Obstetric and perinatal complications in HIV-infected women. Analysis of a cohort of 167 pregnancies between 1997 and 2003.

BACKGROUND: The unquestionable benefit of antiretroviral therapy in reducing the rate of mother-to-child transmission can be lessened by potential maternal or neonatal toxicity. OBJECTIVE: To analyze obstetric and perinatal complications in a cohort of HIV-infected pregnant women and their relationship with maternal antiretroviral therapy. POPULATION: One hundred and sixty-seven HIV-infected pregnant women who delivered at Hospital Universitario La Paz, Madrid, Spain between January 1997 and December 2003. METHODS: Data on the clinical and epidemiological characteristics of HIV-infected patients, previous and current antiretroviral therapy, gestational diabetes mellitus, length of pregnancy, mode of delivery, and weight of the newborn were collected. Pregnancy outcomes were compared with those of all the pregnant women attended at our hospital. MAIN OUTCOME MEASURES: Gestational diabetes mellitus, premature delivery, and low birth weight. RESULTS: Gestational diabetes mellitus was diagnosed in 8.9% of patients. All the cases of gestational diabetes were in the combined antiretroviral therapy group, and the majority were receiving triple antiretroviral therapy with a protease inhibitor. The risk of developing this pathology was greater among women receiving antiretroviral therapy prior to pregnancy. The premature delivery rate was 29% and the low birth weight rate was 28%. CONCLUSION: Gestational diabetes mellitus is more common in HIV-infected women than in the general population and is related to combined antiretroviral therapy, especially the use of protease inhibitors, which suggests the need for close follow-up during pregnancy in HIV-infected patients. Nevertheless, the adverse perinatal consequences observed were more related to maternal factors than to antiretroviral therapy.

Long-term effects of highly active antiretroviral therapy in pretreated, vertically HIV type 1-infected children: 6 years of follow-up.

BACKGROUND: Several studies of children with human immunodeficiency virus (HIV) type 1 infection have demonstrated sustained increases in CD4+ cell count, even when virological failure has occurred after receipt of highly active antiretroviral therapy (HAART), but these studies were of limited duration. Moreover, the CD4+ cell count threshold at which antiretroviral treatment should be initiated is still unsettled. The aim of this study was to define the long-term impact of HAART on CD4+ cell percentage and viral load according to CD4+ cell percentages before HAART was initiated. METHODS: We conducted a retrospective study of 113 pretreated HIV-1-infected children stratified by pre-HAART CD4+ cell percentage (<5%, 5%-15%, 15%-25%, and >25%). The inclusion criteria were as follows: initiating HAART with a protease inhibitor, having 6 years of follow-up after starting HAART, having a CD4+ cell count or viral load recorded before initiation of HAART, and having received mono- or dual-nucleoside therapy before starting HAART. RESULTS: During the first 2 years of HAART, HIV-1-infected children experienced a significant increase in CD4+ cell percentage and a decrease in viral load (P<.05). During their last 4 years of receiving HAART, we found a significant decrease in viral load but not an increase in CD4+ cell percentage, because the CD4+ cell percentage reached a plateau after the second year of HAART. Moreover, children with CD4+ cell percentages of <5% at baseline did not achieve CD4+ cell percentages of >25% after 6 years of HAART. Children with CD4+ cell percentages of 5%-25% at baseline had a strong negative association with achieving CD4+ cell percentages of >30% for at least 6 and 12 months but not with achieving CD4+ cell percentages of >30% for at least 24 months. CONCLUSIONS: Long-term HAART allowed for restoration of CD4+ cell counts and control of viral loads in HIV-1-infected children. However, initiating HAART after severe immunosuppression has occurred is detrimental for the restoration of the CD4+ cell count.