血小板低下癥的區(qū)分及血小板輸注合理評估

1、血小板低下癥的區(qū)分及血小板輸注合理評估,張志升臺灣臺大醫(yī)院輸血醫(yī)學(xué)科2016/6/26,Content,血小板低下癥的原因新生兒血小板低下癥藥物誘導(dǎo)血小板低下癥血栓性血小板低下癥特發(fā)性血小板減少紫癜肝素誘導(dǎo)血小板低下癥,血小板低下癥的原因,骨髓制造血小板的功能減少血小板制造可因放射線、化學(xué)治療或病毒感染等原因受抑制，而骨髓本身疾病，如再生不良性貧血、白血病，骨髓分化不良等皆可引起制造減少。血小板在周邊血液被破壞增加常

2、見的有經(jīng)由產(chǎn)生自體免疫抗體來破壞，如全身性紅斑性狼瘡、特發(fā)性血小板減少性紫斑癥、某些藥物等，而病毒感染也常引起血小板低下，如登革熱病毒、人類免疫缺乏病毒等。此外血小板低下也常見于脾臟腫大病人，如肝硬化病人因門脈高壓引起脾臟腫大，造成血小板破壞增加。,Evaluation of a child with thrombocytopenia,Platelet count3 mouths,CBC, blood smear evaluation,

3、Anemia + thrombocytopenia,pancytopenia,,,Platelet clumps present,pseudothrombocytopenia,,,,,,,,Ill appearing?,No,,,Congenital anomalies?,Yes,No,,,PMN hypersegmentation RBC macroovalocytosis??↓B12 or ↓RBC folate,,,,B12 o

4、r folate deficiency,,Medications Immunizations IrradiationToxins?,,No,Yes,,,Macrothrombocytes,,,Drug-induces Live immunizationIrradiation Toxins,,Yes,No,Other morphologic platelet changes,No other platelet change,Bon

5、e marrow,Cyanotic heart diseaseFanconi anemiaDyskeratosis congenitaTrisomy 13 or 18Syndromes: Kasabach-Merritt TAR Alport variants,Syndromes:May-hegglinHermansky-PudiakGray platelet,,,ITPHereditary thromboc

6、ytopeniaBernard-Soulier,↑NI megakaryocytes,,,,,,,,,,↓megakaryocytes,,,,,LeukemiaAplastic anemiaDrug-induced Amegakaryocytic thrombocytopeniaMyelodysplasia,ITP is a diagnosis of exclusionResponse to therapy, if need

7、ed (corticosteroid, IVIG, anti-D antibody), confirms the diagnosis,,,Yes,PTT, PT, TT,prolonged,DICR/O sepsis,,,,,,See Consumptional coagulopathy,Normal,,↑↑SpleenSigns of portal hypertensionplatelet > 50,000+/-panc

8、ytopenia,MaleEczemaRecurrent infectionSmall platelets,LymphadenopathyHepatosplenomegalySuperior vena cava syndromeAbdominal mass,Chronically ill appearing,Acute, fibrile illness,,,,,,,,WBC enzyme assays Ultrasono

9、graphyThick smear,Biopsy of lymph node, mass or bone marrow consider tumor lysis and superior vena cava syndromes,HIV assayANAU/ARenal function,Blood culture ? antibiotics,,,,,MalariaGaucher diseasePortal hyperte

10、nsionHepatic schistosomiasisCavernoustransformation of the portal vein,Wiskott-Aldrich syndrome,Lymphoma: Hodgkin Non-Hodkin NeuroblastomaleukemiaMyelodysplasia,HIV Autoimmune or connective tissue diseaseHUS/TT

11、P + other microangiopathies Prosthetic cardiac valve,R/O ADMAT-13DATAuto/allo anti-platelet antibody,,,,,,SepsisVaricellaEBVCMVDenque hemorrhagic feverHIVHUSHantavirusParvovirusOther viruses TTP,,Auto/all an

