妊娠合并血小板减少的临床分析

目的:探讨妊娠期血小板减少的病因及处理方法。方法:回顾性分析我院36例妊娠合并血小板减少患者临床资料。结果:妊娠期血小板减少症(PAT)17例占47.2%,特发性血小板减少性紫癜(ITP)12例占33.3%,妊娠高血压综合征(PIH)2例占5.5%,其他病因包括血栓性血小板减少性紫癜2例,上呼吸道病毒感染者2例,Evans综合征1例。血小板减少出现最早孕周为3周,<12周出现5例(13.9%),12～28周出现6例(16.7%),>28周出现25例(69.4%);对血小板减少严重的病例可以应用糖皮质激素、输注浓缩血小板或IVIgG治疗。全部病例无孕产妇死亡。结论:妊娠血小板减少原因较多,应依据不同病情进行处理。对血小板减少严重的病例,根据不同病因,应用糖皮质激素、输注浓缩血小板或IVIgG治疗效果较好。     

Asymptomatic thrombocytopenia developing during pregnancy (gestational thrombocytopenia)--a clinical study.

During pregnancy some women develop unexplained thrombocytopenia (gestational thrombocytopenia). Previous studies have detected abnormal platelet antibodies, suggesting an autoimmune aetiology. To determine whether gestational thrombocytopenia is associated with increased maternal bleeding or adversely affects the fetus, 31 pregnant women with asymptomatic thrombocytopenia were compared with 12 women with thrombocytopenia associated with pre-eclampsia and 34 normal pregnant controls. There was no increase in maternal bleeding in those with asymptomatic thrombocytopenia compared with the normal controls, but pre-eclamptic women experienced more bleeding (mean difference 181 ml, 95 per cent confidence limits 50-312 ml, p < 0.01). There was no difference in the mean weights of the babies or placenta, nor in the APGAR scores between infants born to controls and those with asymptomatic thrombocytopenia. Cord blood platelet levels were measured in 26 women with asymptomatic thrombocytopenia and were normal in 25 and mildly reduced in one. Thus measures used for the treatment and delivery of pregnancies complicated by autoimmune thrombocytopenia are not indicated in gestational thrombocytopenia. Pregnant women should not be considered thrombocytopenic unless the platelet count has fallen below 120 x 10(9)/l.     

Reacting appropriately to thrombocytopenia in pregnancy

The lower limit of normal for the platelet count is considered to be 150,000/cu mm in both pregnant and nonpregnant normal adults. In the absence of preeclampsia, sepsis, drugs, or other apparent causes, the finding of asymptomatic mild thrombocytopenia in pregnant women is compatible with previously unrecognized immune thrombocytopenic purpura (ITP). Because of the risk of fetal/neonatal thrombocytopenia and the subsequent risk of neonatal intracranial hemorrhage in infants born of mothers with ITP, the optimal mode of delivery for an asymptomatic but thrombocytopenic mother is problematic. Conceivably, those gravidas with mild previously unrecognized thrombocytopenia may not have ITP and thus could be spared cesarean section. From the platelet counts of 730 antepartum patients, we found a mean value of 263,900/cu mm with a standard deviation of 66,000/cu mm, yielding 95% confidence limits of 134,500 to 393,300/cu mm. The distribution is statistically indistinguishable from a normal distribution. Of 26 asymptomatic thrombocytopenic patients with no hematologic history, none had infants with hemorrhage or platelet counts less than 100,000/cu mm. Only one patient subsequently had severe glucocorticoid-resistant thrombocytopenia requiring splenectomy several months after delivery. The remaining patients continue to be asymptomatic to date, with platelet counts greater than 100,000/cu mm. We suggest a plan for managing less than normal platelet counts in asymptomatic gravidas without a history of hematologic abnormality.     

