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)

We report a 27-year-old woman with a non-Hodgkin lymphoma in the central nervous system (CNS), showing monoparesis of the right upper extremity during treatment for the galactorrhea amenorrhea syndrome. The MRI demonstrated an infiltrative lesion with an obvious gadolinium-enhancement effect, extending from the pituitary stalk and hypothalamus through the 4th ventricle to the dorsal part of the medulla and upper cervical spinal cord. Because no tumors were detected in any other organ in either a physical examination or radiological investigations, including CT for the chest and abdomen, she was diagnosed as having primary CNS non-Hodgkin lymphoma (B cell origin) on the basis of an open brain biopsy. After the irradiation of the whole brain, followed by chemotherapy (methotrexate + CHOP), the infiltrative tumor disappeared on the MRI with a slight improvement for monoparesis of the right upper extremity. In this patient, primary CNS lymphoma might originate around the hypothalamus and infiltrate the medulla, inducing not only monoparesis of the right upper extremity but the galactorrhea amenorrhea syndrome.
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PMID:[A case of non-Hodgkin lymphoma in the central nervous system, developing during treatment of galactorrhea amenorrhea syndrome]. 1068 43

Lymphocytic hypophysitis is a very unusual disease typically observed in the peripartum period but found also in non-pregnant women or in men. We report the case of a 50-year-old woman with a five-year history of erithema nodosus for which was treated with variable doses of steroids. One year before admission the patient began to complain of headache, amenorrhea and rapidly progressive hypopituitarism. Magnetic resonance imaging showed an expanding sellar mass with homogeneous contrast enhancement while lacking the hyperintense signal of posterior lobe. The MRI findings and the history of autoimmune disease raised the suspicion of hypophysitis. The growth of the lesion and its unresponsiveness to the prolonged steroid therapy made surgery, which is both diagnostic and therapeutic, mandatory. The pathogenesis, diagnosis and management of this unusual clinical condition are discussed.
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PMID:Lymphocytic hypophysitis. Case report. 1081 89

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

In 3 studies brain maturation in 42 preterm infants with no or minor cerebral deviations was examined with MRI. With a scoring system 5 stadia in gyral development were recognized, which corresponded to the gestational age (duration of amenorrhoea of the pregnant woman). At a gestational age between 30 and 34 weeks, myelin was present in many brain stem, diencephalic and cerebellar structures, but only in a few hemispheric structures. Little progress in myelination was noticed up to the gestational age of 46 weeks. Remnants of the germinal matrix formed a sharp contrast with the immature unmyelinated periventricular white matter and had a characteristic appearance on MR images before term age. Broad periventricular zones with subtle change of signal intensity were also physiological in this age group. Zones with more outspoken signal intensity change compared with the rest of the cerebral white matter were, however, not physiological and represent mild ischaemic change of the periventricular white matter.
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PMID:[Diagnostic imaging of brain maturation in premature infants]. 1125 95

We report the case of a 15-year-old girl with amenorrhea and a several-week history of headache. After the diagnosis of membranous obstruction of the foramen of Magendie suggested by MRI, suboccipital craniotomy for removal of the membrane was carried out. The patient made an excellent postoperative recovery, and postoperative phase-contrast MRI demonstrated patent cerebrospinal fluid (CSF) pathways at the level of the foramina of Magendie and Luschka. We believe that this case is of interest because of the unequivocal evidence on MRI studies of the occlusion of the foramen of Magendie preoperatively, and because of the dramatic postoperative MRI findings demonstrating the effectiveness of the surgical procedure both in terms of ventricular size and CSF flow characterization.
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PMID:Membranous obstruction of the fourth ventricle outlet. A case report. 1149 Jan 91

A 32-year-old woman presented with a 10-day history of fever (38.0 degrees C), headaches, nausea, vomiting and a 6-month history of diabetes insipidus and amenorrhoea. Two months previously she had undergone a surgical drilling of the right mastoid area because of mastoiditis. Endocrine investigation showed elevated serum prolactin levels, secondary adrenal and gonadal failure and a normal thyroid function. Cranial MRI scan revealed a contrast enhancing intrasellar mass (approximately 2 cm) of heterogeneous appearance with suprasellar extension and thickening of the pituitary stalk. Lumbar puncture was suggestive of aseptic meningitis. The Ziehl-Neelsen stain of cerebrospinal fluid (CSF) and the tuberculin skin test were both negative. The pituitary mass was removed with a transsphenoidal approach. Histological examination demonstrated destruction of the adenohypophysis by epithelioid granulomas with partial caseous necrosis and microabscess formation, suggestive of a mycobacterial infection. A polymerase chain reaction analysis performed on paraffin-embedded tissue was positive for mycobacterial DNA. According to the individual 16S sequence, it was identified as Mycobacterium malmoense, an atypical nontuberculous mycobacterium (NTM). In conclusion, this is the first case of an isolated pituitary granuloma caused by an NTM infection in a nonimmunosuppressed patient.
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PMID:Isolated pituitary granuloma by atypical Mycobacterium in a nonimmunosuppressed woman. 1184 56

