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Ovarian hyperthecosis

Author: André P van Beek, MD, PhD

Section Editors: Robert L Barbieri, MD, William F Crowley, Jr, MD
Deputy Editor: Kathryn A Martin, MD

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Nov 2017. | This topic last updated: May 19, 2017.

INTRODUCTION — The term hyperthecosis refers to the presence of nests of luteinized theca cells in the
ovarian stroma due to differentiation of the ovarian interstitial cells into steroidogenically active luteinized stromal
cells (picture 1). These nests or islands of luteinized theca cells are scattered throughout the stroma of the ovary,
rather than being confined to areas around cystic follicles as in the polycystic ovary syndrome (PCOS). The
result is greater production of androgens. The precise etiology of ovarian hyperthecosis is still unclear.

The clinical presentation, diagnosis, and treatment of ovarian hyperthecosis are discussed here. The clinical
presentation and diagnosis of PCOS are reviewed separately. (See "Clinical manifestations of polycystic ovary
syndrome in adults" and "Diagnosis of polycystic ovary syndrome in adults".)

CLINICAL PRESENTATION — Ovarian hyperthecosis, a disorder characterized by severe hyperandrogenism

and insulin resistance, is seen primarily in postmenopausal women [1-3]. Women typically present with slowly
progressive acne and hirsutism (eg, excessive male pattern hair growth), and they are likely to be virilized [4].
Thus, many have clitoral enlargement, male pattern baldness, deepening of the voice, and a male habitus.

In almost all cases, insulin resistance and hyperinsulinemia are present [3,5], and women are at increased risk
for type 2 diabetes and cardiovascular disease [2]. Additional physical findings may include central obesity, skin
tags, and acanthosis nigricans.

The ovarian secretion of large amounts of androgens in women with hyperthecosis means that peripheral
estrogen production is increased. As a result, the risk of endometrial hyperplasia and endometrial carcinoma is
increased, especially in postmenopausal women [2,6].

Among premenopausal women who present with hyperandrogenism, the vast majority have polycystic ovary
syndrome (PCOS) and, only rarely, ovarian hyperthecosis. These disease entities may be difficult to distinguish
from each other and may all be part of the same spectrum of hyperandrogenic conditions. However, the hirsutism
and insulin resistance are more severe in women with ovarian hyperthecosis compared with those with PCOS.

Biochemical findings

Patients with hyperthecosis typically have the following biochemical findings:

● Serum total testosterone concentrations >150 ng/dL (>5.2 nmol/L) [7-10]. It is the single most important
biochemical finding, and it should prompt imaging of adrenals and ovaries. It is generally believed that
testosterone below 5.2 nmol/L rules out ovarian hyperthecosis, although no solid data are available to
substantiate this.

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● Insulin resistance and hyperinsulinemia that are sometimes severe; the latter can cause an increase in
ovarian androgen production, which may be mediated by binding to insulin-like growth factor-1 (IGF-1)
receptors [11]. (See "Insulin resistance: Definition and clinical spectrum" and "The metabolic syndrome
(insulin resistance syndrome or syndrome X)".)

● Normal or suppressed luteinizing hormone (LH) and follicle-stimulating hormone (FSH) [12].

● Normal serum dehydroepiandrosterone (DHEA) or dehydroepiandrosterone sulfate (DHEAS)

concentrations.

● Normal 17-hydroxyprogesterone concentrations: basal <6 nmol/L (200 ng/dL); 60 minutes post-corticotropin
(ACTH) (250 mcg) <30 nmol/L (1000 ng/dL). In regularly cycling women, determination of 17-
hydroxyprogesterone is performed in the follicular phase.

● Normal prolactin and IGF-1.

EVALUATION

Imaging — In women who present with hyperandrogenism and an increased testosterone concentration >150
ng/dL (or >5.2 nmol/L), additional imaging is mandatory to find the source of androgen production. (See
'Diagnosis' below.)

