Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyrotropin-secreting pituitary tumors (TSH-omas) are a rare cause of hyperthyroidism and account for less than 1% of all pituitary adenomas. It is however noteworthy that the number of reported cases tripled in the last years as a consequence of the routine use of ultrasensitive immunometric assays for measuring TSH levels. Contrary to previous RIAs, ultrasensitive TSH assays allow a clear distinction between patients with suppressed and those with non-suppressed circulating TSH concentrations, i.e. between patients with primary hyperthyroidism (Graves' disease or toxic nodular goiter) and those with central hyperthyroidism (TSH-oma or pituitary resistance to thyroid hormone action). Failure to recognize the presence of a TSH-oma may result in dramatic consequences, such as improper thyroid ablation that may cause the pituitary tumor volume to further expand. The medical treatment of TSH-omas mainly rests on the administration of somatostatin analogs, such as octreotide and lanreotide. In fact, administration of dopamine agonists failed to persistently block TSH secretion in almost all patients and caused tumor shrinkage only in those with combined hypersecretion of TSH and PRL. On the contrary, somatostatin analogs were effective in reducing TSH and alpha-subunit secretion in more than 90% of cases with consequent normalization of FT4 and FT3 levels and restoration of the euthyroid state in the majority of them. In about one third of patients, a clear shrinkage of tumor mass and vision improvement could be demonstrated. Tachyphylaxis, cholelithiasis and carbohydrate intolerance occurred in a minority of treated patients. Whether somatostatin analog treatment may be an alternative to surgery and/or irradiation in patients with TSH-oma remains to be established. Nonetheless, the long-acting somatostatin preparations represent a useful tool for long-term treatment of such a rare pituitary tumors.
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PMID:Medical management of thyrotropin-secreting pituitary adenomas. 1267 5

Thyrotoxicosis with concomitant thyroid cancer is rare and poorly recognized, which may result in delayed diagnosis, inappropriate treatment and even poor prognosis. To provide a comprehensive guidance for clinicians, the etiology, pathogenesis, diagnosis and treatment of this challenging setting were systematically reviewed. According to literatures available, the etiologies of thyrotoxicosis with concomitant thyroid cancer were categorized into Graves' disease with concurrent differentiated thyroid cancer (DTC) or medullary thyroid cancer, Marine-Lenhart Syndrome with coexisting DTC, Plummer's disease with concomitant DTC, amiodarone-induced thyrotoxicosis with concomitant DTC, central hyperthyroidism with coexisting DTC, hyperfunctioning metastases of DTC and others. The underlying causal mechanisms linking thyrotoxicosis and thyroid cancer were elucidated. Medical history, biochemical assessments, radioiodine uptake, anatomic and metabolic imaging and ultrasonography-guided fine-needle aspiration combined with pathological examinations were found to be critical for precise diagnosis. Surgery remains a mainstay in both tumor elimination and control of thyrotoxicosis, while anti-thyroid drugs, beta-blockers, 131I, glucocorticoids, plasmapheresis, somatostatin analogs, dopamine agonists, radiation therapy, chemotherapy and tyrosine kinase inhibitors should also be appropriately utilized as needed.
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PMID:Thyrotoxicosis with concomitant thyroid cancer. 3102 10