Ovarian hyperthecosis

Ovarian hyperthecosis is a rare endocrine condition characterized by the presence of luteinized theca cells dispersed throughout the ovarian stroma, which are capable of producing increased amounts of androgens and causing hyperandrogenism that is often severe. It is a nonneoplastic form of ovarian androgen excess, distinct both from common polycystic ovary syndrome and from androgen secreting ovarian tumors. Its clinical importance derives from the fact that the ovary, even in the absence of a true dominant tumor mass, becomes a pathological and relatively autonomous androgen source, with significant effects on the skin, metabolism, reproductive function and endometrium.

From a practical perspective, ovarian hyperthecosis is particularly important in women during perimenopause and especially postmenopause, when it may present with progressive hirsutism, androgenetic alopecia, virilization, severe insulin resistance and marked metabolic abnormalities. In these settings, it is one of the main differential diagnoses of organic ovarian hyperandrogenism, and its recognition is essential because definitive treatment is often surgical and provides both treatment and histological confirmation of the diagnosis.

The epidemiology of ovarian hyperthecosis is difficult to define precisely because it is a rare, probably underdiagnosed condition that is often identified only after oophorectomy or bilateral salpingo oophorectomy performed for severe hyperandrogenism. Many patients are initially classified generically as having postmenopausal hyperandrogenism, a suspected androgen secreting ovarian tumor or an extreme form of PCOS, and only histological examination allows the condition to be attributed with certainty to hyperthecosis. This difficulty in classification explains why the disorder is probably more common than published case series suggest.

Age distribution is one of its most characteristic features. Ovarian hyperthecosis occurs mainly after menopause, although cases have been described during reproductive life and, more rarely, during adolescence. In adult clinical practice, recognition is particularly important in women with newly developed or rapidly progressive signs of androgenization after menopause. In this age group, the ovary should no longer exhibit significant physiological follicular activity, so a pathological increase in androgen production immediately carries greater diagnostic significance than it does during reproductive life.

A relevant epidemiological feature is the close association with visceral obesity, hyperinsulinemia, type 2 diabetes mellitus and metabolic syndrome. Many patients with hyperthecosis have a phenotype of severe metabolic dysfunction, with central adiposity, hypertension, impaired glucose tolerance or established diabetes. This association is not merely coincidental, but forms part of the biological profile of the disease, because insulin can amplify ovarian androgen steroidogenesis and reduce SHBG, thereby enhancing the clinical expression of hyperandrogenism.

The relationship with PCOS is complex. In some patients, hyperthecosis has been considered a possible extreme or progressive form of chronic hyperandrogenic ovarian dysfunction, whereas in others it appears to be a distinct stromal disorder rather than a purely follicular one. Epidemiologically, this means that a remote history of menstrual irregularities, subfertility, hyperandrogenism or a diagnosis of PCOS may be present, but is not required. In other words, hyperthecosis should not automatically be interpreted as late PCOS, because the severe postmenopausal phenotype may also emerge without a clear gynecological endocrine diagnosis during reproductive life.

The endocrine context of menopause should be considered among the possible risk factors. Loss of follicular function and granulosa cell aromatase activity makes the net effect of androgens produced by theca and stromal cells more evident. In a predisposed woman, this change in the ovarian microenvironment may unmask pathological androgen production that had previously been less clinically apparent. Metabolic aging, with increasing insulin resistance and abdominal adiposity, also helps create conditions favorable to clinical expression of the disease.

Finally, clinical vulnerability depends not only on the presence of hyperthecosis, but also on the burden of accompanying comorbidities. A woman with diabetes, visceral obesity, hepatic steatosis, hypertension and severe androgenization has a very different overall risk profile from that of a younger patient with isolated hyperandrogenism. The clinical epidemiology of ovarian hyperthecosis is therefore closely linked to the epidemiology of metabolic dysfunction in later life, which explains why its impact extends far beyond terminal hair growth or virilization alone.

Ovarian hyperthecosis is a condition in which the ovarian stromal tissue contains nests of luteinized theca cells capable of persistently producing increased amounts of androgens. Under physiological conditions, theca cells produce androgens as precursors that are subsequently converted into estrogens by granulosa cells. In hyperthecosis, this balance is lost because the ovarian stroma acquires abnormal and diffuse steroidogenic activity. The disorder is therefore not simply an exaggeration of normal follicular physiology, but a pathological reorganization of ovarian stromal function.

