DEL表型是RhD血型系统中D抗原强度最弱的一种变异型。在中国，大约10％-30％的初筛RhD阴性个体具有DEL表型。上海地区，这一频率为17.6％(Li Q， et al. Molecular basis of the RHD gene in blood donors with DEL phenotypes in Shanghai. Vox Sang 2009，97：139-146)。大约0.4％的中国人是初筛阴性，所以，在上海地区DEL在人群中的频率约为0.07％。根据稀有血型的定义，DEL可归于稀有血型。

　　中国国家卫计委和AABB制定的法律与指南，未要求血站/血库的临床实验室筛查DEL。所以在中国的临床实验室DEL筛查不是常规操作。由于中国的临床实验室不对献血者或者患者进行DEL筛查，所有可能的DEL样品均标记为D阴性。

　　中国血站或者血库的研究实验室会使用吸收放散实验检测DEL。如果找到DEL，这些样品会被记为D阳性。这些结果仅供科研使用，不会改变临床实验室的结果。

　　对于如何对待具有DEL表型的个体，目前仍然存在争议。邵超鹏收集了104例产生抗-D的中国孕妇的血样，发现这104人中，没有1人是DEL(Shao CP. Transfusion of RhD-positive blood in "Asia type" DEL recipients. N Engl J Med. 2010 Feb 4;362(5):472-3.)。我们实验室在2004起的一项为期3年的研究中也发现了类似的结果，即15例产生抗-D的孕妇，没有1例是DEL。几乎所有的中国DEL均由RHD (K409K)等位基因控制。邵超鹏认为这种DEL表型可以看做‘亚洲型’DEL，具有这种表型的个体可以安全的输注D阳性血。

　　Günther和同事提出一种假设，认为DEL存在‘部分DEL’，具有这种DEL表型的个体经免疫会产生抗-D。这种部分DEL表型由RHD (IVS5-38del4)等位基因控制(Günther et al. A comprehensive analysis of DEL types: partial DEL individuals are prone to anti-D alloimmunization. TRANSFUSION 2005， 45:1561-1567 )，仅发现于高加索人种，在东亚人群中从未报道。

　　另一方面，Hiroyasu et al. (Yasuda et al. Secondary anti-D immunization by Del red blood cells. Transfusion. 2005 Oct;45(10):1581-4)， Wagner et al. (Wagner et al. Anti-D immunization by DEL red blood cells. Transfusion. 2005 Apr;45(4):520-6.) and Kim et al. (Kim et al. Primary anti-D immunization by DEL red blood cells. Korean J Lab Med. 2009)分别在日本、奥地利、韩国发现了一例D阴性个体输注DEL血液后，产生抗D的案例。对于Wagner的案例，2年后，Inge von Zabern发现这是一个错误，RHD (IVS5-38del4)等位基因不是DEL的编码基因，而是DFR-3这种部分D的一个调控基因(Inge von Zabern & Willy A. Flegel. IVS5-38del4 deletion in the RHD gene does not cause a DEL phenotype: relevance for RHD alleles including DFR-3. TRANSFUSION 2007，Volume 47， 1552-1554)。所以，这个欧洲案例并不是输注DEL血液引起的，而是由部分D所引起。同时，部分DEL也可能是不存在的。对于日本和韩国的报道，这两位患者都超过67岁，有过多次输血史。是否存在其他引发机制还需要进一步研究。

　　目前，有超过10例DEL等位基因被发现。仅仅使用吸收放散技术很难把DEL与一些弱D或部分D区分开。在试验技术改进后，现在的一些DEL可能会被定为弱D或者部分D。

　　综上所述，我们认为，中国DEL个体可以安全的输注D阳性血。中国D阴性个体是否可安全的输注DEL血液，还需要深入研究。我们推测这种情况也是安全的，因为每年中国都有一些D阴性患者接受了DEL血液，但未见有产生抗D的报道。基于RhD阴性血液属于中国的稀有资源，在目前无充分证据显示DEL血型会诱导RhD阴性个体产生抗D的情况下，我们不主张将DEL定为RhD阳性。

