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)

RIA and rosette formation were employed to measure the content of prolactin and lymphocyte populations in the blood of 26 men and 36 women suffering from multiple sclerosis (MS). Hyperprolactinemia was discovered to be attended by a decline of the T lymphocyte count, whereas hypoprolactinemia was marked by the impairment of the ratio of active to total "rosettes". In addition, 16 MS women suffering from persistent galactorrhea-amenorrhea and 40 parturients and lactating women with MS were examined with a special purpose in view. A relationship was demonstrated between exacerbation and development of MS and the status of ++immuno-endocrine regulation.
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PMID:[Pathogenetic role of prolactinemia in multiple sclerosis]. 180 Dec 24

Interviews on changes in the menstrual cycle were taken from 38 women of fertile age, several years after immunosuppressive treatment (IS) with prednisone and cyclophosphamide (CP) for definite multiple sclerosis (MS). Serum FSH, LH and 17-beta-oestradiol levels were determined at the time of interview. MS in itself did not change the experience of menstrual cycles; 17 patients developed hypergonadotrophic amenorrhea during or after IS. Symptoms related to climacterium (c. q. flushing) were present in 15 of these patients. The onset of amenorrhea depended on the age at the time of IS and on the cumulative dose of CP. Older patients developed amenorrhea at a lower cumulative dose of CP than did younger patients. High estrogen oral contraceptives are advocated in oncology to prevent disturbance of ovarian function by anti-mitotic treatment. This policy is advisable in female MS patients treated with drugs like CP or azathioprine.
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PMID:Amenorrhea after immunosuppressive treatment of multiple sclerosis. 312 Apr 88

This article deals with the use of oral contraceptives and IUDs by chronically ill adolescent females. Results of controlled studies of contraceptive choices and problems are reviewed for teenagers with cardiac disease, epilepsy, multiple sclerosis, migraine headaches, asthma, cystic fibrosis, inflammatory bowel disease, hepatitis, diabetes mellitus, thyroid disease, oligomenorrhea and amenorrhea. If oral contraceptives (OC) are prescribed for use in teens with cardiac disease, a contraceptive with 35ug or less of estrogen and the equivalent of 1 mg or less of norethindrone should be used. The low-dose progestin only pill can be prescribed, but should be used in conjunction with a back-up barrier method. Reports to date have failed to reveal increased seizure activity in epileptic pattients on OCs, and there is no significant evidence to date that OCs alter the course of multiple sclerosis. Although the evidence is inconclusive, the physician should use extreme caution in prescribing OCs for teens with prior migraines. Regarding asthmatic patients, no problems have been reported with IUD use except in regard to steroid therapy and its possible effect on reducing IUD effectiveness. No adverse effects 2ndary to the use of OCs in asthmatic patients have been reported. OCs should be avoided or used with extreme caution in the cystic fibrosis patient. Teens with active inflammatory bowel disease should be advised that OCs may be ineffective or dangerous; there are no reports available on the effects of the IUD on the disease. The pill is contraindicated during active liver disease or cirrhosis. The IUD is not highly recommended for contraception in diabetic teenagers, whereas a low-dose combined OC can be used with extreme caution. However, OCs should be avoided in the diabetic patient with nephropathy, vascular complications or retinopathy. There is at present no contraindication for contraceptive use by women with thyroid disease. Finally, patients with prolonged post pill amenorrhea and infertility are generally females with amenorrhea or oligomenorrhea before pill use.
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PMID:Contraceptive use in the chronically ill adolescent female: Part I. 351 58

Changes in sexual function in 47 women with advanced multiple sclerosis are described. Twenty eight (59.6%) of the women reported decreased sexual desire. Seventeen (36.2%) reported decreased lubrication. Five (10.6%) others did not know if they lubricated or not. Eighteen women (38.3%) reported diminished orgasmic capacity and six (12.8%) others had never had an orgasm. Sensory dysfunction in the genital area was experienced by 61.7% of the women and 76.6% had weakness of the pelvic muscles. Sixty six per cent had bowel problems and 89.4% had bladder dysfunction. The changes in sexual function correlated both with neurological symptoms from the sacral segments, such as weakness of the pelvic floor and bladder and bowel dysfunction, and to other symptoms such as ataxia and vertigo as well as with age and the occurrence of amenorrhoea. A significant correlation was found between expanded disability status scale (EDSS) score and cohabitation. Problems with sexual function were reported significantly more often by women with lower EDSS scores. Most women (83%) found the interview a positive experience.
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PMID:Sexual function in women with advanced multiple sclerosis. 760 15

