The distribution of the INHA gene promoter polymorphisms in a Korean POF population was not significantly different from controls, implying that the INHA gene polymorphisms may not be associated with the risk of idiopathic POF.
The association between the INHA promoter variants and POFcould not be replicated, and our results suggest that this discrepancy is likely to be due to the small sample size of previous studies.
Significant reductions in allele frequency were observed for the -16T allele (New Zealand POF) and -124G allele (total POF) and for INHA promoter haplotypes C (New Zealand POF) and D (Slovenian POF).
This study supports the hypothesis that the INHA 769G>A variant may increase susceptibility to POF with impaired inhibin B bioactivity and provides insight into the complex aetiology of POF.
INHA, the gene encoding the inhibin alpha subunit, was recently proposed as a candidate for premature ovarian failure (POF), a syndrome that leads to the cessation of ovarian function under the age of 40 years.