Hemolytic anemia after zopiclone overdose

Introduction. Zopiclone is associated with methemoglobinemia. We report a case of zopiclone overdose manifested with another hematological complication, hemolysis. Case. A 46-year-old woman overdosed with 50–100 tablets of 7.5 mg zopiclone. Oxidative hemolysis was evident by anemia, bite cells, raised unconjugated bilirubin and lactate dehydrogenase, lowered haptoglobin, and reticulocytosis. Discussion. In zopiclone overdose, there may be oxidative stress rendering the development of not only methemoglobinemia but also hemolysis.     

Hemolytic anemia

Hemolysis presents as acute or chronic anemia, reticulocytosis, or jaundice. The diagnosis is established by reticulocytosis, increased unconjugated bilirubin and lactate dehydrogenase, decreased haptoglobin, and peripheral blood smear findings. Premature destruction of erythrocytes occurs intravascularly or extravascularly. The etiologies of hemolysis often are categorized as acquired or hereditary. Common acquired causes of hemolytic anemia are autoimmunity, microangiopathy, and infection. Immune-mediated hemolysis, caused by antierythrocyte antibodies, can be secondary to malignancies, autoimmune disorders, drugs, and transfusion reactions. Microangiopathic hemolytic anemia occurs when the red cell membrane is damaged in circulation, leading to intravascular hemolysis and the appearance of schistocytes. Infectious agents such as malaria and babesiosis invade red blood cells. Disorders of red blood cell enzymes, membranes, and hemoglobin cause hereditary hemolytic anemias. Glucose-6-phosphate dehydrogenase deficiency leads to hemolysis in the presence of oxidative stress. Hereditary spherocytosis is characterized by spherocytes, a family history, and a negative direct antiglobulin test. Sickle cell anemia and thalassemia are hemoglobinopathies characterized by chronic hemolysis.     

Deceased donor neutrophil gelatinase-associated lipocalin and delayed graft function after kidney transplantation: a prospective study

Introduction  

Expanding the criteria for deceased organ donors increases the risk of delayed graft function (DGF) and complicates kidney transplant outcome. We studied whether donor neutrophil gelatinase-associated lipocalin (NGAL), a novel biomarker for acute kidney injury, could predict DGF after transplantation.     

肾移植后贫血因素分析：同一机构10年826例移植者资料回顾

背景：临床上肾移植后贫血发生率为30%-40%,是肾移植后心血管疾病和移植肾失功的重要危险因素,并且是患者死亡的独立预测指标。目的：分析肾移植后贫血发生的相关因素。方法：分析2000-01/2009-12解放军沈阳军区总医院肾移植826例患者资料,其中男541例,女285例,年龄17-71岁;尸体供肾805例,亲体活体供肾21例。根据移植后是否发生贫血将患者分成贫血组与非贫血组,记录可能引起移植后贫血的各项参数,分别用t检验和卡方检验进行单因素分析。结果与结论：826例肾移植患者中发生贫血225例,发生率为27.2%。女性和男性患者贫血发生率分别为23%和37%（P〈0.05）;年龄26~65岁,其中伴有高血压应用血管紧张素转化酶抑制剂或血管紧张素Ⅱ受体拮抗剂类降压药物者46例,伴有慢性糜烂性胃：炎或上消化道溃疡者16例,人存活率为85.3%,肾失功率为25.3%;非贫血组601例,占总例数的72.8%,其中男405例,女196例,年龄17~71岁,伴有高血压应用血管紧张素转化酶抑制剂或血管紧张素Ⅱ受体拮抗剂降压药物者35例,伴有慢性糜烂性胃炎或上消化道溃疡者14例,人存活率为92.1%,肾失功率为12.6%,与贫血组对比差异有显著性意义（P〈0.05）。分析表明,性别、年龄、肾功能、消化道疾病史、药物因素等与肾移植后贫血的发生密切相关。     

