血浆置换术抢救25例蜂毒致急性重度溶血性贫血临床观察

目的：观察血浆置换术（TPE）治疗蜂毒致急性重度溶血性贫血的疗效。方法：对25例已被确诊为蜂毒致急性重度溶血性贫血患者,在应用糖皮质激素的基础上进行TPE治疗,并观察其治疗效果。结果：25例患者中,22例患者经1-2次TPE治疗后,中毒症状很快缓解,血氧饱和度上升到90％～99％,溶血基本控制,血红蛋白尿、高胆红素血症消失,降低了多脏器功能衰竭的发生率,有效率为88％,平均住院12．5d。结论：TPE能快速有效地清除蜂毒及红细胞溶解产物,可阻断因溶血及蜂毒导致的脏器功能衰竭,是抢救蜂毒危重者的有效方法。     

大剂量甲泼尼龙联合血浆置换抢救蜂螫伤急性重度溶血性贫血临床观察

目的观察大剂量甲泼尼龙联合血浆置换（PE）抢救蜂螫伤致急性重度溶血性贫血的疗效。方法对13例蜂螫伤致急性重度溶血性贫血患者,随机分为常规量甲泼尼龙联合血液灌流组（HP组）和大剂量甲泼尼龙联合血浆置换组（PE组）,观察其疗效。结果大剂量甲泼尼龙联合血浆置换组比血液灌流联合常规量甲泼尼龙组疗效好,溶血控制迅速,并发症减少,死亡率下降。结论大剂量甲泼尼龙阻断蜂毒素对红细胞的破坏,抑制体内的炎症反应;血浆置换（PE）能有效清除蜂毒素及红细胞溶解产物,二者联合运用能从不同环节阻碍溶血过程的进行,从而发挥了很好的协同治疗效果,保护脏器功能,是抢救蜂螫伤危重者的有效方法。     

甲基泼尼松龙治疗感染性休克的研究

目的：采用建立感染性休克兔动物模型,给予甲基泼尼松龙（MP）治疗,评价其疗效。方法：选择健康家兔30只,随机分为A、B、c和对照组,分别予甲基泼尼松龙1ms／（ks·d）、甲基泼尼松龙3ms／（kg·d）、休克发生后延迟给甲基泼尼松龙3mg／（kg·d）和对症常规治疗,监测各组血压回升时间、循环改善时间及病情稳定时间。结果：大剂量甲基泼尼松龙治疗组血压回升时间明显缩短,总有效率与对照组比较,差异有统计学意义（P〈0．05）。结论：实验中大剂量甲基泼尼松龙治疗感染性休克安全有效,可根据进一步实验与临床研究推广到临床应用。     

溶血性贫血的60例临床治疗体会

目的探讨溶血性贫血的临床治疗方法与疗效。方法选取2011年溶血性贫血患者60例,对急、慢性溶血者,贫血严重时,输血可迅速改善贫血,祛除病因和诱因,对症治疗。结果经治疗溶血得以控制,血象恢复时间7～20 d,平均13 d。全部病例病情明显好转或治愈出院。结论坚持按时、按量、按疗程用药,定期复查血常规,以便观察病情变化和判断疗效。     

大剂量地塞米松治疗温抗体型难治性自身免疫溶血性贫血6例

6例温抗体型自身免疫溶血性贫血(AIHA)患经泼尼松联合免疫抑制剂治疗无效后，改用大剂量地塞米松(HDD)治疗，6例患溶血症状均得到不同程度的改善，且所有患HDD均耐受良好。     