From an etiological perspective, the disease is not caused by a true neoplasm, but by functional proliferation or transformation of the stroma with theca cell luteinization. Its exact origin is not fully understood. A possible interaction among ovarian aging, persistent gonadotropin stimulation, chronic hyperinsulinemia and individual predisposition of ovarian steroidogenesis has been proposed. This may explain why the disorder emerges mainly in perimenopausal and postmenopausal women with metabolic syndrome and progressive androgen excess.

At the molecular level, hyperfunctioning luteinized theca cells increase the activity of enzymatic pathways involved in androgen biosynthesis. Cholesterol availability, the function of the StAR system and the activity of enzymes such as CYP11A1, 3β-HSD and particularly CYP17A1 are shifted toward excessive production of testosterone and other androgen precursors. Insulin acts as a powerful permissive modulator of this process, enhancing the ovarian steroidogenic response and reducing hepatic SHBG synthesis, with a consequent increase in the free fraction of circulating testosterone.

A decisive pathophysiological aspect is the postmenopausal setting. After menopause, the marked reduction in follicular activity and granulosa cell aromatization makes the intraovarian conversion of androgens into estrogens less effective. Consequently, pathological stromal androgen production becomes much more clinically apparent. This mechanism explains why a nonneoplastic stromal condition can produce a very intense endocrine phenotype, sometimes resembling that caused by a secreting ovarian lesion.

The effects of the disease are systemic. At the cutaneous level, androgen excess increases sebaceous gland activity, promotes conversion of vellus hair into terminal hair and induces miniaturization of scalp follicles. At the reproductive level, women who have not yet reached menopause may develop chronic anovulation and menstrual abnormalities, whereas in postmenopausal women the clinical focus shifts mainly toward the endometrium. Peripheral conversion of androgens into estrogens, particularly in adipose tissue, may expose the endometrium to unopposed proliferative stimulation, increasing the risk of hyperplasia and endometrial disease.

At the metabolic level, hyperthecosis is associated with a vicious cycle involving androgens, visceral adiposity and insulin resistance. Androgens promote abdominal fat accumulation and worsen glucose metabolism, whereas hyperinsulinemia amplifies ovarian steroidogenesis and reduces SHBG. This loop helps explain why many patients have a phenotype of marked metabolic impairment, including diabetes, dyslipidemia and hepatic steatosis. Ovarian hyperthecosis should therefore be interpreted as an integrated endocrine and metabolic disorder, rather than solely as a localized gynecological condition.

Finally, its pathophysiology must be distinguished from that of androgen secreting tumors. In hyperthecosis, excessive production arises from bilaterally altered stroma, often without an evident dominant mass, whereas in tumors the mechanism is sustained by a circumscribed neoplastic clone. This difference is crucial because it explains why imaging findings may be less conspicuous in hyperthecosis and why definitive diagnosis often requires histological confirmation after removal of the ovaries.

The clinical presentation of ovarian hyperthecosis is dominated by hyperandrogenism that is often marked and progressively evolving, but more intense than common functional forms seen during reproductive life. The typical patient is a perimenopausal or postmenopausal woman who reports increasing terminal hair growth on the face and body, worsening androgenetic alopecia and progressive changes in body habitus. The disorder is sometimes initially perceived as a cosmetic problem, but the severity of the phenotype and the metabolic context soon lead to a more detailed endocrine assessment.

In the medical history, the most common symptom is progressive hirsutism, which is often more pronounced than in mild functional forms. Acne, seborrhea and frontoparietal hair thinning may also occur, although acne may be less prominent than alopecia and terminal hair growth in postmenopausal women. The speed of onset is a fundamental clinical feature. In nonneoplastic stromal forms, progression is often gradual but persistent, whereas very rapid virilization over a few months always requires differential diagnosis with an androgen secreting ovarian tumor.

The physical examination may document signs of severe androgenization, including increased terminal hair in androgen dependent areas, advanced androgenetic alopecia, increased muscle mass and sometimes clitoromegaly. Deepening of the voice, reduced breast volume and changes in body fat distribution are also consistent with intense and prolonged androgen excess. These signs are particularly significant because they cannot be regarded as physiological in a woman after menopause.

