Cases reported "Leydig Cell Tumor"

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1/64. Loss of gender difference in serum leptin levels and its slow recovery after successful surgery for Leydig cell tumours in two virilized females.

    One of the factors that predicts serum leptin levels is gender. It has been shown that sex steroid hormones, in particular testosterone, play an important role in the regulation of serum leptin levels. We had the opportunity to examine the effects of acute and chronic changes in serum testosterone levels on serum leptin concentrations in two virilized females harbouring testosterone-secreting ovarian tumours, before and after curative surgery. Chronically elevated basal testosterone levels (46 nmol/l) were associated with suppressed serum leptin levels (1.46 microg/l and 2.56 microg/l) vs. 12 age- and BMI-matched healthy subjects 9.89 /- 0.64 microg/l. leptin levels were determined from pooled serum samples assayed by commercial radioimmunoassay. High testosterone levels abolished the well known sexual dimorphism of serum leptin levels. Two weeks after curative resection of these tumours serum leptin levels were unaltered and started to increase progressively after one month. One patient received parenteral conjugated oestrogens while the other resumed spontaneous menstrual cycles. Three months after curative surgery obvious changes in body composition were registered (DEXA). Six months later further rise in serum leptin concentrations occurred without further changes in body composition. In conclusion, leptin levels did not change in spite of rapid changes in the steroid milieu, but in the long term increase in body fat stores, new steroid milieu and maybe other factors are important determining factors of serum leptin levels.
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2/64. Malignant Leydig cell tumour of the testis.

    A case of malignant Leydig cell tumour is presented. It is a rare primary malignant tumour of the testis and occurs exclusively in adults. The present case is of interest because it occurred at the young age of 25 years which is rare. Histologically it showed almost all features which suggest malignancy and also had metastases to the lungs and liver. The clinical details and pathology of this tumour are discussed.
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3/64. Leydig cell tumour--a rare testicular tumour.

    Although Leydig cell tumour is a rare tumour which constitutes only 1-3% of all testicular tumours, still it is in the focus of interest because of the difficulties in determining its exact nature and subsequently the type of treatment and follow-up. We report a case of Leydig cell tumour with a review of the related literature.
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4/64. testis sparing enucleation of a Leydig-cell tumour in a boy.

    Testicular tumours are very rare in paediatric age, accounting only for 1% of all paediatric tumours. Testicular tumours can originate either from germ cells (77.4%) or from stromal cells (7.1%) or from other cells. Leydig-cell tumours account for 1% of all testicular tumours and 39% of gonadal stromal tumours and in the prepubertal male are responsible for causing precocious pseudopuberty. In the past, orchiectomy has been considered the treatment of choice, but in consideration of the fact that Leydig Cell tumours in children invariably show a benign behaviour, in recent years some authors have suggested a more conservative approach. In the herein reported case, a decision was made to simply enucleate the tumour leaving the testis. After one year, imaging shows a normal testis with no sign of recurrence.
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5/64. Oestrogen secreting Leydig cell tumour and GnRH agonist in-vivo and in-vitro studies.

    OBJECTIVE: The purposes of our study concerning two patients with oestrogen secreting Leydig cell tumour were to determine whether endogenous LH levels are involved in testicular tumour steroidogenesis and whether aromatase activity of oestrogen secreting Leydig cell tumours is directly or indirectly dependent on LH levels. MEASUREMENTS: E2 and T were evaluated after hCG injection (5000 IU) during 96 hours. Bio and immuno LH, T, E2, were determined at the basal state and after administration of D-Trp-6-GnRH agonist (3.75 mg) every 3 weeks. The abnormal testis was removed after the third injection and testicular venous blood was collected during the operation. Testicular tumour was incubated with 4-14C-T. RESULTS: Oestradiol (E2) response to hCG injection (5000 IU) was prolonged and exaggerated while that of testosterone (T) was similar to that of the controls. The aromatase index (E2/T) remained elevated even 96 hours after hCG. Intramuscular injection of the GnRH agonist, D-Trp-6-GnRH (3.75 mg) resulted in a reduction of immunoreactive and bioactive LH. T was decreased to about 10% of baseline levels and E2 fell from 240 to 36 pmol/l. In the blood of the spermatic veins collected in the course of surgery, E2 levels were found to be lower in comparison with the controls. E2 was found to be twofold higher in the spermatic vein draining the tumoral side than in that of the contralateral testis. Incubation of the testicular tumours with 4-14C-T, displayed a reduced aromatase activity (conversion of T to E2: 0.3 and 0.1% in patients 1 and 2 respectively). CONCLUSIONS: The kinetics of E2 response to hCG administration would suggest a modification of the regulation of the aromatase activity in this type of oestrogen secreting tumour. A certain endogenous LH level may be necessary to supply a sufficient quantity of T substrate, and to maintain aromatase activity of such Leydig cell tumours secreting oestrogens. These tumours seem to be responsive to endogenous LH levels.
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6/64. Case report: MRI in the diagnosis of testicular Leydig cell tumour.

