1/20. gynecomastia with sulpiride.OBJECTIVE: Neuroleptic agents have been associated with gynecomastia, but evidence for a causal link is insufficient. We describe a case of unilateral gynecomastia without galactorrhea in a 38-year-old man during sulpiride treatment for generalized anxiety disorder. The patient had been treated with sulpiride (100 mg/day) for about 5 months by a primary care physician. In this patient, no specific endocrine alterations were found, except for a marked increase in prolactin (PRL) level and slight decrease in testosterone (T)/estradiol (E2) ratio. Drug withdrawal led to a reduction of the lump. sulpiride is a substituted benzamide with selective dopaminergic blocking activity. From the marked increase in PRL level and the slight decrease in T/E2 ratio observed during sulpiride therapy, it is proposed that sulpiride may induce gynecomastia by inhibiting hypothalamic-pituitary function directly, and/or indirectly through hyperPRLemia.- - - - - - - - - - ranking = 1keywords = endocrine (Clic here for more details about this article) |
2/20. A case of hypogonadotrophic hypogonadism with anosmia (Kallmann's syndrome) in a male, with familial incidence of a small metacentric chromosome (47,XX, mat? ).A case of Kallmann's syndrome in a male is reported. Besides the classical picture of hypogonadotrophic hypogonadism (demonstrated both by endocrine investigation and a testicular biopsy) with anosmia, a number of other unusual features are present including gynaecomastia, agencies of the anterior brachial muscles, some dental abnormalities, and dyschromatopsy. The karyotype, studied on peripheral lymphocytes, shows, in the propositus as well as in his mother, the presence in all mitoses of an extra small metacentric chromosome; its derivation is uncertain.- - - - - - - - - - ranking = 1keywords = endocrine (Clic here for more details about this article) |
3/20. An oestrogen-producing seminoma responsible for gynaecomastia.In feminising testicular tumours, oestrogens can be either secreted by the tumour itself or produced by normal leydig cells in response to paracrine and/or endocrine stimulation by hCG. Typical hormonal Leydig cell tumour patterns include: plasma oestradiol levels > 300 pmol/l on day 3 following an hCG injection, reduced plasma testosterone, and normal plasma hCG and gonadotrophin levels. Except for elevated plasma oestradiol levels, opposite results are observed in seminomas. We report a case of oestrogen-secreting seminoma mimicking a Leydig cell tumour. A 24-year-old Caucasian patient had complained of gynaecomastia for 6 months before admission. Hormonal pattern was typical of Leydig cell tumour. A 1.4 cm tumour was found in the left testis and confirmed on sonography. Considering the likely diagnosis of Leydig cell tumour, the patient was treated by tumourectomy. Surprisingly, pathological examination revealed a pure seminoma. Perifusion experiments showed that the tumour was able to secrete significant amounts of oestradiol. In addition, hCG induced a two-fold increase in oestradiol production from perifused tumour explants. immunohistochemistry revealed that the tumour was composed of nests of seminoma cells intermingled with lymphoid infiltrates. Tumour cells also expressed aromatase, the hCG/LH receptor and the Leydig cell marker relaxin-like factor, but were betahCG-negative. These results demonstrate that a pure seminoma of the testis is able to synthesise and secrete oestrogens. They also illustrate that the body of proof favouring the diagnosis of feminising Leydig cell tumour of the testis is not rigorously specific.- - - - - - - - - - ranking = 1keywords = endocrine (Clic here for more details about this article) |
4/20. Switch to tacrolimus for cyclosporine-induced gynecomastia in liver transplant recipients.We report herein on two male liver transplant (LT) recipients who presented with cyclosporine (CsA)-related gynecomastia 6 and 10 months after transplantation. The clinical workup showed increased luteinizing hormone (LH), associated with a slight reduction in testosterone blood levels in one patient and increased prolactin levels in the other. After excluding concomitant primary endocrine and/or malignant disease, conversion to tacrolimus (TAC) was performed resulting in clinical improvement of gynecomastia and return of hormone blood levels to normal range within 3 months. Our report confirms a putative role of CsA in post-LT gynecomastia, reversible however upon conversion to TAC.- - - - - - - - - - ranking = 1keywords = endocrine (Clic here for more details about this article) |
5/20. Prepubertal gynecomastia in peutz-jeghers syndrome: incomplete penetrance in a familial case and management with an aromatase inhibitor.BACKGROUND: peutz-jeghers syndrome (PJS) is a rare autosomal-dominant disorder characterized by multiple gastrointestinal hamartomatous polyps, mucocutaneous pigmentation and increased predisposition to various neoplasms. Endocrine manifestations in PJS include gynecomastia due to calcified Sertoli cell testicular tumors usually referred to as large-cell calcifying Sertoli cell tumors (LSCT). OBJECTIVE: To evaluate the value of endocrine markers and aromatase inhibitor treatment in children with PJS and LSCT. DESIGN AND SETTING: Familial cases, followed in a tertiary care center. patients: Two male siblings aged 7 and 9 years with PJS and LSCT. INTERVENTION: Third generation aromatase inhibitor (anastrozole) in one of the patients. MAIN OUTCOME MEASURES: Longitudinal measurements of sex-steroids, gonadotropins, Sertoli cell markers and auxological evaluation. RESULTS: The two male siblings with PJS had similar bilateral multifocal testicular calcifications and biochemical evidence of Sertoli cell dysfunction manifested by elevated plasma inhibin-alpha levels. Only one sibling had gynecomastia. estradiol levels were normal in both. During treatment with anastrozole, estradiol levels, growth and skeletal maturation, as well as Sertoli cell markers (inhibin B, inhibin-alpha and anti-mullerian hormone) decreased. CONCLUSIONS: Inhibin-alpha may be considered as a marker for LSCT in children with PJS, pointing to a specific defect in inhibin regulation in this condition. Moreover, the decrease in Sertoli cell markers during aromatase inhibitor treatment suggests that increased estrogen production is a primary event regulating downstream production of Sertoli cell peptides. Anastrozole is efficient in controlling the clinical features of the disease and should be proposed as an alternative to bilateral orchidectomy, which is often performed in this condition.- - - - - - - - - - ranking = 1keywords = endocrine (Clic here for more details about this article) |