The metabolic profile is often highly evident. Many patients have central obesity, increased waist circumference, type 2 diabetes mellitus, acanthosis nigricans, hypertension and dyslipidemia. This aspect is not secondary, but forms part of the clinical phenotype of the disease. In some cases, worsening glycemic control or the emergence of marked insulin resistance prompts medical assessment before the androgenic disorder has been fully recognized.

Women who have not yet reached menopause may develop oligomenorrhea, amenorrhea, anovulation and infertility, although the classic phenotype remains that of the mature or postmenopausal woman. At this stage of life, the absence of menstruation does not help the clinician recognize endocrine dysfunction, so diagnosis may depend only on the degree of androgenization. Recognition may therefore be delayed unless hyperandrogenism is considered a systemic syndrome.

An important clinical aspect is possible involvement of the endometrium. Peripheral aromatization of androgens into estrogens, particularly in women with obesity, may produce chronic proliferative endometrial stimulation. This may lead to endometrial hyperplasia, abnormal uterine bleeding during perimenopause or the detection of endometrial abnormalities on imaging. In some case series, endometrial abnormalities have been frequent even when virilization was not extremely severe.

Finally, the effect on quality of life is substantial. Severe hirsutism, alopecia and virilization profoundly alter body image and may cause anxiety, social withdrawal, changes in sexuality and depressive symptoms. In ovarian hyperthecosis, this psychological burden adds to the metabolic and cardiovascular burden, making the disease a complex condition that requires management extending far beyond simple control of circulating androgens.

Ovarian hyperthecosis should be suspected particularly in a woman during perimenopause or postmenopause who develops clinically significant androgen excess. The combination of progressive hirsutism, androgenetic alopecia, progressive virilization and elevated testosterone in the absence of clear evidence of an adrenal source strongly suggests a pathological ovarian source. In these cases, the issue is not merely to confirm hyperandrogenism, but to rapidly distinguish hyperthecosis from an androgen secreting tumor.

Suspicion increases further when androgen excess is associated with visceral obesity, insulin resistance, diabetes and acanthosis nigricans. This metabolic profile, particularly when marked, is highly consistent with ovarian hyperthecosis and is less typical of isolated secreting ovarian tumors. Severe metabolic syndrome is therefore not merely a comorbidity, but an important diagnostic clue in the correct clinical assessment.

In women of reproductive age, suspicion is more difficult because differential diagnosis with severe PCOS is complex. In this age group, hyperthecosis should be considered when hyperandrogenism is more intense than expected, with virilization, persistently elevated testosterone and an unsatisfactory response to standard medical strategies used for PCOS. Even in these cases, however, diagnosis often remains probabilistic until histological confirmation.

The presence of virilization always requires acceleration of the diagnostic pathway. Clitoromegaly, a deeper voice, rapid increase in muscle mass and severe alopecia are not manifestations of mild uncomplicated hyperandrogenism and require investigation for an organic cause. Hyperthecosis is fully included among these causes, but the same presentation may occur in androgen secreting ovarian tumors. The initial suspicion should therefore be that of a pathological ovarian source rather than of a single definitive diagnosis.

Another suggestive setting is that of a postmenopausal patient whose ovarian imaging is not overtly neoplastic, but shows enlarged ovaries, a stromal appearance or bilateral involvement, in association with elevated testosterone. In the presence of these characteristics, particularly when DHEAS is not markedly increased, the probability of hyperthecosis rises. Nevertheless, negative or nonspecific imaging does not exclude the diagnosis, because small tumors and diffuse stromal abnormalities may not be readily distinguishable.

Finally, suspicion should remain high even when cutaneous manifestations predominate and the problem is perceived as purely cosmetic. In a woman who has never previously shown clinically relevant androgenization, the development of progressive signs after menopause should not be dismissed. Correct clinical suspicion is decisive because it prevents diagnostic delay in a condition that, although often histologically benign, may have a substantial endocrine, metabolic and endometrial impact.

The diagnosis of ovarian hyperthecosis requires a pathway that begins with biochemical confirmation of hyperandrogenism, excludes the principal alternative diagnoses and localizes the ovarian source of androgen excess. The first level consists of measurement of total testosterone, preferably using reliable methods suitable for the female range, together with assessment of SHBG and, when useful, the free fraction or free androgen index. DHEAS provides guidance in the differential diagnosis because a marked increase shifts suspicion toward an adrenal rather than an ovarian origin.

