Hankins Jane S, Penkert Rhiannon R, Lavoie Paul, Tang Li, Sun Yilun, Hurwitz Julia L
Department of Hematology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA
Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Exp Biol Med (Maywood). 2016 Apr;241(7):749-54. doi: 10.1177/1535370216636723. Epub 2016 Mar 2.
Parvovirus B19 infection causes transient aplastic crisis in sickle cell disease (SCD) due to a temporary interruption in the red blood cell production. Toxicity from hydroxyurea includes anemia and reticulocytopenia, both of which also occur during a transient aplastic crisis event. Hydroxyurea inhibits proliferation of hematopoietic cells and may be immunosuppressive. We postulated that hydroxyurea could exacerbate parvovirus B19-induced aplastic crisis and inhibit the development of specific immune responses in children with SCD. We conducted a retrospective review of parvovirus B19 infection in 330 children with SCD. Altogether there were 120 known cases of aplastic crisis attributed to parvovirus B19 infection, and 12% of children were on hydroxyurea treatment during the episode. We evaluated hematological and immune responses. Children with HbSS or HbSβ(0)-thalassemia treated with hydroxyurea, when compared with untreated children, required fewer transfusions and had higher Hb concentration nadir during transient aplastic crisis. Duration of hospital stays was no different between hydroxyurea-treated and untreated groups. Children tested within a week following aplastic crisis were positive for parvovirus-specific IgG. Immune responses lasted for the duration of the observation period, up to 13 years after transient aplastic crisis, and there were no repeat aplastic crisis episodes. The frequencies of parvovirus-specific antibodies in all children with SCD increased with age, as expected due to the increased likelihood of a parvovirus exposure, and were comparable to frequencies reported for healthy children. Approximately one-third of children had a positive parvovirus B19-specific IgG test without a documented history of transient aplastic crisis, and 64% of them were treated with hydroxyurea. Hydroxyurea may reduce requirements for blood transfusions and may attenuate symptoms during transient aplastic crisis episodes caused by parvovirus B19 infections. Children with SCD, whether treated or untreated with hydroxyurea, generate sustained and protective parvovirus B19-specific immune responses.
细小病毒B19感染会导致镰状细胞病（SCD）患者出现短暂再生障碍危象，原因是红细胞生成暂时中断。羟基脲的毒性包括贫血和网织红细胞减少，这两种情况在短暂再生障碍危象期间也会出现。羟基脲会抑制造血细胞的增殖，并且可能具有免疫抑制作用。我们推测羟基脲可能会加重细小病毒B19诱导的再生障碍危象，并抑制SCD患儿特异性免疫反应的发展。我们对330例SCD患儿的细小病毒B19感染情况进行了回顾性研究。共有120例已知的再生障碍危象病例归因于细小病毒B19感染，其中12%的患儿在发病期间接受了羟基脲治疗。我们评估了血液学和免疫反应。与未接受治疗的患儿相比，接受羟基脲治疗的HbSS或HbSβ(0) -地中海贫血患儿在短暂再生障碍危象期间需要的输血次数更少，血红蛋白浓度最低点更高。羟基脲治疗组和未治疗组的住院时间没有差异。再生障碍危象后一周内进行检测的患儿细小病毒特异性IgG呈阳性。免疫反应在观察期内持续存在，直至短暂再生障碍危象后13年，且没有再次出现再生障碍危象发作。正如预期的那样，由于接触细小病毒的可能性增加，所有SCD患儿中细小病毒特异性抗体的频率随年龄增长而增加，并且与健康儿童报告的频率相当。大约三分之一的患儿细小病毒B19特异性IgG检测呈阳性，但没有记录在案的短暂再生障碍危象病史，其中64%的患儿接受了羟基脲治疗。羟基脲可能会减少输血需求，并可能减轻由细小病毒B19感染引起的短暂再生障碍危象发作期间的症状。无论是否接受羟基脲治疗，SCD患儿都会产生持续且具有保护性的细小病毒B19特异性免疫反应。
