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1.
J Neurosurg Sci ; 51(2): 65-9; discussion 68-9, 2007 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-17571037

RESUMO

Apoplexy of a pituitary adenoma is a rare and under-diagnosed clinical occurrence. It results from either infarction or haemorrhage into an adenoma of the pituitary gland. Its clinical presentation more often includes rapid development of impaired consciousness, severe headache, visual disturbance and variable association of oculomotor nerve palsy. Meningeal irritation signs are considered very rare and usually not reported as presenting symptoms. A 33-year-old male suffered a pituitary macroadenoma apoplexy, clinically indistinguishable from an infectious meningitis at presentation. Three days after surgery, the patient developed a left ophthalmoplegia due to 3(rd) nerve palsy, which fully resolved within 2 months. A right pterional craniotomy was performed during which complete tumour removal was achieved. In conclusion the authors believe that, despite many reports in the literature, encouraging conservative management in pituitary apoplexy by administering intravenous steroids, surgery should be undertaken in order to avoid eventual visual field defects, relieve pituitary gland compression and prevent a possible recurrent apoplectic episode or tumor re-growth.


Assuntos
Adenoma/complicações , Meningite/diagnóstico , Apoplexia Hipofisária/diagnóstico , Hipófise/patologia , Neoplasias Hipofisárias/complicações , Doença Aguda , Adenoma/diagnóstico , Adenoma/fisiopatologia , Adulto , Infarto Encefálico/complicações , Infarto Encefálico/etiologia , Infarto Encefálico/patologia , Diagnóstico Diferencial , Cefaleia/etiologia , Humanos , Hidrocortisona/uso terapêutico , Hipopituitarismo/tratamento farmacológico , Hipopituitarismo/etiologia , Hipopituitarismo/patologia , Imageamento por Ressonância Magnética , Masculino , Cervicalgia/etiologia , Procedimentos Neurocirúrgicos/métodos , Doenças do Nervo Oculomotor/etiologia , Apoplexia Hipofisária/etiologia , Apoplexia Hipofisária/fisiopatologia , Hipófise/irrigação sanguínea , Hipófise/cirurgia , Neoplasias Hipofisárias/diagnóstico , Neoplasias Hipofisárias/fisiopatologia , Complicações Pós-Operatórias/etiologia , Tomografia Computadorizada por Raios X , Resultado do Tratamento , Inconsciência/etiologia , Vômito/etiologia
2.
J Neurooncol ; 67(1-2): 77-81, 2004.
Artigo em Inglês | MEDLINE | ID: mdl-15072451

RESUMO

UNLABELLED: Temozolomide a recent, oral, second generation alkylating agent is a chemotherapeutic with demonstrated efficacy for the treatment of high-grade gliomas; its efficacy has been demonstrated in both pre-clinical and phase I and II studies. The goal of this study is to determine the activity and safety of temozolomide in improving overall survival (OS), progression-free survival (PFS) and health-related quality of life (HQL) in patient with malignant gliomas. Forty-two patients with newly diagnosed glioblastoma, anaplastic astrocytoma and anaplastic oligodendroglioma were studied. The mean follow-up period was 12 months. The overall response rate (only responsive patient) for all histological groups was 40%, 10 patients (24%) showed a stabilization of disease. The median PFS and OS was respectively 8.35 and 14.1 months: time to progression was 34 week ranging from 21 to 47. In all patients, treatment with temozolomide was associated with improvement of performance status including the patient showing disease progression: Karnofski score improved in all patients by a minimum of 10, with a median of 20 at 6 months. No patient stopped the treatment due to side-effects, no major adverse events were recorded. CONCLUSION: Temozolomide appears to be an ideal, first-line, single-agent, with a safe profile and demonstrated HQL benefits in patients with high-grade gliomas.


Assuntos
Antineoplásicos Alquilantes/uso terapêutico , Neoplasias Encefálicas/tratamento farmacológico , Dacarbazina/análogos & derivados , Glioma/tratamento farmacológico , Idoso , Antineoplásicos Alquilantes/efeitos adversos , Neoplasias Encefálicas/mortalidade , Dacarbazina/efeitos adversos , Dacarbazina/uso terapêutico , Intervalo Livre de Doença , Feminino , Glioma/mortalidade , Humanos , Masculino , Pessoa de Meia-Idade , Qualidade de Vida , Temozolomida , Resultado do Tratamento
3.
Metabolism ; 48(11): 1351-6, 1999 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-10582540

RESUMO

We studied the effect of acute administration of the calcium-channel blocker verapamil (VER) in 27 patients with tumoral hyperprolactinemia ([THPRL] prolactinomas and pseudoprolactinomas). We also studied the effect of VER in seven patients with idiopathic hyperprolactinemia (IHPRL) and a small group of patients with normal prolactin (PRL) levels and minimal incidental anomalies shown by magnetic resonance imaging (MRI). The study was performed on 2 separate days: on the first day, all subjects received VER, and on the second they received placebo. Acute administration of VER evoked a remarkable increase in serum PRL in IHPRL (as in normal healthy subjects used as controls), but no response was shown in THPRL, with no overlap between the two conditions. Acute administration of VER stimulated PRL secretion in patients with minimal incidental lesions shown by MRI; however, this increase was smaller in patients whose PRL level consistently reached the upper-normal limit. Although the meaning of such minimal anomalies shown by MRI is unknown, this could suggest that the test is precociously altered. To further elucidate the action of VER on lactotropes, we investigated the effect of VER given intravenously (IV) and compared different oral formulations in healthy subjects. Our data show that the VER test is effective in distinguishing between THPRL and IHPRL, but unfortunately, like other tests, it is not able to individualize patients in whom THPRL is the result of diminished dopaminergic tone (pseudoprolactinoma). From a pathophysiological point of view, calcium influx would appear less important in PRL regulation in chronic disorders of PRL secretion. VER given IV did not stimulate PRL release in normal subjects. This suggests that IV administration could produce a peak with an inadequate duration or that oral formulations may act also by metabolites formed on first-pass metabolism in the liver.