大剂量丙种球蛋白及甲基泼尼松龙冲击治疗小儿暴发性心肌炎32例临床分析

目的:观察分析大剂量丙种球蛋白及甲基泼尼松龙冲击法治疗暴发性心肌炎的临床疗效。方法:采用大剂量丙种球蛋白及甲基泼尼松龙冲击疗法,结合正性肌力药、扩血管、利尿、转换酶抑制剂、扩容、血管活性药物和纠正心律失常以及保护心肌、吸氧、监护等综合措施,治疗暴发性心肌炎患儿32例。结果:暴发性心肌炎病情进展迅速,病死率高,心电图表现多样且易变,可出现心源性休克、传导阻滞、室速及室颤。32例中住院期间死亡3例,转往上级医院途中死亡4例,治愈25例。结论:在综合治疗的基础上,突出大剂量丙种球蛋白及甲基泼尼松龙冲击疗法在暴发性心肌炎治疗方面的作用,能明显纠正休克、传导阻滞、心律失常,提高抢救成功率,降低死亡率。     

14例急性脊髓损伤应用大剂量甲基泼尼松龙联合神经节苷脂临床观察

目的观察大剂量甲基泼尼松龙冲击联合神经节苷脂治疗急性脊髓损伤的疗效。方法对14例急性脊髓损伤患者采用早期大剂量甲基泼尼松龙冲击联合神经节苷脂治疗,观察神经功能恢复情况,并与同期末进行此治疗的11例该病患者进行比较。结果采用甲基泼尼松龙冲击联合神经节苷脂治疗患者的神经恢复速度及程度均优于对照组。结论早期大剂量甲基泼尼松龙冲击联合神经节苷脂治疗急性脊髓损伤,对于抑制脊髓继发性损伤的发生、发展及促进患者神经功能的恢复有积极意义。     

甲基泼尼松龙治疗川崎病23例临床分析

目的：探讨甲基泼尼松龙治疗川崎病的临床疗效。方法：将46例川崎病患儿随机分为观察组和对照组各23例,对照组采用丙种球蛋白＋阿司匹林治疗,观察组在对照组的基础上加用甲基泼尼松龙治疗,比较两组疗效及不良反应。结果：46例患儿均痊愈或好转,观察组3d内退热者23例（100.00%）,对照组3d内退热者20例（89.96%）,两组比较,差异有统计学意义（P〈0.05）;两组在治疗后白细胞（WBC）、血小板（PLT）、C反应蛋白（CRP）、血沉（ESR）值均明显下降,组间比较,差异有统计学意义（P〈0.05）;观察组治疗后21d及3个月后的冠状动脉病变发生率分别为13.04%和4.35%,对照组分别为30.43%和17.39%,组间比较,差异有统计学意义（P〈0.05）。结论：川崎病是一种病因及发病机制目前尚未完全明确的全身性血管炎性疾病,在采用大剂量丙种球蛋白＋阿斯匹林联合治疗的基础上,短期静脉使用甲基泼尼松龙可有效缩短病程,减少冠状动脉病变的发生。     

中剂量甲基泼尼松龙联合丙种球蛋自治疗特发性血小板减少性紫癜12例

目的探讨中剂量甲基泼尼松龙联合丙种球蛋白治疗特发性血小板减少性紫癜的疗效。方法对本科2007年6月～2010年2月采用中剂量甲基泼尼松龙联合丙种球蛋白治疗的特发性血小板减少性紫癜12例进行回顾性分析。结果该组患者治疗后完全缓解者7例（58．3％）,部分缓解者3例（25．0％）,进步1例（8-3％）,无效1例（8．3％）,总有效率为91．6％。结论中剂量甲基泼尼松龙联合丙种球蛋白治疗重症特发。性血小板减少性紫癜起效快,副作用较轻,值得临床应用。     

婴儿自身免疫性溶血的临床分析

目的探讨婴儿自身免疫性溶血性贫血（AIHA）的病因、诱因及治疗方法。方法对32例婴儿AIHA的临床资料进行回顾性分析。结果婴儿AIHA女性多于男性;32例中病因明确者22例;免疫分型以IgG＋C3型多见,且其溶血、贫血程度最重;患者采用肾上腺皮质激素治疗有效率为84．4％。结论自身免疫性溶血性贫血抗体分型与临床特点相关;基础疾病的追查及治疗有重要意义;应重视临床表现及实验室检查特征;皮质激素加免疫抑制剂或加用大剂量免疫球蛋白的治疗效果好。     