Female genital tract anomalies are common (1 to 2% of the female population), and may lead to multiple clinical manifestations: amenorrhea, infertility, spontaneous repeated miscarriage, pelvic pain, endometriosis. They are caused by intra-uterine insults between weeks 6 and 18 of gestation. They are classified according to their embryologic origin. Imaging relies essentially on ultrasound and MRI, and indications for hysterosalpingography are less common. Imaging must classify the malformation and detect complications in order to assess the fertility prognosis and treat complications.
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PMID:[Imaging of gynecologic malformations]. 1191 48

We report successful operations for a meningeal hemangiopericytoma using sufficient amounts of Preoperative Autologous Transfusion (PAT) and Hemodilutional Autologous Transfusion (HAT). A 23-year-old woman with amenorrhea and bilateral visual field disturbance was found to have a huge intracranial tumor. MRI showed a well-enhanced cystic mass in the left middle fossa, suprasellar, intrasellar, sphenoidal sinus, and cavernous sinus. Preoperatively, the tumor was thought to be a cystic pituitary tumor or meningioma. Surgical removal was planned in three steps. The first operation was carried out via the transsphenoidal approach. Total blood loss was 1348 ml and 2 MAP infusion were required to control bleeding. Histopathological diagnosis was hemangiopericytoma. After preparation of PAT 400 ml and HAT 800 ml, we carried out the second partial removal operation mainly via the interhemispheric approach. Total blood loss was 1829 ml and required autologous transfusion only. After preparation of PAT 1200 ml and HAT 400 ml, the last total removal operation was carried out mainly via the pterional and subtemporal approach. Total blood loss was 1813 ml and required autologous transfusion only. We needed 2 MAP infusion in the first operation, but were able to perform total removal successfully without homologous blood transfusion because a sufficient amount of PAT and HAT had been prepared preoperatively. Hemangiopericytoma required postoperative radiation therapy to avoid local recurrence. After successful removal of the tumor surgically, postoperative radiation therapy was able to be carried out efficiently.
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PMID:[Successful treatment of a huge meningeal hemangiopericytoma using Preoperative Autologous Transfusion and Hemodilutional Autologous Transfusion: case report]. 1209 90

The involvement of the hypothalamus and/or pituitary gland by granulomatous, infiltrative or autoimmune diseases is a rare condition of non-tumoral-non-vascular acquired hypothalamic dysfunction and hypopituitarism. In this paper, we present the case of a 26-year-old woman, who showed an amenorrhea-galactorrhea syndrome with hypogonadotropic hypogonadism due to an isolated hypothalamic-peduncular localization of neurosarcoidosis. Acquired GH deficiency was also demonstrated. This clinical case provided the opportunity for a review of the endocrine aspects linked to brain infiltrative diseases that may affect the hypothalamic-pituitary function, with a focus upon neurosarcoidosis. Sarcoidosis is a pathogen-free granulomatous disease that affects both the central and peripheral nervous system in 5-16% of patients. In most cases, such involvement by sarcoidosis occurs within a multi-systemic disease, but disease localization limited to the nervous system may also be observed. Endocrine manifestations of neurosarcoidosis disclose "chameleon-like" clinical pictures, which are usually expressed by the evidence of hypothalamic dysfunction, diabetes insipidus, adenopituitary failure, amenorrhea-galactorrhea syndrome, in isolated fashion or variedly combined. More rarely, inappropriate anti-diuretic hormone secretion, isolated secondary hypothyroidism, adrenal insufficiency or altered counter-regulation of glucose homeostasis have been reported. Neurosarcoidosis is often hard to diagnose, especially when the neurological localization of the disease is not accompanied by other systemic localizations or by specific signs of the disease, and when the lesion is too deep to obtain bioptic confirmation. The study of cerebrospinal fluid and blood lymphocyte sub-populations, integrated by MRI and nuclear scans (67GalIium uptake and 111Indium-pentetreotide, Octreoscan), may be helpful for a correct diagnosis. Therapy with corticosteroid and immunosuppressive drugs, such as cyclosporine A, and other treatment approaches to neurosarcoidosis are also accounted for.
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PMID:Endocrine aspects of neurosarcoidosis. 1215 Mar 44