12、ti-platelet antibodies study,,Heparin-induced thrombocytopenia,,Check PF4,,Thrombocytopenia in the ill neonate,,,Any etiology of thrombocytopenia that occurs in the well child,History, examination, CBC, blood smear evalu

13、ation,,See Thrombocytopenia in the well neonate,,Platelets 100,000~149,000/uL,,,,Platelets < 100,000/uL,If platelets < 50,000? Cranial ultrasound to R/O intracranial hemorrhage resulting from severe TP of any etolo

14、gy,,Follow platelet count,>150,000/uL ? no further evaluation,100,000~149,000? continue to fellow,,,,,,PTT, PT, TT,,,,,,,High Hb,Severe jaundice and low Hb,Prolonged PTT, PT and/or TT +/- microangiopathic hemolytic an

15、emia:Consider D-dimer of FSP, and/or fibrinogen +/- factors II, V and VIII,,,,PolycythemiaCyanotic congenital heart disease,Erythroblastosis fetalisExchange transfusion pphototherapy,DIC,EtologiesAcute infectionAsp

16、hyxiaRDSMeconium aspirationObstetrical complicationsShockThrombosisSevere hemolytic disease of the newbornSevere hepatic disease,TP usually mild enough not to require transfusion except in DIC due to erythroblasto

17、sis fetalis,,,,,,,Treat underlying disease Maintain platelets > 50,000 with transfusionsMaintain fibrinogen > 1.0g/L and PT WNL with FFP +/- cyrorecipitate,,Normal PTT, PT, TT,,,RDSPulmonary hypertansionMeconiu

18、m aspirationMechanical ventilation,Infection ViralBacterial Fungal,Perinatal asphyxia,No other specific etiology identified,Unknown etiology,Ongoing re-evaluation if platelets < 50,000,Acutely ill Usually prematu

19、re Abdominal signs,,,,,,,NEC,,,AcidosisEmesisLethargy,+/- Central venous catheterHematuriaPulseless extremity,Drug useGancyclovirHeparinVancomycin,Metabolic defects,Thrombosis,Drug-induced,Stop drug,Remove cathet

20、er when possibleLMWH??Thrombolytic therapy,,,,,,,Supportive care- Platelet transfusions to maintain count > 20,000 in stable full term neonates, > 50,000 with hemorrhage, surgery, or more extremely preterm infant

21、sObserve for DIC,,,,,,,,,免疫性血小板低下,Neonatal alloimmune thrombocytopenia (NAIT)Platelet transfusion refractoriness (PTR)Post-transfusion thrombocytopenic purpura (PTP)Passive alloimmune thrombocytopenia (PAT)Transplan

22、tation-associated alloimmune thrombocytopenia (TAATP),Alloantigens implicated in allo immune thrombocytopenia,Dr. N.H. Tsuno presented in 24th regional congress of ISBT,血小板相關(guān)抗體疾病或異常,新生兒免疫性血小板減少癥NAITP輸血后紫斑癥PTP血小板輸血無效癥P

23、TR免疫性血小板低下紫瘢癥ITP血栓性血小板低下紫癜TTP肝素刺激血小板低下癥HIT藥物抗體血小板低下癥DIT 嚴(yán)重輸血相關(guān)呼吸窘迫癥候群TRALI,即輸血小板兩次以上無法達(dá)到預(yù)期血小板的增加數(shù)稱為 “ 血小板輸注無療效 ” 成因: 異體免疫, 自體抗體, ABO血型不符, 病人因素 ( 如急性出血或組織移植排斥..等 ), 藥物治療 ( 如抗生素vancomycin..)所引起血小板輸血后的品質(zhì)評估: 1小時(shí)

24、后其 “ 校正血小板增加數(shù) ” > 7000, 此方法亦為偵測有無 “ 異體免疫 ” 的間接方式CCI : ( 輸血后血小板數(shù)-輸血前血小板數(shù)) X BSA/ 輸注血小板量。,血小板輸注無效癥,與血小板抗體有關(guān)之疾病：,Neonatal alloimmune thrombocytopenia 白種人中此病之報(bào)告較多，母體之抗血小板抗體進(jìn)入胎兒內(nèi)，造成新生兒之血小板異常低下，此病可以生于第一胎。西方人報(bào)告中以HPA