Hemolytic anemia and plasma exchange

Hemolytic anemia is a disease caused by autoantibodies and resulting in various complaints and clinical symptoms. In about half of cases, the cause of autoimmune hemolytic anemia can not be determined. Corticosteroids are the first-line treatment option for warm autoantibody-related hemolytic anemia. In patients who develop steroid side effects or do not respond adequately, other immunosuppressives may be preferred. In case a rapid response is required or fulminant hemolysis occur, human immunoglobulins (IVIGs) may be added to treatment. Finally, plasma exchange (PE) may additionally be utilised. The essence of PE is based on the removal of immune complexes, protein-bound toxins, autoantibodies and high molecular weight solutes and protein-bound solutes. The main clinical aim of the removal of solutes is usually to gain a faster response than immunosuppressive therapy. Studies related to hemolytic anemia and PE are usually based on case reports. Our case report is about a patient with severe IgG subtype hemolytic anemia. The treatment was started with 1 mg/kg methylprednisolone; to which there was no response with weekly rituximab 375 mg/m² and IVIG administered. Because of unresponsiveness to all of the immunosuppresives, a total of 5 sessions of PE were added to the treatment procedure every other day. After these sessions, the requirement for transfusions has decreased and the patient underwent splenectomy. The patient is currently being followed up only on oral cyclosporine and the last hemoglobin level was 14.7 g /dl. In severe and refractory anemia, especially in the case of cardiovascular imbalance in fulminant hemolysis, PE may be preferred as a third series option after immunosuppressive treatments and play a role as a bridge to splenectomy.     

肾移植后骨病

肾移植是终末期肾衰的最佳治疗手段，但移植后的并发症也不容忽视，如骨病。肾移植成功后骨病的表现有赖于移植前的骨代谢状态，以及移植及其后治疗所带来的新的因素。     

肾移植后的蛋白尿

背景:蛋白尿的发生与移植肾的远期存活直接相关,是影响移植肾远期存活、导致肾移植患者死亡的独立危险因素。目的:观察应用血管紧张素Ⅱ受体阻断剂联合雷公藤多苷治疗肾移植后蛋白尿的效果。方法:选择肾移植后出现蛋白尿患者45例,分为3组,在常规应用免疫抑制剂基础上,治疗组采用2倍剂量血管紧张素Ⅱ受体阻断剂联合雷公藤多苷1mg/(kg·d)、雷公藤多苷组采用雷公藤多苷1mg/(kg·d),对照组仅维持原有免疫抑制方案治疗。结果与结论:治疗后12个月治疗组和雷公藤多苷组24h尿蛋白定量、环孢素A血药浓度、环孢素A用量均显著低于对照组(P<0.05),治疗后治疗组尿素氮、肌酐浓度显著低于其他两组(P<0.05)。提示血管紧张素Ⅱ受体阻断剂联合雷公藤多苷能明显减少肾移植后蛋白尿的出现,且可减少免疫抑制剂的用量,对移植肾起保护作用。     

超声监测移植肾术后妊娠1例

患者女,32岁,于1997年11月26日因慢性肾炎尿毒症行同种异体肾移植术.     

移植肾动脉血栓1例

患者女,50岁,1年前诊断为慢性肾小球肾炎.此次来我院行异体移植肾手术.手术顺利,术中显示:移植肾质地良好,色泽红润,动脉搏动明显,大约1 min后输尿管有尿液排出.术后一周,尿量偏少,给予利尿治疗,效果不佳,24 h尿量2000 ml.复查肾功能:BUN 20.2 mmol/L、Cr 230μmol/L.二维超声显示:移植肾大小9.9 cm×5.4 cm×5.5 cm,实质回声均匀,边界清楚,无肾积水及肾周围血肿.彩色多普勒血流显示:移植肾上部未见血流充盈,无血流信号;移植肾下部血管充盈完整,血流连续性好.超声意见考虑为移植肾上极动脉血栓形成(见图1).本例病人通过溶栓治疗后,临床症状及实验室检查结果进行性好转;彩色多普勒超声显示移植肾血供恢复正常,经治疗性诊断,说明超声诊断正确.     

