巨噬细胞集落刺激因子与妊高征关系的研究

采用酶联免疫双抗体夹心（ＥＬＩＳＡ）法测定了２１例妊娠高血压综合征（下称妊高征）患者（妊高征组）、２４例正常晚期妊娠妇女（正常妊娠组）及１０例健康非孕妇女（非孕组）的血浆中巨噬细胞集落刺激因子（Ｍ－ＣＳＦ）浓度。结果：血浆Ｍ－ＣＳＦ浓度正常妊娠组显著高于非孕组（Ｐ〈０．００１）,妊高征组显著高于正常妊娠组（Ｐ〈０．０５）,重度妊高征患者显著高于轻、中度妊高征患者（Ｐ〈０．０５）和正常妊娠组（Ｐ〈０     

儿童置入频率适应性起搏器前后药物负荷左室收缩功能的研究

目的　了解儿童完全性房室传导阻滞（ＣＡＶＢ）置入频率适应性起搏器前后左室收缩功能的变化。方法　对６ 例３～１２ 岁ＣＡＶＢ患儿,采用多巴酚丁胺负荷超声心动图技术测定起搏器置入术前及术后３～６ 月的左室短轴缩短率（ＦＳ）、射血分数（ＥＦ）、室壁增厚率（ＬＶＰＷＴ）、应变率（ＭＶＣＦＣ） 、每搏指数（ＳＩ） 及心排指数（ＣＩ）,并与８ 例正常同龄儿童进行对比分析。结果　术前ＦＳ及ＥＦ均随药物浓度增加而稍增大,但与对照组比较无显著差异,Ｐ 均＞ ０－０５;ＬＶＰＷＴ、ＭＶＣＦＣ及ＳＩ于静息状态及低药物浓度时明显高于对照组,Ｐ＜０－０５,随药物浓度增加而无明显增大,Ｐ＞ ０－０５;ＣＩ于静息状态及低药物浓度时与对照组无差异,Ｐ＞０－０５,但随药物浓度增加而出现明显差异,Ｐ＜ ０－０５。术后ＬＶＰＷＴ、ＭＶＣＦＣ、ＳＩ、ＣＩ均随药物浓度增加而增大,与对照组比较无明显差异,Ｐ＞０－０５ 。结论　ＣＡＶＢ 患儿,静息状态下左室收缩功能正常,但药物负荷状态下出现储备功能不足,置入频率适应性起搏器后左室收缩储备功能可达正常。     

脑梗塞患者炎性因子、血管活性肽含量变化及相互关系的研究

目的 探讨ＴＮＦ－α，ＩＬ－２和ＥＴ，ＣＧＲＰ的含量变化与脑梗塞发生的相互关系，方法 应用放射免疫分析法，检测了３４例脑梗塞患得及３０例正常人外用血和脑脊液中ＴＮＦ－αＩＬ－２，ＥＴ，ＣＧＲＰ含量。结果 脑梗塞患者血，脑脊液中ＴＮＦ－α，ＩＬ－２含量均显著高于对照组（Ｐ〈０．００１）。外周血ＥＴ含量显著高于对照组（Ｐ〈０．０５）。脑脊液中ＣＧＲＰ含量则明显低于对照组（Ｐ〈０．０５）。并且血中ＴＮＦ     

城乡维吾尔族及汉族围产期妇女和新生儿巨细胞病毒IgM的检测分析

用生物学－亲和素酶联免疫吸附试验（ＡＢＣ－ＥＬＩＳＡ）法对维吾尔族及汉族围产期妇女（简称围产妇）和新生儿血清进行巨细胞病毒（ＣＭＶ）ＩｇＭ测定和关联分析。维吾尔族围产妇和新生儿感染率与汉族对应组存在显差异（Ｐ〈０．０５），新生儿ＣＭＶ特异性抗体检出率与围产妇近期高感染率密切相关（Ｐ〈０．０５）。农村妊娠晚期妇女和新生儿ＣＭＶ的感染率均高于城市对照组（Ｐ〈０．０５）。研究结果提示：了解孕妇ＣＭＶ感     

