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Published on: September 6, 2019
Lactic acidosis in HIV-exposed infants with perinatal exposure to antiretroviral therapy
1HIV Clinic, Department of Pediatrics, B. J. Wadia Hospital for Children, Mumbai, India. irashah@pediatriconcall.com
Insights
Perinatal exposure to nucleoside reverse transcriptase inhibitors (NRTI) in infants can lead to symptomatic lactic acidosis (LA). Monitoring for LA symptoms in HIV-exposed infants receiving NRTI is crucial.
Area of Science:
- Pediatrics
- Infectious Diseases
- Toxicology
Background:
- Nucleoside reverse transcriptase inhibitors (NRTI) are associated with lactic acidosis (LA) and hepatosteatosis with prolonged use.
- Symptomatic LA in infants due to perinatal antiretroviral therapy (ART) exposure is rarely reported in developing nations.
Observation:
- Three cases of infants developing symptomatic lactic acidaemia following perinatal exposure to zidovudine (ZVD) are presented.
- One HIV-infected infant exposed antenatally and postnatally to ZVD developed liver dysfunction and mental retardation.
- Two HIV-uninfected infants exposed to ZVD, with or without other ART drugs, presented with LA and metabolic acidosis.
Findings:
- Perinatal NRTI exposure, including ZVD, can cause symptomatic LA in HIV-exposed infants.
- The severity of LA varied, with one case presenting as life-threatening metabolic acidosis.
Implications:
- Healthcare providers should monitor HIV-exposed infants for symptoms of LA, especially those with perinatal NRTI exposure.
- Early detection and intervention are essential for managing NRTI-induced LA in infants.
- This highlights a potential risk of ART in developing countries where reporting is scarce.
Background:
Prolonged exposure to nucleoside reverse transcriptase inhibitors (NRTI) is known to be associated with lactic acidosis (LA) and hepatosteatosis. However, perinatal exposure to antiretroviral therapy (ART) and the subsequent development of symptomatic LA in infants, although recognised, is rarely reported in developing countries.
Cases:
Three infants born to HIV-infected mothers and who developed symptomatic lactic acidaemia associated with perinatal exposure to ZVD are reported. The first infant was HIV-infected and developed liver dysfunction and mental retardation at 5 months of age after exposure to 24 weeks of ZVD antenatally and 6 weeks of ZVD plus 4 weeks of ART triple-drug ART postnatally. The second and third infants were HIV-uninfected. The second infant had been exposed to ZVD for 14 weeks antenatally and for 6 weeks postnatally and presented with LA at 6 weeks of age. The third infant was exposed to ZVD, lamivudine and nevirapine for 9 weeks antenatally and 6 weeks of ZVD postnatally, and presented with life-threatening metabolic acidosis at 10 weeks.
Conclusion:
In HIV-exposed infants, perinatal NRTI may lead to symptomatic LA and monitoring for symptoms is therefore essential.
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