TITLE:
The Effects of Plasma Homocysteine in PCOS Women: A Review
AUTHORS:
Pranita Maharjan, Peng Dan Hong
KEYWORDS:
Polycystic Ovary Syndrome, Homocysteine, Insulin Resistance
JOURNAL NAME:
Open Journal of Obstetrics and Gynecology,
Vol.8 No.1,
January
15,
2018
ABSTRACT: Homocysteine is an intermediate
substance formed during the breakdown of the amino acid methionine and may
undergo remethylation to methionine or trans-sulfuration to cystathionine or
cysteine. The metabolism occurs via two pathways:
remethylation to methionine, which requires folate and vitamin B12; and
transsulfuration to cystathionine, which requires pyridoxal-5’-phosphate.
The disturbances in the metabolic pathways lead to the accumulation of Hcy,
either by insufficient transsulfuration (through CBS mutations or vitamin B6
deficiency) or by a blockage of remethylation. In the latter case, folate or vitamin
B12 deficiency may be involved, as well as MTHFR. High levels of
Hcy induce sustained injury of arterial endothelial cells, proliferation of
arterial smooth muscle cells and enhance activity of key participants in
vascular inflammation, atherogenesis, and vulnerability of the established
atherosclerotic plaque. Hyperhomocysteinemia has become the topic of interest
in recent years. It has been highly associated with increased risk for
cardiovascular disorders, such as, atherosclerosis, thromboembolism and dyslipidemia.
Women with PCOS show constellation of metabolic syndromes. Obesity, hyperandrogenemia
and type 2 diabetes mellitus is the hallmark of PCOS which later becomes the
risk factors for cardiovascular disease. Various studies had revealed the
presence of increased Hcy level in PCOS women which may or may not be
associated with other biochemical parameters. Intense treatment for PCOS can
influence homocysteine levels.