Following a report of the efficacy of total lymphoid irradiation (TLI) in the treatment of chronic progressive multiple sclerosis a further randomised double-blind placebo-controlled study was undertaken with the intention of entering 56 patients. In the event it was possible to recruit only 27 patients in a 2.5 year period. Three patients received active treatment openly and 24 were randomised to either active (14) or sham (10) treatment. Treatment was 1980 cGy to the lymphoid system and spleen or sham treatment after full simulation. The primary outcome measure was a comparison of the mean rates of change between treatment groups on the expanded Kurtzke disability scale (EDSS) over the two year follow up period. Patients were also assessed on other clinical outcome measures, psychometry, and serial MRI of the brain. Active treatment resulted in a profound and prolonged fall in T lymphocytes especially those with the CD4 marker and a reversal in CD4:CD8 ratio. No significant benefit was demonstrated on the rate of clinical disease progression (EDSS). A small but significant benefit was found on a score of bladder function. No significant benefit was demonstrated on other clinical or psychometric indices or on subjective visual analogue scales. There was a small but significant difference in the rate of accumulation of lesions on brain MRI favouring the treatment group. The treated group had a higher incidence of clinically relevant side effects, notably amenorrhoea and infections: three deaths (one in the TLI group, two in the sham treated group) occurred. A post hoc calculation indicates that the study had a possible 35% risk of a false negative result using the principal outcome measure. The study fails to confirm the previously reported clinical benefit of TLI although there may be a minor benefit on disease progression as indicated by MRI lesion counts. It is concluded that TLI cannot be recommended for the routine treatment of chronic progressive multiple sclerosis but the beneficial effect on MRI lesions, though modest, suggests that further research into immune modulation of this condition may be worthwhile.
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PMID:Total lymphoid irradiation in multiple sclerosis. 812 97

It has long been suspected that hormonal factors contribute directly and indirectly to the etiology and pathogenesis of multiple sclerosis (MS). The susceptibility of MS is higher in women than in men and women are even more susceptible to hormonal influences when onset occurs at an early or delayed age. Pregnancy has a short-term favorable effect on the course of the disease but there is an increased rate of relapse during the post-partum period. In addition, women often report premenstrual exacerbation of their symptoms with remission during menses. These findings suggest that in women estrogens may exert a stabilizing effect on the clinical manifestations of MS. The role of estrogens is supported also by observations of a higher incidence of cognitive impairment in women than men with MS. A 50 year old woman with a remitting progressive MS experienced profound deterioration in cognitive functions during withdrawal from estrogen therapy which was initiated for the treatment of amenorrhea. Improvement in cognitive functions occurred shortly after she restarted therapy with an estrogen/progesterone preparation and was maintained during long term therapy. Serotonin (5-HT) mechanisms have been implicated in memory functions and estrogens modulate these functions through an interaction with 5-HT2 receptors in the cerebral cortex and limbic system. It is suggested that estrogen withdrawal induces impairment in cognitive functions through dysregulation of 5-HT2 receptor activity and 5-HT neurotransmission. These findings suggest that estrogens have a beneficial influence on cognitive functions in MS patients and that hormonal supplementation might be advised in menopausal and postmenopausal MS patients for the prevention of cognitive deterioration.
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PMID:Estrogen's impact on cognitive functions in multiple sclerosis. 882 57

Patients with multiple sclerosis sometimes show subthalamic lesions presenting syndrome of inappropriate secretion of ADH (SIADH), hypothermia, hyperprolactinemia, weight loss, and cachexia. Hyperprolactinemia also has been found in the patients with active systemic lupus erythematosus, because prolactin can be produced from human activated lymphocytes. We described a case of multiple sclerosis showing galactorrhea-amenorrhea syndrome with hyperprolactinemia. A 31-year-old woman showed a high level of prolactin in the serum (79.6 ng/ml) during remission stage 5 months after the onset of multiple sclerosis. She showed galactorrhea-amenorrhea syndrome 3 years later. She showed dysesthesia in her limbs, relapsing monoparesis, visual disturbance and Gd-enhanced plaques in Brain MRI for 6 years. She was admitted to our hospital on November 24, 1995. A neurological examination showed hyporeflexia of the upper extremities, hyperreflexia of the lower extremities, bilateral ankle clonus, truncal ataxia, and neurogenic bladder. Laboratory tests revealed increased level of serum prolactin, exaggerated secretion of serum prolactin after intravenous injection of 500 micrograms TRH, and marked suppression after oral administration of 2.5 mg bromocriptine. Brain MRI showed demyelinating lesions near the lateral ventricle, and cervical MRI (T2 image) showed high signal intensity lesions in the spinal cord from C2 to C5. In the previous case, galactorrhea-amenorrhea syndrome was found during the exacerbation stage of multiple sclerosis. Hyperprolactinemia may be caused from subthalamic lesions or by activated lymphocytes in multiple sclerosis. We considered that hyperprolactinemia and galactorrhea-amenorrhea syndrome in our patient might be caused from subthalamic lesions because lymphocytes were not activated during the remission stage of multiple sclerosis.
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PMID:[A case of multiple sclerosis with galactorrhea-amenorrhea syndrome]. 936 74

