Final Diagnosis -- Multicystic ovaries secondary to hypothyroidism




Multicystic ovaries secondary to hypothyroidism have been described extensively in the literature especially as case reports (1-9). We report here a case of multicystic ovaries secondary to hypothyroidism in a 9-year-old girl with a history of recurrent bilateral ovarian masses.

Most patients present with symptoms of precocious puberty, vaginal bleeding, abdominal distention, acute abdomen, massive cystic ovarian masses and ovarian torsion (1-10). Since most patients have underlying hypothyroidism, commonly under observation, the ovarian cysts tend to regress rapidly and completely with thyroid replacement therapy, thus there are very few descriptions of the histopathology of these cysts (2,10-11).

The pathophysiology of this entity is unclear. Various mechanisms have been proposed as to the cause of ovulatory dysfunction with formation of cysts, these include altered estrogen metabolism, hypothalamic-pituitary dysfunction, a direct effect on the ovaries or an altered prolactin metabolism (2). Thyroid stimulating hormone (TSH), growth hormone (GH), follicle stimulating hormone (FSH), and luteinizing hormone (LH) have common alpha chains and it is their -chains that confer specificity. Cross-reaction of very high TSH could produce FSH and LH-like activity responsible for the luteinized ovarian cysts (12). In some case reports, the FSH levels have been high, therefore, there may be some action of thyroid releasing hormone on pituitary cells to stimulate gonadotrophin release and hence FSH and LH. An enlarged pituitary gland and pituitary adenomas have been described in hypothyroidism, some of these also with ovarian cysts (9,11,13-14). An animal model of hypothyroid rats suggests yet another mechanism in that there is increased sensitivity to FSH because of an increase in the number of ovarian FSH receptors (15). Combinations of pituitary and local ovarian effects are likely, given the histopathology. Gross descriptions reveal multiple cysts that contain clear fluid. The few histological descriptions documented in the literature have described the cysts as lined by a single layer of ovoid cells with no evidence of luteinization or as follicular cysts (2,10). In our case, the ovarian resection revealed numerous follicular cysts with a compact granulosa cell component, two to three cell layers thick, overlying a slightly luteinized theca interna. Other cysts had a prominent granulosa cell proliferation that had an "immature" appearance with pleomorphism, slightly prominent nucleoli and brisk apoptotic and mitotic activity. The peripheral granulosa cell layer revealed prominent luteinization. Inhibin A and CD 99 staining was intense on these elements confirming their granulosa cell nature. Although these were interpreted as bilateral juvenile granulosa cell tumors at the time, in the light of the documentation of hypothyroidism it is overwhelmingly likely that this case represents the ovarian cysts of hypothyroidism.

Recognition and appropriate diagnosis of this clinical entity by both clinicians and pathologists is extremely important since thyroid hormone replacement therapy is highly effective and prevents unwarranted surgeries.


The patient improved clinically following Synthroid treatment and her pituitary and thyroid tests have normalized.


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Contributed by Akosua B. Domfeh MBChB and Ronald Jaffe, MB.BCh

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