25、-1a 抗體為主(又名anti-plA1)，多發(fā)生于HPA-1a陰性且HLA-DR3*0101之婦人。日本則曾報(bào)告過HPA-4b抗體引起之新生兒血小板減少癥  Post-transfusion purpura (PTP) 輸血后紫斑癥，病人輸血后發(fā)生血小 板異常降低，引起反應(yīng)的血品包括血小板，紅血球等。部份輸血病人體內(nèi)可以驗(yàn)出血小板抗體，文獻(xiàn)報(bào)告中最多的也是HPA-1a抗體(anti-plA1 ),Conte

26、nt,血小板低下癥的原因新生兒血小板低下癥藥物誘導(dǎo)血小板低下癥血栓性血小板低下癥特發(fā)性血小板減少紫癜肝素誘導(dǎo)血小板低下癥,Neonatal Alloimmune Thrombocytopenia (NAIT),NAIT due to anti-HLA antibodiesCase of NAIT suspectedly due to anti-HLA are reported, but the association nee

27、ds to be confirmed.Class I HLA Abs are found in about one third of multiparous women (15~31%), and anti-HPA Abs less frequency; however, platelet destruction is usually caused by the anti-HPA AbsProtective immune mecha

28、nism of the placenta : anti-HLA antibodies adsorbed by the stromal cells of placenta expressing paternal antigens; routinely, the infants are born with normal platelet counts.,Dr. N.H. Tsuno presented in 24th regional c

29、ongress of ISBT,Specificity of HPA Ab in NAIT(Japan),Dr. N.H. Tsuno presented in 24th regional congress of ISBT,,The risk of ICH was the highest with anti-HPA-3,血小板抗體的特異性70 NAITP案例,Dr. G.G. Wu presented in 24th regiona

30、l congress of ISBT,2013 ISBT IPIWP-AR,The risk of ICH was the highest with anti-HPA-3Anti-HPA-4a/4b is the highest rate in NAIT in Japan ( anti-HPA-4a 7%, anti-HPA-4b 52%) HPA-4 incompatible may cause rejection rection

31、 reactions in solid organ transplantation.(Vox Sanguinis, 2010 july, Supplement1,Vol 99)More than 0.5% of CD36 type I deficient individuals are at risk to be immunized through blood transfusion or pregnancy in China.,Th

32、e frequency of CD36 negative,新生兒免疫血小板低下癥(NAIT),NAIT due to anti-HLA antibodiesCase of NAIT suspectedly due to anti-HLA are reported, but the association needs to be comfirmedClass I HLA Abs are found in about one third

33、 of multiparous women (15~31%), and anti-HPA Abs less frequently; however, platelet destruction is usually caused by the anti-HPA Abs.Protective immune mechanism of the placenta: anti-HLA antibodies adsorbed by the str

34、omal cells of placenta expressing paternal antigens; routinely, the infants are born with normal platelet counts.,新生兒血小板低下的評估(NATP),新生兒免疫血小板低下癥的評估診斷,母體血清驗(yàn)血小板抗體PIFTELISA法母體血清和患兒血小板交叉SPRCA, FCM母體血清和父親血小板交叉SPRCA, 流式細(xì)胞

35、儀,This assay can detect HLA, ABO, and platelet specific IgG antibodies. But weak reactions give immediate results.,Solid- phase red cell adherence assay (SPRCA),輸血后紫斑癥,Post-transfusion thrombcytopenia purpuraDeveloped