Asymptomatic Thrombocytopenia Developing During Pregnancy (Gestational Thrombocytopenia) - A Clinical Study

During pregnancy some women develop unexplained thrombocytopenia(gestational thrombocytopenia). Previous studies have detectedabnormal platelet antibodies, suggesting an autoimmune aetiology.To determine whether gestational thrombocytopenia is associatedwith increased maternal bleeding or adversely addressed affectsthe fetus, 31 pregnant women with asymptomatic thrombocytopeniawere compared with 12 women with thrombocytopenia associatedwith pre-eclampsia and 34 normal pregnant controls. There wasno increase in maternal bleeding in those with asymptomaticthrombocytopenia compared with the normal controls, but pre-eclampticwomen experienced more bleeding (mean difference 181 ml, 95per cent confidence limits 50-312 ml, p < 0.01). There wasno difference in the mean weights of the babies or placenta,nor in the APGAR scores between infants born to controls andthose with asymptomatic thrombocytopenia. Cord blood plateletlevels were measured in 26 women with asymptomatic thrombocytopeniaand were normal in 25 and mildly reduced in one. Thus measuresused for the treatment and delivery of pregnancies complicatedby autoimmune thrombocytopenia are not indicated in gestationalthrombocytopenia. Pregnant women should not be considered thrombocytopeniaunless the platelet count has fallen below 120 x 10⁹/l.     

Thrombocytopenia in Pregnancy: Mechanisms and Management

Thrombocytopenia is a common hematologic issue encountered by obstetricians and hematologists, detected in about 10% of all pregnancies. In the vast majority of cases, the thrombocytopenia will be attributed to gestational thrombocytopenia (GT), where the thrombocytopenia is mild, does not necessitate active management, and does not introduce maternal or fetal bleeding risk. Although GT is common, the specific mechanism responsible for it is not known with certainty, and therefore, differentiating it from other causes of thrombocytopenia can be challenging. Previously proposed explanations for GT suggest that a decrease in platelet count is universal in pregnancy, and women diagnosed with GT are simply those with a baseline platelet count on the lower end of normal range. This concept is challenged in this review, and a possible mechanism for GT is proposed. Additionally, a framework for approaching the diagnosis and management of thrombocytopenia in pregnancy is presented.     

妊娠合并血小板减少症28例临床分析

目的 探讨妊娠合并血小板减少的病因和围生期的处理方法.方法 回顾分析28例妊娠合并血小板减少患者的临床资料,使用糖皮质激素、免疫球蛋白及成分输血等治疗方法.结果 28例血小板减少的病因为妊娠期特发性血小板减少13例,HELLP综合征4例、特发性血小板减少性紫癜3例、再生障碍性贫血2例、脾功能亢进1例及不明病因5例.早产3例,阴道分娩6例、剖宫产19例.结论 妊娠合并血小板减少处理的重点是治疗病因,加强监护,适时提升血小板数,防止分娩期出血.     

Fetomaternal alloimmune thrombocytopenia.

Thrombocytopenia is the second commonest haematological abnormality in the neonatal period after anaemia due to iatrogenic blood letting. One to four percent of all newborn babies have a platelet count < 150 x 10(9)/l at birth and approximately 20-40% of neonates in intensive care units are affected by neonatal thrombocytopenia. The most common cause of severe neonatal thrombocytopenia is fetomaternal platelet incompatibility and subsequent alloimmunisation. During the last decade recent advances in molecular techniques have led to rapid and efficient methods for diagnosis. Progress in fetal medicine has enabled accurate determination of fetal status, allowing improvements in fetal diagnosis and therapy. Human platelet antigen (HPA)-1a is by far the most frequently involved platelet antigen system in Caucasians accounting for 90% of cases, followed at a much lower frequency by HPA-5b (5-15%) and HPA-3a. The incidence is estimated to be 1 per 2000 to 1 per 5000 live births, but this is low in comparison to the incidence of fetomaternal platelet antigen incompatibility especially for the HPA-1 alloantigen system in the Caucasian population in whom the estimated frequency of HPA-1b1b individuals is 2%. Retrospective and prospective studies have reported that the immunogenetic background is important, and the chance of HPA-1a alloimmunisation is strongly associated with maternal HLA class II DRB3*0101 (DR52a) type. A significant association (p = 0.004) between severe thrombocytopenia and a third trimester antiHPA titre >1:32 has been observed. It is now possible to genotype the fetus or neonate and the parents, which provides confirmation as to which HPA systems are incompatible between the mother and father. Simultaneous genotyping of HPA-1, 2, 3 and 5 can be carried out using the polymerase chain reaction-sequence specific primers (PCR-SSP) protocol, which has been widely used for HLA class II determination. The platelet count may continue to fall during the first 48 h after birth and the risk of intracranial bleeding is highest during this period. The best option is transfusion of specially selected antigen negative compatible donor platelets or if unavailable, maternal washed platelets. Antenatal screening for the most common form of fetomaternal alloimmune thrombocytopenia (FMAIT), due to antiHPA-1a is under consideration, but there is no established method at present. The Scottish National Blood Transfusion Service started a study in August 1999 on 25,000 pregnancies to carry out a cost benefit analysis of routine antenatal screening. The aims of the study are to determine the frequency of HPA-1b homozygosity; monitor antibody titres during pregnancy and confirm correlation of antibody emergence with HLA-DRB3*0101, and finally to access cost effectiveness of routine screening across Scotland. Of 26,509 women screened in three Scottish regions 501 (1.9%) are HPA-1b homozygous and about 9%, of the consented women are antibody positive.     