In addition to these tests, the initial profile generally includes androstenedione, gonadotropins, prolactin, TSH and morning 17-hydroxyprogesterone, with further targeted investigations when the clinical presentation suggests nonclassic congenital adrenal hyperplasia, Cushing syndrome or other endocrinopathies. In postmenopausal women, the combination of elevated testosterone and a DHEAS concentration that is not proportionally increased is particularly suggestive of an ovarian source. However, this finding alone does not distinguish hyperthecosis from an androgen secreting ovarian tumor and must always be interpreted within the clinical and imaging context.

According to shared diagnostic approaches for severe and postmenopausal female hyperandrogenism, assessment should confirm androgen excess, exclude extragonadal causes and localize the ovarian or adrenal source using dedicated imaging and integrated clinical and biochemical evaluation.

Diagnostic assessment of ovarian hyperthecosis

• Confirmation of androgen excess through measurement of total testosterone, assessment of SHBG and, when indicated, the free fraction, together with DHEAS and androstenedione for differential diagnosis.
• Exclusion of the main alternative causes through medication history, 17-hydroxyprogesterone, screening endocrine tests and assessment of the clinical context.
• Assessment of the ovarian source using transvaginal ultrasound as the first examination, supplemented by pelvic MRI when suspicion remains high or ultrasound findings are uncertain.
• Definitive confirmation, often histological, after removal of the ovaries, particularly in postmenopausal patients with a severe presentation and persistent suspicion of a pathological ovarian cause.

Transvaginal ultrasound is the first line imaging examination. It may show bilaterally enlarged ovaries with prominent stroma or a relatively homogeneous appearance, but it does not always identify a specific lesion. In many patients, the findings are suggestive but not definitive. Pelvic magnetic resonance imaging therefore becomes useful when ultrasound is inconclusive or when small stromal or sex cord tumors need to be excluded. Even with advanced imaging, however, distinguishing hyperthecosis from an androgen secreting ovarian tumor may remain difficult.

The differential diagnosis is the crucial issue. Hyperthecosis must be distinguished from secreting ovarian tumors, androgen secreting adrenal tumors, nonclassic congenital adrenal hyperplasia, iatrogenic hyperandrogenism and functional disorders such as PCOS. In postmenopausal women, the speed of progression, degree of virilization, absolute testosterone level and imaging pattern determine the level of urgency. Severe postmenopausal androgenization generally requires accelerated assessment because tolerance for diagnostic uncertainty should be low.

In selected cases, when biochemical testing and imaging do not reliably localize the source of androgen production, selective venous sampling may be performed in specialist centers. This is a complex approach that is unnecessary in most patients and is reserved for situations in which the therapeutic decision depends on more precise localization. In clinical practice, particularly in postmenopausal women with strong suspicion of an ovarian cause, bilateral surgery may be selected for both curative and diagnostic purposes.

The definitive diagnosis of ovarian hyperthecosis is often histopathological. Histological examination documents luteinized theca cells within the ovarian stroma, frequently with bilateral involvement. This has fundamental practical importance: the clinical diagnosis may be highly probable, but formal certainty is often obtained only after removal of the ovaries. Diagnostic assessment must therefore be sufficiently robust to justify a definitive therapeutic strategy when required by the clinical and biochemical phenotype.

The classification of ovarian hyperthecosis has mainly clinical and pathophysiological value. An initial distinction separates the classic postmenopausal forms, which represent the most typical phenotype, from the rarer forms occurring during reproductive life or adolescence. The former are dominated by severe androgenization, metabolic dysfunction and a frequent indication for surgery. In the latter, the main difficulty is overlap with severe PCOS and greater complexity in reproductive management.

A second classification criterion concerns clinical intensity. Some forms are predominantly hyperandrogenic, with hirsutism and alopecia as the main signs, whereas others are virilizing, with clitoromegaly, deepening of the voice, reduced breast volume and increased muscle mass. This grading has diagnostic and prognostic value because overt virilization indicates a substantial androgen burden and requires particularly careful exclusion of an ovarian secreting lesion.

From a morphological perspective, hyperthecosis may present as diffuse bilateral stromal involvement or in more nodular forms. This variability contributes to the limitations of imaging and explains why some patients have bilaterally enlarged ovaries while others have less conspicuous findings. Bilaterality nevertheless remains common and is useful in distinguishing hyperthecosis from small unilateral androgen secreting ovarian tumors.

