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Original Article
- A Retrospective Review of the Effectiveness of Recombinant Human TSH-Aided Radioiodine Treatment of Differentiated Thyroid Carcinoma.
- Min Ah Na, Sun Hae Shin, Yang Ho Kang, Seok Man Son, In Joo Kim, Yong Ki Kim
- J Korean Endocr Soc. 2006;21(4):274-280. Published online August 1, 2006
- DOI: https://doi.org/10.3803/jkes.2006.21.4.274
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Abstract
PDF - BACKGROUND
The aim of the study was to evaluate the biochemical effects of recombinant human thyroid stimulating hormone (rhTSH) as an adjunct to radioiodine (RI) treatment of a differentiated thyroid carcinoma (DTC). We retrospectively reviewed the clinical response rates of DTC patients treated with RI after thyroid hormone withdrawal and compared with those after rhTSH stimulation. METHOD: We included the patients treated with RI for locally recurrent DTC from February 1, 2002 to August 31, 2005 and followed with diagnostic studies at our hospital. Forty totally (or near totally) thyroidectomized adults were included in this study. Nine patients underwent RI treatment after rhTSH stimulation while euthyoid on L-thyroxine (LT4), and 31 patients were treated with RI after thyroid hormone withdrawal. The clinical response was defined as >25% decrease in serum thyroglobulin (Tg) level on LT4 3 months after the RI treatment. RESULTS: In each group, serum Tg levels were significantly decreased 3 months after the RI treatment. And we found that 77.8 and 71.0% of those prepared by rhTSH and LT4 withdrawal, respectively, had clinical responses 3 months after the RI treatment by our criteria and there was no significant difference in response rates between two groups (P=0.238). CONCLUSIONS: Given the biases that exist in retrospective studies, at the current time we cannot recommend the routine use of rhTSH to prepare RI treatment of DTC. However, our study provided preliminary evidence that rhTSH effectively aided RI treatment of DTC at least to an equivalent degree as LT4 withdrawal.
Case Report
- Reversible Pituitary Dysfunction in a Patient with Cushing's Syndrome due to Adrenal Adenoma.
- Jee Hyun Kong, Kyung Wook Kim, Hei Jin Kim, Ji Sun Nam, Jin A Park, Jong Sook Park, Chul Sik Kim, Byung Soo Moon, Soon Won Hong, Chul Woo Ahn, Kyung Rae Kim
- J Korean Endocr Soc. 2006;21(2):146-152. Published online April 1, 2006
- DOI: https://doi.org/10.3803/jkes.2006.21.2.146
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Abstract
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- A 45-year-old woman who complained of weight gain and irregular menstruation was diagnosed as having Cushing's syndrome due to a 3 cm sized left adrenal adenoma. She underwent left adrenalectomy, and she also underwent combined anterior pituitary tests before and 9 months after the surgery. The growth hormone and adrenocorticotropic hormone levels failed to respond to hypoglycemia before the surgery, but their responses recovered after the surgery. Cortisol and thyroid stimulating hormone failed to respond to hypoglycemia and thyrotropin releasing hormone (TRH) before the surgery, respectively, but these were improved after the surgery. Luteinizing hormone, follicle stimulating hormone, and prolactin adequately responded to gonadotropin-releasing hormone and TRH, respectively, before and after the surgery. However, the basal levels of these hormones were higher after adrenalectomy, suggesting that hypercortisolemia had a significant influence on all the pituitary hormones.
Original Articles
- Hormonal and Cytokine Regulation of ICAM-1 gene in FRTL-5 Thyroid Cells: Cloning and Analysis of 5-Regulatory Region of Rat ICAM-1 Gene.