妊娠合并血小板减少的病因及母婴结局分析

目的 探讨妊娠合并血小板减少（PT）的病因及母婴结局。方法 收集228例PT患者,其中血小板（51 ~ 100）×10⁹/L为轻度组,血小板（30 ~ 50）×10⁹/L为中度组,血小板< 30×10⁹/L为重度组,比较3组患者的病因和母婴结局的差异。结果 228例PT孕妇中,轻度血小板减少159例（69.8%）,中度血小板减少33例（14.5%）,重度血小板减少36例（15.8%）。主要病因有妊娠相关性血小板减少症（63.6%）、特发性血小板减少性紫癜（11.8%）、HELLP综合征（3.9%）、SLE（3.9%）和子痫前期-子痫（2.2%）。轻度组、中度组和重度组的妊娠丢失、早产、产后出血、新生儿血小板减少的发生率及分娩孕周比较差异均有统计学意义（P均< 0.05）,其中重度组的妊娠丢失率、早产率、产后出血率均高于轻度组,分娩孕周短于轻度组（P均< 0.017）。结论 PT的病因复杂多样,病因多见妊娠相关性血小板减少症、特发性血小板减少性紫癜、HELLP综合征、SLE和子痫前期-子痫。血小板< 30×10⁹/L的PT患者发生妊娠丢失、早产、产后出血的概率明显增加。     

孕晚期产妇生殖道B族链球菌感染与胎膜早破及新生儿结局的相关性

目的:探讨孕晚期产妇生殖道B族链球菌(group B Streptococcus,GBS)感染与胎膜早破及新生儿结局的相关性。方法:搜集2017年5月至2019年8月首都医科大学附属北京世纪坛医院产科门诊的2100例孕妇,选取其中122例孕晚期胎膜早破产妇作为观察组,另选取120例同期健康孕晚期产妇作为健康对照组,比较两组GBS感染率,依据观察组患者是否合并GBS感染,将其分为GBS阴性组与GBS阳性组,采用单因素和多因素logistic回归分析影响胎膜早破孕妇GBS感染的危险因素,观察不同组别不良妊娠情况及新生儿结局。结果:健康对照组GBS感染率显著低于观察组(P<0.05);两组孕妇胎位异常、双胎或多胎妊娠和巨大儿发生率比较差异具有统计学意义(P<0.05);经多因素logistic回归模型分析结果显示胎位异常、双胎或多胎妊娠和巨大儿为影响胎膜早破孕妇GBS感染的危险因素(P<0.05)。GBS阴性组早产、产后出血和宫内感染率均显著低于GBS阳性组(P<0.05);GBS阳性组新生儿窒息和新生儿肺炎感染发生率均高于GBS阴性组(P<0.05);两组新生儿感染率比较,差异无统计学意义(P>0.05)。结论:胎位异常、双胎或多胎妊娠和巨大儿均可影响孕晚期胎膜早破产妇GBS感染,GBS感染可致新生儿窒息、新生儿感染和新生儿肺炎的发生,同时引起早产、产后出血和宫内感染等不良妊娠结局的发生。临床需要对孕晚期产妇生殖道GBS感染进行及时监测和处理,以降低其不良母婴结局的发生率。     

Headaches During Pregnancy

Among primary headaches, migraine is the form more sensitive to the ovarian hormonal milieu. Migraine without aura (MO) benefits from the hyperestrogenic state of pregnancy and the lack of hormonal fluctuations, while migraine with aura (MA) presents distinctive features. Indeed, a very strong improvement of MO has been documented across gestation, and only a minority of pregnant women still suffers during the third trimester. On the other hand, fewer women with MA report improvement or remission, and new onset of aura may be observed during pregnancy. After delivery, breastfeeding exerts a protective action on migraine recurrence. The persistence of migraine during gestation seems to affect neonatal outcomes, and several studies indicate a link between migraine and an increased risk of developing gestational hypertension/preeclampsia and other vascular complications.     

