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.