36、after 1-2 weeks after transfusionsCaused by Anti-HPA -1a,Content,血小板低下癥的原因新生兒血小板低下癥藥物誘導(dǎo)血小板低下癥血栓性血小板低下癥特發(fā)性血小板減少紫癜肝素誘導(dǎo)血小板低下癥,藥物誘導(dǎo)血小板低下癥抗體,大部份藥物誘導(dǎo)血小板低下的癥狀輕微，但偶而有危及生命的出血狀況產(chǎn)生。病理原因較藥物誘導(dǎo)紅細(xì)胞溶血性貧血復(fù)雜，至少有六種以上的機(jī)轉(zhuǎn)主要臨床意義在于排除血小

37、板低下原因,J Thromb Haemost. 2009 Jun; 7(6): 911–918.,DIT藥物誘導(dǎo)血小板低下抗體鑒定,血小板交叉配血相容，1Hr CCI>7500, 24 Hr CCI>5000 有效輸血小板1Hr CCI>7500, 24 Hr CCI<5000 infection, fever, non-immune1Hr CCI<7500, 藥物誘導(dǎo)型血小板低下.血小板抗體篩檢陰性

38、，自身血小板抗體陽性( flowcytometry, SPRCA, 近日內(nèi)輸過血小板也可能自身血小板抗體陽性)使用SPRCA法鑒定：血清+藥物及血小板+藥物培溫,Drug induced thrombocytopenia,藥物誘導(dǎo)型血小板低下抗體鑒定流程,血小板低下,篩查血小板骨髓制作功能及最近用藥史,血小板抗體篩檢交叉配血, 1Hr /24 Hrs CCI,,配血相容, 1 hr CCI>7500, 24hrs CCI&g

39、t;5000,配血相容, 1 hr CCI>7500, 24hrs CCI<5000,配血相容, 1 hr CCI<7500,,配血不相容, 1 hr CCI<7500,,執(zhí)行血小板抗體篩檢HPA or HLA class I Ab, or CD36,發(fā)燒等非免疫因素,成功輸血,藥物誘導(dǎo)型血小板低下,跟臨床取得藥物及查詢藥物作用濃度,配制藥物濃度, 執(zhí)行藥物依賴型檢測SPRCA,更改藥物,,,,,,,,,

40、,,藥物誘導(dǎo)型血小板低下抗體鑒定案例,男性68歲大腸癌患者，使用oxaliplastin合并5-FU化療使用，每周一次療程，約使用三星期療程后發(fā)覺血小板從原來17萬/dL, 不明原因降為5.8萬/dL, 無出血現(xiàn)象，也無其他敗血癥及DIC等情形。其他檢查：凝血功能PT/aPTT正常，血小板交叉配血相容，血小板抗體篩檢Pakplus ELISA酶標(biāo)法無血小板抗體。輸血后一小時(shí)CCI 6000.,,,,Negative,Weak po

41、sitive,Positive,疑似藥物誘導(dǎo)溶血性貧血與藥物誘導(dǎo)血小板低下出血案例,一居住在臺灣東部花蓮原住民族男性45歲酒精性肝炎住院患者。之前的病史及輸血史：A型Rh陽性，年輕時(shí)(30歲左右因工作受傷)手術(shù)曾輸過RBC 6U及1U機(jī)采血小板。三四年前曾因急性肺炎住院接受治療，長期使用抗生素(泰巴坦)治療此次住院治療疲倦黃疸，有傷口長期無法愈合不良合并有腎結(jié)石發(fā)燒出血等癥狀實(shí)驗(yàn)室檢查A/pos 抗篩陰性，Hb 6.5, p

42、latelet count 50k, aPTT/PT prolong INR 1.7 blood culture no grow 建議抗生素及輸血治療,疑似DIHA合并DIT輸血治療案例,臨床醫(yī)師建議輸給RBC 4U, 機(jī)采血小板1U, FFP 6U及泰巴坦治療, 抗篩陰性輸血科給予隨機(jī)A型RBC相叉相容RBC 4U 及A型機(jī)采血小板1U, FFP6U 輸注。輸血后第一天Hb 7.2 直抗轉(zhuǎn)陽, Plt 45K 溶血三癥明顯，LDH

