Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After being suspected in the presence of galactorrhoea, it is now easy to prove hyperprolactinism thanks to radioimmunoassay of prolactin. The repercussions of hyperprolactinism on gonad function are now well known, especially in women where they lead to anovulation then amenorrhoea, whereas in man there occurs hypoandrogenism with loss of libido. Hyperprolactinemia may occur in numerous circumstances and may be deduced logically from the mechanism of secretory regulation of this hormone. Among the latter, one cause dominates the others by its therapeutic consequences, I.e. the presence of an adenoma or microadenoma secreting prolactin discovered thanks to tomography of the sella turcica. The treatment of hyperprolactinism has advanced in recent years with the introduction of dopamineric drugs such as bromcriptin which permits one to normalise prolactinemia and thus restore gonad function. It's use requires however certain precautions and neurological and ophthalmic supervision when htere is a microadenoma.
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PMID:[Hyperprolactinism and antiprolactin drugs]. 19 33

Administration of a dopamine (DA) antagonist, metoclopramide (MCP) resulted in dose-related acute increments of circulating levels of LH and FSH in patients with hyperprolactinemic anovulation due to pituitary microadenoma but not in normal cycling women during the early follicular phase. Concomitant PRL responses to MCP in hyperprolactinemic patients were 1/10 those observed in the cycling women. These findings suggest a relative DA excess at the hypothalamic LRF neurons and a relative DA deficiency at the adenoma lactotroph of hyperprolactinemic patients as compared to cycling women.
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PMID:Effects of a dopamine antagonist on the release of gonadotropin and prolactin in normal women and women with hyperprolactinemic anovulation. 42 15

When the pituitary or hypothalamus becomes resistant to steroid negative feedback, a vicious cycle ensues, resulting in chronic hypersecretion of luteinizing hormone (LH) from the pituitary and steroids from the ovaries. In women, LH hypersecretion is implicated in infertility, miscarriages, and development of granulosa cell tumors. Progress in defining the underlying mechanisms of LH toxicity, however, has been limited by the lack of well-defined animal models. To that end, we have developed a new transgenic mouse model (alpha-LHbetaCTP) wherein LH hypersecretion occurs chronically and results in several dire pathological outcomes. Chronic hypersecretion of LH was achieved by introducing a transgene containing a bovine alpha subunit promoter fused to the coding region of a chimeric LHbeta subunit. The alpha subunit promoter directs transgene expression only to gonadotropes. The LHbeta chimera contains the carboxyl-terminal peptide (CTP) of the human chorionic gonadotropin beta subunit linked to the carboxyl terminus of bovine LHbeta. This carboxyl extension extends the half-life of LH heterodimers that contain the chimeric beta subunit. In intact alpha-LHbetaCTP females, serum LH is elevated five- to ten-fold in comparison to nontransgenic littermates. Levels of testosterone (T) and estradiol (E2) also are elevated, with an overall increase in the T-to-E2 ratio. These transgenic females enter puberty precociously but are anovulatory and display a prolonged luteal phase. Anovulation reflects the absence of gonadotropin-releasing hormone (GnRH) and the inability to produce a pre-ovulatory surge of LH. The ovaries are enlarged, with reduced numbers of primordial follicles and numerous, giant, hemorrhagic follicles. Despite the pathological appearance of the ovary, females can be superovulated and mated. Although pregnancy occurs, implantation is compromised due to defects in uterine receptivity. In addition, pregnancy fails at midgestation, reflecting a maternal defect presumably due to estrogen toxicity. When the transgene is in a CF-1 background, all females develop granulosa cell tumors and pituitary hyperplasia by five months of age. They die shortly thereafter due to bladder atony and subsequent kidney failure. When the transgene is placed in other strains of mice, their ovaries develop a luteoma rather than a granulosa cell tumor and the pituitary develops pituitary hyperplasia followed by adenoma. In summary, alpha-LHbetaCTP mice provide a direct association between abnormal secretion of LH and development of a number of ovarian and pituitary pathological responses.
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PMID:Chronic hypersecretion of luteinizing hormone in transgenic mice disrupts both ovarian and pituitary function, with some effects modified by the genetic background. 1103 34

3 conditions may be responsible for absence of menstruation in women taking the minipill: pregnancy, extrauterine pregnancy, or endometrial atrophy which is the most frequent cause but should be treated only after the other 2 possibilities are excluded. The most frequent cause of pregnancy while taking minipills is error in pill consumption due to forgetting, but malabsorption due to vomiting less than 2 hours after taking the pill or an interaction with some other medication may be responsible. The possibility of extrauterine pregnancy should be systematically considered, and the possibility that a micropill and not a minipill is involved should be ruled out. With a sequential minipill contraceptive efficacy does not reach 100% but iatrogenic amenorrhea is infrequent because of the strong dose of ethinyl estradiol. In the case of a preexisting amenorrhea that does not respond to the estrogen or progestin dose, a prolactin adenoma may be suspected. After 2 consecutive beta tests of pregnancy 8 days apart have been negative, it may be concluded that endometrial atrophy is the cause of the amenorrhea. Unprotected sexual relations should be avoided and the patient should be given a fast-acting combined oral contraceptive such as Lutestral to induce bleeding, after which the minipill can be resumed. If unprotected intercourse occurs there is a risk of pregnancy since amenorrhea and anovulation are not synonymous. A morning after pill can be used if the unprotected sexual relations occurred within the last 72 hours. If a pill was forgotten or probably forgotten before the emenorrhea, the most prudent attitude would be to consider the pill to have been ineffective during the preceding 21 days and to test for pregnancy. Unprotected intercourse should be avoided, a fast-acting combination pill should be prescribed to induce bleeding, and the minipill should then be resumed. Amenorrhea in the 1st month of use after an abortion is not significant. This secondary effect of the minipill should be explained to the patient to avoid unnecessary worry.
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PMID:[Do's and don'ts in treating amenorrhea in women taking the minipill]. 1226 2

Hyperprolactinemia means the presence of abnormally high values of prolactin. It's the most common clinical hypothalamic-hypophysis disorder. Amenorrhea and anovulation are the most usual clinical findings but we can find milder alterations of gonadal function as oligomenorrhea or luteal phase alterations. Galattorrhea appears in approx 30% of patients, but its presence in women with ovulation disorders is highly suggestive of hyperprolactinemia. Subjects with primary amenorrhea and delayed puberty can present hyperprolactinemia. Male hyperprolactinemia can cause hypogonadism (decreased testosterone levels), libido decrease, infertility due oligospermia and gynecomastia while galactorrhea rarely occurs. Accurate anamnesis is very important for a correct diagnosis. It's necessary to exclude pregnancy and primary hypothyroidism. The use of many drugs can be associated with hyperprolactinemia but the most common causes are idiopathic hyperprolactinemia and hypophysis secreting adenoma. Diagnostic examinations are: PRL, FT3, FT4, TSH in case of hypothyroidism, testosterone in men, eventually sampling GH, IGF, ACTH, cortisol, free urinary cortisol. Dynamic tests are used just for idiopathic hyperprolactinemia, but today their meaning is widely discussed. CAT and MNR are necessary to observe hypotalamus, hypophysis and optic chiasm. Twenty years ago the sole option for prolactinoma patients was adenomectomy, today idiopathic hyperprolactinemia can be treated with drugs, while prolactinoma can be treated with a pharmacological, surgical or radiological therapy.
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PMID:[Hyperprolactinemia: from diagnosis to treatment]. 1238 43