Mitoxantrone (Novantrone), a synthetic anthracenedione derivative, is an antineoplastic, immunomodulatory agent. Its presumed mechanism of action in patients with multiple sclerosis (MS) is via immunomodulatory mechanisms, although these remain to be fully elucidated. Intravenous mitoxantrone treatment improved neurological disability and delayed progression of MS in patients with worsening relapsing-remitting (RR) [also termed progressive-relapsing (PR) MS] or secondary-progressive (SP) disease. In a pivotal randomised, double-blind, multicentre trial, mitoxantrone 12 mg/m(2) administered once every 3 months for 2 years provided significant improvements in neurological disability ratings, including Kurtzke Expanded Disability Status Scale (EDSS), Ambulatory Index (AI) and Standardised Neurological Status (SNS) scores, compared with placebo. The drug also significantly reduced the mean number of corticosteroid-treated relapses and prolonged the time to the first treated relapse, with the beneficial effects on disease progression supported by magnetic resonance imaging. Post hoc analyses suggest that the benefits associated with mitoxantrone treatment may be sustained for at least 12 months after cessation of treatment, mean changes from baseline at 36 months in EDSS, AI and SNS scores of 0.10, 0.61 and 0.19, respectively, in the mitoxantrone group versus 0.46, 1.13 and 3.38 with placebo. Concomitant intravenous mitoxantrone 20mg plus intravenous methylprednisolone 1g once every month for 6 months was more effective than intravenous methylprednisolone monotherapy in preventing the development of new gadolinium-enhanced lesions in patients with very active RRMS or SPMS. The drug was generally well tolerated in patients with MS. Adverse events were generally mild to moderate in severity and usually resolved upon discontinuation of treatment or with appropriate pharmacotherapy. At the recommended dosage, mitoxantrone appears to have a low potential to cause cardiotoxicity. In conclusion, intravenous mitoxantrone reduces the relapse rate and slows progression of the disease in patients with worsening RRMS, PRMS or SPMS; thus providing a new option for the management of these patients. The drug was generally well tolerated at the recommended dosage, although potential cardiotoxicity limits the total cumulative dose to 140 mg/m(2). Further studies are warranted to determine which patients with worsening RRMS, PRMS or SPMS are most likely to benefit from mitoxantrone treatment and to more fully define the long-term safety and tolerability of mitoxantrone, including the use of concomitant cardioprotectants to extend the therapeutic lifespan of the drug. Pharmacodynamic Profile. Mitoxantrone, a synthetic anthracenedione derivative, is an established cytotoxic, antineoplastic agent. Its presumed mechanism of action in multiple sclerosis (MS) is immunosuppression. In antineoplastic studies, the drug showed several immunomodulatory effects, inducing macrophage-mediated suppression of B-cell, T-helper and T-cytotoxic lymphocyte function. Currently, the pharmacodynamic properties of mitoxantrone have not been investigated to any extent in patients with MS. In one study, 6 months' treatment with intravenous mitoxantrone generally had no effect on the distribution of cytokine-positive peripheral blood monocyte cells in patients with MS. In an animal model of the disease, mitoxantrone suppressed the development and progression of both actively and passively induced acute experimental allergic encephalomyelitis (EAE). It appeared to be 10-20 times more effective than cyclophosphamide in the suppression of EAE. Moreover, mitoxantrone approximately doubled the mean time to onset of EAE versus control animals (279 vs 148 days after immunisation; p < 0.00005). In vitro, mitoxantrone 10 and 100 micro g/L inhibited myelin degradation by leucocytes and peritoneal macrophages derived from mice with acute EAE by approximately 60% and 100%. Pharmacokinetic Profile. Currently, there are no published pharmacokinetic data for intravenous mitoxantrone in pitoxantrone in patients with MS, paediatric patients or in those with renal impairment. All studies, to date, have been in patients with cancer receiving a single, approximately 30-minute intravenous infusion of mitoxantrone 5-14 mg/m(2). The drug exhibits triexponential pharmacokinetics, with a rapid initial distribution (alpha) phase, an intermediate distribution (beta) phase and a much slower elimination (gamma) phase. The mean half-life of the alpha phase appears to be 6-12 minutes and that of the beta phase 1.1-3.1 hours. Mitoxantrone has a high affinity for tissue, with a volume of distribution of up to 2248 L/m(2). Mitoxantrone persists for prolonged periods in tissues and was detectable in autopsy tissue from patients who last received the drug up to 272 days before death. At concentrations of 10-10000 ng/mL, the drug was 70-80 % bound to plasma proteins in dogs. Elimination of mitoxantrone occurs predominantly through biliary excretion and