Ultrasonography — Ultrasonography in women with hyperthecosis usually shows a bilateral increase in

ovarian stroma [13-15]. Unlike polycystic ovary syndrome (PCOS), where the ovaries characteristically have a
multifollicular appearance with 12 or more antral follicles of 2 to 9 mm per ovary and/or ovarian volume >10 cm3
[16], few cysts are seen in severe hyperthecosis and the ovaries appear more solid (image 1) [13]. In
postmenopausal women with hyperthecosis, ovarian size is usually increased compared with normal [17].

MRI — A normal, postmenopausal ovary has a mean volume between 1.25 to 3.7 cm3 [18,19], and in
hyperthecosis, the average volume may be up to 10 cm3 [5,17]. Magnetic resonance imaging (MRI) findings in
ovarian hyperthecosis include symmetric bilateral ovarian enlargement, with homogeneous T2-hypointensity and
mild enhancement of the ovaries [20,21].

Additional testing

● Gonadotropin-releasing hormone (GnRH) agonist testing – We suggest administering a single dose of long-
acting GnRH agonists for diagnostic purposes in patients with increased testosterone concentrations >5.2
nmol/L in whom the diagnosis of hyperthecosis is considered based on biochemical findings and imaging.
This may be especially relevant in the context of a concomitant adrenal "incidentaloma" on imaging, which
may occur in 4 to 10 percent of patients. (See "Clinical presentation and evaluation of adrenocortical
tumors".)

Immediately before and four weeks after intramuscular injection of a GnRH agonist, testosterone, luteinizing
hormone (LH) and follicle-stimulating hormone (FSH) should be determined. Suppression of testosterone
confirms the presence of LH-dependent ovarian testosterone production and may provide evidence for
successful long-term treatment with GnRH agonists [22-25]. However, this test does not distinguish between
hyperthecosis and androgen-secreting ovarian tumors, as some of these are gonadotropin dependent
[22,24,25].

● Ovarian venous sampling – When imaging studies are negative but an ovarian source of androgens is still
suspected, selective catheterization of the ovarian veins may be performed to demonstrate a left-to-right
difference in androgen concentrations. However, this procedure should not be performed routinely, as it is

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technically difficult and there is no consensus on the testosterone gradient that localizes the androgen
source [26]. It should only be performed by an experienced radiologist [26,27].

We only suggest this procedure in premenopausal women interested in future fertility with serum
testosterone >150 ng/dL (5.2 nmol/L) and a negative adrenal computed tomography (CT) scan. In this
instance, localization to one ovary would change management (eg, the patient would undergo a unilateral
rather than a bilateral oophorectomy if a tumor source was located).

In postmenopausal women, androgen-producing Leydig-cell tumors, many of which are located in the hilus
(hilar cell tumors), may be found, but they are often too small to be seen on imaging studies. However, we
do not suggest ovarian vein sampling in this setting, because it is unlikely to change management (bilateral
oophorectomy).

● Women with ovarian hyperthecosis have insulin resistance and are at increased risk for type 2 diabetes
mellitus (see 'Clinical presentation' above). We therefore suggest screening for diabetes with a fasting blood
sugar or glycated hemoglobin (A1C). It is possible that a two-hour oral glucose tolerance test is more
sensitive in this population (as it is in women with PCOS), but this has not yet been established. (See
"Screening for type 2 diabetes mellitus" and "Diagnosis of polycystic ovary syndrome in adults", section on
'Cardiometabolic risk assessment'.)

DIAGNOSIS — Ovarian hyperthecosis should be suspected in women with a longstanding history of hirsutism,
virilization, insulin resistance, and the hormonal pattern described above (see 'Biochemical findings' above).
However, the diagnosis can be confirmed only by histologic examination of the ovaries and demonstration of the
presence of nests of luteinized cells in the ovarian stroma (picture 1) [28-30]. Occasionally, nodules are scattered
throughout the stroma. In practice, the definitive diagnosis is typically made by the pathologist after surgical
removal of the ovary or a portion thereof. (See 'Treatment' below.)