抗菌药物诱发急性溶血性贫血临床特点分析

目的：探讨临床常用抗菌药物诱发溶血性贫血的特点。方法：回顾某科发生的头孢唑肟引起溶血性贫血2例患者临床资料,同时在MEDLINE光盘数据库、中国知网中国期刊全文数据库、中国科技期刊全文数据库及万方数据库检索,搜集114例抗菌药物诱发溶血性贫血病例资料,分析其临床及实验室特点。结果：共搜集116例抗菌药物引起溶血性贫血病例,儿童50例,成人66例。报道最多抗菌药物为头孢菌素,其次为青霉素及磺胺类抗菌药物,喹诺酮类及大环内酯类抗菌药物引起溶血性贫血亦有散在病例报道。溶贫发生时抗菌药物应用时间最短为5 min,最长为21 d,69.8%发生在抗菌药物应用1周内。临床症状不典型,表现多样,发热、恶心呕吐、疲劳、腰背疼痛为常见临床表现,常伴有血清白细胞及乳酸脱氢酶明显增高。最常见并发症为肾功能衰竭,其次可有肝功能异常、凝血异常、血小板减少等。42.3%患者出现初始症状及时停药,57.7%患者未及时停药,最终24例死亡。结论：抗菌药物引起溶血性贫血罕见但可致死,及时识别并停药对于改善预后至关重要,临床医师在抗菌药物应用中应随时警惕这一致命性不良反应发生的可能。     

甲基强的松龙对重症蜂蜇伤患者的治疗分析

【摘要】 目的 探讨重症蜂蜇伤患者血清中肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）、白细胞介素8（IL-8）的水平及甲基强的松龙冲击对其的影响。方法 将蜂蜇伤患者随机分为治疗组与对照组,2组均给予器官功能支持为主的综合治疗;治疗组前三天予以甲基强的松龙0.5g/d静脉滴注。分别于0h、2h观察2组患者的细胞因子（TNF-α,IL-6和IL-8）水平、2组患者入院0h、72h器官功能损害程度、并比较2组患者的死亡率。结果 0h时,治疗组、对照组TNF-α、IL-6和IL-8水平分别为3.21±0.84、113.25±35.61、162.49±79.33;3.17±0.79、109.83±32.58、157.71±73.65,二者比较无统计学差异（P＞0.05）;但在2h时TNF-α、IL-6、IL-8水平分别为8.11±2.34、37.95±11.68、53.99±25.86;15.67±5.21、314.76±86.40、452.07±211.09,存在统计学差异（P﹤0.05）;72h时,甲基强的松龙冲击治疗组患者器官功能损害程度明显低于对照组,存在显著的统计学差异（P﹤0.01或﹤0.05）;甲基强的松龙冲击治疗组患者治愈率明显高于对照组,存在统计学差异（P﹤0.05）. 结论 炎性细胞因子在引起蜂蜇伤患者多器官功能损害中起了重要作用, 甲基强的松龙冲击治疗可以明显减轻蜂蜇伤引起的这种损伤。甲基强的松龙冲击治疗可能降低蜂蜇伤急性期病死率,改善远期预后。     

病毒性肝炎非消化道出血性贫血的原因探讨

目的 探讨病毒性肝炎患者非消化道出血性贫血的原因.方法 对血常规检查伴有贫血而无消化道出血的30例病毒性肝炎患者作骨髓穿刺及溶血方面的检查.结果 检查发现原因不明的溶血性贫血3例,地中海贫血3例,缺铁性贫血2例;骨髓增生减低/明显减低共9例.结论 对病毒性肝炎伴有贫血者,应常规作骨髓穿刺及溶血的相关检查.     

