妊娠合并血小板减少61例临床分析

目的 :探讨妊娠合并血小板减少的病因和围产期的处理方法。方法 :回顾分析 6 1例妊娠合并血小板减少患者的临床资料。结果 :6 1例血小板减少的病因为再生障碍性贫血、特发性血小板减少性紫癜 (ITP)、脾功能亢进、系统性红斑狼疮 (SLE)、抗心磷脂抗体综合征、妊娠高血压综合征及妊娠期肝内胆汁淤积症 (ICP)。治疗方法是使用糖皮质激素、免疫球蛋白与成分输血等。早产 15例 ,阴道分娩 10例 ,剖宫产 5 1例。结论 :妊娠合并血小板减少处理的重点是治疗合并症和并发症 ,加强监护 ,适时提升血小板数 ,防止分娩期出血     

特发性血小板减少性紫癜合并妊娠的临床分析

目的 探讨特发性血小板减少紫癜（ITP）合并妊娠的围产期处理方法。方法 回顾性分析我院1990－1999年间37例ITP合并妊娠的临床处理经验。结果 37例ITP孕妇中阴道分娩16例,剖宫产21例。与ITP有关的围产期并发症有产后出血及产褥感染,发生率分别为8．1％和2．7％。无孕产妇死亡。3例新生儿出现血小板减低,发生率为8．1％。无颅内出血发生。结论 ITP合并妊娠时,如不无科合并症,产妇以阴道分娩为宜;血小板水平极低的情况下,也可在血源充足时行选择性剖宫产;不主张使用干预性措施预防新生儿被动免疫性血小板减少症。     

108例妊娠合并血小板减少临床分析

目的:分析妊娠合并血小板减少(PT)的临床特点与围生期处理。方法:对108例妊娠合并血小板减少患者的临床资料作回顾性研究。结果108例患者中妊娠相关性血小板减少(PAT)占94例(87.9%),妊娠期肝内胆汁淤积症(ICP)3例(2.8%),妊娠高血压疾病(HDCP)2例(1.8%),特发性血小板减少性紫癜(ITP)5例(4.6%),其他病因2例(1.8%)。有出血倾向或血小板计数<50*109/L患者需用糖皮质激素和(或)免疫球蛋白治疗,阴道分娩9例,剖宫产93例,产后出血8例,死亡1例。结论:PAT是PT的最主要病因,糖皮质激素、丙种球蛋白,血小板输注是治疗PT的有效手段,分娩方式视血小板多少及有无产科手术指征而决定,大部分以剖宫产终止妊娠。     

108例妊娠合并血小板减少临床分析

目的:分析妊娠合并血小板减少(PT)的临床特点与围生期处理。方法:对108例妊娠合并血小板减少患者的临床资料作回顾性研究。结果108例患者中妊娠相关性血小板减少(PAT)占94例(87.9%),妊娠期肝内胆汁淤积症(ICP)3例(2.8%),妊娠高血压疾病(HDCP)2例(1.8%),特发性血小板减少性紫癜(ITP)5例(4.6%),其他病因2例(1.8%)。有出血倾向或血小板计数<50*109/L患者需用糖皮质激素和(或)免疫球蛋白治疗,阴道分娩9例,剖宫产93例,产后出血8例,死亡1例。结论:PAT是PT的最主要病因,糖皮质激素、丙种球蛋白,血小板输注是治疗PT的有效手段,分娩方式视血小板多少及有无产科手术指征而决定,大部分以剖宫产终止妊娠。     

妊娠合并血小板减少98例临床分析

目的　探讨妊娠合并血小板减少的病因及围生期处理方法。方法　总结 1994～ 2 0 0 3年间 98例妊娠合并血小板减少患者的临床资料。结果　妊娠合并血小板减少的主要原因包括妊娠相关性血小板减少症(PAT) ,特发性血小板减少性紫癜 (ITP)和妊娠期高血压疾病 (妊高征 )。治疗方法为在治疗原发病的基础上 ,对血小板计数 <5 0× 10 9/L者于分娩前后短期使用糖皮质激素及血小板制剂。 98例中阴道分娩 34例 ,剖宫产 6 4例 ;发生产后出血 12例 ,产后出血发生率为 12 2 % ;胎死宫内 3例。新生儿血小板减少 7例。结论　在针对病因治疗的基础上 ,糖皮质激素及血小板制剂是治疗严重妊娠合并血小板减少的有效手段。     

