Fetal stroke and cerebrovascular disease: Advances in understanding from lenticulostriate and venous imaging,alloimmune thrombocytopaenia and monochorionic twins

Fetal stroke is an important cause of cerebral palsy but is difficult to diagnose unless imaging is undertaken in pregnancies at risk because of known maternal or fetal disorders. Fetal ultrasound or magnetic resonance imaging may show haemorrhage or ischaemic lesions including multicystic encephalomalacia and focal porencephaly. Serial imaging has shown the development of malformations including schizencephaly and polymicrogyra after ischaemic and haemorrhagic stroke. Recognised causes of haemorrhagic fetal stroke include alloimmune and autoimmune thrombocytopaenia, maternal and fetal clotting disorders and trauma but these are relatively rare. It is likely that a significant proportion of periventricular and intraventricular haemorrhages are of venous origin. Recent evidence highlights the importance of arterial endothelial dysfunction, rather than thrombocytopaenia, in the intraparenchymal haemorrhage of alloimmune thrombocytopaenia. In the context of placental anastomoses, monochorionic diamniotic twins are at risk of twin twin transfusion syndrome (TTTS), or partial forms including Twin Oligohydramnios Polyhydramnios Sequence (TOPS), differences in estimated weight (selective Intrauterine growth Retardation; sIUGR), or in fetal haemoglobin (Twin Anaemia Polycythaemia Sequence; TAPS). There is a very wide range of ischaemic and haemorrhagic injury in a focal as well as a global distribution. Acute twin twin transfusion may account for intraventricular haemorrhage in recipients and periventricular leukomalacia in donors but there are additional risk factors for focal embolism and cerebrovascular disease. The recipient has circulatory overload, with effects on systemic and pulmonary circulations which probably lead to systemic and pulmonary hypertension and even right ventricular outflow tract obstruction as well as the polycythaemia which is a risk factor for thrombosis and vasculopathy. The donor is hypovolaemic and has a reticulocytosis in response to the anaemia while maternal hypertension and diabetes may influence stroke risk. Understanding of the mechanisms, including the role of vasculopathy, in well studied conditions such as alloimmune thrombocytopaenia and monochorionic diamniotic twinning may lead to reduction of the burden of antenatally sustained cerebral palsy.     

腔内微波和射频消融闭合大隐静脉主干的疗效及安全性对比分析

目的 探讨血管腔内微波消融（EMA）与射频消融（RFA）闭合大隐静脉主干的疗效和安全性差异。方法 收集2019年1—6月浙江省人民医院收治的316例大隐静脉功能不全患者的临床资料,并按照性别、年龄、病程、体重指数、身高、基础临床表现-病因-解剖-病理生理（CEAP）分级、大隐静脉主干直径的不同将患者筛选并分层配对为EMA组（n=157）和RFA组（n=159）。采用视觉模拟评分法（VAS）评价两组患者术后14 d的大隐静脉主干闭合段疼痛情况和皮肤瘀伤情况;术后第14天、6个月,所有患者均通过超声复查治疗段大隐静脉主干闭合情况。比较两组患者的术后并发症发生情况。结果 RFA组患者的术后VAS最高评分出现在术后第1天,EMA组患者的术后VAS最高评分出现在术后第3天。术后第1～10天,两组患者的VAS评分存在差异;与EMA组患者相比,RFA组患者的术后VAS评分更低。两组患者的皮肤瘀伤最高评分均出现在术后第4天;与EMA组患者相比,RFA组患者的皮肤瘀伤评分较低;术后第5～9天,两组患者的皮肤瘀伤评分差异较大。两组患者术后第14天、6个月的治疗段大隐静脉主干闭合率、术后并发症发生情况比较,...     