Differential diagnosis — In postmenopausal women with severe hyperandrogenism, androgen-secreting

ovarian and adrenal tumors, although rare, are the most important disorders to address in the differential
diagnosis. Serum testosterone concentrations are, in these cases, often considerably higher than those seen
with ovarian hyperthecosis (eg, >150 ng/dL [5.2 nmol/L]), but an important overlap may be found [15]. Women
with androgen-secreting tumors present with rapid onset and progression of hirsutism and virilization. Additional
testing for diabetes is warranted. (See "Clinical presentation and evaluation of adrenocortical tumors" and "Sex
cord-stromal tumors of the ovary: Sertoli-stromal cell tumors" and "Sex cord-stromal tumors of the ovary: Tumors
with granulosa and Sertoli-Leydig elements".)

In premenopausal women, androgen-secreting ovarian and adrenal tumors must also be considered, but they
are very rare. The approach to evaluating pre- or postmenopausal women with severe hyperandrogenemia,
including testing for possible androgen-secreting tumors, is discussed separately. (See "Evaluation of
premenopausal women with hirsutism", section on 'Additional evaluation for severe hyperandrogenemia'.)

The most common disorder in women that causes hirsutism is polycystic ovary syndrome (PCOS). Women with
PCOS have lower serum testosterone concentrations, are not typically virilized, and are typically less insulin
resistant when compared with women with hyperthecosis. In addition, the ultrasound appearance of the ovaries
is different as described above. (See 'Ultrasonography' above.)

PCOS, as well as other disorders that cause hirsutism (such as idiopathic hirsutism and nonclassic 21-
hydroxylase deficiency), are discussed in detail separately. (See "Clinical manifestations of polycystic ovary
syndrome in adults" and "Diagnosis of polycystic ovary syndrome in adults" and "Diagnosis and treatment of
nonclassic (late-onset) congenital adrenal hyperplasia due to 21-hydroxylase deficiency" and "Uncommon
congenital adrenal hyperplasias", section on 'Lipoid congenital adrenal hyperplasia'.)

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The differential diagnosis of hyperandrogenism is presented in the table (table 1).

The approach to evaluation of the patient with hirsutism is reviewed in detail separately. (See "Evaluation of
premenopausal women with hirsutism".)

TREATMENT — Treatment of hyperthecosis should include therapy for hyperandrogenism (hirsutism and
virilization), anovulation, obesity, and insulin resistance. The primary goal of treatment is to eliminate the
excessive testosterone production. However, normalization of hyperandrogenism after surgery for androgen-
secreting ovarian tumors is not always followed by an improvement in body weight or insulin sensitivity [31].

In postmenopausal women and in premenopausal women who have completed childbearing:

● Bilateral oophorectomy, as it provides a definitive solution for the hyperandrogenism.

● Long-term gonadotropin-releasing hormone (GnRH) agonist treatment (with estrogen-progestin add-back) is

an alternative, particularly in women who have an increased risk for surgery due to comorbidities or who are
unwilling to undergo bilateral oophorectomy [3,22,32,33].

In a report of three postmenopausal women with virilization, ovarian hyperandrogenism, and negative
imaging, GnRH agonist treatment resulted in androgen suppression within the first one to three months [23].
Total treatment duration was between 8 and 13 months; after stopping therapy, testosterone concentrations
remained low in two but increased again in the third. Since no histologic diagnosis is available as final
confirmation in women treated medically rather than surgically, it is recommended that all patients treated
with GnRH agonists receive careful follow-up, including periodic testing of androgen levels and ovarian
imaging.

If serum testosterone concentrations do not decrease after several months of GnRH agonist therapy, we
suggest surgery for histologic diagnosis.

In premenopausal women:

Treatment in premenopausal women is essentially the same as in women with the polycystic ovary syndrome
(PCOS). (See "Treatment of polycystic ovary syndrome in adults".)

● It includes treatment of hirsutism mainly by local therapy, oral contraceptives, antiandrogens, or GnRH
agonists combined with estrogen-progestin replacement. (See "Treatment of hirsutism".)

