Altinbaş Akif, Ozkaya Gülşen, Büyükaşik Yahya, Unal Serhat
Hacettepe Universitesi Tip Fakültesi, iç Hastaliklari Anabilim Dali, Ankara.
Mikrobiyol Bul. 2007 Jul;41(3):473-6.
Anemia, which may develop due to direct effect of the virus or indirect effect of zidovudine a widely used antiviral agent for the treatment, is not an uncommon complication in human immundeficiency virus (HIV) infections. In this report, a 26 years old male HIV positive patient who developed rapid anemia in the HAART (Highly active anti-retroviral therapy) protocol including zidovudine, was presented. The patient has been followed since May 2003 without anti-retroviral therapy. He was diagnosed as alpha-thalassemia trait, because of the low mean red blood cell volume (MCV), high red blood cell count and living in an Mediterranian country. However, no treatment for thalassemia had been given in this period, since the other laboratory findings [hemoglobin, hematocrit, red cell distribution width index (RDWI), iron and iron binding capacity, transferrin saturation and ferritin levels] were normal. During the follow-up of patient, HAART protocol with zidovudine, lamivudine and indinavir, was started depending on the findings of low CD4+ T-cell count (443/mm3) and high HIV serum load (1,330,000 copies/ml). In the second month of the therapy the hemoglobin level decreased to 12.9 gr/dL, and then to 9.9 gr/dL in the fourth month, while it was 14.5 gr/dL before anti-retroviral therapy. Although the patient had no hemolysis findings, and his serum folic acid level was normal, folbiol treatment was initiated with the possibility of the presence of folic acid deficiency at cellular level. Anemia resolved with folic acid replacement without discontinuation of zidovudine or a reduction in dosage. It was thought that the presence of alpha-thalassemia co-morbidity has facilitated the development of anti-retroviral-induced anemia in this patient. As a result, it is concluded that thalassemia should be considered in the differential diagnosis of anemia in HIV positive patients, especially for the ones from Mediterranian countries.
贫血可能是由于病毒的直接作用或齐多夫定（一种广泛用于治疗的抗病毒药物）的间接作用而发生，在人类免疫缺陷病毒（HIV）感染中是一种常见的并发症。在本报告中，介绍了一名26岁的男性HIV阳性患者，他在包括齐多夫定的高效抗逆转录病毒治疗（HAART）方案中迅速出现贫血。该患者自2003年5月以来未接受抗逆转录病毒治疗。由于平均红细胞体积（MCV）低、红细胞计数高且生活在地中海国家，他被诊断为α地中海贫血特征。然而，在此期间未对地中海贫血进行治疗，因为其他实验室检查结果[血红蛋白、血细胞比容、红细胞分布宽度指数（RDWI）、铁和铁结合能力、转铁蛋白饱和度和铁蛋白水平]均正常。在患者随访期间，根据低CD4 + T细胞计数（443/mm³）和高HIV血清载量（1,330,000拷贝/ml）的结果，开始使用齐多夫定、拉米夫定和茚地那韦的HAART方案。治疗的第二个月血红蛋白水平降至12.9 gr/dL，第四个月降至9.9 gr/dL，而抗逆转录病毒治疗前为14.5 gr/dL。尽管患者没有溶血表现，且血清叶酸水平正常，但考虑到细胞水平可能存在叶酸缺乏，开始使用叶酸治疗。贫血通过补充叶酸得以缓解，未停用齐多夫定或减少剂量。认为α地中海贫血合并症的存在促进了该患者抗逆转录病毒药物诱导的贫血的发生。因此，得出结论，在HIV阳性患者贫血的鉴别诊断中应考虑地中海贫血，特别是对于来自地中海国家的患者。
