev xwm khi rau glucocorticoid receptors (GR). Cov yam ntxwv ntawm cov qauv no ua rau nws muaj zog mineralocorticoid nrog tsawg cuam tshuam rau cov piam thaj thiab cov protein metabolism.
1. Receptor binding thiab nuclear translocation
Tom qab nkag mus rau lub hom phiaj cell,Fludrocortisone acetate ntsiav tshuajkhi rau mineralocorticoid receptors nyob rau hauv lub cytoplasm, tsim ib tug complex thiab hloov mus rau lub nucleus. Cov complex no ncaj qha tswj cov noob transcription los ntawm kev khi rau cov DNA ib ntus, xws li cov ntsiab lus ntawm cov tshuaj hormones.
2. Synthesis tswj ntawm cov protein tseem ceeb
Sodium channel (ENaC):
Upregulation ntawm EnaC qhia nyob rau hauv lub raum tubular epithelial hlwb txhim khu lub reabsorption muaj peev xwm ntawm sodium ions. Piv txwv li, hauv cov neeg mob uas muaj qhov tsis txaus ntawm adrenal tsis txaus, 0.1mg ntawm dexamethasone ib hnub tuaj yeem txo cov zis sodium los ntawm 50% -70%.
Sodium poov tshuaj ATPase:
Txhawb cov synthesis ntawm sodium poov tshuaj ATPase nyob rau hauv lub raum tubular hauv qab daim nyias nyias, accelerates kev thauj ntawm sodium ions mus rau hauv lub cell thiab secretion ntawm poov tshuaj ions rau hauv lub lumen.
Carbonic anhydrase:
Inhibits carbonic anhydrase kev ua si nyob rau hauv proximal raum tubules, txo hydrogen ion reabsorption, thiab indirectly txhawb sodium retention.
3. Inactive zog ntawm metabolites
Fluhydrocortisone yog oxidized los ntawm cytochrome P450 enzyme (CYP3A4) nyob rau hauv lub siab mus rau inactive 3-keto-4-pregnen-17,21-diol, zam lub sij hawm ntev tsub zuj zuj toxicity. Nws ib nrab-lub neej yog 3.5-4.5 teev, tab sis ib zaug kev tswj hwm txhua hnub tuaj yeem tswj cov ntshav cov tshuaj kom ruaj khov, vim tias cov tshuaj khi rau cov ntshav plasma proteins (feem ntau yog transferrin) ntawm tus nqi ntawm ntau dua 90%, ua rau muaj kev tso tawm tso tawm.
1. Cov kev cai ntawm lub raum dej sodium tshuav nyiaj li cas
Hydrocortisone acetate tuaj yeem ua tiav dej thiab sodium tuav los ntawm kev nce glomerular filtration rate (GFR) thiab reabsorption ntawm sodium thiab chlorine los ntawm lub raum tubules. Cov ntaub ntawv kho mob qhia tau tias:
Ntshav ntim expansion:
Ib koob tshuaj txhua hnub ntawm 0.1mg tuaj yeem ua kom ntshav ntim ntau dua 5% -10% thiab systolic ntshav siab los ntawm 10-15 mmHg.
Electrolyte kho:
Hauv cov neeg mob Addison tus kab mob, cov ntshav sodium tuaj yeem rov qab los<130mmol/L to the normal range within one week of treatment, and blood potassium levels can decrease from>5.5 mmol / L rau 4.0-5.0 mmol / L.
Acid Base Balance tswj:
Los ntawm kev txhawb nqa hydrogen ion excretion, kho metabolic acidosis, thiab nce ntshav pH los ntawm<7.30 to 7.35-7.45.
2. Kev saib xyuas ntawm cov hlab plawv qhov nro
Increased vascular resistance: By dilating blood volume and enhancing the sensitivity of blood vessels to catecholamines, peripheral vascular resistance is increased. For example, in patients with orthostatic hypotension, a daily dose of 0.1-0.2mg/day can reduce the decrease in systolic blood pressure during standing (>20mmHg) thiab txhim kho cov tsos mob xws li kiv taub hau thiab dub.
Kev txhawb nqa kev ua haujlwm ntawm lub plawv: nce myocardial contractility thiab cardiac output, txhim kho cov ntaub so ntswg perfusion hauv cov neeg mob hypovolemic shock.
Txawm hais tias fluorocortisone acetate feem ntau nthuav tawm cov haujlwm mineralocorticoid, nws tseem khaws qee cov khoom siv glucocorticoid thiab tuaj yeem ua rau muaj kev tiv thaiv kab mob los ntawm cov hauv qab no:
1. inhibit qhov tso tawm ntawm cov neeg kho mob inflammatory
Arachidonic acid metabolism: inhibits phospholipase A2 (PLA2) kev ua haujlwm thiab txo qis kev tsim cov tshuaj kho mob xws li prostaglandin E2 (PGE2) thiab leukotriene C4 (LTC4). Piv txwv li, nyob rau hauv ib tug qauv ntawm kev sib cuag dermatitis, lub zos daim ntawv thov ntawm fluoxetine cream yuav txo tau qhov liab thiab o ntawm daim tawv nqaij los ntawm 40% -60%.
Cytokine regulation: Downregulate cov kev qhia ntawm pro-inflammatory cytokines xws li IL-2 thiab IFN - , thiab alleviate cov ntaub so ntswg inflammatory puas.
2. Stabilize lub mast cell membrane
Tiv thaiv kev tso tawm ntawm allergens xws li histamine thiab serotonin, thiab alleviate allergic reactions xws li urticaria thiab allergic rhinitis. Cov kev tshawb fawb soj ntsuam tau pom tias qhov ncauj noj txhua hnub ntawm 0.1mg / hnub tuaj yeem txo tauFludrocortisone acetate ntsiav tshuajCov qhab nia hauv cov neeg mob uas muaj kev tsis haum dermatitis ntau dua 50%.
3. inhibit T lymphocyte activation
Los ntawm kev txo qis kev qhia ntawm co stimulatory molecules nyob rau saum npoo ntawm T hlwb, xws li CD28 thiab CTLA-4, T cell proliferation thiab cytokine secretion tuaj yeem inhibited, yog li txo cov kab mob hauv cov kab mob autoimmune xws li kab mob lupus erythematosus.
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