RESUMO
Acute hyponatremia, following neurosurgery, results from inappropriate antidiuretic hormone secretion (SIADH) or cerebral salt wasting (CSW). CSW is due to abnormally high atrial or brain natriuretic peptides (ANP, BNP), which block all stimulators of zona glomerulosa steroidogenesis, resulting in mineralocorticoid deficiency. A 3 year-old girl presented CSW at day 4, after resection of craniopharyngioma and hypophysectomy. Hyponatremia, hyperkalemia and high natriuresis occurred on day 8, with low renin and aldosterone and elevated BNP 120.3 ng/ml (undetectable before surgery). Fludrocortisone 100 microg/day controlled natriuresis and restored electrolytes within 24 hours. A 5 year-old boy presented CSW at day 6 after partial resection of optic glioma. Fludocortisone 100 microg/day restored electrolytes within 8 hours. ANP was elevated, 60.6 ng/l, aldosterone and renin were low. Fludrocortisone supplementation should be considered in CSW, as excessive natriuresis is controlled, and electrolytes are easily restored, avoiding life-threatening complications of this complex disorder.
Assuntos
Cérebro/cirurgia , Hiponatremia/diagnóstico , Hiponatremia/etiologia , Mineralocorticoides/deficiência , Complicações Pós-Operatórias/diagnóstico , Complicações Pós-Operatórias/etiologia , Fator Natriurético Atrial/metabolismo , Criança , Pré-Escolar , Craniofaringioma/cirurgia , Eletrólitos/análise , Feminino , Fludrocortisona/administração & dosagem , Humanos , Hiperpotassemia/metabolismo , Hiponatremia/metabolismo , Hipofisectomia , Masculino , Peptídeo Natriurético Encefálico/metabolismo , Neoplasias Hipofisárias/cirurgia , Período Pós-Operatório , Cloreto de Sódio/metabolismoRESUMO
Hypoxia-inducible factor 1 alpha (HIF-1alpha) is a transcription factor that was suggested in vitro to promote cell death by modulation of proapoptotic genes. In this report, we tested the hypothesis of an in vivo proapoptotic role of HIF-1alpha after an ischemic insult. For this purpose, HIF-1alpha and procaspase-3 mRNA and protein expressions were examined in rat brain subjected to 12- and 24-h permanent focal ischemia and the presence of an HIF-1 binding activity to the caspase-3 gene promoter was explored. The results showed that HIF-1alpha and procaspase-3 expressions increased with a similar pattern in response to ischemia. In addition, caspase-3 activation was observed in cells that express HIF-1alpha. Moreover, electrophoretic mobility assay revealed a specific HIF-1 binding activity to the caspase-3 gene promoter. Altogether the present data provide strong arguments for a causative relationship between HIF-1alpha and caspase-3 inductions through a functional binding activity to the caspase-3 gene promoter.
