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Kang Woo Lee  (Lee KW) 8 Articles
A Case of Adrenal Teratoma.
Ji young Kim, Youn zoo Cho, Kang Woo Lee, Dong Mee Lim, Keun Young Park, Byung Joon Kim
Endocrinol Metab. 2011;26(3):272-275.   Published online September 1, 2011
DOI: https://doi.org/10.3803/EnM.2011.26.3.272
  • 65,958 View
  • 21 Download
  • 2 Crossref
AbstractAbstract PDF
Teratoma is a congenital tumor containing tissues derived from all germ layers. Teratoma in the region of the adrenal gland is a very uncommon retroperitoneal tumor. Only 7 cases of adrenal teratoma have been reported worldwide, but in Korea, no similar cases have been reported until now. This case report describes an adrenal teratoma in a 38-year-old healthy woman who was incidentally diagnosed with a left adrenal mass on abdominal ultrasonography during a medical inspection. Computed tomographic scans revealed a 9-cm heterogeneous circumscribed round mass, containing primarily fat tissue, and a solid calcification component in the left adrenal gland. Adrenal hormonal assessment results and biochemical markers for gonadal neoplasia were negative. Result of serum laboratory tests were normal. The patient underwent laparoscopic adrenalectomy. Histologic analysis confirmed the diagnosis of a mature teratoma; the obtained specimen measured 5 x 7 x 7.5 cm and weighed 267 g. The surface of the mass was smooth, and sebaceous tissue and hair with hard material were observed on the incisional surface. The patient was discharged on postoperative day 4, without complications. In this case report, we describe the incidental finding of a teratoma occurring in the adrenal gland region in a healthy woman; the teratoma was laparoscopically excised.

Citations

Citations to this article as recorded by  
  • Lipomatous tumours in adrenal gland: WHO updates and clinical implications
    Alfred King-yin Lam
    Endocrine-Related Cancer.2017; 24(3): R65.     CrossRef
  • A Case of Teratoma of Thyroid Gland in Adolescence
    Yu-Chang Lee, Su-Jin Jeong, Sol-Jae Lee, Chong-Hwa Kim, Yong-Hoon Lee, Jung-Eun Lee, Hye-Ji Seo
    International Journal of Thyroidology.2017; 10(1): 61.     CrossRef
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GLP-1 Can Protect Proinflammatory Cytokines Induced Beta Cell Apoptosis through the Ubiquitination.
Dong Mee Lim, Ju Young Kim, Kang Woo Lee, Keun Young Park, Byung Joon Kim
Endocrinol Metab. 2011;26(2):142-149.   Published online June 1, 2011
DOI: https://doi.org/10.3803/EnM.2011.26.2.142
  • 1,618 View
  • 19 Download
AbstractAbstract PDF
BACKGROUND
Proinflammatory cytokines are one of the causes of diabetes mellitus. However, the exact molecular mechanism by which proinflammatory cytokines induce beta-cell death remains to be clearly elucidated. Glucagon-like peptide-1 (GLP-1) affects the stimulation of insulin secretion and the preservation of beta-cells. Additionally, it may exert an antiapoptotic effect on beta cells; however, the mechanism underlying this effect has yet to be demonstrated. Therefore, we investigated the protective effects of GLP-1 in endoplasmic reticulum (ER)-mediated beta-cell apoptosis using proinflammatory cytokines. METHODS: To induce ER stress, hamster insulin-secreting tumor (HIT)-T15 cells were treated using a mixture of cytokines. Apoptosis was evaluated via MTT assay, Hoechst 33342 staining, and annexin/propidium iodide (PI) flow cytometry. The mRNA and protein expression levels of ER stress-related molecules were determined via PCR and Western blotting, respectively. Nitric oxide was measured with Griess reagent. The levels of inducible nitric oxide synthase (iNOS) mRNA and protein were analyzed via real-time PCR and Western blot, respectively. iNOS protein degradation was evaluated via immunoprecipitation. We pretreated HIT-T15 cells with exendin (Ex)-4 for 1 hour prior to the induction of stress. RESULTS: We determined that Ex-4 exerted a protective effect through nitric oxide and the modulation of ER stress-related molecules (glucose-regulated protein [GRP]78, GRP94, and CCAAT/enhancer-binding protein homologous protein [CHOP]) and that Ex-4 stimulates iNOS protein degradation via the ubiquitination pathway. Additionally, Ex-4 also induced the recovery of insulin2 mRNA expression in beta cells. CONCLUSION: The results of this study indicate that GLP-1 may protect beta cells against apoptosis through the ubiquitination pathway.
