Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of a large empty sella was reported, which was intrasellar herniation of the third ventricle associated with a prolactinoma. The patient was a 46-year-old female admitted due to consciousness disturbance with pyrexia and vomiting. She had amenorrhea, galactorrhea and sterility in her past history. On admission, physical and neurological examinations revealed severe dehydration, systemic edema, systemic hypotension, nuchal rigidity, papilloedema and goiter. A spinal tap was performed and revealed an increase in CSF pressure. Laboratory data indicated CSF lymphocytosis, an increase in CSF protein content, high titers of serum microsome test, a low concentration of anterior pituitary hormones in serum except for PRL, and an unusually high concentration of PRL in serum and CSF (4680 and 222ng/ml, respectively). Plain films of the skull showed destructive enlargement of the sella turcica. The patient was diagnosed as having non-bacterial meningitis, chronic thyroiditis and a prolactinoma with hypopituitarism and was then admitted to our department. Except for amenorrhea she was asymptomatic under the administration of levothyroxine, hydrocortisone and bromocriptine. CT scan, MRI, pneumoencephalography and CT cisternography as further examinations disclosed the intrasellar herniation of cisterns and the third ventricle, which were surrounded by an intrasellar parenchymal layer. This layer was thought to be still viable prolactinoma tissue. We supposed the third ventricle entered the enlarged sellar cavity following the spontaneous degeneration of the large prolactinoma. Although we could find some documented reports of similar cases, the complete herniation of the third ventricle secondary to degeneration of an adenoma might be rare.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Empty sella as an intrasellar herniation of the third ventricle secondary to spontaneous degeneration of a prolactinoma]. 813 65

A 21 year-old woman was found to have a pituitary macroadenoma following an episode of haemophilus meningitis. Biochemical TSH and GH excess was noted, although with no clear clinical correlates. She was treated with a somatostatin analogue (SSA), which restored the euthyroid state and controlled GH hypersecretion, but she re-presented with a further episode of cerebrospinal fluid (CSF) leak and recurrent meningitis. Histology following transsphenoidal adenomectomy revealed a Pit-1 lineage plurihormonal adenoma expressing GH, TSH and PRL. Such plurihormonal pituitary tumours are uncommon and even more unusual to present with spontaneous bacterial meningitis. The second episode of CSF leak and meningitis appears to have been due to SSA therapy-induced tumour shrinkage, which is not a well-described phenomenon in the literature for this type of tumour. Learning points: Pit-1 lineage GH/TSH/PRL-expressing plurihormonal pituitary adenomas are uncommon. Moreover, this case is unique as the patient first presented with bacterial meningitis. Inmunohistochemical plurihormonality of pituitary adenomas does not necessarily correlate with biochemical and clinical features of hormonal hypersecretion. Given that plurihormonal Pit-1 lineage adenomas may behave more aggressively than classical pituitary adenomas, accurate pathological characterization of these tumours has an increasing prognostic relevance. Although unusual, a CSF leak and meningitis may be precipitated by SSA therapy of a pituitary macroadenoma via tumour shrinkage.
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PMID:Plurihormonal Pit-1 lineage adenoma presenting as meningitis with recurrence after somatostatin analogue. 3089 48