There is also an implicit classification according to the burden of the metabolic component. Some patients have a phenotype in which metabolic syndrome is almost as prominent as virilization, with diabetes, central obesity and severe insulin resistance. In others, the presentation is dominated by androgenic changes affecting the skin and its appendages. This difference does not alter the histological definition of the disease, but substantially changes therapeutic priorities and long term follow up.

Severity also includes the relationship with the endometrium. In patients with substantial peripheral aromatization of androgens, particularly those with obesity, endometrial risk may become clinically relevant and should be considered part of the overall severity of the disease. Hyperthecosis associated with endometrial hyperplasia or abnormal uterine bleeding is more complex than isolated androgen excess because it directly influences the surgical strategy and gynecological assessment.

Finally, classification must always retain a differential perspective with androgen secreting ovarian tumors. In practical terms, hyperthecosis lies among nonneoplastic ovarian disorders with high endocrine activity. This intermediate position explains why it can clinically mimic a neoplasm and why the diagnostic boundary may remain subtle before histological examination. Correct classification therefore serves not only to describe the condition, but also to determine the urgency and type of therapeutic intervention.

Treatment of ovarian hyperthecosis depends on age, menopausal status, severity of androgen excess, presence of virilization, reproductive goals and metabolic burden. In a postmenopausal woman, the standard treatment is generally bilateral salpingo oophorectomy, because it removes the androgen source, permits histological confirmation and simultaneously addresses the differential diagnostic concern of small secreting ovarian neoplasms that cannot always be reliably distinguished before surgery. In this population, surgery therefore serves both therapeutic and diagnostic purposes.

The surgical rationale is strong. Hyperthecosis is frequently bilateral, the pathological stroma may not be localized within a well defined mass, and observation alone or limited surgery may fail to resolve the endocrine disorder. After bilateral removal, testosterone levels tend to decline rapidly, retrospectively confirming the ovarian origin of hyperandrogenism. However, reversibility of the clinical signs is not uniform. Seborrhea and certain cutaneous manifestations improve relatively quickly, whereas longstanding hirsutism, alopecia and particularly changes in voice pitch may regress only partially.

Management is more complex in women of reproductive age. When suspicion of hyperthecosis is high but fertility remains an objective, treatment decisions must be highly individualized and require a difficult balance between definitive control of the androgen source and preservation of ovarian function. More conservative strategies may be considered in selected cases with localized or nodular involvement, but the rarity of the disorder and difficulty of localization often require a specialist approach in experienced centers.

Medical treatment plays a role mainly in symptom control or as a bridging strategy. Antiandrogens and combined contraceptives may reduce the clinical expression of hyperandrogenism in women who are not postmenopausal, whereas GnRH analogues have been used in some cases as a temporary option to suppress ovarian steroidogenesis when surgery is not immediately feasible or must be postponed. However, these strategies do not represent the typical definitive solution for a postmenopausal woman with established bilateral stromal disease.

An essential part of care concerns the metabolic component. Weight reduction, treatment of insulin resistance and management of diabetes, hypertension and dyslipidemia are indispensable because hyperthecosis is not merely an ovarian source of androgens, but a complex endocrine and metabolic syndrome. Metformin may be useful in patients with hyperinsulinemia and diabetes or prediabetes, but its main purpose is to improve the metabolic background rather than independently resolve the ovarian origin of hyperandrogenism.

Endometrial assessment is an integral part of treatment. In patients with abnormal uterine bleeding, a thickened endometrium or major risk factors, the therapeutic pathway should include investigation and management of the endometrium because peripheral conversion of androgens may have caused chronic estrogenic stimulation. In some patients, ovarian surgery therefore forms part of a broader gynecological treatment strategy that also considers endometrial safety.

Finally, treatment should include realistic counselling regarding the timing and limits of recovery. Biochemical normalization may be rapid, but clinical improvement requires months and not all signs are fully reversible. This information is crucial for avoiding unrealistic expectations and for promptly integrating cosmetic, trichological, metabolic and psychological strategies into the care pathway. Effective management of ovarian hyperthecosis therefore does not end with surgery, but continues through multidisciplinary follow up aimed at the patient’s overall recovery.

Follow up of ovarian hyperthecosis aims to document regression of hyperandrogenism, assess the metabolic response, monitor associated gynecological problems and evaluate medium term clinical recovery. After surgical treatment, the first step is confirmation of the reduction in testosterone and other androgen markers that were abnormal before the procedure. This assessment has practical value because it verifies correct identification of the ovarian source and excludes persistent androgen excess from another site.