妊娠合并血小板减少208例临床分析

目的:探讨妊娠合并血小板减少的病因及围生期的处理方法。方法:回顾性分析1996年1月至2005年12月收治的妊娠合并血小板减少患者208例临床资料。结果:208例孕妇中妊娠期血小板减少症(PAT)88例(42.31%),特发性血小板减少性紫癜(ITP)58例(27.88%),妊娠期高血压疾病32例(15.38%),系统性红斑狼疮12例(5.77%),再生障碍性贫血(AA)10例(4.81%),妊娠期肝内胆汁淤积症(ICP)2例(0.96%),血栓性血小板减少性紫癜(TTP)2例(0.96%),Evan’s综合征1例(0.48%),病因不明3例(1.44%)。结论:多种原因可引起妊娠期孕妇血小板减少,PAT是最常见类型。血小板<50×109/L,应在术前输注浓缩血小板后行剖宫产;血小板计数>50×109/L的孕妇,如无产科指征,应阴道分娩为主。     

妊娠合并血小板减少85例临床分析

目的探讨妊娠期血小板减少的原因及对围产结局的影响。方法回顾性分析安徽省立医院2008—2014年间足月分娩的85例妊娠合并血小板减少患者的临床资料,并选取同一时期血小板计数正常的85例妊娠妇女作为对照。结果妊娠合并血小板减少的患者中妊娠期血小板减少症(GT)69例(占81.2%),其中自然分娩58例,剖宫产11例;特发性血小板减少性紫癜(ITP)10例(占11.7%),其中自然分娩3例,剖宫产7例;其他原因引起的血小板减少6例(占7.1%),其中自然分娩2例,剖宫产4例。产后出血GT组4例(5.7%),ITP组4例(40.0%),其他病因组2例(33.3%)。对照组自然分娩70例,剖宫产15例,产后出血1例(1.2%)。结论妊娠合并血小板减少患者的分娩方式取决于血小板水平、原发病的情况及产科因素。严重血小板减少患者剖宫产率及产后出血率增加。     

妊娠合并特发性血小板减少性紫癜110例临床分析

目的：探讨妊娠合并特发性血小板减少性紫癜（idiopathic thromboeytopenic purpura,ITP）的诊断、治疗及其对母婴的影响。方法：回顾性分析1997年1月—2011年4月间住院分娩110例妊娠合并ITP患者的临床资料。结果：阴道分娩68例,剖宫产42例。其中发生产后出血3例,无死亡病例。予以单纯糖皮质激素治疗33例,糖皮质激素联合丙种球蛋白治疗25例,糖皮质激素联合丙种球蛋白治疗效果不佳或入院时血小板极低因产科因素需急诊剖宫产予以血小板悬液输注48例。除1例新生儿出生后外周血小板计数＜100×109/L外,其余均在正常水平（＞100×109/L）,无颅内出血及其他血小板减少或相关疾病。结论：妊娠合并ITP时,若处理及时得当,对母婴影响很小。糖皮质激素联合丙种球蛋白为有效的治疗方法,分娩方式由产科情况决定,若无产科指征,以阴道分娩为宜;若治疗无效或血小板水平极低,也可在血源充足时行选择性剖宫产。     

妊娠期血小板减少63例临床分析

目的:探讨妊娠期血小板减少的病因、治疗及预后。方法:对我院2006年1月至2010年12月就诊63例妊娠期合并血小板减少患者进行回顾性资料分析。结果:血小板减少症(PAT)占80.95%,特发性血小板紫癜(ITP)占7.94%,妊娠高血压疾病(PIH)占9.52%。根据不同病因,给予强的松或者地塞米松、免疫球蛋白、输注血小板或全血等措施治疗。正常阴道分娩者约73.02%,剖宫产约占26.98%,产妇及新生儿均未发生大出血。结论:妊娠期血小板减少要积极寻找病因,根据不同病因治疗,患者及新生儿预后良好。     

妊娠期血小板减少56例临床分析

目的探讨妊娠期血小板减少的主要原因和相关治疗。方法回顾分析1997～2003年北京妇产医院56例妊娠期血小板减少的临床资料。结果56例中，15例依据骨穿或血小板抗体检查诊断为特发性血小板减少性紫癜（ITP）合并妊娠，10例为妊娠期血小板减少症，1例为再生障碍性贫血合并妊娠，1例为药物所致血小板减少，其余为临床疑似ITP合并妊娠。给予糖皮质激素或免疫球蛋白治疗或输注血小板的例数为40例。56例中剖宫产48例，阴道分娩8例，产后大出血3例。3例新生儿出现血小板减低，但无出血征象。结论妊娠期血小板减少以ITP合并妊娠多见，当血小板持续下降或≤50×10^9／L，应行骨髓穿刺及血小板抗体检查，并给予相应治疗。分娩方式取决于血小板水平及产科相关情况，血小板极低时，可在补充血小板后或在血源充足的情况下行剖宫产。不主张预防性治疗新生儿血小板减少。     

