肾病综合征合并肾静脉血栓形成:病因及抗栓治疗进展

肾病综合征患者具有明显的高凝倾向,肾静脉血栓形成是其常见且严重的并发症之一。文中阐述了肾病综合征患者高凝状态的病理生理学基础,对肾静脉血栓的抗栓治疗也做了详尽的综述。     

五叶参抗血栓形成作用的研究

用人血进行体外实验研究证实,五叶参水煮制备液能明显抑制APD、复合诱聚剂诱导的血小板1min、5min、最大聚集率,并促进解聚发生(P均<0.05);该药还对体外血栓形成具有显著的抑制作用(P<0.05);五叶参水煮液与PPP混合后,尚能抑制多种凝血因子活性,使KPTT、PT、TT、AT、RVV-RT、RVV-CT等凝血试验时间延长(P均<0.05);此外,五叶参有加速红细胞电泳速度的作用。上述结果表明,五叶参是一种具有抑制血小板功能、凝血功能及红细胞聚集性等多个环节的抗血栓形成药物,值得进一步研究探讨。     

可控性丝线留置术治疗体表难治性海绵状静脉畸形的实验及临床研究

目的研究可控性丝线的致栓效果及其治疗体表难治性海绵状静脉畸形的初步疗效。方法将丝线一端留置于不同管腔大小的静脉内,另一端挂于血管壁埋于皮下,实现其可控性,用经过不同处置的丝线,分别留置于兔耳缘静脉、股静脉,观察其引起血管栓塞的效果。选择致栓效果较好的丝线组,用于临床治疗难治性体表海绵状静脉畸形的患者。结果几种经不同处置的丝线,均能不同程度地起到闭塞血管的作用,对于管腔稍大,血流较快的静脉(兔股静脉),浸泡丝裂霉素并打结的丝线组,致栓效果最好;临床初步应用证实,可控性丝线治疗体表难治性静脉畸形,安全有效。结论可控性丝线静脉内留置术,是一种安全、有效、损伤小、操作简便的治疗体表难治性海绵状静脉畸形的新方法。     

长脉冲Nd:YAG激光非侵入性治疗皮肤浅表静脉畸形

目的前瞻性研究长脉冲1064nm Nd:YAG激光非侵入性治疗皮肤浅表静脉畸形的疗效。方法22例不同部位皮肤浅表静脉畸形患者接受长脉冲1064nm Nd:YAG激光治疗,6mm直径光斑,7～8ms双脉宽,脉冲间隔20ms,140～150J/cm2能量,接触式冷却,治疗间隔3周至1个月,治疗后1、6个月随访,评价病灶清除率分为五级。结果22例患者完成治疗,最多治疗5次。随访6个月,96.3%浅表静脉畸形获得76%～100%的清除,37%获得病灶的完全清除,未见复发。治疗部位无一例发生紫癜,治疗后8例(38.1%)出现红斑,1d至1个月消退。无色素改变和形成。结论长脉冲1064nm Nd:YAG激光能有效安全地治疗皮肤浅表静脉畸形,选择性地清除浅表血管,并使用接触冷却系统保护表皮,减少紫癜发生及色素改变和瘢痕的形成,达到理想的美容效果。     

MR血管成像在诊断下肢深静脉血栓形成中的价值并与DSA对照研究

目的探讨下肢深静脉血栓形成MR血管成像（MRA）的临床价值。方法对30例怀疑下肢深静脉血栓形成的患者进行了MRA和DSA检查，MRA采用二维时间飞越法（2DTOF）。对MRA与DSA表现进行对照分析。结果下肢深静脉血栓形成的MRA表现有1静脉充盈缺损（14例）、静脉闭塞和中断（8例）、静脉再通（3例）、侧支循环形成（25例）。以DSA为标准，MRA诊断出所有病变，但有1例假阳性。结论MRA作为无创性检查，是诊断下肢深静脉血栓有效的检查方法之一。     

Co-segregation of the PROS1 locus and protein S deficiency in families having no detectable mutations in PROS1.

Inherited deficiency of protein S constitutes an important risk factor of venous thrombosis. Many reports have demonstrated that causative mutations in the protein S gene are found only in approximately 50% of the cases with protein S deficiency. It is uncertain whether the protein S gene is causative in all cases of protein S deficiency or if other genes are involved in cases where no mutation is identified. The aim of the current study was to determine whether haplotypes of the protein S gene cosegregate with the disease phenotype in cases where no mutations have been found. Eight protein S-deficient families comprising 115 individuals where previous DNA sequencing had failed to detect any causative mutations were analyzed using four microsatellite markers in the protein S gene region. Co-segregation between microsatellite haplotypes and protein S deficiency was found in seven of the investigated families, one family being uninformative. This suggests that the causative genetic defects are located in or close to the protein S gene in a majority of such cases where no mutations have been found.     