Epidermal innervation in type 1 diabetic patients: a 2.5-year prospective study after simultaneous pancreas/kidney transplantation

OBJECTIVE—To assess the effect of normoglycemia following simultaneous pancreas/kidney transplantation (SPK) on neurological function and intraepidermal nerve fiber density (IENFD) in patients with type 1 diabetes.RESEARCH DESIGN AND METHODS—We performed vibration perception threshold (VPT) testing and autonomic function testing (AFT) and assessed IENFD in skin biopsies from the lower thigh and upper calf in 14 healthy control subjects and 18 patients with type 1 diabetes at the time of and at 21–40 (median 29) months post SPK.RESULTS—At baseline, significantly increased VPTs, pathological AFT results, and severe reduction in IENFD were present in SPK recipients. After SPK, an increase of IENFD in the thigh of more than one epidermal nerve fiber per millimeter was noted in three patients (median 4.1, range 1.9–10.2), but changes were not significant for the group as a whole.CONCLUSIONS—We conclude that either irreversible nerve damage might be present in some SPK recipients or that longer periods of normoglycemia might be needed to allow nerve regeneration.Diabetic neuropathy is a common diabetes complication that may result in serious consequences such as pain, foot ulcers, and amputations. Although optimal glycemic control is considered an effective preventive measure, intervention studies in advanced stages of diabetic neuropathy have been almost uniformly unsuccessful (1). Only arrest of progression of diabetic neuropathy could be achieved in patients after pancreas transplantation (2). To assess nerve regeneration following pancreas transplantation, Kennedy et al. (3) proposed the use of skin biopsies with quantification of intraepidermal nerve fiber density (IENFD). Previously, we documented severe IENFD reduction in lower-limb skin biopsies performed at the time of pancreas transplantation (4). Here we present assessment of IENFD following a mean of 2.5 years of normoglycemia.     

肾移植后贫血的改善

背景:肾移植后随着肾功能的逐渐恢复,大部分患者移植成功后贫血能够得到纠正。目的:观察肾移植前后受者血清促红细胞生成素、铁蛋白、血红蛋白、铁水平的变化,并分析其与移植后贫血改善的关系。设计、时间及地点:病例对照观察,于2005-05/12在中南大学湘雅三医院移植中心完成。对象:纳入肾移植患者20例,根据血清铁蛋白值分为2组,铁正常组(血清铁蛋白≥100μg/L)11例,低铁组(血清铁蛋白<100μg/L)9例。另外选择20例同期健康体检者作为对照。方法:肾移植前1d、移植后3,5,7d,第2,3,4周测定血清促红细胞生成素、铁蛋白、血红蛋白、铁水平,所有患者在移植后1个月内未予铁剂治疗。主要观察指标:以放射免疫法测定血清促红细胞生成素含量,以免疫浊度法测定转铁蛋白含量,以酶联免疫法测定血清铁蛋白含量,按标准实验室方法测定血红蛋白、血清铁水平。结果:肾移植后患者血清促红细胞生成素水平逐渐上升,并在移植后3周达到高峰,明显高于移植前及正常对照组(P<0.01)。低铁组肾移植患者血清铁、血清铁蛋白含量明显低于铁正常组(P<0.05,0.01)。低铁组患者贫血纠正时间比铁正常组显著延长(P<0.01)。6例患者出现急性排斥反应,并出现肾功能恢复、血清促红细胞生成素高峰及贫血纠正延迟。结论:肾移植后贫血的纠正可能与移植后血清促红细胞生成素、铁代谢水平及移植肾功能恢复情况有关。     

Hemolytic anemia with impaired hexokinase activity

Analyses of key glycolytic intermediates in freshly drawn red cells from six related individuals suggest that decreased hexokinase activity underlies the hemolytic process in the two members with overt hemolysis. Low red cell glucose 6-phosphate (G6P) was observed not only in the anemic patients but in the presumptive heterozygotes as well and served as a useful marker for the presence of the trait. Hexokinase activity was labile in distilled water hemolysates but was only slightly low when protected by glucose, mercaptoethanol, and ethylenediaminetetraacetate (EDTA). Normal red cell hexokinase was demonstrated to be dependent on glucose for maintenance of activity after heating to 45 degrees C. The cells of the proposita are unable to utilize glucose efficiently at glucose concentrations lower than 0.2 mmole/liter whereas normal cells maintain linear glucose consumption to at least 0.05 mM glucose. These qualitative abnormalities could result from the presence of a mutant hexokinase with an abnormally reactive sulfhydryl group and altered substrate affinity in the red cells of this kindred.