车前番泻复合颗粒治疗功能性便秘的临床观察

目的 观察车前番泻复合颗粒治疗功能性便秘的有效性和安全性。方法 将80例确诊为功能性便秘患者分为两组,每组40例。治疗组给予车前番泻复合颗粒5 g口服,每日1次, 对照组则给予淀粉颗粒5 g口服,每日1次,共2周,观察两组患者治疗前后排便次数、大便性状、排便困难症状评分、伴随症状评分、胃肠传输时间及不良反应。结果 对照组排便次数、大便性状、排便困难症状评分、伴随症状评分、胃肠传输时间治疗前后差异无统计学意义(P＞0.05), 而治疗组上述各指标治疗前后比较,差异有统计学意义(P<0.05)。且治疗后两组上述指标比较,差异亦有统计学意义(P<0.05)。两组均无明显不良反应发生。结论 车前番泻复合颗粒能显著增加功能性便秘患者的排便次数、改变大便性状、缓解排便困难症状及伴随症状、缩短胃肠传输时间, 并具有较好的安全性和耐受性。     

新疆维吾尔族霍奇金淋巴瘤HLA—A高分辨基因多态性分析

目的：研究人类白细胞抗原（humanleukocyteantigen,HLA—A）高分辨等位基因型与新疆地区维吾尔族霍奇金淋巴瘤（hodgkin’Slymphoma,HL）易感性的关系,以揭示遗传因素在HL发病中的作用。方法：采用病例一对照的研究设计和DNA测序分型（SBT）法,对45例维吾尔族HL患者和110名健康者进行HLA—A基因座位的精确分型,计算HLA_A基因座位等位基因的相对频率（RF）及基因频率（AF）。结果：1）病例组共检出33个高分辨等位基因型,对照组中共检出44个高分辨等位基因型,HLA-A基因座位上等位基因频率分布均满足Hardy-Weninberg遗传平衡检验,P=0．61。2）与新疆地区维吾尔族人群比较,维吾尔族HL患者中等位基因HLA-A＊01：01：01：01（45．48％＂US16．04％）、A＊03：01（39．68％VS18．35％）、A＊01：01（33．91％vs18．35％）、A＊02：07（28．18％VS13．73％）高分辨等位基因分布频率较高,差异有统计学意义,P〈0．01。HLA—A＊02：01（69．05％vs85．47％）和A＊1l：01（16．81％VS32．34％）则相对较低,差异有统计意义,P〈0．01。3）新疆地区维吾尔族HL患者与维吾尔族健康人抗原型均以A2最为多见,各型在病例组与对照组之间分布差异无统计学意义,P〉0．05。结论：HLA-A＊01：01：01：01、A＊03：01、A＊01：01和A＊02：07基因型与维吾尔族HL存在阳性关联,可能为维吾尔族HL发病的易感基因,而HLA-A＊02：01、A＊ll：01可能为维吾尔族HL发病的拮抗基因。     

Maternal mortality in the United States

Despite a significant improvement in the US maternal mortality ratio since the early 1900s, it still represents a substantial and frustrating burden, particularly given the fact that - essentially - no progress has been made in most US States since 1982. Additionally, the US Centers for Disease Control and Prevention has stated that most cases are probably preventable. Two disheartening issues within this topic include a gross underestimation of the magnitude of maternal mortality - particularly before 1987, but which likely persists to a lesser degree today - and the continued significant racial disparity in maternal mortality. Explanations for the plateau in maternal mortality include the recent trend of delayed childbearing, with the potential accompanying complications associated with older reproductive age (particularly over 35 years) and multiparity. The impressive increase in multifetal pregnancies related to delayed childbearing and assisted reproductive technology also plays a role. Finally, peripartum cardiomyopathy has become an increasingly recognized source of maternal mortality. Pregnancy-related mortality is largely accounted for by thromboembolic disease, hemorrhage, hypertension and its associated complications, and infection. However, since the inclusion of maternal deaths occurring after 42 days post-delivery as pregnancy related, traumatic injuries - including homicides and suicides - are an alarming source of maternal mortality. An especially important contemporary issue to consider within this topic is cesarean delivery "on maternal request", opponents of which cite concerns not only for immediate morbidity and mortality increased over that associated with a vaginal birth, but also for potential morbidity and mortality associated with future pregnancies. One particularly appealing opportunity to reduce maternal mortality is to recognize, examine, and learn from so-called "near-miss" cases.     