磁共振成像对脑静脉畸形的诊断价值

目的 探讨磁共振成像各种方法对脑静脉畸形的诊断价值。方法 收集本院6例脑静脉畸形病例，均进行过磁共振T1WI、T2WI扫描，其中部分病例做过DWI、T2FLAIR、MRA、MRV、T1WI增强扫描及DSA。结果 幕上4例，幕下2例，T1WI、T2WI表现：引流静脉均为流空的低信号，深髓静脉为细条状长T1、长T2信号。其中1例DWI引流静脉及深髓静脉区域低信号；1例T2 FLAIR引流静脉流空的低信号，深髓静脉高信号；2例MRA均阴性，但MRV显示深髓静脉汇入引流静脉；2例T1 WI增强扫描：深髓静脉呈轮辐状汇入引流静脉；1例DSA：动脉期阴性，静脉期见典型的“海蛇头”征。结论 磁共振能明确诊断脑静脉畸形，T1WI增强扫描及MRV均较敏感，DSA为诊断脑静脉畸形金标准。     

Compliance with recommended prophylaxis for venous thromboembolism: improving the use and rate of uptake of clinical practice guidelines

Summary.  Although several authoritative, evidence-based, guidelines for the prevention of venous thromboembolism (VTE) have been published, the use of VTE prophylaxis in routine clinical practice varies markedly. Even in orthopedic surgery, the indication for which prophylaxis is used most often, a significant proportion of surgeons do not use routine prophylaxis. When prophylaxis is used, guideline recommendations are often not followed. A number of factors may contribute to the under-use of guidelines. Physician-related factors include: a lack of awareness of, or familiarity with, the guidelines; a perception that VTE is not a significant problem or that VTE prophylaxis is ineffective; and concern about potential bleeding risks. The guidelines may also be perceived to be too complicated or difficult to apply in a routine manner. In addition, a lack of facilities or resources may also present a barrier to implementation of the guidelines. A number of strategies are being investigated in an attempt to improve compliance with guidelines for VTE prophylaxis. For example, the Investigators Against Thromboembolism (INATE) initiative has developed a simplified pocket guideline on VTE prophylaxis in orthopedic and trauma surgery in order to raise awareness of the current guideline recommendations.     

Thalidomide protects endothelial cells from doxorubicin-induced apoptosis but alters cell morphology

Summary.  Antiangiogenesis agents are now being used in clinical trials to reduce the risk of recurrence of cancer. Several of these agents, however, are associated with thrombosis, especially when used in combination with chemotherapy. Antiangiogenesis and thrombosis are both endothelial-related activities, and we therefore evaluated one presumed antiangiogenesis agent (thalidomide) on intact cultured endothelial cells, and on cultured endothelial cells injured by preincubation with doxorubicin. We evaluated cell viability, caspase-3 activation, morphology of cells using light microscopy, and protease activated receptor-1 (PAR-l) expression. In our experiments, doxorubicin induced a dose- and incubation time-dependent and caspase-3-mediated apoptosis of endothelial cells. Thalidomide alone caused no changes in intact endothelial cells in terms of morphology, cell viability or activation of caspase-3. In contrast, when thalidomide was added to doxorubicin-injured endothelial cells, there was protection from cell death, increase in viability of endothelial cells, induction of differentiation and formation of neotubules. Doxorubicin reduced the expression of thrombin receptor, PAR-1, as evaluated by immunostaining and flow cytometry. Thalidomide did not alter PAR-1 expression in untreated cells but restored its expression reduced by doxorubicin. These findings suggest that thalidomide may be procoagulant, not by enhancing doxorubicin-mediated endothelial cell injury, but by altering the expression of PAR-1 on injured endothelium and resulting in endothelial dysfunction, which may explain hypercoagulability in patients treated with chemotherapy followed by thalidomide.     

Cerebral perfusion during human liver transplantation

Summary. During transplantation of the liver cerebral perfusion was monitored by transcranial Doppler determined middle cerebral artery mean flow velocity (V_mean) and pulsatility index (PI) in six fulminant hepatic failure patients and 11 patients with chronic liver disease. In both groups of patients V_mean, PI and central haemodynamic variables were recorded during (1) the last preanhepatic hour; (2) the anhepatic phase; (3) the first 15 min of reperfusion; and (4) for the following 45 min of reperfusion. No significant differences were detected between the two groups of patients with respect to changes of variables with time. The V_mean (40±13 cm s^-1 [mean±SD]), thoracic electrical impedance (TI) (30±7 Ohm), heart rate (97±19 beats min^-1), mean arterial pressure (84±9 mmHg) and arterial carbon dioxide tension (PaCO₂, 4.5±0.4 kPa) remained stable in the anhepatic phase, while cardiac output (CO, 7.6±2.7 to 5.4±1.41 min^-1), stroke volume (SV, 79±26 to 56±15 ml) and PI (1.2±0.3 to 0.9±0.2) decreased (P<0.05). During reperfusion, CO (9.9±4.01 min^-1), SV (105±40 ml), Pa_CO2 (5.5±0.6 kPa), Vmean (57±17 cm s^-1) and PI (1.2±0.2) became elevated. Taken together, during the anhepatic phase of the liver transplantation a maintained central blood volume as indicated by the constant TI served for a stable blood pressure and in turn cerebral perfusion, whereas revascularization of the graft increased cerebral perfusion concomitant with an elevated carbon dioxide tension.