6/20. The endocrinopathy of poems syndrome.We describe the clinical features and post mortem findings in a patient with poems syndrome (P--polyneuropathy, O--organomegaly, E--endocrinopathy, M--M protein, S--skin changes), with particular emphasis on the evolution of the endocrinopathy over a three year period. In addition to gynaecomastia this case exhibited primary hypothyroidism and primary and secondary adrenal and gonadal failure. The widespread nature of the endocrine changes suggests that a circulating substance interferes with the action of trophic hormones, possibly by inhibiting second messenger production.- - - - - - - - - - ranking = 1keywords = endocrine (Clic here for more details about this article) |
7/20. Clinical and endocrinological characterization of two subjects with Reifenstein syndrome associated with qualitative abnormalities of the androgen receptor.The androgen receptor in fibroblasts cultured from a biopsy of scrotal skin from 1 subject with Reifenstein syndrome has been found to be normal in amount and to bind dihydrotestosterone with normal affinity but to be qualitatively abnormal as evident by thermolability and instability upon ultracentrifugation. The family study of this subject and endocrine studies document androgen resistance in the index patient and his affected uncle. These findings provide evidence for X-linkage of this disorder, and suggest that the mutations that give rise to this phenotype are probably allelic to the mutations of the androgen receptor that cause testicular feminization.- - - - - - - - - - ranking = 1keywords = endocrine (Clic here for more details about this article) |
8/20. Pseudogynecomastia secondary to injection of heroin into breast tissue.A 50-year-old man who has a heroin addict developed bilateral, symmetrical swelling of the breasts as a result of injecting himself directly into the breasts for several years. Results of histologic examination of the breast tissue showed granulomatous inflammation and a foreign body reaction without gynecomastia or tumor. liver and endocrine functions were generally normal.- - - - - - - - - - ranking = 1keywords = endocrine (Clic here for more details about this article) |
9/20. Feminizing leydig cell tumor: endocrine and incubation studies.A 32-year-old patient with a history of surgery for left gynecomastia four years previously presented with right gynecomastia; a tumor in the left testis proved to be a leydig cell tumor. Preoperative investigations showed elevated but variable levels of plasma estradiol (E2) and estrone (E1), and reduced serum LH and FSH and plasma testosterone (T). After hCG stimulation, E2 response was increased and abnormally prolonged; T reached normal values, which has predictive value for a return to normal of post-operative T level. After left orchiectomy, gynecomastia regressed within a few days, gonadotropins increased by day 2, estrogens dropped by day 2 and were normal at day 7, T and 5 alpha-dihydrotestosterone dropped at day 2 but reached normal levels at day 16. Pathophysiology of these hormonal data are discussed. An incubation procedure with 3H testosterone showed an aromatase activity 21 times greater in the tumor than in normal peritumoral tissue, while the percentage of the volume occupied by leydig cells was 34 times higher. This suggests that the aromatase activity of a single tumor cell is very similar to that of a normal Leydig cell. Furthermore, evidence of juxtatumoral Leydig cell hyperplasia in areas where the tumor was well encapsulated suggests the existence of a factor stimulating Leydig cell multiplication.- - - - - - - - - - ranking = 4keywords = endocrine (Clic here for more details about this article) |
10/20. Feminizing testicular leydig cell tumor: hormonal profile before and after unilateral orchidectomy.The effect of chronic hyperestrogenism on gonadal function was studied in three men who had estrogen-secreting Leydig cell tumors before unilateral orchidectomy and for 11-43 months after surgery. All three men had low plasma gonadotropin and testosterone levels and increased estradiol levels. Impairment of testicular steroidogenesis was also suggested by increased progesterone to 17-hydroxyprogesterone and 17-hydroxyprogesterone to androstenedione ratios in both spermatic venous plasma and the medium of Leydig tumor cells from one patient incubated in vitro. Before surgery, spermatogenesis was abnormal in two men. Testicular endocrine function and spermatogenesis did not return to normal after surgery. During the follow-up period, plasma gonadotropin levels were high in all three men, and testosterone was low normal. estradiol levels decreased to normal immediately after surgery and then returned to the upper normal limit. The response to hCG stimulation in one man was subnormal. We conclude that chronic hyperestrogenism produced hypothalamo-pituitary inhibition as well as direct steroidogenic blockade at the testicular level. Long term impairment of both endocrine and exocrine testicular functions may be secondary to slowly reversible (or irreversible) estrogen-induced damage to tubular and leydig cells.- - - - - - - - - - ranking = 2keywords = endocrine (Clic here for more details about this article) |
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