43、↑↑，疑輸血后溶血癥，輸血科啟動(dòng)輸血反應(yīng)調(diào)查SOP。輸血科輸血反應(yīng)調(diào)查：輸血后樣本抗篩陰性，直抗轉(zhuǎn)陽，放散液抗篩陰性和原獻(xiàn)血者樣本交叉相容，重復(fù)輸血后樣本對照輸血前樣本交叉配血，輸血后樣本的主側(cè)配血AHG有1+凝集，凝聚胺配血相合，輸血前樣本配血均相容。臨床醫(yī)師建議再次輸血RBC 4U, Plt 1機(jī)采血小板.輸血科再次配血相容RBC 4U及1U 機(jī)采血小板輸注。輸血后第二天溶血評估加劇，疑似引發(fā)DIC ( D-dimer, FDP

44、上升) Hb5.0, plt 8k, 無大量出血現(xiàn)象.,疑似DIHA合并DIT輸血治療案例-cont.,輸血科再次啟動(dòng)輸血反應(yīng)調(diào)查作業(yè)，同時(shí)間病患出現(xiàn)EV bleeding 輸血科緊急供應(yīng)交叉配血相容RBC 及機(jī)采血小板, FFP, Cryo。最后輸血不及, 病患死亡事后調(diào)查: 血小板抗體篩檢陰性( Genprobe Pakplus ELISA), auto-platelet Ab.陽性( FIPA, Flowcytometry流式

45、細(xì)胞儀)DAT : polyAHG 3+, IgG AHG 3+, C3d negative, 放散液抗篩陰性重測抗篩陰性, 紅細(xì)胞主交叉: 相容.,DITP的治療,立即停藥；血小板輸注；大劑量IVIG；短期使用糖皮質(zhì)激素；避免再次使用該藥物,Content,血小板低下癥的原因新生兒血小板低下癥藥物誘導(dǎo)血小板低下癥血栓性血小板低下癥特發(fā)性血小板減少紫癜肝素誘導(dǎo)血小板低下癥,栓塞性血小板低下紫斑癥TTP,形成的原因仍

46、不清楚，多數(shù)學(xué)者認(rèn)為是一種病毒傳染后毒素所造成的反應(yīng)。但臨床上可發(fā)覺正常金屬蛋白酵素（metalloprotease,ADAMTS-13）可以分解超大von Willebrand’s體。它具有類似thrombospondin-1單元（thrombospondin-1–like domains），并藉此與內(nèi)皮細(xì)胞上的thrombospondin接受體結(jié)合，并由此固定于內(nèi)皮細(xì)胞上。固定于內(nèi)皮細(xì)胞上的ADAMTS 13，使可以分解旁邊的超大V

47、on Willebrand's氏因子聚合體。栓塞性血小板低下紫斑癥患者，其金屬蛋白酵素（metalloprotease－ADAMTS 13）于此時(shí)的活性若嚴(yán)重通常趨近于零，無法分解旁邊的超大Von Willebrand's氏因子聚合體，所導(dǎo)致的微血管內(nèi)血小板凝集，因而表現(xiàn)出所謂的pentad：包括微血管病變?nèi)苎载氀⒀“宓拖?、發(fā)燒、神經(jīng)學(xué)癥狀、以及腎功能不全等五種特征。,The ADAMTS-13 assay is

48、 based on fluorescence resonance energy transfer (FRET) technology. A synthetic fragment of the von Willebrand Factor protein is used as the Substrate. Cleavage of this peptide between two modified residues releases the

49、fluorescence quenching capabilities.This assay is based on quantifying the cleavage of a small fragment of von Willebrand Factor by the ADAMTS-13 protease. The cleavage of this synthetic substrate is detected by reading

