摘要
Background： Thyrotropin-secreting pituitary adenomas （TSHomas） are a rare cause of hyperthyroidism. Somatostatin （SST） analogs work by interacting with somatostatin receptors （SSTRs）. This study aimed to evaluate short-term preoperative octreotide （OCT） use in TSHoma patients and to investigate SSTR2 and SSTR5 expression and observe structural changes in tumor tissue. Methods： We reviewed records and samples from eight TSHoma patients treated between July 2012 and July 2015. We tested immunohistochemically for SSTR2/5 expression and examined TSHoma cells for morphological changes. Signed rank sum test was used to compare the efficacy of short-term preoperative OCT treatment. Results： OCT treatment （median time： 7.9 days, range： 3-16 days; median total dose： 1.8 mg, range： 0.94.2 mg） led to significant decrease in all patients＇ thyroid hormone levels （FT3 [nmol/L]： 8.33 [7.02, 12.29] to 4.67 [3.52, 5.37] [P = 0.008]; FT4 [pmol/L]： 25.36 [21.34, 28.99] to 16.66 [14.88, 21.49] [P = 0.016]; and TSH [gU/ml]： 5.80 [4.37, 6.78] to 0.57 [0.19, 1.24] [P = 0.008]）. All the eight tumor specimens expressed high SSTR2 protein levels; 5/8 expressed high SSTRS, but 3/8 that expressed low SSTR5 presented a significantly higher TS H suppression rate （P = 0.036）. Electron microscopy showed subcellular level impairments, including clumped nuclear chromatin and reduced cytoplasmic volume. Golgi complexes were observed in the OCT-treated TSHoma specimens. Conclusions： OCT can control hormone levels and damage the ultrastructure of tumor cells and organelles. Short-term response to OCT may be related to SSTR5 expression. Preoperative SST analog treatment for TSHoma could be considered as a combination therapy.
Background： Thyrotropin-secreting pituitary adenomas （TSHomas） are a rare cause of hyperthyroidism. Somatostatin （SST） analogs work by interacting with somatostatin receptors （SSTRs）. This study aimed to evaluate short-term preoperative octreotide （OCT） use in TSHoma patients and to investigate SSTR2 and SSTR5 expression and observe structural changes in tumor tissue. Methods： We reviewed records and samples from eight TSHoma patients treated between July 2012 and July 2015. We tested immunohistochemically for SSTR2/5 expression and examined TSHoma cells for morphological changes. Signed rank sum test was used to compare the efficacy of short-term preoperative OCT treatment. Results： OCT treatment （median time： 7.9 days, range： 3-16 days; median total dose： 1.8 mg, range： 0.94.2 mg） led to significant decrease in all patients＇ thyroid hormone levels （FT3 [nmol/L]： 8.33 [7.02, 12.29] to 4.67 [3.52, 5.37] [P = 0.008]; FT4 [pmol/L]： 25.36 [21.34, 28.99] to 16.66 [14.88, 21.49] [P = 0.016]; and TSH [gU/ml]： 5.80 [4.37, 6.78] to 0.57 [0.19, 1.24] [P = 0.008]）. All the eight tumor specimens expressed high SSTR2 protein levels; 5/8 expressed high SSTRS, but 3/8 that expressed low SSTR5 presented a significantly higher TS H suppression rate （P = 0.036）. Electron microscopy showed subcellular level impairments, including clumped nuclear chromatin and reduced cytoplasmic volume. Golgi complexes were observed in the OCT-treated TSHoma specimens. Conclusions： OCT can control hormone levels and damage the ultrastructure of tumor cells and organelles. Short-term response to OCT may be related to SSTR5 expression. Preoperative SST analog treatment for TSHoma could be considered as a combination therapy.
