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Anhaptoglobinemia in the tropics has long been considered as a genetic phenomenon (Allison et al 1968; Sulton et al 1959). However, between 1963 and 1968, several other workers found a close relationship between anhaptoglobinemia and hemolytic diseases, thus bringing to question the genetic hypothesis which had earlier existed. The object of our study was to verify the following in a area that was endemic both for malaria and sickle cell disease: if anhaptoglobinemia was present in both populations, if it was proportional to the parasite load or the amount of hemolysis, if anhaptoglobinemia could be used either as a marker for malaria studies or for diagnosis of intravascular hemolysis. Anhaptoglobinemia turned out not to be present in all patients suffering from malaria, but was proportional to the parasite load and hemolysis. In patients with malaria, it was undetected after malarial prophylaxis but reappeared one month after cessation of treatment, while, in sickle cells patients, it disappeared at the end of their crisis. This was evidence of high reticulocyte regeneration. These findings highlight the problem of the existence of the HpO phenotype.