Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002453 (amenorrhea)
 6,245 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prolactin secretion from the anterior pituitary is mediated via dopaminergic pathways. Any process that alters dopamine production or transport in the central nervous system may lead to hyperprolactinemia. Most cases of hyperprolactinemia are due to prolactin secreting pituitary tumors or to medications which alter dopamine production. Prolactinomas cause amenorrhea, galactorrhea and infertility in women and impotence and neurological deficits in men. Dopamine receptor agonists are the mainstay of therapy for hyperprolactinemia as they rapidly lower serum prolactin and cause tumor shrinkage. In this paper we review the regulation of prolactin secretion, the clinical features and causes of hyperprolactinemia, and the use of dopamine agonists.
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PMID:Pituitary production of prolactin and prolactin-suppressing drugs. 1172 91

Despite increasing sales of gold supplements, and claims of benefits for neurological and glandular conditions, gold has received little attention in modern medical literature except as a drug for rheumatoid arthritis. Historically, however, gold had a reputation as a "nervine," a therapy for nervous disorders. A review of the historical literature shows gold in use during the 19th century for conditions including depression, epilepsy, migraine, and glandular problems such as amenorrhea and impotence. The most notable use of gold was in a treatment for alcoholism developed by Keeley (1897). In the modern medical literature, gold-containing medicines for rheumatoid arthritis are known to have occasional neurotoxic adverse effects. There are also a few studies suggesting a role for gold as a naturally occurring trace element in the reproductive glands. One small recent study demonstrated a possible positive effect of gold on cognitive ability. There is a need for more experimental and clinical research of the neuropharmacology and neurochemistry of gold, and for the exploration of gold's possible role as a trace element.
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PMID:Gold and its relationship to neurological/glandular conditions. 1215 4

Much information has been gathered on the role of human prolactin in both physiological and pathological lactation since it was identified in 1971. Although estrogens increase the number and activity of the prolactin-secreting cells, they block the action of prolactin on the breast. As a result, circulating prolactin levels rise 20-50 fold during pregnancy, but lactation does not start until estrogen levels have fallen after delivery. Prolonged breast feeding maintains high serum prolactin levels. After suckling there is an additional rise. These high serum prolactin levels act to impair fertility by several mechanisms: the ovaries are resistant to gonadotropin stimulation; the frequency of pulsatile pituitary gonadotropin secretion is reduced, and there is suppression of the normal pre-ovulatory gonadotrophin surge in response to rising estradiol levels. The contraceptive effect of lactation has proved unreliable in individual women. Small amounts of prolactin circulate in males and non-pregnant females but have no identified function. Sustained hyperprolactinemia causes galactorrhea and hypogonadism in both sexes: amenorrhea or infertility in females and relative or absolute impotence in males. Sustained hyperprolactinemia is most often the result of a prolactin-secreting pituitary tumor. The management of hyperprolactinemic patients calls for consideration of the endocrine abnormalities and of the pituitary tumor if 1 has been found.
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PMID:Prolactin and gonadal function. 1231 Sep 75

Novel antipsychotics (clozapine, risperidone, olanzapine, quetiapine) are effective in treating psychotic symptoms, also in neurological disease. Hyperprolactinemia is a side effect related to antipsychotics that can cause galactorrhea, gynecomastia, amenorrhea, anovulation, impaired spermatogenesis, decreased libido and sexual arousal, impotence, and anorgasmia, consequent to removal of tonic dopaminergic inhibition of prolactin secretion via hypothalamic dopaminergic receptor blockade in the tuberoinfundibolar tract. Hyperprolactinemia occurs more frequently during treatment with risperidone and olanzapine compared with clozapine and quetiapine. The therapeutic algorithm to antipsychotic-relatedhyperprolactinemia is the following: reduction in antipsychotic dose, addition of cabergoline, bromocriptine, amantadine, and/or switch to another antipsychotic. We propose switching to quetiapine in symptomatic hyperprolactinemia related to antipsychotics and describe five cases.
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PMID:Switch to quetiapine in antipsychotic agent-related hyperprolactinemia. 1252 80

Hyperprolactinemia is one of the most common endocrinological disorders. The main clinical symptoms are limited to hypogonadism, which manifests as fertility disturbances, oligo- or amenorrhea in women, and libido loss, impotence, and fertility disturbances in men, as well as bone density disturbances (osteopenia, osteoporosis) and alactorrhea. Hyperprolactinemia is caused in most cases by drugs or it has an organic etiology (pituitary tumor:--prolactinoma). Differentiation between these two causes is very important for both therapeutic decisions and prognosis. In the medical treatment of a hyperprolactinemic condition dopamine receptors type D2 agonists are used. Such drugs have well-established high therapeutic efficiency (in the vast majority of patients they cause normalization of PRL serum level, tumor shrinkage, and withdrawal of the hyperprolactinemia-related symptoms and tumor mass). This is why they are the first line treatment for prolactinoma. In cases of a lack of pharmacological effect, drug intolerance or resistance, large tumors with accompanying compression symptoms' (tumor mass effect), dynamic tumor enlargement, or if a macroprolactinoma-affected woman desires pregnancy neurosurgery should be considered. Radiotherapy is used mainly as a supplement to surgical treatment.
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PMID:[Hyperprolactinemia: etiology, clinical symptoms, and therapy]. 1576 82