● For the treatment of anovulation and subsequent infertility in hyperthecosis, there is no evidence from
clinical trials. First-line treatment to induce ovulation should be clomiphene or letrozole, although in a small
series of women with hyperthecosis, this was reported to be unsuccessful [12]. In cases of clomiphene
failure, gonadotropins can be used. (See "Overview of ovulation induction".)

As follicular development may be inhibited by the high intraovarian androgen concentrations, GnRH agonist
pretreatment may reduce intraovarian androgen levels and result in restoration of sensitivity to exogenous
gonadotropins with subsequent ovulation [32].

● There are no published reports on the success of ovarian drilling in restoring ovulation, and procedures
aiming at reducing ovarian stromal volume should be discouraged and considered as a last resort only.

Additional treatment recommendations:

● Obesity and insulin resistance – Weight reduction in obese women with hyperthecosis results in an increase
in insulin sensitivity [34]. As a result, ovarian androgen secretion may decrease.

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● Additionally, in women with type 2 diabetes or impaired glucose tolerance, metformin treatment should be
part of the treatment. (See "Treatment of polycystic ovary syndrome in adults".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries
and regions around the world are provided separately. (See "Society guideline links: Hirsutism".)

SUMMARY AND RECOMMENDATIONS

● The term hyperthecosis refers to the presence of nests of luteinized theca cells in the ovarian stroma due to
differentiation of the ovarian interstitial cells into steroidogenically active luteinized stromal cells, causing
hyperandrogenism with typical testosterone levels >5.2 nmol/L (150 ng/dL). (See 'Biochemical findings'
above.)

● A serum total testosterone concentration <5.2 nmol/L (150 ng/dL) is likely to rule out hyperthecosis.

● Hyperthecosis must be differentiated from several other diseases, most importantly malignant androgen-
producing ovarian or adrenal tumors, congenital adrenal hyperplasia (CAH), and Cushing's disease.
Premenopausal women with polycystic ovary syndrome (PCOS) have lower serum testosterone
concentrations, are not typically virilized, and are typically less insulin resistant when compared with women
with hyperthecosis. In addition, the ultrasound appearance of the ovaries is different. (See 'Differential
diagnosis' above and 'Ultrasonography' above.)

● Imaging of the ovaries (ultrasound and magnetic resonance imaging [MRI] if needed) and adrenals (by
computed tomography [CT] scan and/or MRI) is recommended to rule out testosterone-producing tumors. A
single dose of long-acting GnRH agonists can be used for diagnostic purposes to confirm the ovarian origin
of androgens. (See 'Imaging' above and 'Additional testing' above.)

● Treatment of hyperthecosis depends on age, degree of virilization, and pregnancy goals. In postmenopausal
women and premenopausal women who have completed childbearing, the main aim is to lower androgen
levels by bilateral oophorectomy or gonadotropin-releasing hormone (GnRH) agonist treatment. In
premenopausal women, symptomatic treatment of hirsutism and ovulation induction for infertility may be
indicated. Additional treatment should aim at reducing weight and insulin resistance. (See 'Treatment'
above.)

ACKNOWLEDGMENTS — The editorial staff at UpToDate would like to acknowledge Manubai Nagamani, MD,
and Jolande Land, MD, PhD, who contributed to earlier versions of this topic review.

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

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5. Krug E, Berga SL. Postmenopausal hyperthecosis: functional dysregulation of androgenesis in climacteric

