Cases reported "Leydig Cell Tumor"

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11/44. Hilus cell pathology and hirsutism.

    Hilus cell abnormalities are uncommon causes of hirsutism with virilization. Although hilus cell tumours have been well described, hilus cell hyperplasia is rare and is poorly defined clinically. We describe three cases of hilus cell hyperplasia and compare them with a case of hilus cell tumour. Both pathologies were associated with increased testosterone and oestradiol secretion. Suppression of testosterone to the 'normal range' in response to exogenous oestrogen was seen only in the cases with hyperplasia; only partial responsiveness was seen in the case with hilus cell tumour. Bilateral oophorectomy offers the potential for cure for both hilus cell hyperplasia and tumour.
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12/44. Ossifying malignant Leydig (interstitial) cell tumour of the testis.

    An ossifying malignant Leydig cell tumour of the testis in a patient with associated gynaecomastia is presented. The criteria for diagnosing malignancy in these tumours are briefly discussed.
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13/44. A malignant Leydig cell tumour associated with testicular trauma and prostatic carcinoma.

    A case of metastatic Leydig cell carcinoma without sex hormone overproduction is reported. The patient had had a prior testicular contusion trauma on the same side after which the testicle had been swollen and firm. The possible aetiological role of extreme trauma is discussed. Radical orchidectomy is recommended for large tumours because of the difficulty in predicting malignant potential, and routine follow-up with retroperitoneal ultrasound scanning for 10 years in all cases.
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14/44. Ovarian Sertoli-Leydig cell tumour with raised serum alpha fetoprotein. A case report.

    A case of ovarian Sertoli-Leydig cell tumour with a raised serum alpha fetoprotein is reported. The patient first presented at the age of 27 years with a history of 6 years' amenorrhoea followed by 3 months irregular vaginal bleeding. A ovarian tumour was found and excised and shown microscopically to be a spindle cell malignant tumour. The patient was treated with chemotherapy and had a complete response. Thirty months after first presentation there was a recurrence in the pelvis which microscopically showed the typical features of a Sertoli-Leydig cell tumour. Six months later a second recurrence had the microscopic appearance of a lipid cell tumour. A raised serum alpha fetoprotein was found at the time of the second recurrence and immunohistochemistry showed this protein in the Leydig and luteinized cells of the recurrent tumours but not in the spindle cells of the original ovarian neoplasm.
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15/44. Localization of S-100 protein in a Leydig and Sertoli cell tumour of testis.

    A Sertoli-Leydig cell tumour of testis presented some diagnostic difficulties. The tumour cells showed strong expression of S-100 antigen. Preliminary study of non-neoplastic testis suggests that leydig cells and, to a lesser extent, sertoli cells express S-100 antigen; its localization may be of value in the diagnosis of sex cord-stromal tumours of testis.
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16/44. Bilateral testicular tumours in congenital adrenal hyperplasia: a continuing diagnostic and therapeutic dilemma.

    Bilateral testicular tumours are a rare but well described complication of congenital adrenal hyperplasia (CAH). It can be extremely difficult to distinguish histologically between Leydig cell tumours and adrenocortical rest hyperplasia which may lead in some cases to unnecessary orchidectomy in young men. A 26-year-old male in whom CAH had been diagnosed neonatally, was referred for further investigation of a craggy mass in the left testis. Six months earlier, right orchidectomy had been performed after presentation with bilateral enlarged, hard testes and azoospermia. The tumour was interpreted to be a malignant interstitial cell tumour of the testis. Our investigations revealed that his CAH was inadequately controlled and that the hormonal secretion from the remaining left testicular mass was ACTH dependent. Percutaneous venous sampling revealed high concentrations of cortisol and other adrenocortical hormones coming from the gonadal vein. dexamethasone suppressed these adrenal hormones and reduced the size and softened the consistency of the testicular mass. Total disappearance of the mass was achieved by using dexamethasone, given in a reverse circadian rhythm regimen. spermatogenesis returned and the patient's wife became pregnant after 6 months; she gave birth to a normal male infant. To our knowledge, this is the first time in this clinical setting that fertility has been achieved. This case highlights the need for both a functional and histological assessment of such 'tumours' in CAH prior to orchidectomy.
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17/44. Gynaecomastia and occult Leydig cell tumour of the testis.

    Two patients with Leydig cell tumours of the testis are described. Both presented with gynaecomastia, but on initial examination had apparently normal testes. The causative tumour did not become obvious for some months, despite being carefully sought. review of the literature suggests that gynaecomastia preceding a readily palpable tumour is a recognised problem. The detection and management of Leydig cell tumours of the testis are discussed.
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18/44. Isosexual precocious pseudopuberty secondary to a testosterone-secreting Leydig cell testicular tumour: true isosexual development early after surgery.

    The paper reports on a 6-year-old boy with precocious pseudopuberty due to androgen hypersecretion by a testicular interstitial cell tumour. Steroidogenesis, characterized by high testosterone, dihydrotestosterone, androstenedione, dehydroepiandrosterone and 17-hydroxyprogesterone plasma levels, was not modified by ACTH, dexamethasone or HCG administration. gonadotropins were subnormal and unresponsive to LRH stimulation. TSH and prolactin levels were normal both in basal and dynamic conditions. The hormonal profile progressively returned to prepubertal value and persisted normal for 6 months after removal of the tumour. The patient entered puberty spontaneously at 7,6/12 years showing a normal pubertal basal and LRH stimulated FSH and LH and a pubertal circadian rhythm of both gonadotropins and testosterone.
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19/44. Endocrine investigations in two cases of feminizing Leydig cell tumour.

    Two patients, aged 32 and 35 years, presented with gynaecomastia and a unilateral testicular tumour which proved to be a Leydig cell tumour. Pre-operative samples taken at 08.00 h on different days showed marked elevation of plasma oestradiol in the first patient, and very slight irregular oestradiol elevation in the second, plasma oestrone within the normal range in both patients, reduced plasma testosterone in the first patient and reduced or normal testosterone in the second, and low or low-normal serum LH and FSH in both patients. One of the patients received an oral dose of 100 mg of clomiphene citrate for 3 consecutive days which induced a rise in LH and FSH and a decrease in the 17-hydroxyprogesterone/androstenedione ratio. These data suggest the inhibiting effect of endogenous hyperoestrogenism on testicular steroidogenesis owing to both the reduction of gonadotropin secretion and a direct local negative effect on C 17,20-lyase. After human chorionic gonadotropin stimulation, oestradiol response was increased and abnormally prolonged, a finding which may be helpful when diagnosing a feminizing Leydig cell tumour; testosterone reached normal values. After removal of the tumoural testis, gynaecomastia regressed within a few days, gonadotropins increased, oestrogens dropped, testosterone and 5 alpha-dihydrotestosterone normalized in one patient but remained low in the other at day 30. The leydig cells outside the tumour appeared morphologically normal, but the count gave evidence of juxtatumoural Leydig cell hyperplasia in areas where the tumour was well encapsulated while showing a significant reduction at a distance from the tumour and in the contralateral testis by comparison with control testes.(ABSTRACT TRUNCATED AT 250 WORDS)
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20/44. Long-term suppression of a testosterone-producing ovarian tumour by oestrogen/progestogen therapy.

    A 44-year-old lady presenting with hirsutism was found to have a testosterone-secreting Leydig cell tumour of the right ovary. serum testosterone levels were adequately suppressed for 8 years by combined oestrogen/progestogen preparation (Microgynon 30, Schering, West Sussex). The fall in gonadotrophin and testosterone levels during therapy and their rise after stopping therapy suggests that the tumour was gonadotrophin dependent.
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