自体骨髓移植后血清TNF—α,IFN—α活性研究

应用ＴＮＦ－α和ＩＦＮ－α依赖细胞ＭＴＴ比色分析法，研究了５例自体骨髓移植（ＡＢＭＴ）病人血清中ＴＮＦ－α、ＩＦＮ－α活性，。处于完全缓解期的急性粒细胞性白血病（ＡＭＬ）血清中ＴＮＦ－α生显著的高于正常成人（ＰＢｓ）组（Ｐ〈０．０５）；ＩＦＮ－α活性明显低于ＰＢｓ组（Ｐ〈０．０１）。ＡＢＭＴ前血清中的ＴＮＦ－α、ＩＦＮ－α活性显著高于ＡＢＭＴ后９－１０天（Ｐ〈０．０５）和２１天（Ｐ〈０．０５）；与     

充血性心力衰竭时单核细胞诱生肿瘤坏死因子-α测定及临床意义

目的：研究外周血单核细胞诱生肿瘤坏死因子－α（ＴＮＦ－α）在充血性心力衰竭（ＣＨＦ）发病中的作用。 方法：体外培养１１３例心脏疾病患者（无ＣＨＦ组３７例,严重ＣＨＦ组５０例,ＣＨＦ并恶病质组２６例）外周血单核细胞,用固相酶放大敏感免疫法测定其培养液中外周血单核细胞经脂多糖诱生的ＴＮＦ－α（ＰＢＭＣ－ＴＮＦ－α）及血清ＴＮＦ－α浓度。 结果：①严重ＣＨＦ组血清ＴＮＦ－α浓度较无ＣＨＦ组明显增高（Ｐ＜０．０５）,ＣＨＦ并恶病质组增高更为显著（Ｐ均＜０．０１）;②无ＣＨＦ组、严重ＣＨＦ组、ＣＨＦ并恶病质组３组ＰＢＭＣ－ＴＮＦ亦有显著性差异（Ｐ均＜０．０１）;③ＰＢＭＣ－ＴＮＦ与心功能分级呈明显正相关（ｒ＝０． ４８,Ｐ＜０．０１）;④ＰＢＭＣ－ＴＮＦ－α与血清 ＴＮＦ－α浓度无明显相关性。 结论：外周血单核细胞的激活是ＣＨＦ的临床特征之一,其分泌的ＴＮＦ－α至少部分参与ＣＨＦ及ＣＨＦ恶病质的病理生理过程。     

胃良性病变患者血清及胃粘膜组织中白细胞介素—1水平检测及其临床意义

采用细胞生物反应法测定了慢性浅表胃炎（ＣＳＧ）、胃溃疡（ＧＵ）及慢性萎缩性胃炎（ＣＡＧ）患者血清及胃组织的白细胞介素－１（ＩＬ－１）含量。结果显示，各组间血清ＩＬ－１水平无显著差异（Ｐ〉０．０５）。组织中ＩＬ－１水平ＣＳＧ组低于ＣＡＧ组（Ｐ〈０．０５），但与对照组、ＧＵ组比较无差异（Ｐ〉０．０５）；ＧＵ组低于正常组（Ｐ〈０．０５）；ＣＡＧ组高于Ｎ组，ＣＳＧ组、ＧＵ组（Ｐ〈０．０１）。提示局部胃粘膜     

自发性细菌性腹膜炎病人腹水G-CsF和CRP检测的临床意义

目的：探讨自发性细菌性腹膜炎（ＳＢＰ）病人腹水中粒细胞集落刺激因子（Ｇ－ＣＳＦ）和Ｃ－反应蛋白（ＣＲＰ）水平的变化和临床意义。方法：采用双抗体夹心ＥＬＩＳＡ法测定Ｇ－ＣＳＦ,快速免疫消浊比浊法测定ＣＲＰ。结果：２８例ＳＢＰ病人血清和腹水Ｇ－ＣＳＦ和ＣＲＰ水平明显高于２０例漏出性腹水病人（Ｐ〈０．０１）。ＳＢＰ病人腹水中的Ｇ－ＣＳＦ和ＣＲＰ水平明显高于血清中的水平。随着感染的控制,腹水中Ｇ－ＣＳＦ和ＣＲＰ水平逐渐下降（Ｐ〈０．０５）。结论：腹水Ｇ－ＣＳＦ和ＣＲＰ的检测有助于对ＳＢＰ的诊断和疗效观察。     

