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

The evolution of the endoscopic endonasal transsphenoidal technique, which was initially reserved only for sellar lesions through the sphenoid sinus cavity, has lead in the last decades to a progressive possibility to access the skull base from the nose. This route allows midline access and visibility to the suprasellar, retrosellar and parasellar space while obviating brain retraction, and makes possible to treat transsphenoidally a variety of relatively small midline skull base and parasellar lesions traditionally approached transcranially. We report our current knowledge of the endoscopic anatomy of the midline skull base as seen from the endonasal perspective, in order to describe the surgical path and structures whose knowledge is useful during the operation. Besides, we describe the step-by-step surgical technique to access the different compartments, the "dangerous landmarks" to avoid in order to minimize the risks of complications and how to manage them, and our paradigm and techniques for dural and bony reconstruction. Furthermore, we report a brief description of the useful instruments and tools for the extended endoscopic approaches. Between January 2004 and April 2006 we performed 33 extended endonasal approaches for lesions arising from or involving the sellar region and the surrounding areas. The most representative pathologies of this series were the ten cranioparvngiomas, the six giant adenomas and the five meningiomas; we also used this procedure in three cases of chordomas, three of Rathke's cleft cysts and three of meningo-encephaloceles, one case of optic nerve glioma, one olfactory groove neuroendocrine tumor and one case of fibro-osseous dysplasia. Tumor removal, as assessed by post-operative MRI, revealed complete removal of the lesion in 2/6 pituitary adenomas, 7/10 craniopharyngiomas, 4/5 meningiomas, 3/3 Rathke's cleft cyst, 3/3 meningo-encephalocele. Surgical complications have been observed in 3 patients, two with a craniopharyngioma, one with a clival meningioma and one with a recurrent giant pituitary macroadenoma involving the entire left cavernous sinus, who developed a CSF leak and a second operation was necessary in order to review the cranial base reconstruction and seal the leak. One of them developed a bacterial meningitis, which resolved after a cycle of intravenous antibiotic therapy with no permanent neurological deficits. One patient with an intra-suprasellar non-functioning adenoma presented with a generalized epileptic seizure a few hours after the surgical procedure, due to the intraoperative massive CSF loss and consequent presence of intracranial air. We registered one surgical mortality. In three cases of craniopharyngioma and in one case of meningioma a new permanent diabetes insipidus was observed. One patient developed a sphenoid sinus mycosis, cured with antimycotic therapy. Epistaxis and airway difficulties were never observed. It is difficult todav to define the boundaries and the future limits of the extended approaches because the work is still in progress. Such extended endoscopic approaches, although at a first glance might be considered something that everyone can do, require an advanced and specialized training.
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PMID:Extended endoscopic endonasal approach to the midline skull base: the evolving role of transsphenoidal surgery. 1838 14

Pituitary apoplexy is a rare but potentially life-threatening clinical syndrome characterized by ischemic infarction or hemorrhage into a pituitary tumor. The diagnosis of pituitary tumor apoplexy is frequently complicated because of the nonspecific nature of its signs and symptoms, which can mimic different neurological processes, including meningitis. Several factors have been associated with apoplexy, such as dopamine agonists, radiotherapy, or head trauma, but meningitis is a rarely reported cause. We describe the case of a 51-year-old woman with acromegaly due to a pituitary macroadenoma. Before surgical treatment, she arrived at Emergency with fever, nausea, vomiting and meningismus. Symptoms and laboratory tests suggested bacterial meningitis, and antibiotic therapy was initiated, with quick improvement. A computerized tomography (CT) scan at admission did not reveal any change in pituitary adenoma, but a few weeks later, magnetic resonance imaging (MRI) showed data of pituitary apoplexy with complete disappearance of the adenoma. Currently, her acromegaly is cured, but she developed hypopituitarism and diabetes insipidus following apoplexy. We question whether she really experienced meningitis leading to apoplexy or whether apoplexy was misinterpreted as meningitis. In conclusion, the relationship between meningitis and pituitary apoplexy may be bidirectional. Apoplexy can mimic viral or bacterial meningitis, but meningitis might cause apoplexy, as well. This fact highlights the importance of differential diagnosis when evaluating patients with pituitary adenomas and acute neurological symptoms.
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PMID:Spontaneous remission of acromegaly: apoplexy mimicking meningitis or meningitis as a cause of apoplexy? 2472 69

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

Carcinoma ex pleomorphic adenoma (Ca ex PA) is a rare malignant transformation of a benign primary pleomorphic adenoma (PA). We report the case of a 62-year-old male who presented with a swelling over his left temple. Imaging revealed a lytic lesion over the left orbital wall with soft tissue extension suggestive of malignancy. He underwent an en bloc resection of the mass with orbital exenteration, craniotomy, and reconstruction. Pathology demonstrated a lacrimal gland ductal adenocarcinoma arising from a PA which led to the diagnosis of ductal adenoCa ex PA. Postoperatively, he received chemotherapy with 6 cycles of cisplatin and concurrent radiation therapy (RT), but his course was complicated by recurrent bacterial meningitis and abscesses and he ultimately opted for comfort measures. Patients with PA of the lacrimal gland experience an insidiously enlarging painless swelling of the orbit with transformation to Ca ex PA highlighted by a rapid onset of bulbar enlargement, displacement, and often proptosis. Ductal adenoCa ex PA is aggressive with a poor prognosis and has no established standard of care. This case highlights the rarity of this condition and the need for more literature to help direct treatment.
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PMID:Ductal Adenocarcinoma Ex Pleomorphic Adenoma of the Lacrimal Gland: a Rare and Morbid Malignancy. 3208 22