Comparison of placenta structure in preterm deliveries between HIV infected and uninfected women in Kenya.
Background: Preterm birth (PTB) is a major cause of infant morbidity and mortality in developing countries. The underlying structural mechanisms by which PTB occur are largely unknown. Whereas the association between maternal HIV infection and adverse obstetric outcomes is known, there is a paucity of data that investigate the structural changes in the placenta amongst HIV infected versus uninfected women. This data could be useful in interpreting whether specific lesions are related to increased risk of pre or perinatal HIV transmission besides providing a further understanding of biology of preterm placenta in vertical transmission of HIV and PTB. Objective: To compare the structural features of the placenta delivered by HIV infected and uninfected women with preterm births. Material and methods: This was a descriptive cross-sectional laboratory based study of placenta delivered by mothers at Kenyatta National and Pumwani maternity hospitals. Forty-three and thirty-eight preterm placentas from HIV seronegative and seropositive women respectively who delivered between 28 and 37 weeks of gestation were analyzed. The samples were obtained after relevant ethical and administrative approvals. Ten placentas each from HIV positive and negative mothers with term deliveries were also studied for comparative purposes. Placentas were examined grossly for obvious color change, shape, diameter, weight, umbilical cord insertion thrombosis and infarction. Samples were then processed for paraffin wax embedding at Lancet Laboratories and studied in a blinded fashion for light microscopy, morphometry and stereology at the University of California San Francisco. Observations were recorded in preformatted data sheets and photomicrographs of various placental sections taken. Clinical data included age, gestational age, recent CD4 count, HIV viral load, status of antiretroviral therapy (ART). This information was then correlated with the placental findings and analyzed using SPSS version 20. Results: Preterm HIV seropositive placenta were significantly associated with thrombosis, infarction, anomaly in cord insertion and unusual colour of the membranes (p<0.001, p=0,041, p=0.022, p=0.43 respectively). Comparatively only infarction and anomaly in cord insertion were significantly associated with term HIV seropositive placenta (p=0.028, p=0.022 respectively). Preterm placenta from HIV seronegative women appeared to be significantly thicker (p=0.010) than those from matched HIV seropositive placenta. There was, however, no significant difference in cord diameter, cord length, weight and great diameter of the placenta between the two preterm groups. Microscopically, preterm placentas were in general associated with immature villi, syncytial knotting, villitis and deciduatis. Main findings associated with preterm HIV seropositive placenta included massive fibrinoid deposition with villi degeneration, syncytiotrophoblast delamination, increased red cell adhesion to the terminal villi and increased neoangiogenesis. Compared to term and preterm HIV seronegative placenta, HIV preterm seropositive placentas showed significantly smaller villous area (p<0.05) being also fewer per unit area, increased vascularity and diminished perimeter. Conclusion: These results imply that HIV is associated with salient morphological changes in preterm placentas that could potentially exacerbate preterm birth. The unique villous architectural changes may signify hypoxia effects in placentas related to HIV infected and/or ART use putting the pregnancy at greater risk of PTB. Further research to explore potential mechanisms will help elucidate these pathways, and could lead to interventions to decrease the risk of PTB