PATHOGENESIS AND PATHOPHYSIOLOGY OF ANEMIA IN HIV-INFECTION

Anemia occurs frequently among patients seropositive for human immunod eficiency virus (HIV), but its multifactorial origin complicates its d ifferential diagnosis and adequate treatment. In addition, the etiolog y of anemia in HIV infection often remains unclear. In recent years se veral attempts have been undertaken to elucidate the mechanisms leadin g to HIV-associated anemia. Direct infection of erythroid progenitors has been discussed, but could not be proven. Furthermore, soluble fact ors like HIV proteins and cytokines have been suggested to inhibit gro wth of hematopietic cells in the bone marrow of HIV-infected patients. However, so far no statements can be made whether these factors are d irectly involved in myelosuppression or mediate their effect by inhibi ting growth-factor synthesis. Opportunistic complications represent th e underlying cause for anemia in a large number of HIV-infected patien ts. Next to this rather obvious reason for anemia, iatrogenic anemia i nduced by myelosuppressive drugs is also very common. It is of note, h owever, that modern dosages of < 600 mg zidovudine (ZDV) daily rarely cause anemia. Instead, other drugs that,can induce anemia itself or by enhancing ZDV plasma concentrations must be considered important cont ributing factors. Deficiency of vitamin B12, folate and iron are frequ ently reported in HIV patients. However, specific investigations revea led appropriate storage amounts of these micronutrients. Supplementati on may be beneficial in some patients, but often fails to reverse anem ia in this population. In anemic HIV patients reticulocytopenia is a c onsistent finding. Additionally, inadequately low endogenous erythropo ietin concentrations have been repeatedly reported. Thus, it is specul ated that a blunted erythropoietin feedback mechanism contributes subs tantially to the pathogenesis of anemia in HIV patients.