We present a 31-year-old woman of multiple sclerosis. At age 28, she was admitted with complaints of echolalia and a gradual onset of weakness affecting the right upper and bilateral lower limbs. Brain MRI showed high intensity areas in the bilateral frontal gyri, lobuli paracentralis, and left anterior thalamus. Although she had been in remission for 3 years, she developed dysesthesia of left upper and lower limbs. Cervical T2 weighted MRI showed a new high signal intensity lesion in the spinal cord from the C2 to C3 level. The combination of the cerebral, thalamic and spinal cord lesions with remission and excerbations allowed the diagnosis of clinically MS to be made. She suffered amenorrhea from the onset of her illness. Serum prolactin was within the normal range. The LH and FSH basal secretions were decreased and there were low delayed secretions of LH and FSH after intravenous injection of 100 micrograms LHRH. We consider that her amenorrhea was caused by the hypothalamic lesion, supported by MR findings of dilatation of the third ventricle.
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PMID:[A case of multiple sclerosis with hypothalamic amenorrhea]. 1088 39

A mild prevalence of multiple sclerosis (MS) is present in females (2:1). To elucidate the pathogenetic role of sex steroids on the disease, we studied 76 women affected by MS, compared to 50 healthy women (mean age +/- SD, 34.9 +/- 0.9 vs. 33.4 +/- 1.7 years). The menarche was at mean age of 12.3 +/- 0.2 vs. 12.4 +/- 0.2. Interval between menses was 28.0 +/- 0.3 vs 27.8 +/- 0.3 days, with duration of menstrual flow of 5.0 +/- 0.2 vs. 5.0 +/- 0.2 days. Oligo- or amenorrhea was present in 20% of patients and in 16% of controls. Oral contraceptives were assumed by 21% of patients and 34% of controls (n.s.). Premenstrual symptoms were found in 43% of patients and in 46% of controls (n.s.). The incidence of hyperandrogenism (greasy skin, acne and hirsutism), evaluated by a specific questionnaire, was higher and statistically significant in MS patients than in controls (28% vs. 10%, p<0.05). Further studies, including a complete clinical and laboratory evaluation of gonadal function, are necessary in order to clarify whether hyperandrogenism may influence MS disease activity.
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PMID:High incidence of hyperandrogenism-related clinical signs in patients with multiple sclerosis. 1152 31

Mitoxantrone (MX) has been approved by the Food and Drug Administration (FDA) for the treatment of patients with worsening relapsing-remitting (RR) or secondary progressive (SP) multiple sclerosis (MS). However, indications should be refined and mitoxantrone reserved as a rescue therapy to: (1) patients in the relapsing-remitting phase with frequent and disabling exacerbations likely leading to permanent severe disability and (2) to patients in the secondary progressive phase whose disability progression rate increases by one EDSS point or more per year and who do not respond to other current therapies. An induction phase with the monthly intravenous administration of 12 mg/m(2) followed by a maintenance phase with 12 mg/m(2) every 3 months for 2 years seems the most effective and safe treatment regimen, not exceeding the maximum cumulative dose of 140 mg/m(2). Given the potent myelosuppressive activity of mitoxantrone, dosage should be carefully adapted to the body surface and hematological changes. Long-term toxicities (amenorrhoea and therapy-related leukemia) seem acceptable but a valid evaluation will need a longer follow-up in more patients. Cardiotoxicity, the major long-term toxicity, is clearly dose-dependent and is a strict treatment duration limiting factor. To reduce the risk of cardiac events, the drug should be administered by slow infusion (over 30 min). Analogs of mitoxantrone with a much lower cardiotoxicity are currently investigated in animal experimental models.
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PMID:Mitoxantrone in progressive multiple sclerosis: when and how to treat? 1255 12


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