血透相关因素对维持性血透患者外周血单个核细胞产生IL－1β、TNFα的影响

观察了１５名正常人及１４例维持性血液透析（ＭＨＤ）患者外周血单个核细胞（ＰＢＭＣ）在脂多糖（ＬＰＳ）刺激下产生和分泌白细胞介素－Ｉβ（ＩＬ－１β）、肿瘤坏死因子α（ＴＮＦα）的情况，以及铜仿膜和血仿膜、醋酸盐和碳酸盐透析液对ＰＢＭＣ产生和分泌ＩＬ－１β、ＴＮＦα的影响。结果表明，ＭＨＤ患者ＰＢＭＣ在ＬＰＳ刺激下，产生和分泌ＩＬ－１β、ＴＮＦα的量明显高于正常人（Ｐ＜０．０５）。铜仿膜透析组，血透５ｍｉｎ时ＩＬ－１β、ＴＮＦαｍＲＮＡ的表达达高峰，与透前及正常对照组相比，有显著性差异（Ｐ＜０．０５），其生物活性或蛋白质水平也相应升高，较正常对照组及透前水平均有显著性差异（Ｐ＜０．０５）。血仿膜组ＩＬ－１β、ＴＮＦα的表达和蛋白质水平虽较正常对照组升高，但无统计学差异（Ｐ＞０．０５）。碳酸盐与醋酸盐组无明显差异。提示ＬＰＳ是引起ＰＢＭＣ产生和释放ＩＬ－１β、ＴＮＦα的重要因素；铜仿膜透析器亦可促进细胞因子的产生     

老年人红细胞膜唾液酸含量与红细胞免疫功能的相关性

目的探讨老年人红细胞膜唾液酸（ＲＢＣｍ－ＳＡ）与红细胞免疫功能的相关性。方法采用Ｂｉａｌｓｃｈｅ试剂法检测ＲＢＣｍ－ＳＡ，Ｆ－８８３６化学比色法检测血浆唾液酸（Ｐ－ＳＡ），红细胞免疫粘附试验观察红细胞Ｃ３ｂ受体花环率（ＲＲＣＦ）。结果老年急性心肌梗死（ＡＭＩ）组和脑梗塞（ＡＣＩ）组的ＲＢＣｍ－ＳＡ分别为３０．８±４．３和３１．３±４．４μｇＮＡＮＡ／ｍｇ膜蛋白，ＲＲＣＦ分别为１６．７％±３．５％和１６．０％±３．６％，均低于老年对照组（Ｐ＜０．０１或０．０５），老年对照组均低于非老年对照组（均为Ｐ＜０．０５）；ＡＭＩ和ＡＣＩ患者的Ｐ－ＳＡ分别为２．４±０．４和２．４±０．３ｍｍｏｌ／Ｌ，均高于老年对照组（均为Ｐ＜０．０５），老年对照组则高于非老年对照组（Ｐ＜０．０５）。老年患者和老年对照组的ＲＢＣｍ－ＳＡ与ＲＲＣＦ均呈正相关，而ＲＢＣｍ－ＳＡ与Ｐ－ＳＡ均呈负相关。结论老年人红细胞Ｃ３ｂ受体花环率降低与ＲＢＣｍ－ＳＡ代谢障碍有关。     

The role of parathyroid hormone-related protein in intra-tracheal fluid

Parathyroid hormone-related protein (PTHrP), a multi-functional protein, is produced by many tissues in fetus. PTHrP concentration in amniotic fluid is reported to be significantly higher than in either fetal or maternal plasma. Other investigators have reported that PTHrP in amniotic fluid is derived mainly from amnion. The aim of this study was to investigate the contribution of fetus to PTHrP in amniotic fluid and the role of PTHrP in human fetal lung tissue. Samples of amniotic fluid, neonatal intra-tracheal fluid, gastric fluid, and the first urine of neonates were obtained at the time of elective cesarean section (n=11), and the concentrations of PTHrP were measured. The PTHrP level in intra-tracheal fluid (41.0+/-19.6 pmol/l, mean+/-SD) was significantly higher than the levels in amniotic fluid (22.1+/-0.8), neonatal gastric fluid (13.5+/-2.5), first urine (0.95+/-0.6), umbilical cord venous and arterial plasma (1.35+/-0.2, 1.63+/-0.3) and maternal plasma (1.05+/-0.1). PTHrP and PTH/PTHrP receptor mRNA were detected in human lung tissue obtained from a fetus stillborn at 36 weeks of gestation. The effects of PTHrP on fetal lung maturation were studied in H441 cells from a human lung epithelial cell line. PTHrP (10(-7)M) significantly suppressed cell proliferation (p<0.05) to approximately 80% of the control level, while administration of PTHrP significantly increased surfactant protein A production (p<0.01). We first demonstrated the high concentration of PTHrP in intra-tracheal fluid that may suggest the positive production of this protein from the fetal lung. The results obtained by in vitro study using a human lung epithelial cell line suggest that PTHrP derived from the fetal lung might modulate its own maturation.     

