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polycystic ovary
Monday 13 March 2017
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polycystic ovary
Pseudo-precocious puberty
Rarely, multiple follicular cysts may be the cause of pseudo-precocious puberty, although more often they are the result of central causes of pseudoprecocity.
Juvenile hypothyroidism
As many as 75% of girls with juvenile hypothyroidism have multicystic ovaries, and, rarely, the ovarian enlargement may be the presenting sign leading to a diagnosis of hypothyroidism.
Clinically, affected patients may show varying degrees of sexual precocity and galactorrhea due to increased secretion of pitu-itary gonadotropins and prolactin.
Treatment with thyroxin results in regression of the ovarian cysts as well as the other symptoms.
Polycystic ovary syndrome (PCOS)
Multiple follicular cysts should be distinguished from polycystic ovary syndrome (PCOS), which involves 3% to 8% of the female population.
PCOS is responsible for 25% of cases of primary amenorrhea and is the most common cause of delayed puberty and heavy anovulatory bleeding in adolescent females.
It is characterized by inappropriate gonadotropin secretion, hyperandrogenemia, increased peripheral conversion of androgens to estrogens, chronic anovulation, and sclerocystic ovaries.
The diagnostic criteria for PCOS were established in 2004 by the Rotterdam criteria, although this has been heavily debated subsequently.
Affected patients often have a history of premenarcheal obesity, secondary amenorrhea or oligomenorrhea, infertility, and hirsutism.
These features may occur alone or in any combination and the clinical spectrum is broad.
The unopposed estrogenic stimulation may cause menometrorrhagia and endometrial hyperplasia.
Currently, the underlying etiology of PCOS is widely debated; however, the resulting clinical manifestations are known to be heavily impacted by environmental factors such as diet.
While several genes have been linked with PCOS, the evidence supporting this linkage is weak.
Grossly, the ovaries of PCOS are enlarged two- to five-fold and have smooth or nodular white surfaces, with multiple cysts located beneath the thickened cortex.
Histologically, multiple follicle cysts, atretic follicles, a prominent theca interna with luteinization, and medullary stromal overgrowth are the principal histologic features.
The superficial cortex is fibrotic and hypocellular.
Maturing follicles up to midantral stage and atretic follicles showing prominent luteinization of the theca interna may be twice as numerous as in normal ovaries.
Primordial follicles are often decreased in number.
It is important to remember that these findings are not specific and may accompany adrenal lesions such as Cushing syndrome, congenital adrenal hyperplasia, virilizing adrenal tumors, primary hypothalamic disorders, ovarian lesions that produce excessive quantities of estrogens or androgens and hypothyroidism.
Long-term sequelae of PCOS include infertility, endometrial carcinoma, an increased risk for cardiovascular disease due to type 2 diabetes mellitus, dyslipidemia, and systolic hypertension.
See also
polycystic ovary syndrome
ovarian anomalies
- ovarian cysts
