Abstract
Immune reconstitution syndrome (IRIS) is an uncommon complication seen in patients living with human immunodeficiency virus (HIV) characterized by the decline in a pre-existing condition or a new diagnosis of a masked disease. It is associated with a significant inflammatory component that occurs after starting antiretrovirals, being most frequent in those with severe immunosuppression. Thereby, different types of opportunistic diseases such as non-tuberculous mycobacteria are more frequent in this group of patients, especially those with low lymphocyte counts of below 50 cells/µL. Here, we present the case of an HIV-positive patient who developed lymphadenitis caused by Mycobacterium intracellulare as an unmasked IRIS after initiating treatment for HIV.
Highlights
It is well known that highly active antiretroviral therapy (HAART) leads to immunovirological control in the treatment of human immunodeficiency virus (HIV) infection, decreasing the frequency of opportunistic diseases and improving survival
We present the case of an HIV-positive patient who developed lymphadenitis caused by Mycobacterium intracellulare as an unmasked immune reconstitution syndrome (IRIS) after initiating treatment for HIV
There is a temporal association between the initiation of HAART and the onset of symptoms, with patients presenting with a reduction in the HIV viral load and a rise in the CD4 lymphocyte count, the latter not being a necessary condition [2]
Summary
It is well known that highly active antiretroviral therapy (HAART) leads to immunovirological control in the treatment of human immunodeficiency virus (HIV) infection, decreasing the frequency of opportunistic diseases and improving survival. A 22-year-old heterosexual male with a history of daily tetrahydrocannabinol use was diagnosed with HIV in 2019 He was lost to follow-up after the first medical visit but returned in May 2020 when he decided to start HAART with tenofovir disoproxil 300 mg + efavirenz 600 mg + emtricitabine 200 mg; suspending it three days later because of marked intolerance with no reintroduction after this episode. During the few months, there was no clinical response, despite the fact that the patient was adherent to his treatment, and drug interactions were ruled out, triggering the possibility of non-tuberculous mycobacteria This was confirmed by the definitive culture results and a new molecular test (GenoType) isolating Mycobacterium intracellulare with an absence of rrl and rrn gene mutations (macrolide and aminoglycoside sensibility). Rapid response was seen within a month during the follow-up visit
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