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14. Nagamani M, Chilvers R. Ultrasonography and diagnosis of polycystic ovary syndrome. In: Ultrasonograph
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15. Yance VRV, Marcondes JAM, Rocha MP, et al. Discriminating between virilizing ovary tumors and ovary
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18. Hall DA, McCarthy KA, Kopans DB. Sonographic visualization of the normal postmenopausal ovary. J
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20. Rosenkrantz AB, Popiolek D, Bennett GL, Hecht EM. Magnetic resonance imaging appearance of ovarian
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21. Fujii S, Kiyokawa T, Tsukihara S, et al. Magnetic resonance imaging findings of ovarian stromal
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23. Vollaard ES, van Beek AP, Verburg FA, et al. Gonadotropin-releasing hormone agonist treatment in
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24. Chico A, García JL, Matías-Guiu X, et al. A gonadotrophin dependent stromal luteoma: a rare cause of
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28. Brown DL, Henrichsen TL, Clayton AC, et al. Ovarian stromal hyperthecosis: sonographic features and
histologic associations. J Ultrasound Med 2009; 28:587.
29. Baldini M, Semprini E, Orsatti A, et al. Reduction of insulin resistance after correction of nonneoplastic
ovarian virilization. J Endocrinol Invest 1993; 16:285.
30. Manieri C, Di Bisceglie C, Fornengo R, et al. Postmenopausal virilization in a woman with gonadotropin
dependent ovarian hyperthecosis. J Endocrinol Invest 1998; 21:128.
31. Pelusi C, Forlani G, Zanotti L, et al. No metabolic impact of surgical normalization of hyperandrogenism in
postmenopausal women with ovarian androgen-secreting tumours. Clin Endocrinol (Oxf) 2013; 78:533.
32. Steingold KA, Judd HL, Nieberg RK, et al. Treatment of severe androgen excess due to ovarian
hyperthecosis with a long-acting gonadotropin-releasing hormone agonist. Am J Obstet Gynecol 1986;
154:1241.
33. Parr JH, Abraham RR, Seed M, et al. The treatment of a hyperandrogenic and virilizing state in an elderly
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GRAPHICS

Ovarian hyperthecosis

Light micrograph from a woman with ovarian hyperthecosis shows nests of

steroidogenically active luteinized theca cells in the ovarian stroma. These cells,
which are large and lighter looking (arrows), are derived from differentiation of
the ovarian interstitial cells. Hematoxylin and eosin x 400.

Courtesy of Manubai Nagamani, MD.

Graphic 75548 Version 3.0

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Ovarian stroma

Sagittal ultrasound image from a patient with ovarian hyperthecosis: No antral

follicles are visible in the ovary; there is an increase in homogeneous,
hyperechogenic ovarian stroma.

Courtesy of Manubai Nagamani, MD.

Graphic 68176 Version 3.0

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Differential diagnosis of clinical hyperandrogenism

Age of
Frequency Time of onset to Menstrual
Diagnosis onset Virilization
(percent) presentation disturbance
years
PCOS and >95 15 to 25 Years +/- Rare
related
disorders

CAH 1 to 2 Congenital Birth/adolescence/adulthood + +/-

Adrenal tumor <1 Any time Weeks-months + +

Ovarian tumor <1 Any time Weeks-months + +

Cushing's <1 Any time Months-years + +/-

syndrome

Hyperthecosis <1 Pre- to post- Months-years + +

ovary menopause

PCOS: polycystic ovary syndrome; CAH: congenital adrenal hyperplasia; (+): present; (-): absent; (+/-): present or absent.

From: Dennedy MC, Smith D, O'Shea D, McKenna TJ. Investigation of patients with atypical or severe hyperandrogenaemia
including androgen-secreting ovarian teratoma. Eur J Endocrinol 2010; 162:213. Copyright © Society of the European Journal
of Endocrinology 2010. Reproduced by permission.

Graphic 83495 Version 1.0

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Contributor Disclosures
André P van Beek, MD, PhD Nothing to disclose Robert L Barbieri, MD Nothing to disclose William F
Crowley, Jr, MD Consultant/Advisory Boards: Juniper Pharmaceuticals [Endocrinology (Vaginal progesterone)];
Quest Diagnostics [Reproductive endocrinology]. Other Financial Interest: Stock ownership: Juniper
Pharmaceuticals [Endocrinology (Transvaginal ring delivery systems)]. Kathryn A Martin, MD Nothing to
disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
UpToDate standards of evidence.

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