Eun Kyung Lee, Yea Eun Kang, Young Joo Park, Bon Seok Koo, Ki-Wook Chung, Eu Jeong Ku, Ho-Ryun Won, Won Sang Yoo, Eonju Jeon, Se Hyun Paek, Yong Sang Lee, Dong Mee Lim, Yong Joon Suh, Ha Kyoung Park, Hyo-Jeong Kim, Bo Hyun Kim, Mijin Kim, Sun Wook Kim, Ka Hee Yi, Sue K. Park, Eun-Jae Jung, June Young Choi, Ja Seong Bae, Joon Hwa Hong, Kee-Hyun Nam, Young Ki Lee, Hyeong Won Yu, Sujeong Go, Young Mi Kang, MASTER study group
Endocrinol Metab. 2021;36(3):574-581. Published online May 26, 2021
Background Postoperative thyroid stimulating hormone (TSH) suppression therapy is recommended for patients with intermediate- and high-risk differentiated thyroid cancer to prevent the recurrence of thyroid cancer. With the recent increase in small thyroid cancer cases, the extent of resection during surgery has generally decreased. Therefore, questions have been raised about the efficacy and long-term side effects of TSH suppression therapy in patients who have undergone a lobectomy.
Methods This is a multicenter, prospective, randomized, controlled clinical trial in which 2,986 patients with papillary thyroid cancer are randomized into a high-TSH group (intervention) and a low-TSH group (control) after having undergone a lobectomy. The principle of treatment includes a TSH-lowering regimen aimed at TSH levels between 0.3 and 1.99 μIU/mL in the low-TSH group. The high-TSH group targets TSH levels between 2.0 and 7.99 μIU/mL. The dose of levothyroxine will be adjusted at each visit to maintain the target TSH level. The primary outcome is recurrence-free survival, as assessed by neck ultrasound every 6 to 12 months. Secondary endpoints include disease-free survival, overall survival, success rate in reaching the TSH target range, the proportion of patients with major cardiovascular diseases or bone metabolic disease, the quality of life, and medical costs. The follow-up period is 5 years.
Conclusion The results of this trial will contribute to establishing the optimal indication for TSH suppression therapy in low-risk papillary thyroid cancer patients by evaluating the benefit and harm of lowering TSH levels in terms of recurrence, metabolic complications, costs, and quality of life.
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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.
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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.
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
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.
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.
Chang Won Lee, Hyun Ju Yoon, Won Min Hwang, Jung Kyu Kim, Hoon Sup Koo, Dong Mee Lim, Eu Gene Choi, Moon Jun Na, Do Yeun Cho, Bum Kyeong Kim, In Seok Choi, Keun Young Park
J Korean Endocr Soc. 2004;19(4):446-451. Published online August 1, 2004
An adrenocortical carcinoma is a rare malignancy, which is associated with a poor prognosis. Eighty percent of adrenal tumors are functional, and commonly secrete glucocorticoids alone (45%), glucocorticoids and androgens (45%) or androgen alone (10%). Less than 1% of all cases secrete aldosterone. A case of a 75 year old female patient was experienced, presenting with anadrenocortical carcinoma and associated concurrent Cushing's syndrome and primary aldosteronism. She had complained of left flank pain for 5 months, and also showed clinical features of Cushing's syndrome, hypertension, hypokalemia and a left abdominal mass. An abdominal CT* demonstrated a large left adrenal mass, with necrosis, and a hemorrhage in the left upper abdomen. The plasma renin activity was 0.51 ng/ml/hr, and the serum aldosterone level was increased by 46.4 ng/dL. A low and high dose dexamethasone suppression test revealed no suppression. Histologically, the tumor was diagnosed as a adrenocortical carcinoma. After complete removal of the mass, she received mitotan and prednisolone as adjuvant therapies. Liver and bone metastasis occurred after 6 months of treatment, so was treated with palliative radiotherapy for the bone metastasis