MEASUREMENT OF TSH IN HUMAN AMNIOTIC FLUID: DIAGNOSIS OF FETAL THYROID ABNORMALITY IN UTERO

Using a highly sensitive immunoradiometric assay kit for human TSH, we measured TSH concentrations in unconcentrated amniotic fluids in normal pregnancies and those complicated for example by maternal hyper- and hypothyroidism, and compared them with those in maternal and cord sera. In normal pregnancies the mean concentration of TSH in amniotic fluid samples was 0.129 microU/ml, ranging from 0.065 to 0.278 microU/ml. In patients with premature delivery, the amniotic fluid TSH concentration was higher at 0.218 microU/ml. In four patients with abnormal thyroid function, TSH in amniotic fluid changed in parallel to that in cord serum, and there was a significant positive correlation between the two. No such correlation was observed between the concentrations of TSH in amniotic fluid and maternal serum. These results suggest that TSH in human amniotic fluid reflects fetal rather than maternal thyroid function and that the determination of TSH levels in amniotic fluid is useful in the diagnosis of abnormal thyroid function in fetuses.     

羊膜腔输液及羊水置换治疗妊娠晚期羊水过少临床研究

将126例妊娠晚期羊水过少患者随机分为两组,治疗组经腹羊膜腔穿刺输液或经宫颈羊膜腔输液(AI),并记录输液量及输液后羊膜腔容积与胎儿情况.对照组给予吸氧、输液等一般宫内复苏方法.结果显示,治疗组在B超引导下行AI,其中8例羊水粘稠者行羊水置换,症状改善97.06%;对照组症状改善仅10.34%,两组差异有显著性(P＜0.01).治疗组剖宫产率13.24%,新生儿窒息率14.71%;对照组分别为51.72%、46.55%,明显高于治疗组(P均＜0.01).对照组新生儿胎粪吸入6例,新生儿死亡2例,畸形儿4例,而治疗组无1例发生.两组产褥病率比较无显著性(P＞0.05).认为对妊娠末期羊水过少患者进行AI或羊水置换,降低了新生儿病率及剖宫产率,是减少围产期母婴病率的有效方法.     

Relationship between maternal and fetal corticotrophin-releasing hormone-41 and ACTH levels in human mid-trimester pregnancy

Samples of maternal blood, amniotic fluid and umbilical arterial and venous blood were collected from 11 women at 16-24 weeks of pregnancy. Corticotrophin-releasing hormone-41 (CRH-41) and ACTH were measured by immunoradiometric assay. The mean levels of ACTH were 11 pmol/l in maternal plasma, 12 pmol/l in fetal plasma and 9.7 pmol/l in amniotic fluid. The mean levels of CRH-41 were 1.6 pmol/l in maternal plasma and 0.7 pmol/l in fetal plasma. There was a positive correlation between maternal and fetal plasma CRH-41 and between maternal CRH-41 and ACTH. In fetal plasma there was a weak inverse correlation between CRH-41 and ACTH. This is the first demonstration of CRH-41 in the circulation of the mid-trimester human fetus, but on the basis of the present findings it is not possible to specify the exact source (fetal, placental or maternal).     

Measurement and characterization of insulin-like growth factor binding protein-3 in human biological fluids: discrepancies between radioimmunoassay and ligand blotting.