Clinical monitoring should assess the progression of hirsutism, alopecia, seborrhea and signs of virilization. Not all parameters improve at the same rate. Cutaneous manifestations related to sebaceous activity may diminish relatively quickly, whereas established terminal hair requires months before perceptible improvement occurs. Structural signs such as deepening of the voice may be only partially reversible, and this should be discussed clearly with the patient before surgery.

Metabolic surveillance is a central component of follow up. Many patients with hyperthecosis have diabetes, abdominal obesity, hypertension and dyslipidemia that do not disappear automatically after correction of hyperandrogenism. Glucose, glycated hemoglobin, lipid profile, body weight, waist circumference and blood pressure should therefore be monitored, with adjustment of metabolic treatment over time. The quality of follow up is also determined by its ability to reduce residual cardiovascular risk, not merely normalize testosterone.

In patients with previous endometrial disease or risk, gynecological monitoring remains important even after correction of the androgen source. When abnormal bleeding, endometrial thickening or hyperplasia was present, follow up should assess regression or the need for further intervention. This is particularly relevant in women with obesity, in whom peripheral aromatization may have exerted long term proliferative stimulation on the endometrium.

In the rare patients managed using temporary or conservative medical strategies, follow up should be even more frequent. Persistent or increasing testosterone, worsening virilization or inadequate metabolic control require reassessment of the strategy and often return surgery to the center of the therapeutic decision. In these cases, monitoring is not merely observation, but an active part of decision making.

A final element concerns quality of life. Severe androgenization often leaves a psychological impact that does not automatically resolve with biochemical normalization. Follow up should therefore include the patient’s subjective perception of improvement, residual body image distress, the need for additional dermatological or trichological treatment and possible psychological support. Effective monitoring of ovarian hyperthecosis must assess not only laboratory results, but also the patient’s true physical and psychosocial recovery.

The prognosis of ovarian hyperthecosis is generally favorable from an endocrine perspective when the condition is correctly recognized and definitively treated. Removal of the ovarian source usually leads to rapid biochemical normalization of androgen levels, followed by gradual clinical improvement. However, overall prognosis depends greatly on the duration of androgen exposure and the burden of associated metabolic comorbidities. Correction of the ovarian source does not automatically eliminate all systemic consequences that developed during the preceding years.

The most important complications are metabolic. Type 2 diabetes mellitus, severe insulin resistance, visceral obesity, dyslipidemia and hypertension represent a substantial proportion of the clinical burden of the disease. Even after definitive treatment, these conditions may persist and continue to cause cardiovascular risk and organ damage. Prognosis should therefore be assessed not only as an endocrine outcome, but also as an overall cardiometabolic prognosis.

A second group of complications involves the endometrium. Peripheral aromatization of androgens into estrogens may promote endometrial hyperplasia and, in selected settings, increase the risk of more advanced endometrial disease. This is particularly relevant in patients with obesity and prolonged exposure to unopposed peripheral estrogenic stimulation. Prevention and early recognition of these complications are therefore an integral part of management.

Dermatological and phenotypic complications may leave residual effects. Chronic hirsutism tends to improve slowly and may require cosmetic or laser treatment to achieve satisfactory recovery. Advanced androgenetic alopecia may not be fully reversible, particularly when follicular miniaturization has become established over time. Voice changes, when present, are among the least reversible features and represent an important prognostic issue to discuss with the patient.

From a therapeutic perspective, complications also depend on the strategy adopted. Ovarian surgery, although generally curative, carries the risks inherent in the procedure and perioperative management. In women of reproductive age, reproductive prognosis must also be assessed carefully when surgery that reduces the ovarian reserve becomes necessary. In postmenopausal patients, this issue is less relevant, and surgical prognosis is more directly linked to control of the androgenic phenotype and resolution of the diagnostic uncertainty.

Finally, there is a cross cutting complication involving quality of life. Ovarian hyperthecosis may alter body image, sexuality, social relationships and psychological wellbeing for years. Even when the hormonal profile normalizes, subjective recovery may remain incomplete or require a long period. The best prognosis is therefore achieved when diagnosis is early, definitive treatment is provided when indicated and follow up explicitly addresses not only androgen excess, but also its metabolic, gynecological and psychosocial consequences.