Endocrinology and Metabolism

Kyu Sang Song (Song KS)

2 Articles

A Case of Giant Cell Granulomatous Hypophysitis with Recurrent Hypoosmolar Hyponatremia.: Yun Hyeong Lee, Yong Bum Kim, Ju Hee Lee, Kyoung Hye Jeong, Min Kyeong Kim, Kyu Sang Song, Young Suk Jo; Endocrinol Metab. 2010;25(4):347-353. Published online December 1, 2010; DOI: https://doi.org/10.3803/EnM.2010.25.4.347

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A 39-year-old woman presented with a 20 day history of recurrent hypoosmolar hyponatremia. Because her volume status seemed to be normal, the most suspected causes of her hyponatremia were adrenal insufficiency and hypothyroidism. Endocrinologic examination, including a combined pituitary function test, showed TSH and ACTH deficiency without GH deficiency, and hyperprolactinemia was also present. Sella MRI showed a pituitary mass, stalk thickening and loss of the normal neurohypophysial hyperintense signal on the T1 weighted image. Pathologic exam demonstrated granulomatous lesions and Langhans' multinucleated giant cells with inflammatory cell infiltration. After high dose methylprednisolone pulse therapy (1 g/day for 3 days) with subsequent prednisolone and levothyoxine replacement, there was no more recurrence of the hyponatremia. The sella MRI on the 6th month showed decreased mass size, narrowed stalk thickening and the reappearance of the normal neurohyphophysial hyperintense signal. She is currently in a good general condition and is receiving hormone replacement therapy.

Citations

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Primary Granulomatous Hypophysitis Presenting with Panhypopituitarism and Central Diabetes Insipidus
Hyun Jin Oh, Ji Young Mok, Ji Eun Kim, Sung Bae Cho, Sang Ah Chang, Ji Hyun Kim, Jung Min Lee
Korean Journal of Medicine.2015; 88(5): 581. CrossRef
Idiopathic granulomatous hypophysitis: a systematic review of 82 cases in the literature
Benjamin H. M. Hunn, William G. Martin, Steven Simpson, Catriona A. Mclean
Pituitary.2014; 17(4): 357. CrossRef

The Neuroprotective Effect of Growth Hormone on Neuronal Injury of Brain in Pilocarpine induced Status Epilepticus.: Ren Zhe An, Jae Hong Yu, Kyu Sang Song; J Korean Endocr Soc. 2001;16(1):26-38. Published online February 1, 2001

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Abstract PDF: BACKGROUND
Several growth factors, including growth hormone (GH) and Insulin like growth factor-I, have been reported to have a neuroprotective effect in experimental models of hypoxic ischemia. This study is aimed at assessing the clinical significance of growth hormone for neuroprotection in status epilepticus induced neuronal cell deaths. METHODS: Pilocarpine induced status epilepticus (SE) was studied in rats (male, Sprague-Dawley). Rats were divided into pre- or post-treatment groups that had either a low (5 U/kg/day) or high (10 U/kg/day) dose of recombinant human GH (Eutropin, LGCI, Korea), and then subdivided into 24 hour, 72 hour and 1 week groups. This was done in the pretreatment groups for 5 days before SE and in the post-treatment groups for 5 days after 2 hrs of SE injection, after SE, the GH was daily injected via intraperitoneal route. Status epilepticus was induced by pilocarpine (360 mg/kg) with scoplamine (1 mg/kg) 30 minutes before pilocarpine injection using a stereotaxic instrument and EEG monitoring. Rats were killed at 24 and 72 hours after the SE in the pretreatment groups and at 1 week after the SE in the post-treatment groups for pathology studies. Neuronal injuries in the rat brain were studied by Hematoxylin & Eosin stain and the TUNEL method. RESULTS: Neuronal necrosis was found in the hippocampal CA1 and CA3 regions in all experimenatal groups after SE, and was more severe in the CA3 region. Apoptosis was found only in the pre-GH treated group and there were TUNEL-positive and morphologically necrotic cells in the hippocampal CA1 and CA3 regions at 72 hours after SE. Neuronal necrosis and apoptosis were significantly decreased in the high dose GH treated groups (p<0.05) compare to controlsd, but not in the low dose GH hormone treated groups (p>0.05). CONCLUSION: Growth hormone has a neuroprotective effect in neuronal cell death (necrosis and apoptosis) that is caused by pilocarpine induced status epilepticus in a dose dependent manner and prevents the activation of apoptosis by SE in neurons which eventually become necrotic.

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