孕晚期胎儿心脏室壁厚度与妊娠期糖尿病孕妇HbA1c水平控制状态的关系

目的观察孕晚期胎儿心脏室壁厚度与妊娠期糖尿病孕妇HbA1c水平控制状态的关联并讨论其临床意义。方法随机择2015年1月~2019年6月我院接受孕检的罹患妊娠期糖尿病的122例单胎妊娠孕妇及其胎儿为研究对象。收集母亲孕早期、孕中期以及孕晚期HbA1c信息,借助超声检测收集孕晚期胎儿心室壁厚度信息等相关资料信息,分析孕晚期胎儿心脏室壁厚度与母亲孕期HbA1c水平控制状态的关联情况。结果孕早期受试对象的HbA1c水平为（5.80±1.60）%,孕中期为（5.91±1.61）%,孕晚期为（5.97±1.86）%,3个时期测定水平差异无统计学意义（P>0.05）,不同孕期HbA1c控制情况分布特征差异无统计学意义（P>0.05）;孕早期、孕中期和孕晚期不同HbA1c控制水平的孕妇,在孕晚期经超声测定胎儿的心室壁厚度和室间隔厚度比较可见,孕早期和孕中期不同HbA1c控制水平的胎儿舒张晚期、收缩晚期左右心室以及室间隔的厚度差异无统计学意义,但是绝对数字可见血糖水平控制不佳的孕妇胎儿心室壁和室间隔厚度均相对更高;孕晚期母亲血糖水平对胎儿收缩晚期左心室壁厚度影响相对较大,孕晚期母亲HbA1c控制水平不佳者均可见胎儿收缩晚期左心室壁厚度更大（P < 0.05）;孕晚期母亲HbA1c水平控制不良与孕晚期胎儿测定的舒张晚期左心室厚度、收缩晚期左心室厚度以及舒张晚期室间隔厚度呈正相关关系（r=0.404、0.361、0.332,P < 0.05）。结论罹患妊娠糖尿病的孕妇,血糖控制不佳会影响引发胎儿心室壁和室间隔增厚,有可能对胎儿心脏发育造成不良影响,基于此建议尽量有效控制孕妇血糖水平处于良好范围,特别是孕晚期控制血糖水平,以便减低胎儿和新生儿的心脏损害。     

Thrombocytopenia

Thrombocytopenia is defined as a platelet count of less than 150 × 103 per μL. It is often discovered incidentally when obtaining a complete blood count during an office visit. The etiology usually is not obvious, and additional investigation is required. Patients with platelet counts greater than 50 × 103 per μL rarely have symptoms. A platelet count from 30 to 50 × 103 per μL rarely manifests as purpura. A count from 10 to 30 × 103 per μL may cause bleeding with minimal trauma. A platelet count less than 5 × 103 per μL may cause spontaneous bleeding and constitutes a hematologic emergency. Patients who present with thrombocytopenia as part of a multisystem disorder usually are ill and require urgent evaluation and treatment. These patients most likely have an acute infection, heparin-induced thrombocytopenia, liver disease, thrombotic thrombocytopenic purpura/hemolytic uremic syndrome, disseminated intravascular coagulation, or a hematologic disorder. During pregnancy, preeclampsia and the HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome are associated with thrombocytopenia. Patients with isolated thrombocytopenia commonly have drug-induced thrombocytopenia, immune thrombocytopenic purpura, pseudothrombocytopenia, or if pregnant, gestational thrombocytopenia. A history, physical examination, and laboratory studies can differentiate patients who require immediate intervention from those who can be treated in the outpatient setting. Treatment is based on the etiology and, in some cases, treating the secondary cause results in normalization of platelet counts. Consultation with a hematologist should be considered if patients require hospitalization, if there is evidence of systemic disease, or if thrombocytopenia worsens despite initial treatment.     