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A Case of Coexistence of Parathyroid and Papillary Thyroid Carcinoma.
Yoon Shick Yom, Myung Jun Lee, Hyun Woo Lim, Jeong Ho Park, Sung Tae Kim, Yu Mi Lee, Dong Ju Yang, Youn Zoo Cho, Moon Il Park, Kang Woo Lee, Keun Young Park, Dong Mee Lim, Byung Joon Kim
J Korean Endocr Soc. 2010;25(1):61-67.   Published online March 1, 2010
DOI: https://doi.org/10.3803/jkes.2010.25.1.61
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AbstractAbstract PDF
Primary hyperparathyroidism is usually caused by a parathyroid adenoma, occasionally by primary parathyroid hyperplasia and rarely by parathyroid carcinoma. Coincidental occurrence of thyroid carcinoma in parathyroid adenoma is not uncommon, but synchronous parathyroid and thyroid carcinoma is extremely rare. Here, we describe a case of synchronous parathyroid carcinoma and papillary thyroid carcinoma.
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A Case of Prolonged Hypoglycemia Post Topiramate Treatment an Anti-convulsant, in a Type 2 Diabetic Patient.
Myung Jun Lee, Yoon Shick Yom, Hyun woo Lim, Sung Tae Kim, Yu Mi Lee, Youn Zoo Cho, Kang Woo Lee, Byung Joon Kim, Keun Young Park, Dong Mee Lim
J Korean Endocr Soc. 2009;24(4):277-280.   Published online December 1, 2009
DOI: https://doi.org/10.3803/jkes.2009.24.4.277
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  • 92 Download
AbstractAbstract PDF
Topiramate is a drug used to treat epilepsy, and is known for its effects including reduced appetite resulting in lower body weight, and the lowering of neutral fat. In addition, topiramate is known to reduce blood sugar levels by increasing insulin sensitivity and by increasing insulin secretion by glucose stimulation. The authors report a case of persistent hypoglycemia, in a patient who had been administrating topiramate, as a treatment for epilepsy following an episode of cerebral infarction.
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Central Diabetes Insipidus Surmised as from Post-obstructive Diuresis after Decompression Treatment for Neurogenic Bladder.
Kang Woo Lee, Chul Woo Yang, Dong Jun Lim, Hyuk Sang Kwon, Mi Ja Kang, Eun Sook Kim, Kun Ho Yoon, Ho Young Son, Bong Yun Cha
J Korean Endocr Soc. 2009;24(2):144-147.   Published online June 1, 2009
DOI: https://doi.org/10.3803/jkes.2009.24.2.144
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  • 25 Download
  • 1 Crossref
AbstractAbstract PDF
Post-obstructive diuresis after treatment for neurogenic bladder-induced obstructive kidney disease is a common symptom. As polyuria may develop in many other conditions as well, the present case is about a patient with a chief complaint of polyuria accompanied by nocturia, that was initially diagnosed as hydronephrosis due to the presence of neurogenic bladder and bladder dysfunction. The result of the water deprivation test, which was conducted for persistent diluted polyuria, yielded a final diagnosis of central diabetes insipidus, notwithstanding the strong impression of post-obstructive diuresis initially made because of a sudden increase in urine output after an indwelling catheter was inserted for bladder decompression.

Citations

Citations to this article as recorded by  
  • A Case of Septo-Optic Dysplasia Resulting in Central Diabetes Insipidus and Nonobstructive Bilateral Hydronephrosis
    Jong Hyun Kim, Kwang Bok Lee, Jeonghun Lee, Soo Min Nam, Kang-Woo Lee, Eu Gene Hwang, Geon Gil
    Korean Journal of Medicine.2014; 87(2): 209.     CrossRef
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A Patient with Primary Amyloidosis Misrecognized as Thyrotoxicosis-induced Heart Failure.