　　The Clinic usage of DEL blood in China

　　The DEL phenotype， which expresses the weakest D antigen， is one of the D variants in RhD blood system. In China， about 10％~30％ apparent D-negative individuals are DEL phenotypes. The rate is 17.6％ in Shanghai (Li Q， et al. Molecular basis of the RHD gene in blood donors with DEL phenotypes in Shanghai. Vox Sang 2009，97：139-146). Only about 0.4％ Chinese are apparent D-negative， so the DEL rate in Shanghai is about 0.07％， and is identified as one of the rare blood type

　　Because the laws and guidelines made by China National Health and Family Planning Commission or AABB do not require the blood center or blood bank to determine DEL for clinic usage. The DEL identification is not routine test in China clinic lab. As donors and patients are not detected DEL in China clinic lab， all the potential DEL are marked as D-negative.

　　The DEL is tested by absorption and elution assay in research lab of blood center or blood bank in China. When the DEL is found， it will be marked as D positive. The results are only for research usage， and will change the results made by clinic lab.

　　There are still debates existed about how to deal with the person with DEL phenotype. Shao collected blood samples from 104 Chinese pregnant women who produced anti-D， none of the 104 women showed DEL phenotype (Shao CP. Transfusion of RhD-positive blood in "Asia type" DEL recipients. N Engl J Med. 2010 Feb 4;362(5):472-3.). Our lab also found the same results form 15 Chinese pregnant women who were anti-D alloimmunization through a 3-year work beginning from 2004. As almost all the Chinese DELs are caused by RHD (K409K) allele， Shao suggested that persons with "Asia type" DEL can safely receive transfusions from RhD-positive donors.

　　Günther and colleagues put forward a hypothesis that some DEL can be termed as ‘partial DEL’， and individuals with such DEL are prone to anti-D alloimmunization. The partial DEL is caused by RHD (IVS5-38del4) allele (Günther et al. A comprehensive analysis of DEL types: partial DEL individuals are prone to anti-D alloimmunization. TRANSFUSION 2005， 45:1561-1567)， which was only found in Caucasian and never be reported in East Asia population.

　　On the other hand， Hiroyasu et al. (Yasuda et al. Secondary anti-D immunization by Del red blood cells. Transfusion. 2005 Oct;45(10):1581-4)， Wagner et al. (Wagner et al. Anti-D immunization by DEL red blood cells. Transfusion. 2005 Apr;45(4):520-6.) and Kim et al. (Kim et al. Primary anti-D immunization by DEL red blood cells. Korean J Lab Med. 2009) found 3 D-negative individuals produced anti-D after transfused blood form DEL donors in Japan， Austria and South Korea， respectively. To Wagner’s case， two years later， Inge von Zabern found that was a mistake that the RHD (IVS5-38del4) allele does not cause DEL but a partial D (DFR-3) (Inge von Zabern & Willy A. Flegel. IVS5-38del4 deletion in the RHD gene does not cause a DEL phenotype: relevance for RHD alleles including DFR-3. TRANSFUSION 2007，Volume 47， 1552-1554). So the Europe patient produced anti-D was not induced by DEL but partial D， and the partial DEL might be not existed. To the Japanese and Korean cases， the two patients were all old than 67， and had received many blood transfusions. Whether there was another mechanism existed is still unknown. Nowadays， more than 10 DEL alleles have been described. It is very hard to distinguish DEL from some weak D or partial D by absorption and elution assay. Some DEL may be termed as weak D or partial D by advanced technique in the future.

　　Above all， we think that Chinese DEL individuals can safely receive transfusions from RhD-positive donors. Whether truly D-negative Chinese can receive blood from DEL donors need to be further analyzed. We presume Chinese D-negative persons also can be transfused with DEL blood safely， as every year some truly D-negative Chinese received DEL blood， and no case of anti-D alloimmunization was reported. As D-negative blood is rare resource in China， and there is no evidence shows DEL blood can cause D-negative recipient produce anti-D， we do not hope DEL phenotype to be termed as D positive in Clinic.