The inability to detect insulin-like growth factor binding protein-3 (IGFBP-3) in some circumstances by Western ligand blot analysis has emphasized the need to characterize IGFBPs by both ligand binding and immunological techniques. In this study, we have: 1) characterized and quantified IGFBP-3 in nonpregnancy, pregnancy, and fetal cord serum, follicular, peritoneal, and amniotic fluid, seminal plasma, cerebrospinal fluid (CSF), and urine; 2) established a new IGFBP-3 RIA that detects both intact and fragments of IGFBP-3; 3) identified both intact and fragments of IGFBP-3 by Western immunoblot techniques; and 4) addressed the discordance between Western ligand blot analysis and RIA by assessing fluids for IGFBP proteolytic activity. All fluids examined, except pregnancy serum, CSF, and amniotic fluid, displayed a 44-34-kilodalton (kDa) IGFBP-3 doublet by Western ligand blot analysis. Western immunoblot analysis using specific IGFBP-3 antiserum showed a 44-34-kDa IGFBP-3 doublet and a 28-kDa fragment in nonpregnancy serum, fetal cord serum, follicular fluid, and peritoneal fluid. The immunoreactive 42-38-kDa doublet was faint in urine and seminal plasma. IGFBPs in CSF did not cross-react with IGFBP-3 antiserum. Pregnancy serum and amniotic fluid contained only the 28-kDa fragment when compared against equal volumes of nonpregnancy serum. With the development of an IGFBP-3 RIA, IGFBP-3 could be accurately measured; urine, CSF, and seminal plasma contained the lowest levels of IGFBP-3 at 27 +/- 3 ng/ml (mean +/- SEM), 110 +/- 26 ng/ml, and 209 +/- 56 ng/ml, respectively. In increasing concentration: fetal cord serum contained 753 +/- 101 ng/ml; peritoneal fluid, 1124 +/- 130 ng/ml; follicular fluid, 2356 +/- 211 ng/ml; nonpregnancy serum, 3556 +/- 508 ng/ml; pregnancy serum, 3718 +/- 842 ng/ml; and amniotic fluid, 5150 +/- 688 ng/ml. The measurable concentrations of IGFBP-3 in CSF and the high concentrations measured in pregnancy serum and amniotic fluid conflicted with Western blot analysis. Thus, fluids were assessed for IGFBP proteolytic activity by incubation with a source of IGFBP-3, either nonpregnancy serum or purified IGFBP-3. All fluids displayed some proteolytic activity with either assay. Fluids with little protease activity (nonpregnancy serum, follicular fluid, and urine) showed a close relationship between immunoassayable IGFBP-3 by RIA and IGFBP-3 band intensity by Western ligand blot. Fluids with high proteolytic activity (pregnancy serum, CSF, seminal plasma, peritoneal fluid, and amniotic fluid) gave discrepant IGFBP-3 values between RIA and Western ligand blot.(ABSTRACT TRUNCATED AT 400 WORDS)     

Water and salt conservation in the human fetus and newborn. I. Evidence for a role of fetal prolactin

A study was performed on 94 women delivering at 34-44 weeks gestation, whose pregnancies were uncomplicated to determine the role of PRL in human fetal and neonatal salt and water conservation. Ultrasonic estimation of amniotic fluid (AF) volume and sampling of maternal blood, AF, cord blood, and 2-h neonatal blood were performed to analyze PRL, osmolality, sodium ion concentration ([Na]), and blood solids [hematocrit (Hct), total serum solids (tss), and total protein concentration]. In this report, which addresses the role of fetal PRL, Pearson correlations showed the following significant relationships: 1) approximation of cord serum osmolality and [Na] in cord and maternal serum, as well as parallel changes in cord blood Hct, tss, and total protein; 2) reduced estimated AF volume and increased AF osmolality in the face of elevated cord serum osmolality and [Na]; 3) a shift toward normal in cord Hct and tss over the first 2 h of neonatal life after an initially increased or decreased cord serum osmolality, [Na], Hct, or tss; and 4) relationship between fetal pituitary PRL levels of 230 micrograms/L or less and cord serum osmolality, [Na], and Hct. The entire range of cord serum PRL levels correlated with changes in AF osmolality and [Na] as well as with neonatal changes in Hct and tss. These findings support the hypotheses that osmotic equilibrium exists between maternal and fetal circulations; that disturbances in this balance lead to changes in fetal and neonatal water excretion; and that fetal PRL, stimulated by increases in cord serum osmolality and [Na], acts as an antidiuretic, leading to restoration of the offspring's extracellular fluid volume.     

