What is the role of AMH and MIS hormone testing in the workup of granulosa cell tumors (GCTs) of the ovaries

Updated: Aug 30, 2018
  • Author: David C Starks, MD, MPH; Chief Editor: Warner K Huh, MD  more...
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Answer

This hormone is produced exclusively by granulosa cells in postnatal females and both prenatally and postnatally by the Sertoli cells in the male testis. This hormone functions in male fetuses to induce regression of the mullerian system. Normally, MIS/AMH is found in low levels in reproductive-aged females and functions as a paracrine inhibitory factor decreasing resting ovarian follicle response to follicle stimulating hormone (FSH). This insures the emergence of a single dominant follicle. Serum MIS/AMH may be a marker of ovarian reserve and typically disappears from the serum after menopause or bilateral oophorectomy. However, in patients with GCTs, levels have been shown to parallel the extent of disease. [7]

Lane et al found that 76% of patients with GCTs had elevated MIS/AMH levels preoperatively. [8] No patient with levels within the reference range postoperatively experienced recurrence, whereas 6 of 15 patients with elevated levels had a recurrence. On average, elevated levels were detected 3 months before clinical evidence of recurrence was found. In 2000, Long et al used an ultrasensitive ELISA and found that AMH levels became undetectable in 15 of 16 women treated for GCTs and were elevated in 14 of 15 women (sensitivity 93%) with recurrent granulosa cell tumors. [9]

Anttonen et al reported that MIS gene expression was significantly decreased in 87% of tumors greater than 10 cm. [10] This inverse relationship between MIS expression and tumor size raised concerns that MIS/AMH may not be a useful marker in advanced cases of GCT.

Serum MIS/AMH levels correlate well with tumor presence in patients with GCTs. This marker is highly specific for GCT in postmenopausal or oophorectomized women. It may also be elevated in women with Sertoli-Leydig cell tumors of the ovary, but is not typically produced by other gonadal or extragonadal tumors. This is in sharp contrast to inhibin and estradiol levels, both of which may be elevated in a variety of other extraovarian disorders. This makes AMH/MIS attractive as a marker for diagnosis and prospective follow-up of patients with GCTs. However, studies have been limited to retrospective trials. With widespread clinical availability of AMH testing, this marker may gain ground in the management of women with GCTs and perhaps could be a molecular target in the future.


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