Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029089 (ophthalmoplegia)
 3,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acromegaly is caused by GH-secreting pituitary adenomas and, in rare cases, by ectopic production of GRH with resultant hypersecretion of GH. Important systemic manifestations include acral enlargement, swelling, disfigurement, glucose intolerance and diabetes, hypertension, nerve entrapment, arthropathy, and cardiac disease. Tumor-related major manifestations are visual impairment, oculomotor paralysis, and hypopituitarism. Morbidity is substantial, and mortality is increased. Diagnosis should be made as early as possible by measuring plasma GH after an oral glucose load and plasma somatomedin C levels. Assessment of a pituitary lesion is best made by CT scanning in the coronal plane. Therapy is mandatory and consists of surgical removal of the pituitary adenoma (usually by the transsphenoidal route) or of the ectopic source of GRH (carcinoids or islet cell tumors). Adjunctive radiation and/or drug therapy is often necessary if complete surgical ablation of the adenoma is not possible. Radiation therapy can be administered as conventional supervoltage x-ray treatment or in the form of heavy particle beams. Drugs effective in partially lowering GH levels are bromocriptine and (not yet released) somatostatin analogues. Long-term follow-up of treated patients is important to guard against recurrence, progression, or development of hypopituitarism.
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PMID:Acromegaly. 331 99

Neuroendocrine tumor metastases to the pituitary gland are very rare. There are few case reports of carcinoid tumor metastases to the pituitary, but no cases of pancreatic neuroendocrine pituitary metastases have been reported. In this report we present a 55-year-old female with a sellar mass, ophthalmoplegia and headaches initially thought to represent an invasive null cell pituitary adenoma. However a histological (trans-sphenoidal and liver biopsies) and systemic investigation proved it to be a metastasis of an undiagnosed pancreatic neuroendocrine tumor. Our patient was unique in respect to the location of the metastasis and the uncharacteristically high proliferative index of her tumor. She received conventional therapy consisting of Sandostatin, chemotherapy and radiotherapy as well as labeled somatostatin following an avid uptake on octreotide scanning. Despite a radiological improvement the patient suffered progressive clinical deterioration and died.
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PMID:Metastatic pancreatic neuroendocrine tumor presenting as a pituitary space occupying lesion: a case report. 1763 85