000 02208cam a2200181 4500
001 NMDX6627
008 120401t2008 xxu||||| |||| 00| 0 eng d
022 _a15216934
100 _aOkolo, S.
240 _aBest Practice & Research. Clinical Obstetrics & Gynaecology.
245 _aIncidence, aetiology and epidemiology of uterine fibroids.
260 _c2008
500 _aNMUH Staff Publications
500 _a22
520 _a<span style="font-size: 10pt;"><span style="line-height: 17.999801635742188px;">Uterine fibroids are the most common benign tumour of the female genital tract. However, their true prevalence is probably under-estimated, as the incidence at histology is more than double the clinical incidence. Recent longitudinal studies have estimated that the lifetime risk of fibroids in a woman over the age of 45 years is more than 60%, with incidence higher in blacks than in whites. The cause of fibroids remains unclear and their biology poorly understood. No single candidate gene has been detected for commonly occurring uterine fibroids. However, the occurrence of rare uterine fibroid syndromes, such as multiple cutaneous and uterine leiomyomatosis, has been traced to the gene that codes for the mitochondrial enzyme, fumarate hydratase. Cytogenetic abnormalities, particularly deletions of chromosome 7, which are found in up to 50% of fibroid specimens, seem to be secondary rather than primary events, and investigations into the role of tumour suppressor genes have yielded conflicting results. The key regulators of fibroid growth are ovarian steroids, both oestrogen and progestogen, growth factors and angiogenesis, and the process of apoptosis. Black race, heredity, nulliparity, obesity, polycystic ovary syndrome, diabetes and hypertension are associated with increased risk of fibroids, and there is emerging evidence that familial predisposition to fibroids is associated with a distinct pattern of clinical and molecular features compared with fibroids in families without this prevalence.</span></span>
856 _uhttp://www.ncbi.nlm.nih.gov/pubmed/18534913
856 _uhttp://ferriman.wufoo.com/forms/journal-article-request/
999 _c75784
_d75784