may be impaired in patients with hepatic dysfunction or third space abnormalities (e.g. ascites). The mean terminal elimination half-life of mitoxantrone ranged from 23 hours to 215 hours. Renal clearance accounts for 10 % of the total clearance of the drug. Total clearance of mitoxantrone ranged from 13 to 34.2 L/h/m(2) and renal clearance from 0.9 to 2.7 L/h/m(2). The drug appears to have a low potential for interaction with other concomitantly administered agents. Therapeutic Efficacy. Intravenous mitoxantrone (infusion of > or = 5 minutes), either as monotherapy or in combination with intravenous methylprednisolone, delayed the progression of the disease in patients with secondary-progressive (SP) or worsening relapsing-remitting (RR) MS (the latter is also termed progressive-relapsing MS) in comparative, randomised, multicentre trials. In a double-blind, monotherapy trial (Mitoxantrone In Multiple Sclerosis [MIMS] trial), mitoxantrone 12 mg/m(2) (n = 60) once every 3 months for 2 years significantly improved neurological disability relative to placebo (n = 64), as assessed by changes in mean Kurtzke Expanded Disability Status Scale (EDSS) score, mean Ambulatory Index (AI) score and mean Standardised Neurological Status (SNS) score. The drug also significantly reduced the mean number of corticosteroid-treated relapses per patient and prolonged the time to the first treated relapse. A Wei-Lachin multivariate analysis of these five efficacy variables indicated that the global difference between the two treatment groups was 0.30 (p < 0.0001). Mitroxantrone was also more effective than placebo according to secondary endpoints in this study, with fewer mitoxantrone recipients experiencing a relapse, a deterioration of > or =1 EDSS point or a confirmed deterioration in EDSS score over a 3-month period. Mitoxantrone recipients also showed less deterioration in quality-of-life ratings and had fewer hospital admissions, whereas more placebo recipients had new gadolinium-enhanced lesions at study end (the latter parameter was assessed using magnetic resonance imaging [MRI] in a subgroup of 110 patients, including 40 patients who received an exploratory 5 mg/m(2) dose). Furthermore, post hoc analyses indicated that the beneficial effects of mitoxantrone treatment on EDSS, SNS and AI scores were sustained for at least 12 months after cessation of treatment, with mean changes from baseline at 36 months in EDSS, AI and SNS scores of 0.10, 0.61 and 0.19, respectively, in the mitoxantrone group versus 0.46, 1.13 and 3.38 with placebo. Preliminary data from a cost-minimisation analysis based on results from the MIMS trial indicated that approximately half of the cost of mitoxantrone was offset by cost savings in other areas associated with the treatment of MS (direct and indirect major costs), with a total annual incremental cost for mitoxantrone of dollar 1661 per patient. Combination therapy once-monthly with intravenous mitoxantrone 20mg plus intravenous methylprednisolone 1g was more effective than intravenous methylprednisolone 1g once every month in preventing the development of gadolinium-enhanced lesions in patients with very active RRMS or SPMS (double-blind assessment using MRI scans). After 6 months, significantly more combination therapy recipients had no new gadolinium-enhanced lesions (90.5% vs 31.3% with monotherapy; p < 0.001) [primary endpoint]. There were also significant reductions in both the mean number of new enhancing lesions and the total number of gadolinium-enhanced lesions in patients receiving combination therapy versus methylprednisolone monotherapy.Tolerability. Mitoxantrone was generally well tolerated in patients with MS. Treatment-emergent adverse events occurring significantly more frequently with mitoxantrone (12 mg/m(2) once every 3 months for 2 years) than placebo were nausea, alopecia, menstrual disorders, urinary tract infection, amenorrhoea, leucopenia and elevated gamma-glutamyltranspeptidase levels. Adverse events were usually mild to moderate in severity and generally resolved with discontinuation of treatment or when treated with appropriate pharmacotherapy. Eight percent of patients discontinued treatment in the mitoxantrone 12 mg/m(2) group due to an adverse event versus 3% of placebo recipients. The incidence of drug-related acute myelogenous leukaemia was very low (0.12%) in a cohort of 802 patients with MS receiving mitoxantrone. Evidence suggests that the risk of cardiotoxicity is low in patients with MS. After 1 year of monotherapy, 3.4% of mitoxantrone recipients had a reduction in left ventricular ejection fraction (LVEF) to < or =50% compared with 0% of placebo recipients; at the end of the second year, respective incidences were 1.9% and 2.9% (total cumulative dose of mitoxantrone per patient was 96 mg/m(2) after 2 years' treatment). (ABSTRACT TRUNCATED)
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PMID:Mitoxantrone: a review of its use in multiple sclerosis. 1508 10


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