The placenta contributes to activation of the renin angiotensin system in twin-twin transfusion syndrome

The renin-angiotensin system (RAS) in twin-twin transfusion syndrome (TTTS) is up-regulated in the donor fetus's kidneys, but down-regulated in the recipient's. Ultrasonographic and echocardiographic features suggest that the recipient is also exposed to RAS components. In this study we investigated the role and origin of RAS components in the recipient fetus. Monochorionic diamniotic (MCDA) pregnancies were recruited from a tertiary fetal medicine service. Cord blood was collected from MCDA twins (TTTS and control non-TTTS) at delivery for renin and angiotensin II immunoassays. Placental tissue was flash-frozen for mRNA and protein expression or formalin-fixed for immunohistochemistry. Archival placenta and kidney samples were used for immunohistochemistry and in-situ hybridization. Plasma renin levels were elevated (p<0.05) in recipients (median 201pg/ml, range 54-315pg/ml) and donors (125pg/ml, 25-296) with TTTS compared to controls (2.5pg/ml, 1.1-1.5pg/ml). The same was found with angiotensin II with high levels in both recipients (300.5pg/ml, 86.1-488pg/ml) and donors (239pg/ml, 76.6-422) compared to controls (169.5pg/ml, 89-220pg/ml, p<0.05). Renin mRNA expression, and protein appeared qualitatively higher in the placental territory of the recipient compared to that of the donor and non-TTTS controls. We conclude that both fetuses in TTTS are exposed to high levels of RAS components; these appear to be produced from different sites, namely the kidney of the donor, and the placenta of the recipient. Given the markedly different phenotypes in the genetically identical fetuses with TTTS, we suggest that the source of RAS components may influence their clinical manifestations.     

Twin pregnancies in Cardiff and Vale of Glamorgan over four decades: natural twinning is on the increase

Objective

To assess trends in twinning over four decades using a population-based registry.

Design

Ecological study to conduct trend analysis of twin pregnancies in a geographically defined area over 40 years.

Setting

All pregnancies in the Cardiff and Vale of Glamorgan area of South Wales from 1965 to 2004, as recorded in the Cardiff Birth Survey (CBS) database.

Methods

Trends of the incidence of all twin pregnancies (≥18 weeks of gestation) were calculated in 5-year increments, beginning with 1965–1969 and ending in 2000–2004. Natural twinning rates could only be calculated for the terminal five time periods (i.e., 1980–1984, 1985–1989, 1990–1994, 1995–1999, and 2000–2004), when information regarding non-spontaneous (iatrogenic) twinning was first collected in the database. All results were adjusted for maternal age.

Results

The total twinning rate was 13.1 per 1000 pregnancies in the 1st time period (1965–1969). Subsequently, there was a gradual reduction in twinning, reaching a nadir of 10.3 per 1000 for the time period 1980–1985 (Z = 3.15, P value < 0.001). This was followed by a gradual increase in twinning, reaching a maximum of 15.7 per 1000 for both 1995–1999 and 2000–2004 (Z = −5.18, P value < 0.0001). After exclusion of the cases of iatrogenic pregnancies, the natural twinning rate showed a continuous and gradual increase from 10 per 1000 spontaneous pregnancies in 1980–1984 to 13.3 per 1000 in 2000–2004 (Z = −5.08, P value < 0.0001).

Conclusion

The data showed a gradual, continuous increase in natural twinning rates over the last two decades. Such an increase cannot be attributed to the rise in maternal age alone.     

ACE and MTHFR gene polymorphisms in unexplained recurrent pregnancy loss

AIM: To assess the association between polymorphisms in angiotensin converting enzyme and methylene tetrahydrofolate reductase genes and recurrent pregnancy loss by a case-control study in South Indian women. METHODS: DNA was extracted from peripheral blood leukocytes of 104 women with Recurrent Pregnancy Loss (RPL) and 120 controls. Genotyping of ACE Insertion Deletion and MTHFR C677T polymorphism were carried out by PCR and PCR-RFLP, respectively. RESULTS: No statistically significant difference was observed in the distribution of genotypes between cases and controls for ACE and MTHFR polymorphisms. Further, the combination of MTHFR and ACE genotypes failed to reveal an association. CONCLUSION: In conclusion, the present study reveals lack of association of MTHFR C677T and ACE I/D polymorphisms in RPL in South Indian women. However, we cannot exclude the possibility that other polymorphisms of ACE and MTHFR genes could be associated with the disease and might be clinically useful as a marker to assess risk for RPL.