Tardive dyskinesia (TD) may occur in never-medicated patients with psychotic illness, indicating the existence of non-medication, possibly disease-related, causes. We tested the hypothesis that, independent of the antipsychotic-induced rise in prolactin, the incidence of TD would be associated with the incidence of prolactin-related sexual disturbances (PRSD), which would be suggestive of a common pathology involving multiple dopamine tracts. Simple, global measures of TD and PRSD (loss of libido, amenorrhea, gynaecomastia, impotence, and galactorrhea) were rated in a prospective, observational European Health Outcomes Study (SOHO). New onset of TD and new onset of PRSD at 3, 6, and 12 months was analyzed in a risk set of 4263 patients using a Cox proportional hazard model yielding adjusted hazard ratios (aHR). Incidence of TD was significantly and linearly comorbid with the incidence of PRSD in both men and women. Compared to those with no PRSD, the risk for TD was 2.0 (95% CI: 1.1, 3.7) with one PRSD, 2.4 (95% CI: 1.3, 4.5) with two PRSD, and 3.6 (95% CI: 1.1, 11.8) with three PRSD. Associations were stronger in those who only had received prolactin-sparing medications (aHR per unit PRSD increase=2.0, 95% CI: 1.2, 3.3) than in those who only had received prolactin-raising medications (aHR=1.3, 95% CI: 0.9, 1.9). In people with schizophrenia, TD and PRSD show comorbidities that are independent of antipsychotic-induced alterations in plasma prolactin. This may suggest a shared, pandopaminergic pathological mechanism associated with schizophrenia itself, rather than only a medication effect.
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PMID:Tardive dyskinesia in schizophrenia is associated with prolactin-related sexual disturbances. 1648 82

The European SOHO (Schizophrenia Outpatient Health Outcome) study is an observational, naturalistic study of the outpatient treatment of schizophrenia. The patient recruitment and assessment began in September 2000 and finished in early 2005. A total of 10 972 adult patients from ten European countries who were initiating or changing antipsychotic medication for the treatment of schizophrenia within the normal course of care have been enrolled. The patients have been followed at regular intervals over the 3-year timeframe of the study. Evaluation includes clinical severity, measured with the Clinical Global Impression (CGI) scale; health-related quality of life; social functioning; and medication tolerability. The 6- and 12-month results have been published so far and have demonstrated that the patients in whom treatment was initiated with olanzapine or clozapine or who were started on more than one antipsychotic of any class at baseline tended to have somewhat greater improvement than patients treated with other atypical or typical antipsychotics, both in terms of symptoms measured with the CGI and quality of life. Numbers of social contacts increased with the treatment, but other aspects of social functioning did not show any significant change. Atypical antipsychotics as a class were associated with a lower frequency of extrapyramidal symptoms (EPS) and anticholinergic use than typical antipsychotics. The frequency of EPS was lowest in the clozapine-, quetiapine- and olanzapine-treated patients, at around 10%. The atypical antipsychotics also conferred a lower risk for tardive dyskinesia than the typical antipsychotics. Weight gain occurred in all treatment cohorts over the first 12 months of treatment and was statistically significantly greater in the patients who started treatment with olanzapine and clozapine. Prolactin- and sexually-related adverse events were frequent at baseline assessment: amenorrhoea was present in around one- third of women, impotence in around 40% of men, and loss of libido in 50% of both male and female patients. Patients treated with olanzapine, clozapine and quetiapine were significantly less likely to have sexual/endocrine-related dysfunctions after 6 months of treatment (the 12-month results of this parameter are yet to be published) than those in the other treatment cohorts (typical antipsychotics, risperidone and amisulpride). Concomitant medication use during the study has been high, ranging from 5% to 29% for anticholinergics, 8% to 23% for antidepressants, 22% to 37% for anxiolytics and 7% to 19% for mood stabilisers, depending on the type of antipsychotic prescribed. Fewer olanzapine-, quetiapine- and clozapine-treated patients used concomitant anticholinergics or anxiolytics/hypnotics. The current results from the SOHO study indicate that differences in effectiveness and tolerability do exist between the antipsychotics. Future results from the study will be published during the coming months and years, and will allow patterns of antipsychotic use in routine clinical practice (including how often and why changes are made) to be determined. This important information is likely to impact on the future use of antipsychotics and will assist clinicians in refining the use of these drugs and improving the outcome of patients to whom they are prescribed.
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PMID:The SOHO (Schizophrenia Outpatient Health Outcome) study: implications for the treatment of schizophrenia. 1659 47

