Publication

Title: Pre-eclampsia: the role of highly active antiretroviral therapy and immune markers
Authors: Phoswa WN, Naicker T, Ramsuran V, Moodley J.
Journal: Inflamm Res.,doi: 10.1007/s00011-018-1190-3: (2018)
Number of citations (Google Scholar): 5

Abstract

PURPOSE OF THE REVIEW: This review highlights the role immune cells and markers such as natural killer (NK) cells, cytokines and human leukocyte antigen (HLA-G) play in predisposing HIV-infected women who are on HAART to develop PE, thus contributing to a better understanding and early diagnosis of PE with a subsequent reduction in maternal foetal and neonatal deaths.

RECENT FINDINGS: Pregnant women infected with the Human Immunodeficiency Virus (HIV) have a 25% risk of mother to child transmission. This risk, however, decreases to 2% if the women is on treatment. Highly active antiretroviral therapy (HAART) is the recommended treatment for both pregnant and non-pregnant women infected with HIV. Treatment with HAART is reported to potentiate predisposition to the development of hypertensive disorders of pregnancy such as pre-eclampsia (PE). Pre-eclampsia accounts for 7-10% of abnormal pregnancies worldwide. Studies demonstrate that pregnant women with HIV have PE at lower frequencies than uninfected women, however, the converse is observed upon HAART initiation. HIV-infected women on HAART exhibit a greater tendency to develop PE, emanating from immune reconstitution induced by HAART. There is paucity of information as to the pathogenesis of PE upon HAART initiation and there are, therefore, controversial data as to whether HAART predisposes women to a lower, equal or higher risk of PE development compared to the general population, further investigations on the impact of HIV infection and HAART on the immune response and rate of PE development in HIV infected pregnant women are urgently needed.

Download: Full text paper

Citation: Phoswa WN, Naicker T, Ramsuran V, Moodley J. Pre-eclampsia: the role of highly active antiretroviral therapy and immune markers Inflamm Res.,doi: 10.1007/s00011-018-1190-3: (2018).