Cases reported "Hypogonadism"

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1/12. diabetic ketoacidosis and hypogonadotropic hypogonadism in association with transfusional hemochromatosis in a man with beta-thalassemia major.

    We report a 23-year-old man with beta-thalassemia major and transfusional hemochromatosis, which manifested as diabetic ketoacidosis and hypogonadotropic hypogonadism. This unusual presentation of diabetic ketoacidosis in hemochromatosis has rarely been reported. magnetic resonance imaging of the abdomen showed decreased signal intensity in the liver, spleen, and pancreas. In addition, the pituitary gland also showed heterogeneous low signal intensity, compatible with hemochromatosis. He was treated with insulin supplements and pulsatile human chorionic gonadotropin administration. Clinical improvement was noted after hormone replacement. Intensive iron chelation therapy was given to prevent cardiac complications, and to restore his gonadal function. During follow-up, the patient experienced improvement in libido and sexual potency.
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2/12. Sex steroids and sexual desire in a man with a novel mutation of aromatase gene and hypogonadism.

    sexual behavior was investigated by a sexological interview in a man with aromatase deficiency and hypogonadism. The study was performed at the end of a long testosterone treatment, during transdermal estradiol treatment and during estradiol and testosterone associated treatment. sexual behavior did not show abnormalities. As assessed by a sexological interview and by a sexological questionnaire gender-identity was male, sexual orientation was heterosexual and libido was normal. Sexual function was limited to masturbation and was seemingly unaffected by testosterone or estradiol alone; only the associated treatment induced a great increase in libido and in frequency of masturbation and sexual fantasies when both testosterone and estradiol reached the range of normality. sexual behavior is mainly under the control of cognitive functions in men, but sex steroids may modulate some aspects of male sexuality. Our findings suggest that in men estrogens could play a role in sexual activity.
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keywords = libido
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3/12. testosterone replacement-induced hyperprolactinaemia: case report and review of the literature.

    Half of all men with prolactin (PRL)-producing macroadenomas present with hypogonadism, decreased libido and impotence, and therefore require testosterone replacement. However, very little is known about the effect of testosterone on prolactinomas. We report a case of an 18-year-old obese man who presented with hypogonadism and hyperprolactinaemia and underwent a transphenoidal hypophysectomy after a computer tomography scan showed the presence of a suprasellar macroadenoma. On separate occasions, we documented a rise in PRL when testosterone replacement was started and a fall in PRL when testosterone replacement was stopped (r = 0.6090, P = 0.0095). Furthermore, imaging studies suggested the possibility of tumour re-growth after testosterone therapy. We hypothesize that the exogenous testosterone was aromatized to oestradiol, which stimulated the release of PRL by the anterior pituitary. This was supported by the increase in oestradiol levels after testosterone replacement, although statistical significance was not achieved due to the availability of only a few data points. This case highlights the need to be aware of testosterone-replacement-induced hyperprolactinaemia, an under-recognized complication of androgen replacement in this setting. The use of aromatase inhibitors together with testosterone-replacement therapy or the use of non-aromatizable androgens might be indicated in such patients. Taken together, this report and previous studies show that dopamine agonists apparently do not suppress the hyperprolactinaemia induced by testosterone replacement.
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4/12. Hypogonadotropism with elevated serum testosterone: reversible causes of secondary infertility.

    BACKGROUND: A 33-year-old man presented with secondary infertility, increased libido, and extreme oligospermia. Testicular volumes were reduced, but no gynecomastia was apparent and androgen abuse was denied. INVESTIGATIONS: physical examination, semen-volume and sperm-density assessment, laboratory tests for serum levels of luteinizing hormone, follicle-stimulating hormone, testosterone, and dehydroepiandrosterone sulfate, karyotyping, testicular ultrasound, pelvic and abdominal CT, assessment for serum testicular tumor markers (alpha-fetoprotein and human chorionic gonadotropin), and histologic examination of testicular tissue. diagnosis: Benign Leydig-cell adenoma. MANAGEMENT: Left orchidectomy.
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5/12. Transdermal testosterone treatment of hypogonadal men.

    hypogonadism, either primary or secondary, results in diminished libido and/or impotence. Conventional treatment consists of periodic intramuscular injections (usually bimonthly) of a depot testosterone preparation or daily oral ingestion of methyl testosterone. These conventional treatments may be associated with side effects, such as gynecomastia, liver function abnormalities and edema. A new method of administering testosterone is by daily application of a transdermal therapeutic system. We studied the efficacy and safety of the transdermal therapeutic system in 4 hypogonadal men. Three patients were treated for 12 weeks and 1 for 7 weeks, and they were evaluated weekly. Of 4 patients 3 had improvement in erectile and/or sexual function. Mean plasma testosterone levels increased significantly compared to pre-treatment values during 7 of 12 treatment weeks. There were no adverse effects of the transdermal therapeutic system as indicated by serial physical examinations, daily reports, blood chemistry studies, liver function tests, urinalysis and hematological profiles. This preliminary report of transdermal testosterone delivery indicates that it may provide an effective alternative method of gonadal steroid replacement.
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6/12. Primary hypogonadism associated with o,p' DDD (mitotane) therapy.

