{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T23:55:46Z","timestamp":1788306946659,"version":"build-2803163510"},"reference-count":28,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2013,10,23]],"date-time":"2013-10-23T00:00:00Z","timestamp":1382486400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Endocrinology"],"published-print":{"date-parts":[[2014,5]]},"abstract":"Summary<\/jats:title>Objective<\/jats:title>We recently reported that paradoxical GH<\/jats:styled-content> response to TRH<\/jats:styled-content> administration reflects biological characteristics in patients with acromegaly. The aim of this study is to elucidate the relationship between gsp<\/jats:italic> mutations and the paradoxical GH<\/jats:styled-content> response to TRH<\/jats:styled-content>.<\/jats:p><\/jats:sec>Patients<\/jats:title>Sixty\u2010seven patients with acromegaly were included for analysis. Paradoxical increase in serum GH<\/jats:styled-content> level to TRH<\/jats:styled-content>, GH<\/jats:styled-content> suppression by octreotide and bromocriptine, radiological profiles and histopathological findings were analysed with respect to tumour gsp<\/jats:italic>\u2010mutation status.<\/jats:p><\/jats:sec>Results<\/jats:title>Twenty\u2010six (38\u00b78%) gsp<\/jats:italic> mutations were detected, and the number of paradoxical GH<\/jats:styled-content> responders to TRH<\/jats:styled-content>, defined as an increase of 100% or more in GH<\/jats:styled-content> after TRH<\/jats:styled-content>, was 49 (73\u00b71%). Among the paradoxical GH<\/jats:styled-content> responders to TRH<\/jats:styled-content>, 21 patients (42\u00b79%) had a gsp<\/jats:italic> mutation and 28 patients (57\u00b71%) did not. The percentage of paradoxical GH<\/jats:styled-content> responders to TRH<\/jats:styled-content> in gsp<\/jats:italic>\u2010positive and gsp<\/jats:italic>\u2010negative patients was not significantly different (80\u00b78% and 68\u00b73%, respectively). The gsp<\/jats:italic>\u2010positive group showed a significantly higher paradoxical increase in serum GH<\/jats:styled-content> level by TRH<\/jats:styled-content> administration (1830% vs<\/jats:italic> 650% GH<\/jats:styled-content> increase, P<\/jats:styled-content>\u00a0<\/jats:italic>=\u00a0<\/jats:italic>0\u00b7045) and greater GH<\/jats:styled-content> suppression by octreotide (88\u00b77% vs<\/jats:italic> 75\u00b74% GH decrease, P<\/jats:styled-content>\u00a0<\/jats:italic>=\u00a0<\/jats:italic>0\u00b7003) than the gsp<\/jats:italic>\u2010negative group.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>Paradoxical GH<\/jats:styled-content> response to TRH<\/jats:styled-content> was observed regardless of gsp<\/jats:italic> mutation, although the rate of increase was significantly higher in gsp<\/jats:italic>\u2010positive patients. These results suggest that gsp<\/jats:italic> mutation is not sufficient to cause the paradoxical GH<\/jats:styled-content> response to TRH<\/jats:styled-content>, while other unidentified factors have a strong influence on paradoxical GH<\/jats:styled-content> response to TRH<\/jats:styled-content> in patients with acromegaly.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cen.12336","type":"journal-article","created":{"date-parts":[[2013,10,11]],"date-time":"2013-10-11T22:17:34Z","timestamp":1381529854000},"page":"714-719","source":"Crossref","is-referenced-by-count":7,"title":["Gsp<\/i> mutation in acromegaly and its influence on TRH<\/scp>\u2010induced paradoxical GH<\/scp> response"],"prefix":"10.1111","volume":"80","author":[{"given":"Yuko","family":"Goto","sequence":"first","affiliation":[{"name":"Department of Neurosurgery Osaka University Graduate School of Medicine Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manabu","family":"Kinoshita","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Osaka University Graduate School of Medicine Osaka Japan"},{"name":"Department of Neurosurgery Osaka Medical Center for Cancer and Cardiovascular Diseases Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Satoru","family":"Oshino","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Osaka University Graduate School of Medicine Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hideyuki","family":"Arita","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Osaka University Graduate School of Medicine Osaka Japan"},{"name":"Department of Neurosurgery National Cancer Center Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tetsuhiro","family":"Kitamura","sequence":"additional","affiliation":[{"name":"Department of Metabolic Medicine Osaka University Graduate School of Medicine Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michio","family":"Otsuki","sequence":"additional","affiliation":[{"name":"Department of Metabolic Medicine Osaka University Graduate School of Medicine Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Iichiro","family":"Shimomura","sequence":"additional","affiliation":[{"name":"Department of Metabolic Medicine Osaka University Graduate School of Medicine Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshiki","family":"Yoshimine","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Osaka University Graduate School of Medicine Osaka 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