OSCST is the most common cause of hyperandrogenism, which leads to various virilization symptoms, including progressive hirsutism, acne, hoarseness, amenorrhea, breast atrophy, and male-type baldness . Both ovarian and adrenal lesions can cause hyperandrogenism. Sexual cord-stromal tumors are the most common ovarian functional tumors that cause hyperandrogenemia. Hyperandrogenism caused by adrenal tumours is due to the secretion of DHEAS, while LCT primarily secretes testosterone . The average age of onset of adrenal tumours that cause hyperandrogenism is 58 years, but these tumours can also occur in children and women aged 40–50 years . The adrenal tumours are usually large and invasive, progress rapidly, and are fatal when accompanied by Cushing syndrome . When a postmenopausal women suddenly exhibit a gradual rise in androgens and normal dehydroepiandrosterone levels, we should strongly suspect that their androgens originate from functional ovarian tumours.
Some functioning ovarian tumours, such as LCT, SCT-NOS, and mature teratomas, can cause hyperandrogenism. Of these, LCT is most frequently found in postmenopausal women and accounts for less than 0.1% of all ovarian tumours. Androgen-producing Leydig cells are present in the ovaries of more than 80% of women . The age at onset of SCT-NOS ranges from 3 to 93 years, with a mean age at diagnosis of 47 years . Its clinical manifestations are determined by the steroid hormone produced by the tumour[10–11]. In most patients (56–77%), the tumour secretes testosterone and causes virilization. Excessive oestrogen was seen in 6% of patients, which leads to menorrhagia or postmenopausal bleeding and eventually to endometrioid adenocarcinoma. Approximately 25% of SCT-NOS tumours do not produce any hormones. Mature teratoma is the most common germ cell tumour, but it does not frequently cause hyperandrogenism. In most cases, mature teratoma contains non-secretive tissue and rarely produces testosterone-induced virilization [12–13].
Certain scholars believe that imaging studies are not helpful for the detection and diagnosis of small ovarian tumours. Hofland  believes that even negative imaging test results cannot exclude the existence of LCT or Leydig cell hyperplasia. He reported a case of Leydig's hyperplasia for which both MRI and ultrasound showed normal ovarian size, with enhanced perfusion only in the left ovary. However, postoperative pathology confirmed bilateral proliferation of ovarian Leydig cells. Palha  believes that because LCTs are extremely small, these ovarian tumours lack typical imaging features and there is a lack of diagnostic consistency between imaging and histology. Of the 3 cases of LCT she discussed (all of which involved tumours smaller than 3 cm), 2 cases included negative ultrasound and CT results. In the remaining case, ultrasound and CT only showed bilateral ovarian enlargement, but surgery confirmed LCT in the left ovary.
TVS is the first choice for imaging and diagnosis of ovarian tumours due to its convenience, speed, and non-invasiveness. But TVS for LCT in postmenopausal women is still challenging. First, almost all LCTs are less than 5 cm in diameter . Small LCTs (usually < 3 cm) may be invisible on ultrasound and CT scans . Secondly, it can be divided into leydig cell hyperplasia (< 1 cm) and LCT (> 1 cm) according to the difference in size and growth pattern, and because the hyperplasia is usually widely nodular, it is difficult to distinguish them[16−17]. Besides, due to decreased oestrogen level and insufficient ovarian arterial blood flow, ovaries shrink rapidly in menopausal women, the thin cortex and the altered cortex-to-medulla ratio cause the ovary to appear solid and hyperechoic; on colour Doppler flow imaging (CDFI), with no blood flow visible . TVS in this case showed uterine and ovarian atrophy. The ovaries were significantly small and slightly hypoechoic, with diameters of approximately 2.13 cm (right) and 2.0 cm (left), but no obvious space-occupying lesions were detected in the adnexal areas and no obvious blood flow signal in CDFI. Postoperative, the stored images were re-examined and a slightly hyperechogenic nodular lesion (1.23 cm)was found in the right ovary (Fig. D). The boundary between nodule and peripheral atrophic ovarian tissue was unclear. Combined with pelvic enhanced CT and MRI images as well as surgical and pathological findings, we concluded that the slightly hyperechogenic nodular lesion in the right ovary was LCT, which was previously not diagnosed. In summary, an ovarian tumour with a diameter of more than 1 cm but less than 3 cm may exhibit poor visibility on ultrasound examination. Additionally, when LCTs show a slightly hypoechogenic or hyperechogenic nodule may lack a sharp boundary with the surrounding atrophic ovarian tissue; thus, ultrasound physicians who have little experience with LCTs can easily treat lesions as part of the atrophic ovarian tissue, potentially causing false-negative ultrasound results and leading to missed diagnoses.
Demidov et al.  reported 5 cases of LCT, all of which were solid and small. They found that moderate or high blood flow signals could be seen in CDFI of these tumours. In this case, the intensification did appear in enhanced CT and MRI. Based on known imaging findings, we believe that although ovarian LCTs are difficult to distinguish from normal atrophic ovarian tissue in postmenopausal women, blood flow signals in the tumour on CDFI and enhanced perfusion in the tumour on CT or MRI may be used to identify ovarian LCT and reveal important imaging features of atrophic ovarian tissue. Given the principles of CEUS , we believe that CEUS of the ovary may be helpful for distinguishing between atrophic ovarian tissue and small ovarian tumours and for understanding the microcirculatory perfusion status of lesions. We performed a CEUS of ovarian in a case involving a suspected hyperechoic lesion in the ovary of an elderly woman at 10 years after menopause. In this patient, a suspicious lesion of approximately 1 cm in size was found in the left ovary on TVS. The boundary between the lesion and atrophic ovarian tissue was not clear. CDFI showed little blood flow signal in the lesion(Fig. E). Enhanced CT showed no abnormal ovaries. We injected 2.4 ml of contrast agent (Sono Vue) through peripheral blood vessels. Real-time TVS observation showed that the intra-ovarian lesion rapidly increased in the arterial phase and subsided significantly in the late phase. The boundary between the lesion and the surrounding atrophic ovarian tissue was extremely clear. Using CEUS, we definitively established that the patient had a small tumour in the left ovary and unimpeded blood supply (Fig. F). The patient's sex hormone levels did not show abnormal changes. Postoperative pathology suggesting that the lesion was a mature teratoma. Based on this examination, we believe that CEUS can help us distinguish between atrophic ovarian tissue and small ovarian tumours in postmenopausal women and understand the microcirculation perfusion status of lesions. CEUS is especially advantageous for assessing tumours with an approximate diameter of only 1 cm, while CDFI does not show rich blood flow signals; for such tumours, this technique can be the most beneficial for avoiding imaging misdiagnosis. Moreover, when combined with consideration of the patient's clinical manifestations and changes in hormone levels, CEUS will greatly facilitate the clinical diagnosis of postmenopausal ovarian LCT.