    mitotane is a drug which is concentrated largely in adipose tissue and the adrenal glands. It has a remarkable specificity for the adrenal cortex and can produce necrosis of that organ; consequently, it has been used as a therapeutic agent for adrenocortical carcinoma. Because of the similarity between adrenocortical and testicular tissue, mitotane could be expected to cause testicular damage; however, there is sparse support for this in the literature. We recently studied a patient who developed impotency due to primary testicular failure at the time that he was treated with mitotane. A testicular biopsy, performed about four months after the drug was discontinued, showed normal appearing leydig cells and atrophy of the seminiferous tubules with the picture of a maturation arrest. In the four and one half years since he last received mitotane, the patient's libido has slowly improved and his plasma testosterone, gonadotropins and LH response to gonadotropin-releasing hormone have become essentially normal. We propose that mitotane can be cytotoxic to the testis as it is to the adrenal cortex.
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7/12. Hypogonadotropic hypogonadism in hemochromatosis: recovery of reproductive function after iron depletion.

    We studied the effect of iron depletion on reproductive function in a 37-yr-old man with hypogonadotropic hypogonadism due to idiopathic hemochromatosis. Before therapy, he was impotent and had no libido, and seminal fluid analysis revealed no spermatozoa. Testicular biopsy showed marked impairment of spermatogenesis, but no iron load deposits. Sixteen months after institution of aggressive phlebotomy therapy, serum LH, FSH, and testosterone were normal, and potency and libido had returned. Twenty months after diagnosis the patient fathered another child. Seminal fluid analysis at that time revealed an average of 65 million spermatozoa/mL. Thus, recovery of reproductive function, documented by hormone measurements, testicular biopsy, and semen analysis, was complete. We conclude that phlebotomy alone may be adequate treatment for hypogonadotropic hypogonadism in men with hemochromatosis.
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keywords = libido
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8/12. hypogonadism, hyperprolactinaemia, and temporal lobe epilepsy in hyposexual men.

    Previously unrecognised temporal lobe epilepsy (TLE) was diagnosed in 11 of 16 hyposexual men. 6 had neuroendocrine abnormalities (hypogonadism in 4 and hyperprolactinaemia in 2). 4 men with hypogonadism and TLE had persistently subnormal serum testosterone, with a blunted luteinising hormone (LH) response to luteinising hormone releasing hormone (LHRH) in 2 and, in these men, unlike those with isolated hypogonadism, there was no improvement in libido or potency when parenteral testosterone was given. Men with TLE and hyperprolactinaemia had normal serum testosterone and an enhanced serum LH response after LHRH, but effective doses of the dopaminergic agonists, bromocriptine or pergolide, did not produce sustained normoprolactinaemia. In the men with neuroendocrine dysfunction and TLE the most effective therapeutic sequence was first to treat the epilepsy with anticonvulsants and then to add appropriate neuroendocrine therapy. In 2 men hormone levels became normal and sexual function was restored on anticonvulsant therapy alone.
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9/12. Chronic pulsatile low dose GnRH therapy for induction of testosterone production and spermatogenesis in a man with secondary hypogonadotropic hypogonadism.

    Prolonged intermittent treatment with low doses of GnRH was given to a 23-yr-old man with secondary hypogonadotropic hypogonadism. The patient had experienced sudden onset of diabetes insipidus followed by progressive decrease of gonadotropins and gonadal function. Modern radiological techniques did not reveal any organic genesis. A small portable computerized infusion pump connected to a sc catheter was used for the 220-day GnRH therapy. One microgram gnRH was administered every 90 min during the first 90 days and 5 micrograms GnRH every 90 min during the following 130 days. During the prolonged GnRH treatment testosterone secretion normalized, libido and potency improved, and ejaculation returned. spermatogenesis became close to normal and the subject's wife became pregnant after 181 days of treatment. The prolonged treatment with the small infusion pump was well accepted and did not interfere with the patient's daily life activations. Thus, chronic pulsatile low dose GnRH treatment can restore normal pituitary-gonadal function in idiopathic male hypogonadotropic hypogonadism.
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10/12. Effects of preceding androgen therapy on testicular response to human pituitary gonadotropin in hypogonadotropic hypogonadism: a study of three patients.

    There is some uncertainty about the choice of initial therapy to induce virilization in men with hypogonadotropic hypogonadism (HH) who may subsequently desire fertility. Three patients with HH and azoospermia are described. All had received long-term androgen therapy in fully virilizing doses, and two also received interval androgen therapy. spermatogenesis occurred in all three patients after treatment with human chorionic gonadotropin and human pituitary gonadotropin, and the wives of all three conceived. For two patients conception occurred three times in response to gonadotropin therapy, and libido and potency were maintained with testosterone between each conception. It is concluded that preceding long-term therapeutic doses of androgen do not impair subsequent induction of spermatogenesis in patients with HH.
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