[Lopinavir/ritonavir in patients with human immunodeficiency virus infection in special situations].

Enferm Infecc Microbiol Clin

Unidad de Enfermedades Infecciosas y Servicio de Medicina Interna, Hospital Universitario La Fe, Valencia, España. Electronic address:

Published: November 2014

AI Article Synopsis

  • Ritonavir-boosted lopinavir (LPV/r) is an antiretroviral treatment for HIV, is safe for patients with renal failure, and doesn't require dosage adjustments since it is metabolized in the liver.
  • Compared to other antiretroviral therapies, LPV/r shows a lower incidence of renal disease and crystalluria, making it a favorable option for patients on combination therapies.
  • LPV/r is effective in addressing neurocognitive issues associated with HIV, achieves sufficient concentrations in the cerebrospinal fluid, and while liver toxicity can occur, it is generally mild and often linked to pre-existing liver conditions.

Article Abstract

Ritonavir-boosted lopinavir (LPV/r) is a protease inhibitor used for the treatment of human immunodeficiency virus (HIV) infection in both normal patients and in certain situations. In patients with renal failure, LPV/r does not require dosage adjustment because it is metabolized in the liver. Cohort studies have shown that the incidence of varying degrees of renal disease and/or crystalluria related to combination antiretroviral therapy with tenofovir and some protease inhibitors (PI) does not appear with LPV/r or that the incidence is much lower with this combination. Neurocognitive impairments are described in a high proportion of patients with HIV infection and viral replication or related inflammatory activity in the subarachnoid space. In these patients, LPV/r is one of the therapeutic options. A score has been published that rates antiretroviral drugs according to the concentration attained in the cerebrospinal fluid (CSF). LPV/r levels reached in CSF exceed the IC50 of wild-type HIV and has a valuable score (score 3) of the drugs currently used. The most important comorbid condition is chronic hepatitis, due to its frequency and because the biotransformation of LPV/r occurs in the liver. In these circumstances, it is important to evaluate the influence of liver failure on blood drug levels and how these values may cause liver toxicity. LPV/r dose modification has not been established in the presence of liver failure. LPV/r-induced liver toxicity has only been reported with a certain frequency when liver enzymes were elevated at baseline or in patients with chronic hepatitis C, although most cases of liver toxicity were mild.

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http://dx.doi.org/10.1016/S0213-005X(14)70163-6DOI Listing

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