Management of pregnant women complicated with idiopathic thrombocytopenic purpura

Idiopathic thrombocytopenic purpura(ITP) is occasionally manifested during pregnancy by routine prenatal screening for blood cell counts. Since ITP can potentially cause serious hemorrhage both in mother and fetus, the accurate assessments as well as appropriate clinical managements are necessary for successful delivery. Several guidelines were introduced to manage the maternal thrombocytopenia by ITP in pregnancy and in labor. However, there still remain several controversies regarding the indication of measurement of fetal platelet counts by fetal blood sampling, especially by percutaneous umbilical blood sampling, to decide mode of delivery. The current obstetrical managements and their potential limitation are discussed in this review.     

妊娠合并血小板减少78例临床分析

目的探讨妊娠合并血小板减少的临床特点及围生期处理。方法对1997-2007年共78例妊娠合并血小板减少的患者进行回顾性分析。结果妊娠合并血小板减少中,33．3％为妊娠相关性血小板减少（PAT）,12．8％为妊娠高血压疾病,23％为ITP。PAT不需特殊处理,妊娠高血压疾病以输血小板为主,ITP组以皮质激素及免疫球蛋白为主,全部病例无产妇死亡及新生儿血小板减少。结论妊娠期血小板减少原因很多,应依据不同病情进行不同处理。     

西安地区正常妊娠妇女孕早中晚期血常规检测指标参考区间的调查分析

目的建立西安地区妊娠女性孕早、中、晚期血液学相关参数的参考区间。方法选取空军军医大学第一附属医院2017年3月至2018年2月门诊妊娠女性1 197例,按照孕周分为孕早、中、晚期;选择同期体检健康的非孕育龄期女性300例作为健康人对照组;分别检测白细胞计数(WBC)、红细胞计数(RBC)、血红蛋白(Hb)、血细胞比容(Hct)、红细胞平均体积(MCV)、平均红细胞血红蛋白含量(MCH)、平均红细胞血红蛋白浓度(MCHC)、血小板(PLT)并进行统计分析,建立参考区间。结果妊娠女性在不同孕期RBC、Hb、HCT、MCV、MCH、MCHC的水平均低于健康人对照组,孕晚期下降达孕期最低水平(P0.05),不同孕期之间比较差异有统计学意义(P0.05)。妊娠女性WBC水平随孕周的增加逐渐升高,至孕晚期达最高水平,不同孕期之间WBC比较差异有统计学意义(P0.05)。妊娠女性PLT水平较健康人对照组降低,在孕晚期达最低水平(P0.05)。结论妊娠女性血液学相关参数不同于育龄期健康非孕女性,各临床实验室应建立女性妊娠各期血液学相关参数参考区间。     

GBS阳性孕妇阴道微生态与妊娠不良事件的相关性

目的 研究B族链球菌(GBS)阳性孕妇阴道微生态与不良妊娠事件间的相关性.方法 前瞻性选取2017年6月至2019年6月间于恩施州土家族苗族自治州中心医院行常规孕检并分娩的880例孕妇纳为研究对象,分别在孕早期(孕8～12周)及孕晚期(孕37周)使用胶体金免疫层析法行GBS检测.使用五联阴道试剂盒检测阴道微生态,同时记...     

Thrombocytopenia caused by platelet destruction,consumption or abnormal pooling

In this article, we refer to thrombocytopenia caused by increased destruction/consumption of platelets(immune thrombocytopenia and non-immune thrombocytopenia), abnormal pooling, and dilutional loss. The cause of idiopathic thrombocytopenic purpura (ITP) is a accelerated platelet destruction due to autoimmune mechanism. Differential diagnosis is important between ITP and other thrombocytopenic disorders, because the treatment and prognosis are distinct. Drug-induced thrombocytopenia is the most common among secondary autoimmune thrombocytopenia and clinically important. The immediate cessation of all suspect drugs is necessary when drug-induced thrombocytopenia is suspected. Thrombocytopenia of disseminated intravascular coagulation(DIC) and thrombotic microangiopathy(TMA) occur in diffuse intravascular coagulation and induce thrombocytopenia by the consumption of the platelet.     

