Severe delayed haemolytic anaemia associated with artemether-lumefantrine treatment of malaria in a Japanese traveller

Delayed haemolytic anaemia has been reported in association with intravenous artesunate treatment in patients with severe Plasmodium falciparum malaria, and furthermore, oral artemisinin-based combination therapies including artemether-lumefantrine (AL) have also been incriminated. However, definite cases of delayed haemolytic anaemia associated with AL appear to be scarce, as reported cases were often treated concomitantly with other anti-malarials. In this study, we report a severe case of delayed haemolytic anaemia following AL alone in a Japanese traveller with severe parasitaemia caused by numerous P. falciparum parasites and a few P. vivax parasites. We also stress the need by further studies to differentiate between delayed haemolytic anaemia and blackwater fever, the latter being another malaria-related haemolytic condition, more clearly than they are now.     

Haemolytic anaemia caused by anti-Pra following rubella infection

Summary. A 24-year-old male was admitted to Kansai Medical University Hospital, complaining of fever, skin exanthema, jaundice, brown urine and lymphadenopathy.
The patient was diagnosed as having haemolytic anaemia caused by a cold agglutinin following rubella infection.
The cold agglutinin of the patient reacted strongly with group OI red blood cells (RBC), Oi cord RBC, Oi adult RBC and neuraminidase-treated RBC, and much weaker with protease (papain, ficin, bromelin)-treated RBC; it was identified as anti-Pr^a.
Cold agglutinins of anti-Pr^a specificity following rubella infection in adults have rarely been reported.     

Glucose-6-phosphate dehydrogenase (G-6-PD) Hamburg, a new variant with chronic nonspherocytic haemolytic anaemia

Abstract. A new variant of G-6-PD with chronic non-spherocytic haemolytic anaemia and very low activity, named G-6-PD Hamburg, was partially purified and biochemically characterized. It was found to have very high lability, an unusually high Km for G-6-P (2000 μM), increased utilization rates for 2-desoxy G-6-P (133%) and galactose-6-phosphate (87%) and an abnormal pH-activity curve. The electrophoretic mobility seemed to be normal. The leukocytes also revealed diminished G-6-PD activity. No impairment of bactericidal activity of neutrophilic granulocytes, as shown by a normal nitroblue tetrazolium reduction, could be demonstrated.     

Gemcitabine-induced haemolytic uremic syndrome,although infrequent,can it be prevented: A case report and review of literature

Gemcitabine is an antineoplastic used to treat several malignancies including pancreatic cancer. Its toxicity profile is well known with myelotoxicity, increased vascular permeability and peripheral oedema as most frequent adverse events. However, several cases of acute renal failure have been reported and haemolytic uremic syndrome (HUS) seems to be the underlying process. The cause of HUS remains unknown but its consequences can be lethal. Therefore, a high grade of suspicion is crucial to diagnose it and promptly treat it. This hopefully will reduce its morbidity. HUS is characterized by progressive renal failure associated with microangiopathic haemolytic anaemia and thrombocytopenia. The primary event is damage to endothelial cells and thrombotic microangiopathy (TMA) is the histopathological lesion. TMA affects mainly renal microvasculature. However, some cases evolve with central nervous or cardiovascular systems involvement. We present here a case of gemcitabine-induced HUS, with renal and cardiovascular system affected at the time of diagnosis which to our knowledge this is the first time of such case to be reported.     

Transcytosis of IgG anti-D by human term trophoblast cells in culture

Placental trophoblast cells were cultured on filters that allow access to medium bathing the apical and basal surfaces of cells. Purified human IgG was added to either the apical or the basal chambers and sampled at intervals of up to 100 min for determination of IgG concentration by ELISA. Using this experimental system, transport of IgG1 and IgG3 monoclonal anti-D, affinity-purified polyclonal anti-D and human polyclonal IgG were shown to occur primarily in the apical to basal (i.e. maternal to fetal) direction. The overall transport of monoclonal and polyclonal anti-D was less than 10% in 45 min, several times lower than that of IgG. There was no difference in the rate or percentage of transport between IgG1 (BRAD-5) and IgG3 (BRAD-3) monoclonal anti-D. The possibility that the Fc receptor mediating transcytosis of IgG anti-D through human trophoblast cells in culture is the placental hFcRn is proposed.     