Hypopituitarism is the partial or complete insufficiency of anterior pituitary hormone secretion and may result from pituitary or hypothalamic disease. The reported incidence (12-42 new cases per million per year) and prevalence (300-455 per million) is probably underestimated if its occurrence after brain injuries (30-70% of cases) is considered. Clinical manifestations depend on the extent of hormone deficiency and may be non specific, such as fatigue, hypotension, cold intolerance, or more indicative such as growth retardation or impotence and infertility in GH and gonadotropin deficiency, respectively.A number of inflammatory, granulomatous or neoplastic diseases as well as traumatic or radiation injuries involving the hypothalamic-pituitary region can lead to hypopituitarism. Several genetic defects are possible causes of syndromic and non syndromic isolated/multiple pituitary hormone deficiencies. Unexplained gonadal dysfunctions, developmental craniofacial abnormalities, newly discovered empty sella and previous pregnancy-associated hemorrhage or blood pressure changes may be associated with defective anterior pituitary function.The diagnosis of hypopituitarism relies on the measurement of basal and stimulated secretion of anterior pituitary hormones and of the hormones secreted by pituitary target glands. MR imaging of the hypothalamo-pituitary region may provide essential information. Genetic testing, when indicated, may be diagnostic.Secondary hypothyroidism is a rare disease. The biochemical diagnosis is suggested by low serum FT4 levels and inappropriately normal or low basal TSH levels that do not rise normally after TRH. L-thyroxine is the treatment of choice. Before starting replacement therapy, concomitant corticotropin deficiency should be excluded in order to avoid acute adrenal insufficiency. Prolactin deficiency is also very rare and generally occurs after global failure of pituitary function. Prolactin deficiency prevents lactation. Hypogonadotropic hypogonadism in males is characterized by low testosterone with low or normal LH and FSH serum concentrations and impaired spermatogenesis. Hyperprolactinemia as well as low sex hormone binding globulin concentrations enter the differential diagnosis. Irregular menses and amenorrhea with low serum estradiol concentration (<100 pmol/l) and normal or low gonadotropin concentrations are the typical features of hypogonadotropic hypogonadism in females. In post menopausal women, failure to detect high serum gonadotropin values is highly suggestive of the diagnosis. In males, replacement therapy with oral or injectable testosterone results in wide fluctuations of serum hormone levels. More recently developed transdermal testosterone preparations allow stable physiological serum testosterone levels. Pulsatile GnRH administration can be used to stimulate spermatogenesis in men and ovulation in women with GnRH deficiency and normal gonadotropin secretion. Gonadotropin administration is indicated in cases of gonadotropin deficiency or GnRH resistance but is also an option, in alternative to pulsatile GnRH, for patients with defective GnRH secretion.
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PMID:Hypopituitarism. 1707 46

SOHO is a 3-year, prospective, observational study of schizophrenia patients who started a new antipsychotic in 10 European countries. Cohorts of patients were defined according to the antipsychotic started at baseline: olanzapine, risperidone, quetiapine, amisulpride, clozapine, oral typical and depot typical antipsychotics. Tolerability in terms of rates of extrapyramidal symptoms (EPS), tardive dyskinesia (TD), anticholinergic use, loss of libido/impotence, amenorrhoea/galactorrhoea/gynaecomastia, and weight change was assessed in 4939 patients who started monotherapy. Logistic regression models related medication initiated at study entry to adverse events over follow-up, adjusting by baseline differences among treatment cohorts. Patients taking typical antipsychotics or risperidone were more likely to experience EPS and TD during follow-up than patients taking olanzapine. Patients taking olanzapine were less likely to have loss of libido/impotence during follow-up than patients in the risperidone, amisulpride, clozapine, oral typical and depot typical cohorts. Weight gain occurred in all groups, but was greater with olanzapine. In conclusion, antipsychotics have different tolerability profiles in terms of the adverse events we monitored. Results should be interpreted conservatively due to the observational study design.
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PMID:Tolerability of outpatient antipsychotic treatment: 36-month results from the European Schizophrenia Outpatient Health Outcomes (SOHO) study. 1950 Sep 49

Reproductive problems, such as delayed menarche, amenorrhea, early menopause, infertility, impotence, hypogonadism, recurrent abortions, and low-birth-weight or preterm deliveries, are now known to be among the atypical symptoms of coeliac disease (CD). The pathogenesis of reproductive disorders in CD is unclear, but some hypotheses have been suggested, including autoimmunity and macro- and/or micronutrient deficiency. Recent investigations which have focused on tissue transglutaminase are promising with respect to the clarification of the mechanism of infertility and poor pregnancy outcomes in CD. In this review, the effects of CD on male and female reproductive disorders and pregnancy outcomes are discussed and the need for CD screening in the case of reproductive problems is emphasized.
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PMID:Coeliac disease and reproductive disorders. 2001 9


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