Assuntos
Bloqueadores dos Canais de Cálcio/administração & dosagem , Bloqueadores dos Canais de Cálcio/farmacologia , Hiperprolactinemia/sangue , Prolactina/sangue , Prolactinoma/complicações , Verapamil/administração & dosagem , Verapamil/farmacologia , Administração Oral , Química Farmacêutica , Humanos , Hiperprolactinemia/etiologia , Infusões Intravenosas , Prolactinoma/sangue
4.
Minerva Anestesiol ; 55(4): 199-201, 1989 Apr.
Artigo em Italiano | MEDLINE | ID: mdl-2515484

RESUMO

The response of prealbumin was studied in 15 neurosurgical patients following 7 days of enteral nutrition by Nutrisond. Baseline values were compared to day 4 and 7 to assess the degree of change. The prealbumin of day 7 versus baseline value showed a significant increase in the mean serum concentration (16.49 +/- 4.0 vs 19.75 +/- 4.2 mg %). All the patients tolerate well the enteral nutrition with Nutrisond.


Assuntos
Encéfalo/cirurgia , Nutrição Enteral , Alimentos Formulados , Pré-Albumina/metabolismo , Adulto , Idoso , Estudos de Avaliação como Assunto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade
5.
Cancer Genet Cytogenet ; 27(1): 145-59, 1987 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-3472644

RESUMO

Cytogenetic studies on 31 human meningiomas revealed clonal abnormalities in 14 of them. Monosomy 22 was present in three cases as the only abnormality, and in five it was associated with monosomy 18, monosomy 14, loss of X, loss of Y, and trisomy 20, respectively. We found a number of rearrangements involving chromosome #22: an i psu dic(22)(pter----q11::q11----pter) in two cases and a t(18;22)(q12;q11) in another case. Two cases showed a complex translocation involving #7 and #14: t(2;7;14)(q23;q36;q22) and t(1;7;14)(q25;q32;q22), respectively. Other clonal chromosome abnormalities were del(1p) (present in two cases); der(9)t(9;?)(q34;?); der(7)t(7;?)(q31;?); der(22)t(22;?)(q11;?); and a 9p+ chromosome. The relevance for the pathogenesis of human meningiomas of these chromosome anomalies is also discussed with reference to the previous literature. The possible involvement of recessive cancer genes present on the long arm of chromosome #22 is also discussed.


Assuntos
Aberrações Cromossômicas , Genes Recessivos , Neoplasias Meníngeas/genética , Meningioma/genética , Adulto , Idoso , Bandeamento Cromossômico , Feminino , Marcadores Genéticos , Humanos , Cariotipagem , Masculino , Pessoa de Meia-Idade
6.
Minerva Med ; 75(26): 1589-99, 1984 Jun 23.
Artigo em Italiano | MEDLINE | ID: mdl-6738909

RESUMO

Empty sella syndrome is an anatomoclinical condition in which the herniation of the chiasmatic cavities inside the sella turcica causes deformation of the bone and compression of the hypophysis and its peduncle, often in association with neurological and endocrine symptoms. Over the past four years 22 patients with primary empty sella syndrome were studied at Pisa University's Department of Neurosurgery with particular emphasis on clinical and radiological pictures and hypophyseal function. Pneumocisternography and computerised tomography of the cranium and cavities were used to verify the diagnosis. Radiology showed alterations to the sella turcica in all cases, principally sellar enlargement, doubled sellar floor and erosion of the clinoid processes. Many patients were obese hypertensives with a long history of headaches. Most of the women revealed amenorrhoea, oligomenorrhoea or early menopause. The study of hypothalamus and hypophysis function shows endocrine alterations in almost all cases.


Assuntos
Síndrome da Sela Vazia/diagnóstico por imagem , Sistema Hipotálamo-Hipofisário/fisiopatologia , Adolescente , Corticosteroides/sangue , Adulto , Idoso , Androgênios/sangue , Síndrome da Sela Vazia/sangue , Síndrome da Sela Vazia/fisiopatologia , Estrogênios/sangue , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Neuro-Hipófise/fisiopatologia , Hormônios Tireóideos/sangue , Tomografia Computadorizada por Raios X
7.
Surg Neurol ; 20(5): 373-8, 1983 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-6635925

RESUMO

An unusual case of pituitary metastasis from renal cell carcinoma mimicking an adenoma is reported. Panhypopituitarism and chiasmal compression were the first manifestations of the tumor. The clinical, endocrinologic, and pathologic features of pituitary carcinomatous metastasis are discussed.


Assuntos
Adenocarcinoma/secundário , Neoplasias Renais/diagnóstico , Neoplasias Hipofisárias/secundário , Adenocarcinoma/diagnóstico , Adenocarcinoma/metabolismo , Adenocarcinoma/patologia , Humanos , Masculino , Pessoa de Meia-Idade , Hormônios Hipofisários/metabolismo , Neoplasias Hipofisárias/diagnóstico , Neoplasias Hipofisárias/metabolismo , Neoplasias Hipofisárias/patologia
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