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Session 129 Poster Abstracts
Treatment in Pregnant Women and Children: Toxicity
Wednesday, 1:30 - 3:30 pm
Poster Hall


941    
Lactic Acid Levels in Infants Exposed to ART during Fetal Life
C Giaquinto*1, O Rampon1, S Torresan1, E Ruga1, A De Rossi2, A Burlina1, M Sturkenboom3, and R D' Elia1
1Univ. of Padova, Italy; 2Inst of Oncology, Univ. of Padova, Italy; and 3Erasmus Univ. Med Sch., Rotterdam, The Netherlands

Background:  Nucleoside-analogue reverse-transcriptase inhibitors (NRTI) reduce mother-to-child-transmission of HIV by about 70%. NRTI are also substrates for DNA polymerase, the enzyme required for replication of mitochondrial DNA (mtDNA). Our first objective was to describe and compare the level and occurrence of elevated lactate levels between children from HIV+ and HIV- mothers. The second objective was to assess the association between prenatal use of NRTI and the occurrence of elevated lactate.

Methods:  We conducted a cohort study comprising 24 children born to HIV- mothers and 100 children from HIV+ mother; 81 children were followed from birth and had a first lactic acid measurement within 90 days. For HIV+ mothers, all medications that were administered prenatally and during labour were recorded and categorized as PPI/NNRTI/NRTI. The risk of elevated lactate levels (>2.5 mmol/L) was calculated and the association with prenatal treatment was estimated through logistic regression analysis.

Results:  The mean lactate level was significantly lower in control children (HIV- mothers) (1.65±0.42 mmol/L) than in children of HIV+ mothers (3.20±1.58 mmol/L). None of the control children had lactate levels above 2.5, among the children of HIV+ mothers the prevalence of elevated lactate was 64.5% in the first month after birth, 40.5% in those measured for the first time in the second month after birth and 60.9% in those measured between the second and third month. Two children were HIV+‑neither mother had been treated during pregnancy; both received AZT during delivery. Of the 79 mothers not treated during pregnancy, 10 had HIV- children, 16 received PI plus NRTI (mostly NFV and/or SQV) and 25 received NVP plus NRTI. All elevated lactic acid levels returned to normal during follow-up and none of the children developed severe mitochondrial damage. Perinatal exposure to  NRTI significantly increased the risk of elevated lactate (OR = 6.7, 95%CI:  2.4 to 18.4) after adjustment for other prenatal drug exposure.

Conclusions:  In this study we observed that infants who were exposed to prenatal HIV treatment had higher lactate levels than children of HIV- mothers. Furthermore prenatal use of NRTI increased the risk of increased lactate levels during the first 3 months of life but no children developed any neurological symptoms during the follow-up period.

 

Keywords: Mother to child transmission; children; Lactic Acid