Analyses of Methadone and Other Drugs in Maternal and Neonatal Body Fluids: Use in Evaluation of Symptoms in a Neonate of Mother Maintained on Methadone

A former heroin addict treated with methadone maintenance throughout pregnancy, with rapid dose reduction from 110 mg to 9 mg during the last five weeks pre-partum, was evaluated in late pregnancy, at time of labor and delivery, and post-partum; her child was also evaluated. Using gas and thin-layer chromatography and mass spectroscopy, methadone levels were measured, and other drugs looked for in (1) plasma during late pregnancy, (2) mixed cord blood, (3) amniotic fluid at delivery, (4) maternal plasma and milk post-partum (on 50 mg methadone), (5) neonatal plasma and urine. Low levels of methadone were present in amniotic fluid and neonatal urine but not in mixed cord blood or neonatal plasma. Levels of methadone present in breast milk during moderate dose maintenance were also low. Unexpectedly, pentobarbital was identified in amniotic fluid. Neonatal infection was also diagnosed. Multiple factors may have contributed to symtoms observed in the neonate.     

Association between pulmonary and gastric inflammatory cells on the first day of life in preterm infants

It has been shown that inflammatory cells in the newborn lung are fetal in origin, whereas those in the amniotic fluid are maternal. In order to explore the relationship between fetal amnionitis and neonatal pneumonitis, we collected paired samples of gastric aspirate within 2 hours of birth, and bronchoalveolar lavage fluid within 24 hours of birth from intubated preterm infants. Leukocyte counts in bronchoalveolar lavage fluid correlated with the duration of membrane rupture (r = 0.68, P = 0.0001). There was a high degree of correlation between leukocyte counts in the two fluids (r = 0.86, P = 0.0001). The factors responsible for this association are unknown. Pediatr Pulmonol. 1993; 16:59–61. © 1993 Wiley-Liss, Inc.     

The relationship between maternal plasma leptin levels and fetal growth restriction

Leptin is a satiety hormone secreted from the adipose tissue and human placenta. We previously demonstrated that severe preeclampsia up-regulated leptin mRNA expression in the placenta and elevated maternal plasma leptin concentrations. Preeclampsia is frequently related to generation of small for gestational age (SGA) infant especially in cases with severe preeclampsia. However, it is still controversial whether the increase in maternal plasma leptin levels is associated with fetal growth restriction without complication of preeclampsia. Therefore, the aim of the present study was to explore the relationship between maternal plasma leptin levels and fetal growth in non-preeclamptic (n = 98) and preeclamptic (n = 40) women. In non-preeclamptic pregnant women, plasma leptin levels in SGA group (n = 11) were significantly higher than those in appropriate for gestational age (AGA) group (n = 87, P<0.05). In pregnant women with preeclampsia, likewise, plasma leptin levels in SGA group (n = 15) were significantly higher than those in AGA group (n = 25, P<0.05). In multiple linear regression analysis, maternal BMI, mean arterial blood pressure and Delta SD of neonatal body weight were significant factors for determining maternal plasma leptin levels in all population studied. Maternal BMI and Delta SD of neonatal body weight showed positive correlation with maternal plasma leptin levels when analysis was performed in non-preeclamptic subjects alone. In conclusion, maternal plasma leptin levels reflect, at least partly, deterioration in fetal growth.     

Thrombopoietin levels in cord blood plasma and amniotic fluid in fetuses with alloimmune thrombocytopenia and healthy controls

To extend our knowledge of the kinetics of fetal thrombopoietin (TPO), we studied TPO levels in cord blood plasma and amniotic fluid collected from 15 fetuses considered to be at risk of fetomaternal alloimmune thrombocytopenia and also from 10 healthy controls at caesarean delivery. In the plasma of all 25 fetuses and newborn infants studied, TPO was detected above the lower limit of detection (7 pg/ml) and correlated inversely with platelet counts (r = -0.53, P = 0.006). At term, TPO detected in amniotic fluid was at significantly lower levels (7 pg/ml; range 0-22 pg/ml) than simultaneously obtained cord plasma TPO (114 pg/ml; range 43-201 pg/ml; P < 0.001). There was no correlation between levels of TPO in amniotic fluid and cord plasma or platelet counts. In the serial samples collected from the five fetuses with HPA-1a alloimmunization before 37 weeks' gestation, the TPO levels in amniotic fluid were significantly higher than at term (P = 0.013): from 22 to 28 weeks' gestation, 42 pg/ml (30-78 pg/ml); from 32 weeks', 24 pg/ml (17-33 pg/ml); at term, 8 pg/ml (4-13 pg/ml), correlating inversely with gestational age (r = -0.81, P = 0.003). Thus, TPO is present in amniotic fluid at levels apparently inversely related to gestational age. Whether these high levels seen early in pregnancy are normal or are associated with the HPA-1 alloimmunization remains to be shown.