Specific recognition of hydatid cyst antigens by serum IgG,IgA using Western blot

Diagnosis of hydatid disease in humans relies on the detection of specific antibodies against antigens of the matacestode from Echinococcus granulosus. The specificity and sensitivity of current immunological techniques based on specific serum IgG rely on the way antigens are purified. We used Western immunoblotting to detect specific IgG, IgE, and IgA antibodies in serum from patients with hydatid disease using either crude antigen preparations (total hydatid fluid), purified fractions enriched in Antigens 5 and B, and glycoproteins from hydatid fluid. Depending on whether crude HF or purified antigen fractions were used, IgG and IgE recognized specifically low-to-medium MW bands between 12 and 42 kDa. IgA recognized specifically 110 kDa band in crude hydatid fluid and in the glycoprotein fraction of hydatid fluid, and a 42 kDa band in all antigen samples used. Besides the advantage of detecting specific IgA in crude hydatid fluid, these results offer the possibility of simplifying future immunological tests if specific secretory IgA can be similarly detected. J. Clin. Lab. Anal. 11:154–157, 1997. © 1997 Wiley-Liss, Inc.     

新型光敏剂M007剂量及光剂量与红细胞溶血率的相关性研究

目的通过光敏剂剂量和光剂量与红细胞溶血率相关性的研究,为将光化学技术应用于血液中肿瘤细胞灭活的实验研究提供理论基础。方法将光敏剂M007加入Hct 40%的红细胞悬液中,经单波长630～660 nm红光光照后,测定红细胞溶血率。实验分为实验组(M007-PCT,加入光敏剂后光照)、光敏剂对照组(M007,加入光敏剂后避光)、光照对照组(L,仅光照)与空白对照组(C,不加入光敏剂,避光)。光敏剂剂量范围(4～40)μmol/L,光剂量范围(2.16～6.48))J/cm2。结果光剂量2.16 J/cm2,光敏剂浓度(4～40)μmol/L范围内,M007-PCT组及M007组红细胞均发生溶血,2组红细胞溶血率分别从(0.108±0.003)%、(0.092±0.001)%升至(1.032±0.074)%、(1.022±0.053)%,明显大于同剂量L组及C组(P0.05)。L组与C组相比红细胞未发生溶血(P0.05)。光剂量(2.16～6.48))J/cm2,M007-PCT组红细胞溶血率(28、32、36、40μmol/L)分别从(0.920±0.042)%、(0.945±0.054)%、(1.035±0.052)%、(1.032±0.074)%升至(1.489±0.315)%、(1.506±0.110)%、(1.484±0.308)%、(1.502±0.264)%。随暗反应时间延长M007组红细胞溶血率增加。结论 M007-PCT所致红细胞溶血率的变化与光敏剂剂量及光剂量具有相关性(r=0.956、r=0.946),光敏剂剂量及光剂量的增加均能导致红细胞溶血率的增加,实验剂量下最大溶血率1.7%。     

Direct quantitation of IgG subclasses 1, 2, and 3 bound to red cells by Rh1 (D) antibodies

The authors developed quantitative radioimmunoassays to allow direct measurement of total human IgG and individual IgG subclasses among antibodies bound to cell surfaces. The assays use four mouse monoclonal radioiodinated antibodies, one that reacts equally well with all four human IgG subclasses and three that are specific for human IgG subclasses 1, 2, or 3. The assays were used to analyze IgG subclass composition in 21 high-titer anti-D samples from Rh-negative volunteers immunized for Rh immunoglobulin production. Anti-D activity was restricted primarily to the IgG1 and IgG3 subclasses. Eleven of 21 sera demonstrated red cell antibodies with a marked predominance of IgG1 (87 +/- 3.6% of total IgG antibody, +/- SEM) and low levels of IgG3 (1.4 +/- 0.73%). In the remaining 10 sera, IgG3 made up a greater proportion of total IgG antibody (32 +/- 3.8%), although IgG1 was still predominant (61 +/- 4.1%). This observed dichotomy in the IgG subclass profiles of different anti-D sera may be a consideration in the selection of anti-D sera for the production of the immunoglobulin used in the prophylaxis of Rh-incompatible pregnancies.     