- Min Ho Song, Young Tae Shin, Young Kun Kim, Heung Kyu Ro
- J Korean Endocr Soc. 1997;12(3):393-409. Published online January 1, 2001
- 1,588 View
- 17 Download
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Abstract
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- BACKGROUND
We have found abnormal expression of ICAM-1 in thyroid follicular cells from patients with Graves disease and Hashimoto disease. In this report, we present the hormonal regulation of ICAM-1 mRNA expression and the primary structure of 5-regulatory region which is important for transcriptional regulation of ICAM-1 gene. A I.S kb fragment of the 5-regulatory sequences are identified and linked to luciferase as a reporter. METHOD: Those reporter constructs were used to evaluate the expression in response to cytokines and hormones. Deletion analysis of 1.8 kb fragment of ICAM-1 promoter in FRTL-5 cells provide the evidence for the existence of several regulatory elements of enhancer and silencer in ICAM-1 gene transcription in thyroid cells. RESULTS: ICAM-1 mRNA is easily detected by Northern analysis using total RNA from FRTL-5 cells regardless of culture conditions. The transcripts of rat ICAM-1 showed single band of 2.6 kb in length. The FRT cells which was come from early FRTL cell culture did not show ICAM-1 mRNA with usual Northern analysis, We found differential regulation of ICAM-1 RNA level in different culture condition in FRTL-5 cells, The cells maintained at 3H (no hydrocortisone, no insulin, no TSH) condition showed the highest expression level compared to 4H, 5H, or 6H medium. Hydrocortisone markedly decreased the ICAM-1 RNA and insulin partially recovered the hydrocortisone induced repression. TSH which is important in growth and function of FRTL-5 cells could independently downregulate the ICAM-1 RNA levels. Forskolin (10 mM) could mimic the action of TSH on ICAM-1 mRNA. TNF-a and interferon-y increase ICAM-1 expression in FRTL-5 thyroid cells. TSH/forskolin inhibited maximal expression of ICAM-1 by TNF-a and interferon-r. Promoter activity of the ICAM-1 gene was positively regulated by cytokines, TNF-a and IFN-r and negatively regulated by thyroid stimulating hormone. The addition of TSH and FSK caused a 50% decrease in ICAM-1 promoter activity within 24 hour. The TSH and FSK action was mapped at 175 bp and 97 bp of the start of translation. The mutant construct pCAM-175 delGAS which has no GAS sequence showed no TSH mediated suppression of promoter activity. CONCLUSION: These findings suggested that hormones and cytokines differentially regulated the ICAM-1 gene expression and TSH downregulated ICAM-1 gene transcription by inhibiting the activation of IFN-r induced transcription factors which can bind the GAS of ICAM-1 promoter.
- Effect of Acute Hyperglycemia - and Isoproterenol - induced Hypothalamic Somatostatin Release on the Thyroid Hormone Releasing Hormone - induced Thyroid Stimulating Hormone Secretion.
- Cheol Young Park, In Myung Yang, Seung Joon Oh, Deog Yoon Kim, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi
- J Korean Endocr Soc. 2000;15(4-5):486-492. Published online January 1, 2001
- 2,068 View
- 18 Download
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Abstract
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- BACKGROUND
Acute hyperglycemia stimulates somatostatin (SRIH) release from the hypothalamus, and which in turn suppress growth hormone (GH) secretion and thyroid stimulating hormone (TSH) from the anterior pituitary gland. Beta-adrenergic pathway is known to stimulate the hypothalamus SRIH release. Recently, We demonstrated that isoproterenol, a beta-adrenergic agonist, had an additional suppressive effect on the suppression by glucose of GHRH-stimulated GH response. Therefore, the present study aimed to determine whether isoproterenol has an additional suppressive effect on the suppression by glucose of TRH-stimulated TSH response. METHODS: Seven healthy young men, aged 24 to 27 years, were studied. Four different TRH stimulation tests were carried out. (Test 1) TRH (Hoechst AG, Germany), 200 microgram bolus, was given intravenously at 0 minute. (Test 2) Glucose, 100 g, was given orally 30 min before TRH administration. (Test 3) Isoproterenol(Isuprel, Sanofi Winthrop, USA), 0.012 pg/kg, was infused continuously for 120 min after TRH administration. (Test 4) After pretreatment with glucose as Test 2, isoproterenol and TRH were administered as Test 3. RESULTS: Oral glucose ingestion significantly suppressed the TRH-stimulated TSH secretion. Isoproterenol infusion significantly suppressed the TRH-stimulated TSH secretion. Glucose-induced suppression of the TSH response was significantly greater than that by isoproterenol. 1soproterenol infusion after glucose pretreatment did not show any additional suppressive effect on the glucose-induced suppression of TSH response to TRH. CONCLUSION: The results suggest that isoproterenol infusion in addition to glucose pretreatment before the TRH stimulation test is not necessary for the development of stronger stimulation test for the hypothalamic somatostatin secretion.
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