UPDATE ON POLYCYSTIC OVARIAN DISEASE
Dalia Ibrahim Ahmed;
Abstract
Summary
Polycystic ovarian disease is an cugonadotropic hyperandrogenic anovulatory state with thc presence of polycystic ovaries by ultrasonography,in addition to the symptoms of oligomenorrhoca, obesity and hyperandrogenism (acne, hirsutism and alopecia).
The prevalence of polycystic ovarian disease is about 5% of the population and it constitutes approximately 70% of cases of ovulatory dysfunction (Franks, 1995).'
Despite the nomenclature of polycystic ovaries, normal appearing ovaries were found in 40% of patients with clinical PCOD, and no thickening of the tunica in 46% of those who did manifest gross ovarian enlargement (Solomon, 1998)
Additionally the morphological changes can occur unilaterally with a normal appearing ovary in one side and a polycystic appearing ovary in the other (Battaglia et al,1999)'.
Though no definite cause has been identified for PCOD, several etiological factors have been suggested. These include; hereditary, endorinological, metabolic and psychological factors. Metabolic factors recently have received a great deal of attention as 50 % of women with PCOD are obese, and about 50% to 70% of women with PCOD have variable degrees of insulin resistance. This secondary hyperinsulinemia appears to underlie many of the endocrine features of PCOD. In a large
proportion of such patients IGF I receptors arc increased, and are activated
by insulin leading to increased androgen production in theca cells (
Ovalle andAziz, 2002).
Polycystic ovarian disease is an cugonadotropic hyperandrogenic anovulatory state with thc presence of polycystic ovaries by ultrasonography,in addition to the symptoms of oligomenorrhoca, obesity and hyperandrogenism (acne, hirsutism and alopecia).
The prevalence of polycystic ovarian disease is about 5% of the population and it constitutes approximately 70% of cases of ovulatory dysfunction (Franks, 1995).'
Despite the nomenclature of polycystic ovaries, normal appearing ovaries were found in 40% of patients with clinical PCOD, and no thickening of the tunica in 46% of those who did manifest gross ovarian enlargement (Solomon, 1998)
Additionally the morphological changes can occur unilaterally with a normal appearing ovary in one side and a polycystic appearing ovary in the other (Battaglia et al,1999)'.
Though no definite cause has been identified for PCOD, several etiological factors have been suggested. These include; hereditary, endorinological, metabolic and psychological factors. Metabolic factors recently have received a great deal of attention as 50 % of women with PCOD are obese, and about 50% to 70% of women with PCOD have variable degrees of insulin resistance. This secondary hyperinsulinemia appears to underlie many of the endocrine features of PCOD. In a large
proportion of such patients IGF I receptors arc increased, and are activated
by insulin leading to increased androgen production in theca cells (
Ovalle andAziz, 2002).
Other data
| Title | UPDATE ON POLYCYSTIC OVARIAN DISEASE | Other Titles | الجديد فى مرض تكيسي المبايض | Authors | Dalia Ibrahim Ahmed | Issue Date | 2003 |
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