Lamivudine induced pure red cell aplasia and HIV-1 drug resistance-associated mutations: a case report.

Adverse effects linked to antiretroviral therapy (ART) may contribute to poor adherence on the patient's side. Consequently, human immunodeficiency virus (HIV) drug resistance mutations could emerge, negatively impacting the body's immune system. Meanwhile, severe immunosuppression can lead to several conditions, including anemia. The cause of anemia in HIV infection is multifactorial, and can be mainly explained by deleterious direct effects of the virus on the bone marrow, and opportunistic infections such as Parvovirus B19. Other causes include blood loss resulting from neoplasms and gastrointestinal lesions. Moreover, anemia can also be caused by antiretroviral drugs. We report a case of persistent anemia after ART initiation, kidney injury and treatment failure following a lengthy period of non-adherence to ART. The anemia was classified as Pure Red Cell Aplasia (PRCA). With treatment modification, the anemia resolved and the patient attained virologic suppression. Lamivudine (3TC) was pointed out as the cause of PRCA, which resolved after its withdrawal from the ART regimen. This rare side effect should be investigated in patients on 3TC who present with recurrent anemia.

A case of undisclosed prior exposure to antiretroviral therapy (ART) and early virologic failure that improved on a pre-emptive third-line ART regimen.

Introduction: The test and treat strategy recommends starting ART on the same day of diagnosis; yet, in Namibia neither baseline viral load (VL) nor genotypic resistance testing (GRT) are recommended prior to ART initiation. However, some clients return to care having defaulted ART and undergo HIV testing as "new" clients without disclosing their previous exposure, which predisposes them to primary virologic failure. Case report: A 53-year-old man tested HIV positive in 2019 without disclosing his prior exposure to ART from 2010-2015 and who stopped medication from 2015-2019 due to religious advice. He was thus initiated of first-line ART on the same day of his new diagnosis with a nadir CD4 count of 102 cells/mm3. He had a negative cryptococcal serum antigen, a normal creatinine clearance but with hepatitis B coinfection. He presented later with a primary virologic failure (VL >1000 copies/mL) and severe immunosuppression. The in-depth discussion revealed previous exposure to ART. He consequently benefited from a presumptive third-line ART that suppressed his VL while a GRT was being processed which later confirmed ART resistance. Conclusions: In poor resource settings where GRT is not performed regularly, undisclosed exposure to ART might lead to subtherapeutic treatment and primary virologic failure. In such patients where primary virologic failure is suspected despite good adherence, presumptive third-line ART can be considered in severely immunocompromised patients while waiting for GRT.