IgG titer, subclass, and light-chain phenotype of pregnancy-induced HPA-5b antibodies that cause or do not cause neonatal alloimmune thrombocytopenia

BACKGROUND: The most common pregnancy-induced platelet-specific antibody is HPA-5b. Neonatal alloimmune thrombocytopenia that results from anti-HPA-5b may cause severe hemorrhage in only a few infants, but the sequelae for the affected children can be severe. It is therefore essential that infants at risk for neonatal alloimmune thrombocytopenia are identified. STUDY DESIGN AND METHODS: The IgG titer, subclass, and light-chain composition of pregnancy-induced anti-HPA-5b were determined by the monoclonal antibody-specific immobilization of platelet antigens assay. Sera were from 12 mothers, who among them had 16 pregnancies that resulted in an HPA-5-mismatched fetus (positive for HPA-5b). Eight mothers gave birth to an infant with a normal platelet count. Three maternal sera were obtained after delivery of a severely thrombocytopenic infant. Three alloimmunized women were followed repeatedly during the course of a subsequent pregnancy, again with an HPA-5-mismatched infant. RESULTS: There was no difference in the antibody titer or its subclass in mothers who had a thrombocytopenic child and the titer or subclass in mothers compared with those who had a child with a normal platelet count. All pregnancy-induced HPA-5b antibodies were of a predominant, lambda, light-chain type. The IgG subclass did not change during pregnancy. CONCLUSION: Neither the antibody titer nor the subclass composition predict the occurrence of thrombocytopenia in a newborn whose mother is alloimmunized against HPA-5b.     

Assessment of iodine intake in mildly iodine-deficient pregnant women by a new automated kinetic urinary iodine determination method.

Maternal iodine deficiency can compromise the thyroid status of the mother, fetus and newborn child. Therefore, it is important to assess the iodine excretion level of groups of pregnant women. In this study we aimed to determine iodine intake in pregnancy using a recently reported automated kinetic method for urinary iodine determination. Urinary iodine measurements of 123 pregnant women (18 first, 28 second and 77 third trimester) were carried out using a new automated kinetic assay based on the Sandell-Kolthoff reaction at 37 degrees C and its kinetic measurement at 340 nm in a random-access automated analyzer after ammonium persulfate digestion at 95 degrees C in a water bath with +/-0.1 degree C precision. Statistical analyses were carried out using SPSS software. Whole group, first trimester, second trimester and third trimester urinary iodine concentrations (mean+/-SD) in pregnant women were 1.13+/-0.81, 1.08+/-0.71, 0.86+/-0.58 and 1.27+/-0.87 micromol/L, respectively. The urinary iodine concentration significantly increased with gestational age (p<0.05). We found that our study group was mildly iodine-deficient according to WHO criteria. Furthermore, the pregnant women were found to be mildly iodine-deficient in the first and third trimesters and moderately so in the second trimester. The only statistical difference was between second and third trimester values (p<0.05). Even though the increased iodine deficiency in the second trimester is not useful for early detection of iodine deficiency in pregnancy, the severity of this deficiency in the second trimester may lead to important effects on thyroid metabolism for both mother and fetus. Our study suggests that the iodine excretion of pregnant women living in iodine-deficient areas could be assessed using this fast and automated method.     

Measurement of four tumor marker antigens in the sera of pregnant women

We sought to determine the maternal serum levels of four tumor-associated antigens during the three trimesters of pregnancy in healthy women. CEA, CA 228, CA 15-3, and Her2/neu oncogene product p105 assay values were determined for 90 healthy pregnant women during the three trimesters of pregnancy at five participating evaluation sites. Results were compared to means and cut-off values determined for healthy nonpregnant women. Differences in assay values in the 1st and 3rd trimester were analyzed for statistical significance (Student's t-test). CEA, CA 228 and CA 15-3 assay values in general were found to be within the normal range. CA 15-3 and Her2/neu p105 serum assay values were above the cut-off (3.3% and 8.2%, respectively) and were significantly elevated in the 3rd trimester as compared to the 1st trimester of pregnancy (P < 0.05 and P < 0.001, respectively). CEA and CA 228 may be of potential value in monitoring pregnant women with malignant disease. Normal elevations in 3rd trimester serum Her2/neu p105 and CA 15-3 assay values should be considered when monitoring a pregnant patient with malignant disease.