Seok Ju Lee, Seung Hwan Lee, Jung Yeon Chin, Youn Mi Song, Sung Won Lee, Min Hee Kim, Mi Ja Kang, Kang Woo Lee, Hyuk Sang Kwon, Kun Ho Yoon, Ho Young Son, Bong Yun Cha
J Korean Endocr Soc. 2008;23(5):332-336.   Published online October 1, 2008
DOI: https://doi.org/10.3803/jkes.2008.23.5.332
  • 1,711 View
  • 20 Download
AbstractAbstract PDF
Amyloidosis is caused by deposition of insoluble amyloid protein in the extracellular space of organs and tissues. The causes of amyloidosis are classified as primary, secondary, and hereditary, and symptoms develop according to which organ is involved. Cardiac amyloidosis induces cardiomyopathy and is developed by deposition of amyloid proteins in cardiac tissue. We diagnosed a patient with rhabdomyolysis and thyrotoxicosis with underlying Graves' disease 5 years ago. The patient was readmitted recently complaining of general weakness and mild dyspnea, and was diagnosed as relapsed thyrotoxicosis. An echocardiogram was performed for the evaluation of dyspnea and the findings were compatible with infiltrative cardiomyopathy due to amyloidosis. A biopsy of the abdominal subcutaneous fat and rectal mucosa was performed, and diagnosis was amyloidosis with histologic findings. The cause of heart failure was therefore cardiac amyloidosis rather than thyrotoxicosis. This case indicates the importance of evaluating the cause of heart failure in patients with thyrotoxicosis.
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A Case of Pneumocystis Carinii Pneumonia and Cutaneous Nocardiosis Associated with Ectopic ACTH Syndrome.
Hee Sun Jung, Seung Hwan Lee, Hee Yeon Kim, Eun Ho Chu, Kang Woo Lee, Mi Ja Kang, Ji Hyun Kim, Hyuk Sang Kwon, Kun Ho Yoon, Bong Yun Cha, Ho Young Son
J Korean Endocr Soc. 2008;23(1):44-50.   Published online February 1, 2008
DOI: https://doi.org/10.3803/jkes.2008.23.1.44
  • 1,758 View
  • 19 Download
AbstractAbstract PDF
Cushing's syndrome is characterized by hypercortisolism and impairment of cell-mediated immune function, increasing the risk of opportunistic infection, as occurs in other immunocompromised groups such as organ transplant recipients, patients with lymphoreticular malignancy, or acquired immunodeficiency syndrome. We report a case of a 68-year-old woman who was affected with pneumocystis carinii pneumonia (PCP) 8 years ago and cutaneous nocardiosis this year. The patient was diagnosed with ectopic ACTH syndrome 8 years ago, but no ectopic ACTH secreting focus was found in radiologic imaging studies. She recovered from PCP and cutaneous nocardiosis after antibiotic (trimethoprim-sulfamethoxazole) administration. After the infection resolved, she underwent laparoscopic bilateral adrenalectomy and was not longer hypercortisolemic.
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Primary Hyperaldosteronism with Increased Plasma Renin Activity due to Secondary Hypertensive Renal Impairment.
Kang Woo Lee, Hyuk Sang Kwon, Dong Il Shin, Chee Ho Noh, Jung Min Lee, Jong Min Lee, Kun Ho Yoon, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang
J Korean Endocr Soc. 2003;18(4):433-438.   Published online August 1, 2003
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  • 18 Download
AbstractAbstract PDF
An increased plasma aldosterone concentration, with suppressed plasma renin activity (PRA), is an abnormal finding in primary hyperaldosteronism. A suppressed PRA is caused by aldosterone- dependent sodium retention and extracellular volume expansion. A case of primary hyperaldosteronism, due to adenoma, with increased PRA, was observed. An adrenalectomy and intraoperative renal biopsy was performed. In our patient, histologically proven renal arteriosclerosis was the probable cause of the escape of the PRA from the suppression by an aldosterone-producing adenoma. Normal blood pressure was not attained after the adrenalectomy. However, the blood pressure was then controlled by small doses of antihypertensive drug before resection of the tumor. In this case, the patient was treated with spironolactone, but the blood pressure was not correctly controlled. After the adrenalectomy, the blood pressure was well controlled with smaller dose of calcium channel blockers. So, an early adrenalectomy may be beneficial as soon as the diagnosis of an aldosterone-producing adenoma is confirmed, even in patients with hypertensive nephrosclerosis.
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