An epidemic of maternal thrombocytopenia associated with elevated antiplatelet antibody. Platelet count and antiplatelet antibody in 116 consecutive pregnancies: relationship to neonatal platelet count

Twenty-eight (24%) of 116 pregnant women studied prospectively during an 8-month period in 1983 had platelet counts of less than 150,000/mm3 at least once during pregnancy. Thirteen of these were thrombocytopenic in both the prenatal and the peripartum period. Eighteen were restudied 3 to 12 months after delivery. One woman, who was pregnant again, had a platelet count of 140,000/mm3. In the others, platelet counts were in the normal range. Platelet-associated immunoglobulin G and serum antiplatelet antibody levels were elevated in 79% and 61%, respectively, of these 28 women on at least one occasion. However, 59% of 73 pregnant nonthrombocytopenic women had increased platelet-associated immunoglobulin G levels and 59% had positive serum antiplatelet antibody test results. Twenty women who had increased platelet-associated immunoglobulin G levels and positive serum antiplatelet antibody test results were normal 6 to 10 months after delivery. Of 105 infants studied, 10 were thrombocytopenic. Neonatal thrombocytopenia was not predicted by maternal platelet count, platelet-associated immunoglobulin G, or serum antiplatelet antibody. By the fall of 1984, the incidence of thrombocytopenia had dropped to two in 280 consecutive pregnancies. We conclude that (1) epidemics of thrombocytopenia can occur in pregnant women and (2) if a women is found to be thrombocytopenic for the first time during pregnancy, she should not be subjected to the measures advocated for the management of pregnancy in women with autoimmune thrombocytopenic purpura.     

Low neonatal risk of thrombocytopenia in pregnancy associated with immune thrombocytopenic purpura.

OBJECTIVE: To estimate the risk of neonatal thrombocytopenia in infants born to mothers with immune thrombocytopenic purpura (ITP). METHODS: During the years 1993-1997, there were 6,082 deliveries. There were 32 infants born to 31 mothers with ITP. Cordocentesis was performed between 34 and 41 weeks of gestation in 16 mothers with ITP. The cord blood platelet count was checked in all cases at delivery. RESULTS: In mothers with ITP, 5 neonates (15.6%) had mild thrombocytopenia and 7 neonates (21.9%) moderate thrombocytopenia. Severe thrombocytopenia was not observed in any neonate born to mothers with ITP. CONCLUSIONS: The means of delivery in pregnant women with ITP can be determined solely on the basis of obstetric indications because the incidence of severe fetal and neonatal thrombocytopenia is very rare, neonatal intracranial hemorrhage is unlikely to be related to the mode of delivery and percutaneous umbilical blood sampling is technically difficult with a risk of fetal death.     

Management of immune thrombocytopenic purpura in pregnancy

Chronic immune thrombocytopenic purpura (ITP) is an autoimmune disease characterized by a low platelet count and mucocutaneous bleeding. Pregnancy does not increase the incidence of ITP nor does it exacerbate a preexisting disease. Although pregnant women with ITP may experience several maternal and fetal complications, in most cases even with a very low platelet count, there is neither maternal nor fetal morbidity or mortality. Corticosteroids are the first line of therapy in pregnant women; intravenous immune globulin is commonly used in steroid resistant patients. Other treatments such as intravenously administered anti-D (Rhogam) and splenectomy during pregnancy have been reported. Antiplatelet IgG antibodies can cross the placenta and can induce fetal thrombocytopenia. In most women there is no indication to assess fetal platelet counts during the pregnancy. The mode of delivery is determined by obstetrical considerations.     

Maternal antiplatelet antibodies in predicting risk of neonatal thrombocytopenia

Objective: To determine the incidence of maternal antiplatelet antibodies in cases of thrombocytopenia during pregnancy, using the monoclonal antibody–specific immobilization of platelet antigens assay; and to assess the usefulness of this assay for predicting risk of neonatal thrombocytopenia.Methods: A total of 6770 pregnant women were included in the study, and the monoclonal antibody–specific immobilization of platelet antigens assay was done when platelet counts were less than 150 × 10⁹/L. Platelet counts were determined in 6103 newborns.Results: The incidence of maternal thrombocytopenia was 11.6% (95% confidence interval [CI] 10.8, 12.4). Among newborns, 1.3% (95% CI 0.5, 2.7) born to thrombocytopenic mothers were thrombocytopenic, compared with 0.4% (95% CI 0.2, 0.6) born to nonthrombocytopenic women. Antiplatelet antibodies were detected in 37 (8.6%) of 430 thrombocytopenic women; autoantibodies were detected in 28 cases (circulating or bound to platelets), alloantibodies in eight cases, and an association of alloantibodies and autoantibodies in one case. The positive and negative likelihood ratios for predicting neonatal thrombocytopenia were 4.6 and 0.7, respectively.Conclusion: The monoclonal antibody–specific immobilization of platelet antigens assay did not predict the risk of neonatal thrombocytopenia in an unselected population of thrombocytopenic pregnant women.     