50、 the fluorescence that results when the substrate is cleaved.,測定ADAMTS-13的原理,TECHNOZYM® ADAMTS-13 ACTIVITY,PE對TTP的療效,一般血漿交換術(shù)PE對TTP的臨床反應(yīng)可謂是十分之迅速且明確。Bukowski報(bào)告2-3天，Petitt報(bào)告約36小時(shí)。血小板約2~5 PE可見成效，但血色素較略顯緩慢。LDH恢復(fù)則較慢。對不同

51、病因的TTP之臨床反應(yīng)速度快慢差異頗大，有約連續(xù)5天療程即完成療效，有近一個(gè)月或以上連續(xù)QD PE才完成療效。以大量血漿﹝新鮮血漿，新鮮冷凍血漿，冷凍血漿﹞補(bǔ)充效果較佳，開始PE療程QD實(shí)施，超過一個(gè)blood volume的血漿置換術(shù)﹝急性期治療常使用120%﹞，以platelet count評估成效。,PE & PI 對TTP的療效,Plasma infusion (PI)bas been used as an alter

52、native to PE.Studies observed no difference in response or survival between PE and PI.The risks of fluid overload with PI and the potential for PE to remove ADAMTS13 have resulted in PE being preferred to PI,TTP之血漿療法,自

53、1977年血漿療法的臨床應(yīng)用已顯著地改善血栓性血小板減少性紫斑癥(TTP)之愈后。使用血液成份分離機(jī)及血漿分離術(shù)或者是血漿輸注法plasma infusion可治愈大部分的TTP病人。唯此兩種血漿療法之相互優(yōu)劣比較及引發(fā)TTP之致病假說，仍尚無定論。1997年新光醫(yī)院溫武慶/葉建宏等發(fā)表一例TTP，交互使用雙重過濾血漿分離術(shù)DFPP配合血漿輸注療法，及血漿交換術(shù)的案例報(bào)告：初期以連續(xù)16次DFPP配合每天之血漿輸注療法，病人之臨床征

54、狀卻依然持續(xù)惡化，只得改用傳統(tǒng)血漿交換術(shù)。結(jié)果在二天之內(nèi)血小板數(shù)目及神智狀態(tài)明顯進(jìn)步。比較此二種血漿療法之個(gè)別差異，發(fā)現(xiàn)血漿交換術(shù)中每次使用之血漿量大約是血漿輸注法之三倍，因此，大量的血漿輸注應(yīng)是治療成功的主因。﹝臺灣醫(yī)學(xué) Formosan J Med 1997;6:710-5﹞,Cryo-poor plasma(cryosupernatant),laboratory indices of complete and stable res

55、ponse (platelet count, serum lactate dehydrogenase level) did not normalize in concert with clinical improvement.,PE of TTP in NTUH,2006.01.~2008計(jì)十五名疑似TTP﹝如下一張slide﹞。其中一名E先生，癥狀十分疑似，但ADAMTS-13測出達(dá)80%normal，執(zhí)行四次PE換血漿64U后停止

56、PE治療，使用傳統(tǒng)platelet transfusion可回復(fù)到180k。其他十二名, 男3名﹝平均52.5歲﹞，女9名﹝平均32.1歲﹞H女士只執(zhí)行一次PE，臨床癥狀十分吻合，原高度懷疑為TTP，但ADAMTS-13測出達(dá)78%最后確認(rèn)是Trousseaus syndrome 。,2005~2008 TTP案例報(bào)告,ADAMTS-13對TTP的鑒別,H女士：Poor prognosis was informed. Pupil d

57、ilate, unconsciousness and no gag reflex were found. Held PLT transfusion due to suspect TTP. FFP was kept as hematologist suggestion. However, vaginal bleeding and oral bleeding persisted. The ADAMT13 was about 80%. TT

58、P was not likely. Elevated CA 125 was found.The abdomen CT showed ovarian cancer and endometrial hyperplasia. Trousseaus syndrome was suspected.,ADAMTS-13對TTP的鑒別(二),某君從新店慈濟(jì)轉(zhuǎn)入本院急診，疑似TTP的案例。臨床癥狀及實(shí)驗(yàn)室檢查疑似TTP：LDH↑，Bilirubin

