Yasuda Hiroyasu, Ohto Hitoshi, Sakuma Shizue, Ishikawa Yoshihide
Division of Blood Transfusion and Transplantation Immunology, Fukushima Medical University School of Medicine, 1 Hikariga-oka, Fukushima City, Fukushima, Japan.
Transfusion. 2005 Oct;45(10):1581-4. doi: 10.1111/j.1537-2995.2005.00579.x.
Recent molecular studies of the RHD gene have revealed that D(el) individuals retain a grossly intact RHD gene or have a portion of RHD in their genomes. No D(el) phenotype has yet been shown to induce a primary or secondary alloanti-D immunization, however.
A 67-year-old D- Japanese woman with a history of allosensitization from transfusion of D+ red blood cells (RBCs) was negative for anti-D at admission. After she received RBCs from 19 apparently D- donors, she developed anti-D with an 8-fold titer. The titer of anti-D increased further to 128-fold after transfusions of cross-match-compatible D- negative RBCs from 40 donors over the next 2 years. Two of 59 donors were found to be RHD gene-positive and antigen D- with a D(el) phenotype, that is, RHD(K409K).
This is the first case in which RBCs having the D(el) phenotype induced a secondary alloanti-D immunization. A D- donor with the RHD(K409K) allele was associated with the development of anti-D. Adverse episodes or evidence of hemolysis was not observed after the transfusion of RHD(K409K) RBCs. Further clinical evidence is needed to reveal whether the D(el) phenotype has a clinically relevant potential for anti-D immunization.
近期对RHD基因的分子研究表明,D(el)个体的RHD基因大体上保持完整,或者其基因组中存在部分RHD基因。然而,尚未有研究表明D(el)表型会引发原发性或继发性同种抗-D免疫反应。
一名67岁的日本D型阴性女性,有因输注D型阳性红细胞(RBC)导致同种免疫的病史,入院时抗-D检测为阴性。在接受了19名明显为D型阴性供血者的红细胞后,她产生了效价为8倍的抗-D。在接下来的2年中,她又接受了40名供血者交叉配血相容的D型阴性红细胞输注,之后抗-D效价进一步升至128倍。59名供血者中有2名被发现RHD基因阳性但抗原D阴性,具有D(el)表型,即RHD(K409K)。
这是首例D(el)表型红细胞引发继发性同种抗-D免疫反应的病例。携带RHD(K409K)等位基因的D型阴性供血者与抗-D的产生有关。输注RHD(K409K)红细胞后未观察到不良事件或溶血证据。需要更多临床证据来揭示D(el)表型在抗-D免疫方面是否具有临床相关潜力。