Immune thrombocytopenic purpura in pregnancy: a reappraisal of management

Management and, particularly, mode of delivery of the pregnant patient with immune thrombocytopenic purpura (ITP) are controversial. We reviewed our experience with 31 pregnancies in 25 women with ITP over a 10-year period. Fourteen infants were born vaginally and 18 by cesarean. Six major complications occurred among mothers delivered by cesarean, whereas none occurred among those born vaginally (P = .028). Three of 32 infants were born with moderate thrombocytopenia (platelet count 51-100 x 10(9)/L) and two with severe thrombocytopenia (platelet count 50 x 10(9)/L or less); there were no clinically significant complications in these infants. No maternal characteristic could be used to predict the neonatal platelet count. In an analysis of 474 infants of mothers with ITP reported in the literature and including the present series, 10% were born with moderate thrombocytopenia and 15% with severe thrombocytopenia. The overall rate of intracranial hemorrhage in newborns with moderate or severe thrombocytopenia was 3%. No significant association was found between the rate of intracranial hemorrhage and delivery mode for moderately and severely thrombocytopenic neonates together (weighted odds ratio 1.69, 95% confidence interval 0.14-44.6) or for those with severe thrombocytopenia (crude odds ratio 1.38, 95% confidence interval 0.07-84.67). We conclude that the mode of delivery may not affect the rate of intracranial hemorrhage in thrombocytopenic newborns.     

Pregnancy outcome in patients with idiopathic thrombocytopenic purpura

Objective

To study the outcome of pregnancy in women with idiopathic thrombocytopenic purpura.

Materials and methods

A retrospective analysis of 30 pregnancies in 26 women with idiopathic thrombocytopenic purpura was carried out at a tertiary hospital in India. The courses of the disease, maternal and perinatal outcome in these pregnancies were studied.

Results

Mean age of pregnant women with idiopathic thrombocytopenic purpura was 27.3 years and 61.5 % was primigravidae. Out of 26 patients with idiopathic thrombocytopenic purpura, 16 were already diagnosed while the other 10 were diagnosed during pregnancy. The incidence of bleeding episodes in antenatal period, severe thrombocytopenia and hemorrhagic complications at the time of delivery was 30, 37 and 11.1 %, respectively. Oral steroids were required in 40 % of pregnancies. Two patients received intravenous immunoglobulin therapy. Severe thrombocytopenia at the time of delivery was more commonly seen in women in whom ITP was diagnosed during pregnancy as compared to those in whom ITP was diagnosed prior to pregnancy (P = 0.04). Severe thrombocytopenia was seen in 18.5 % of neonates and intracranial hemorrhage was detected in 1 neonate. There were no still births or maternal mortality.

Conclusion

Pregnancy outcome in patients with idiopathic thrombocytopenic purpura is generally good.     

Predictors of idiopathic thrombocytopenic purpura in pregnant women presenting with thrombocytopenia.

OBJECTIVE: Idiopathic thrombocytopenic purpura (ITP) and gestational thrombocytopenia (GT) are common causes of thrombocytopenia during pregnancy. Despite an ever-increasing experience with these disorders, differentiation between the two entities still remains a diagnostic challenge. The current study attempted to identify the antenatal predictors of ITP for pregnant women. METHODS: Between January 1999 and June 2005, a total of 58 pregnant women with a presumptive diagnosis of either ITP or GT were recruited for the study. All of them had platelet counts of less than 100 x 10(9)/L. The predictors of ITP were evaluated by comparison between the two disorders. RESULTS: The detection of thrombocytopenia prior to 28 weeks of gestation and platelet counts <50 x 10(9)/L at its diagnosis remained independently predictive of ITP (P<0.001 and P=0.004, respectively). The combined analysis of these two factors provided a 96.0% sensitivity and a specificity of 75.8%. CONCLUSION: The onset time of thrombocytopenia and platelet count at its presentation remain the strongest predictors of ITP for pregnant women. The combination model using these factors may be useful for the early prediction of ITP.