Virilizing nodular ovarian stromal hyperthecosis, diabetes mellitus and insulin resistance in a postmenopausal woman. Case report

Abstract

A 69-year-old woman (gravida 2, para 2) was referred with a 15-year history of progressive hirsutism. She shaved on alternite days and had scvcre fronto-temporal balding. Her menarche had been at 13 years, with an uneventful menopause at SO years of age. Non-insulin-dependent diabetes mellitus (NIDDM) had been diagnoscd 2 years before presentation and was well controlled with gliclazide and diet therapy. There was no family history of diabctcs or hirsutism.She was thin and had scvere frontal and teniporal balding. Hirsutism affected the face, shoulders, anterior chest, anterior abdominal wall and back. Blood pressure was 150175 mmHg. She had a small multinodular goitre, but abdominal, breast and pelvic examination was normal. Therc was no clitoromcgaly.A number of investigations were performed and the results are given in Table 1. Serum was analysed for a circulating inhibitor of post-binding insulin action using the method described by Harrison et al. (1985). There was no difference bctwecn the dcgrcc of inhibition of insulin-stimulated lipogenesis (conversion of [3-"] glucose to [jH] lipid i n rat fat cells) produced by the patient's serum and control serum.Because the plasma testosterone was in the Low male range and the plasma dehydro-

Ovarian Thecoma with Virilizing Manifestations

“…It is generally agreed that thecomas are benign although most of them are solid. Nonmalignant disorders usually follow a more slowly progressive benign course, as compared with the rapid progressive virilization seen with underlying malignancy 9. It has been suggested that a simple clinical assessment and a single serum testosterone measurement may be sufficient to differentiate between benign and malignant virilizing tumors in women presenting with hirsutism and androgenetic features 10.…”

Paradoxical glycaemic response to surgical treatment of ovarian hyperthecosis in a patient with type 2 diabetes

“…3 Another case of postmenopausal hyperthecosis with type 2 diabetes reported improvement of HbA1c following oophorectomy, from 10.1% to 8.2%, which required cessation of gliclazide due to hypoglycaemia. 2 More data are available in patients with PCOS, which is associated with increased androgens (albeit at lower levels), and insulin resistance. Studies of the treatment of PCOS with anti-androgen therapies are however contradictory, often depending on the exact agent used, demonstrating improvement, no change and worsening of hyperinsulinism.…”

“…1 Improvement of diabetic control in hyperthecosis has been reported following oophorectomy, perhaps secondary to normalisation of the hyperandrogenaemia. 2 This is a report of worsening diabetes following oophorectomy. The case and possible explanations for the response are described.…”

Postmenopausal Hyperandrogenism of Ovarian Origin

“…the crystalloid-nega tive lutein cell mimicking the theca interna, the crystal loid-positive Leydig cell and the adrenocortical cell [22], Like its relative, the hilus cell, this highly steroidogenic cell is affected by hyperplasia and neoplasia. Diffuse, focal or nodular hyperplasia of the crystalloid-negative and crystalloid-positive steroid cell gives rise to hyperthecosis [ 1,[15][16][17] and stromal Leydig cell hyperplasia [5,6], respectively. These two androgenic states are only distin guished by the presence or absence of Reinke crystalloids and can be primary or secondary to a variety of primary or metastatic ovarian tumors [9], Primary neoplasms of these steroid cells, which used to be called lipid or lipoid cell tumors, are now classified according to their morphologic and functional expression [1,3].…”

“…Postmenopausal hyperandrogenism with overt clinical manifestations is rare and often related to an assortment of ovarian disorders including: (1) primary sex-cord-stromal tumors, steroid cell (lipoid cell) tumors [1][2][3], stromal luteomas [4], luteinized thecomas [5], Sertoli-Leydig tu mors or androblastomas [6], intraovarian Leydig cell tumors [7,8] and cystic granulosa cell tumors [9]; (2) tu mors of the extraovarian hilus cells [10][11][12]; (3) primary ovarian tumors with reactive stromal hyperplasia [13][14][15][16]; (4) secondary ovarian tumors with reactive stromal hyperplasia [17,18]; (5) hyperplastic states, stromal hy- testosterone 5.500 ng/dl (normal 15-52); androstenedione 600 ng/dl (normal 85-290); estradiol 163pg/ml (normal 10-50); normal DHEA levels; hemoglobin 18.6 g/dl. She had a total abdominal hys terectomy and bilateral salpingo-oophorectomy followed by rapid normalization of androgen levels and slow regression of her viriliza tion.…”