INTRODUCTION
Sideroblastic anemias (SAs) encompass a group of bone marrow disorders
characterized by the abnormal accumulation of iron in the mitochondria
of erythroid precursors. This leads to the formation of ring
sideroblasts, where iron-laden mitochondria surround the nuclei of
erythroblasts 1. Ring sideroblasts can be present in
various pathological conditions, including both congenital and acquired
forms of sideroblastic anemias 2. The underlying
mechanisms leading to different forms of sideroblastic anemias are
diverse. However, in all cases, the abnormal accumulation of iron is
attributed to disruptions in mitochondrial proteins involved in
regulating heme synthesis or Fe/S cluster synthesis. Additionally,
impairment in translating mitochondrially encoded proteins contributes
to this iron deposition. Consequently, these alterations give rise to
ineffective erythropoiesis and iron accumulation in tissues, leading to
tissue iron overload 1. It has been associated with
antituberculin agents, chloramphenicol, and ethanol. While several
etiological factors have been implicated in acquired sideroblastic
anemia, including genetic mutations and exposure to
toxins3, the association between antiretroviral
therapy and the development of Acquired sideroblastic anemia (ASA) is
rare and has not been reported to date. Here we report the development
of sideroblastic anemia in a patient who was on Dolutegravir therapy.
Dolutegravir, an integrase strand transfer inhibitor (INSTI) exerts its
antiviral activity by binding to the active site of HIV integrase
preventing the stand transfer step crucial in the retroviral DNA
integration process thus reducing viral load and slowing down disease
progression 4. The association of ASA with
Dolutegravir has not been established in the current literature. Naranjo
method for estimating the probability of Adverse Drug Reaction (ADR) was
used to show the casual association.5