Achievements and limitations of complement inhibition by eculizumab in paroxysmal nocturnal hemoglobinuria: the role of complement component 3

Paroxysmal nocturnal hemoglobinuria (PNH) is a hematological disorder characterized by complementmediated hemolytic anemia, thrombophilia and bone marrow failure. The clinical hallmark of PNH is evident chronic hemolysis due to the absence of the complement regulators CD55 and CD59 on PNH erythrocytes. Intravascular hemolysis drives the major clinical features of PNH, including anemia, hemoglobinuria, fatigue and other hemolysisrelated disabling symptoms, such as painful abdominal crises, dysphagia and erectile dysfunction. A peculiar thromboembolic risk has been associated with the hemolysis in PNH, but its pathophysiologic cause remains unclear. The treatment of PNH has remained supportive until a few years ago, when the first complement inhibitor, designated eculizumab, became available. Chronic treatment with eculizumab results in sustained control of intravascular hemolysis, leading to hemoglobin stabilization and transfusion independence in half of the patients. However, residual anemia may persist in a substantial fraction of patients. Recent observations by different groups, including our own, have demonstrated that residual hemolysis may be due to persistent activation of the early phases of the complement cascade, leading to progressive C3-deposition on PNH erythrocytes and possible subsequent extravascular hemolysis through the reticuloendothelial system. Here we critically review the available clinical results of eculizumab treatment for PNH patients, pointing out the recent insights into the pathophysiology of the disease. We discuss the role of the different components of the complement cascade leading to hemolysis, in both the absence and presence of the terminal effector pathway inhibition by eculizumab. Finally, we provide a theoretical rationale for the development of novel strategies of complement inhibition which could in the future further improve on the already substantial efficacy of eculizumab.     

对头孢唑肟钠致3例溶血的分析

目的：对临床发生的3例头孢唑肟钠致溶血进行分析,为临床合理、安全使用该药提供参考。方法：收集本院2015年1月至2017年12月上报的3例头孢唑肟钠致溶血性贫血不良反应（ADR）报告,探讨发生原因。结果：溶血性贫血是头孢唑肟钠少见的不良反应,但老年患者仍需加强重视,防止漏诊、误诊。结论：使用头孢唑肟钠时需避免超剂量、超适应症用药,使用过程中对患者用药情况监护,防止溶血性贫血造成严重危害。     

Acute hemolysis after receiving oxaliplatin treatment: a case report and literature review

Objective To report a case of immune mediated hemolysis occurring after oxaliplatin infusion in a patient with rectal cancer. Case summary We report a 69 year old male patient who presented with acute onset anemia after infusion of oxaliplatin as chemotherapy. A positive direct Coombs test and good response to steroids treatment underlined the diagnosis of immune related hemolytic anemia. The patient was switched to irinotecan-based chemotherapy regimen for further treatment. Discussion To our knowledge, there has been less than 10 cases of hemolysis occurring after oxaliplatin treatment in the medical literature. In all cases, immune mediated hemolysis has been proven with a positive coombs test. As oxaliplatin based chemotherapy regimen has become a standardized first line treatment for metastatic colorectal adenocarcinoma, this phenomenon warrants a higher level of physician awareness. Conclusions Oxaliplatin related hemolytic anemia is a rare reported phenomenon. Patient under oxaliplatin treatment presenting with sudden hemoglobin decrease should prompt further investigation of hemolysis.     