    We report the appearance of three cases of Leydig cell tumours on MRI. This imaging method showed well-defined and peripheral intratesticular tumours displaying marked and homogeneous enhancement when contrast medium was used. This latter finding was only observed in Leydig cell tumours when they were compared in a series of 104 patients with different scrotal pathologies.
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7/64. Non islet cell tumor hypoglycaemia in a metastatic leydig cell tumor.

    Non islet cell tumour hypoglycaemia (NICTH) is a rare cause of hypoglycaemia associated with malignancy and can be considered as a paraneoplastic syndrome. The hormonal factor associated with this condition is big IGF II, which exerts negative feedback effect and decreases the production of growth hormone and insulin. Due to low growth hormone levels, hepatic production of IGFBP 3 (the main binding protein of IGF II) is impaired. Excess free big IGF II is thus available for binding with insulin receptors to cause hypoglycaemia. Treatment options are either surgical removal of the tumour, administration of growth hormone, glucocorticoids or combination of treatments. A case of metastatic Leydig cell tumour causing NICTH has been discussed and the mechanism of NICTH hypoglycaemia and the treatment is outlined.
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8/64. Intraoperative venous blood sampling to localize a small androgen-producing ovarian tumor.

    BACKGROUND: Among other causes of virilization, ovarian tumors can be the cause of excessive androgen production. We report the case of a leydig cell tumor of the ovary where diagnostic attempts to localize the source of hyperandrogenism preoperatively failed owing to relatively small tumor size. CASE: A 36-year-old woman presented with clinical signs of severe virilization including progressive balding, increased hirsutism, secondary amenorrhea and enlargement of the clitoris. Extensive work-up included endocrinological tests, pelvic ultrasound, magnetic resonance imaging, chromosomal analysis, norcholesterol scintigraphy and selective venous sampling, without direct localization of the source of hyperandrogenism. Persistently high plasma testosterone prompted an explorative laparotomy. Intraoperative selective blood sampling of the ovarian veins and palpation gave evidence of a right ovarian tumor, which was then removed. Histological examination revealed the presence of a pure leydig cell tumor. CONCLUSION: Exploratory laparotomy with intraoperative selective blood sampling of the ovarian veins might be a useful approach in patients without accurate preoperative localization of androgen-producing tumors of the ovaries.
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ranking = 8.8156896804965E-6
keywords = plasma
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9/64. leydig cell tumor estrogen secretion: suppression by a gonadotropin releasing hormone agonist.

    A 35-year-old patient and a 48-year-old patient with a benign feminizing leydig cell tumor were treated just before orchiectomy with a GnRH agonist, respectively buserelin, administered subcutaneously for 7 days (500 micrograms/8 h) and intranasally for the following 7 days (400 micrograms/8 h), and long acting detryptoreline in a single im injection of 3.75 mg. After 10 days of treatment, breast pain was relieved. In the first patient, serum immunoassayable FSH and LH first rose and reached a peak by the first day, then decreased to nearly basal values; they unexpectedly rose again and the second peak was as high as the first one; they again decreased just before orchiectomy. The bioassayable to immunoassayable LH ratio rose and reached a peak on day 3; then it decreased and reached a nadir before orchiectomy. In the second patient, after the initial increase, FSH and LH decreased regularly with no subsequent increase. In both patients, an increase in plasma testosterone (T) and estradiol (E2) followed the first gonadotropin peak, then T and E2 decreased progressively and reached castration levels. It was thus possible to strongly inhibit both E2 tumoral secretion and T secretion. Our findings suggest that E2 tumoral secretion inhibition by GnRH agonists might be proposed as an alternative treatment to surgery, i.e. for patients who refuse orchiectomy or for whom surgery is contraindicated.
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ranking = 8.8156896804965E-6
keywords = plasma
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10/64. Unusual hyperechoic ultrasound appearance of testicular Leydig cell tumour.

    patients with a testicular mass are usually investigated by ultrasound and the ultrasound appearances have been correlated with the histology. The authors describe two patients with Leydig cell tumours. The first had bilateral tumours which although histologically typical of Leydig cell tumours, had differing ultrasound appearances, one with a previously unreported hyperechoic appearance. The second patient had an impalpable tumour with similar ultrasound appearances to those previously described. The paper illustrates the difficulty of giving an accurate diagnosis of solid testicular lesions and also shows that the previously described appearance of Leydig cell tumour is not pathognomonic.
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ranking = 1.75
keywords = cell tumour
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