59、↑，Hb↓，Platelet↓,Coombs’test: negative, unconsciousness ,唯PT, aPTT prolong,留檢體評估ADAMTS-13。病人隨即CPR，ADAMTS-13 assay: 5%,suspected terminal TTP.,血栓性血小板低下的區(qū)分(TTP),Content,血小板低下癥的原因新生兒血小板低下癥藥物誘導(dǎo)血小板低下癥血栓性血小板低下癥特發(fā)性血小板減少紫癜

60、肝素誘導(dǎo)血小板低下癥,ITP特發(fā)性血小板減少癥,ITP的治療主要是在降低臨床重大出血的風(fēng)險(xiǎn)。嚴(yán)重出血的ITP患者，輸血仍是最直接有效的，但缺乏評估輸血1小時(shí)后的有效的血小板數(shù)的循證IVIG 1g/kg (<5000/mL, 每日追蹤)Glucocorticoids (1g IV, 每日3dose),ITP的實(shí)驗(yàn)室診斷,取auto platelet 測auto antibodyELISA PakAuto kit, flow

61、cytometry, SPRCA最近無施打IVIG, 無輸過血小板，采SPRCA: ,<50000 plat count, 抽40cc EDTA，制成PRP,This assay can detect HLA, ABO, and platelet specific IgG antibodies. But weak reactions give immediate results.,Solid- phase red cell a

62、dherence assay (SPRCA),Content,血小板低下癥的原因新生兒血小板低下癥藥物誘導(dǎo)血小板低下癥血栓性血小板低下癥特發(fā)性血小板減少紫癜肝素誘導(dǎo)血小板低下癥,肝素介導(dǎo)的血小板減少（HIT）,機(jī)制： 肝素與血小板因子4(PF4)結(jié)合形成抗原結(jié)構(gòu)，抗體通過Fab段識別PF4/肝素結(jié)合于血小板，F(xiàn)c段連接單核細(xì)胞，迅速、猛烈地引起血小板激活以及促凝微粒的釋放。類似機(jī)制的藥物：魚精蛋白 魚精蛋白

63、-肝素-IgG-血小板FcγRIIa,EDTA依賴假性血小板低下Vs.HIT,HIT的抗體偵測：血清素釋放試驗(yàn)serotonin release assay SRA(高特異性,低敏感性), 抗體-肝素-PF4免疫復(fù)合體試測酶標(biāo)法(高敏感性低特異性性),血小板輸血參考指標(biāo)IPF,IPF是Immature platelet fraction(未成熟血小板比例), 可作為評估骨髓造血小板功能恢復(fù)的參考指標(biāo)化療或干細(xì)胞移植后, IPF開始上

64、升代表骨髓造血小板功能逐漸恢復(fù)，約一周內(nèi)血小板會顯著上升。降低不必要的血小板輸血,IPF與造血小板功能,IPF可早期評估骨髓造血小板功能,評估停上血小板輸血時(shí)機(jī)降低輸血成本降低輸血造成感染的風(fēng)險(xiǎn),美國紅十字會與英國輸血組織移植聯(lián)盟血小板配型流程,Crossmatch with 8 random donors,All donors negative: Use random donors for PLT Tx,8 Crossmatc

65、h positive,Positive and negative donors,Select negative donor for PLT TX,HLA/HPA antibody test,Anti-HPA +Anti-HLA -,Anti-HPA -Anti-HLA +,Anti-HPA +Anti-HLA +,HPA typing of recipient,HLA-identical or compatible PLT,Cro

66、ssmatch with HPA compatible donor,HPA typing of recipient,Crossmatch with HLA/HPA compatible donor,二次以上輸隨機(jī)血小板無效,HLA class I 篩查,positive,Negative或持續(xù)對HLA相容血小板輸注無效,病患的HLA-I分型,提供HLA相容配型血小板,持續(xù)對HLA及HPA配血相容血小板輸注無效,考慮非免疫問題或藥物誘導(dǎo)型