甲氧基聚乙二醇修饰红细胞解决自身免疫性疾病所致配血困难研究

目的观察红细胞(RBC)经甲氧基聚乙二醇-琥珀酰亚胺丙酸酯(mPEG-SPA)修饰后对血型抗原的遮蔽作用,评估其解决自身免疫性疾病等所致配血困难的效果。方法以mPEG-SPA体外修饰正常人RBC,用微柱凝胶血型卡检测对A、B、RhD、RhC、RhE血型抗原的免疫遮蔽作用,并比较不同分子量不同浓度mPEG-SPA的遮蔽效果;观察修饰前后RBC的变形性、渗透脆性、自身溶血率,判断修饰对RBC功能的影响;比较修饰前后自身抗体阳性患者血清与相同ABO血型标本交叉配血时的凝集情况。结果mPEG-SPA修饰不影响RBC的变形性、渗透脆性、自身溶血率等特性,对A和B血型抗原基本没有遮蔽作用,而分子量20000的mPEG-SPA浓度达2mmol/L或分子量10000的mPEG-SPA为6mmol/L时,能有效地遮蔽RhD、RhC和RhE抗原,可有效消除受血者自身抗体和其他相应抗体所致的凝集现象。结论mPEG-SPA修饰可有效遮蔽Rh血型抗原并解决自身抗体所致的配血困难。     

不同吸附剂对肝衰竭患者血浆总胆红素、血氨及胆汁酸的吸附作用对比研究

目的比较几种吸附剂对肝衰竭患者血浆总胆红素、胆汁酸及血氨的吸附作用。方法收集4名肝衰竭患者血浆，将每位患者血浆分为6份，分别用以下6种吸附材料进行血浆灌注：丽珠HA330吸附树脂（HA330组）；用人血白蛋白包被的活性炭（活性炭＋HSA组）；AB-8大孔吸附树脂（AB8组）；用人血白蛋白包被经化学处理的AB-8大孔吸附树脂（化学处理的AB-8＋HSA组）；人血白蛋白包被乙基纤维素（EC＋HSA组）；用人血白蛋白包被经化学处理的乙基纤维素（化学处理的EC＋HSA组）。观察各组吸附剂对总胆红血素、胆汁酸和血氨的吸附效果并进行比较。结果除EC＋HSA组外其余各组对总胆红素、胆汁酸的吸附均有效（P〈0．05），其中化学处理的EC＋HSA组对总胆红素的吸附率最高（10．82±1．24）％，活性炭＋HSA组对胆汁酸吸附率最高（9．85±1．50）％；各组对血氨的吸附均有效（P〈0．05），化学处理的EC＋HGA组的吸附率最高（33．83±2．51）％。结论化学处理的EC＋HSA组对总胆红素、血氨、胆汁酸有较好的吸附效果。     

Effects of dipyridamole, soluflazine and related molecules on adenosine uptake and metabolism by isolated human red blood cells

Summary— The suggestion that adenosine may have beneficial effects on post reperfusion survival following cardiac ischaemia has led to the search for agents which increase the concentration of this substance in the ischemic region as a possible therapeutic approach to the treatment of angina and myocardial infarction. In the present study, dipyridamole, soluflazine and lidoflazine, known inhibitors of the nucleotide exchange system, have been shown using an HPLC method to prevent the decrease in the concentration od added adenosine outside human red blood cells in vitro. However, the results suggest that this effect was due to inhibition of adenosine deaminase rather than inhibition of nucleotide exchange as had previously been suggested. The selective inhibitor of adenosine deaminase erythro-9-(2 hydroxy-3-nonyl adenosine) exhibited the same profile of activity in the human red blood cell assay. pIC₅₀ values for the four compounds named above were found to be 6.80 ± 0.09, 6.95 ± .03, 6.10 ± 0.14 and 7.39 ± 0.05 vs adenosine disapearance observed in the extracellular incubation medium respectively. Thus, as the disappearance of adenosine outside the cells was not due to its uptake but to its catabolism, this in vitro method does not appear to be predictive for the ability of compounds to act on adenosine uptake into cardiac myocytes. Any antiischemic action of these agents is more readily explained by an inhibition of the catabolism of adenosine and not by the inhibition of its transport across the membrane of cardiac myocytes.