The effect of lead on oxidative hemolysis and erythrocyte defense mechanisms in the rat

The effect of chronic lead exposure on oxidative hemolysis and on biochemical defense mechanisms against such hemolysis was examined. The interaction between lead (Pb) and phenylhydrazine (PHZ) was studied using four groups of adult male rats treated with lead acetate in a combined oral-ip dosage regimen. After 27 days of exposure the blood lead (PbB) concentrations were (mean ± SD) 2.3 ± 1 (control), 33 ± 4, 67 ± 13, and 104 ± 17 μg/100 ml. On Day 27, PHZ (45 mg/kg sc) was administered to half of the rats in each group, and hemoglobin (Hb) and hematocrit (Hct) determinations were performed on tail blood drawn on Days 28, 29, 34, and 40. The results showed that in the acute hemolytic phase after PHZ both lead alone and PHZ alone reduced Hb and Hct but that the lead-PHZ interaction was not synergistic. A synergistic interaction did occur during the compensatory phase of anemia. The effect of in vivo lead exposure on in vitro hemolysis and biochemical defense mechanisms was studied in a second experiment, the results of which showed that lead caused a dose-dependent increase in oxidative hemolysis in vitro. Superoxide dismutase activity was decreased, whereas pentose shunt activity was increased. The effect of lead on reduced glutathione concentrations and glutathione peroxidase activity was biphasic, being increased at the intermediate dose but returning to baseline at the highest dose. We conclude that the in vivo interaction between Pb concentrations of up to approximately 100 μg/100 ml blood and oxidative hemolytic anemia was due to the ability of lead to inhibit compensatory hematopoiesis after an acute hemolytic episode. The more sensitive in vitro hemolysis test showed that lead caused a dose-dependent increase in oxidative hemolysis, and the biochemical changes observed were consistent with the hypothesis that in vivo lead exposure exerts a moderate pro-oxidant effect on rat erythrocytes.     

Development of tolerance to 2-butoxyethanol-induced hemolytic anemia and studies to elucidate the underlying mechanisms.

Early work demonstrated that a single administration of 2-butoxyethanol (BE) causes acute hemolytic anemia in rats. Current studies were undertaken to investigate the effect of repetitive daily dosing of BE on the hematologic parameters of male F344 rats. Treatment of rats with BE daily (125 mg/kg/day) for 1 to 3 consecutive days resulted in a time-dependent increase in the hemolysis of erythrocytes. However, when daily treatment with BE continued beyond 3 days, the number of erythrocytes began to rebound and approached pretreatment levels within 12 days despite continued daily exposure, suggesting development of tolerance to the hemolytic effect of BE. In vivo and in vitro studies were designed to investigate the underlying mechanism(s) of tolerance to the hematotoxicity of BE. Rats were treated with 125 mg BE/kg/day for 3 days followed by a 7-day recovery. At the end of this recovery period, rats were challenged with a single 125 or 250 mg BE/kg dose and the hematologic profiles were assessed at 2, 8, and 24 hr later. A significant decline in the sensitivity of BE-pretreated/recovered rats compared to vehicle-pretreated rats was observed. Further, in vitro incubation of blood obtained from BE-pretreated/recovered with the hematotoxic metabolite of BE, 2-butoxyacetic acid (BAA), revealed that erythrocytes obtained from these rats were significantly less sensitive to BAA than those obtained from normal rats. These studies suggested that tolerance is due, at least in part, to the lesser sensitivity of young erythrocytes formed during the regeneration process. In another study, rats were rendered anemic by bleeding followed by a 7-day recovery. BE administration to bled/recovered rats demonstrated that these rats were less sensitive than rats which were not subjected to bleeding. In vitro incubation of blood obtained from the bled/recovered animals with BAA demonstrated that erythrocytes were significantly less sensitive to BAA than those obtained from control rats. This further confirmed that young erythrocytes, formed during the regeneration process, were less sensitive to BAA than older erythrocytes. Current data also suggested that it is unlikely that tolerance is caused by modification of BE metabolism in rats repetitively exposed to this chemical. In conclusion, chronic exposure to BE would be expected to result in tolerance to BE-induced hemolytic anemia. The mechanisms responsible are likely related to the fact that older cells are more susceptible to BE and BAA and that hemolysis of these cells during the initial exposure followed by their replacement with less susceptible younger cells may account for tolerance development.