Comparative analysis of the efficacy of omega-3 fatty acids for hypertriglyceridaemia management in Korea H.-S. Kim, H. Kim, Y. J. Jeong, S. J. Yang, S. J. Baik, H. Lee, S.-H. Lee, J. H. Cho, I.-Y. Choi, H. W. Yim, K.-H. Yoon Journal of Clinical Pharmacy and Therapeutics.2016; 41(5): 508. CrossRef
Ji Young Park, Ji In Lee, Alice Hyun Kyung Tan, Hye Won Jang, Hyun Won Shin, Young Lyun Oh, Jung Hee Shin, Jung Han Kim, Ji Soo Kim, Young Ik Son, Sun Wook Kim, Jae Hoon Chung
J Korean Endocr Soc. 2009;24(3):165-173. Published online September 1, 2009
BACKGROUND The outcomes of papillary thyroid carcinoma (PTC) variants have been described in a limited number of studies. The purpose of this study was to compare patient outcomes of PTC variants with those of patients with classic PTC. METHODS: A single-institution retrospective analysis was performed to review 2,366 patients with classic PTC and 159 patients with PTC variants diagnosed between 1994 and 2004. PTC variant patients were divided into two groups, favorable (n = 119, 119 follicular variants including 14 encapsulated follicular variants) and aggressive (n = 40, including 13 diffuse sclerosing, 11 tall cell, six solid, six oncocytic, and four columnar cell variants). RESULTS: Compared with classic PTC, the favorable and aggressive variants had a significantly larger tumor size (P<0.001). The favorable variants had significantly lower rates of bilaterality, multifocality, extrathyroidal invasion, cervical lymph node metastasis, stage III and IV disease, and greater male to female ratio (P<0.05). In particular, the encapsulated follicular variant showed no bilaterality, multifocality, extrathyroidal invasion, lymph node metastasis, and distant metastasis. However, the disease-specific survival and recurrence-free survival of patients with favorable PTC were not different from the patients with classic PTC. The aggressive variants had significantly higher rates of bilaterality and cervical lymph node metastasis compared to the classic PTC (P<0.05). They had significantly reduced disease-specific survival and recurrence-free survival rates (P<0.01). CONCLUSIONS: Knowledge of the nature of PTC variants, especially aggressive types, is important in predicting patient outcome and providing appropriate treatment. Further study is needed to better understand PTC variants.
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Ultrasonographic Characteristics of the Follicular Variant Papillary Thyroid Cancer According to the Tumor Size Eon Ju Jeon, Young Ju Jeong, Sung Hwan Park, Chang Ho Cho, Ho Sang Shon, Eui Dal Jung Journal of Korean Medical Science.2016; 31(3): 397. CrossRef
Follicular Variant of Papillary Thyroid Carcinoma: Distinct Biologic Behavior Based on Ultrasonographic Features Sun Jung Rhee, Soo Yeon Hahn, Eun Sook Ko, Jae Wook Ryu, Eun Young Ko, Jung Hee Shin Thyroid.2014; 24(4): 683. CrossRef
BACKGROUND In patients with hypoglycemia due to endogenous hyperinsulinemia such as insulinoma or insulin autoimmune syndrome, little is known about the counterregulatory hormone response to spontaneous hypoglycemia. We therefore compared hormone responses during spontaneous hypoglycemia due to endogenous hyperinsulinemia with those at the end of a 72-hour fast. METHODS: We measured glucagon, epinephrine, cortisol, and growth hormone responses during spontaneous hypoglycemia in 8 patients with insulinoma and 18 patients with insulin autoimmune syndrome. We also assessed these responses in 13 normal control subjects who underwent a 72-hour fast. RESULTS: In patients with insulinoma (median serum glucose level, 35.0 mg/dL), plasma glucagon levels (median, 42.9 vs. 76.2 pg/mL, respectively; P < 0.05) were lower than those in control subjects (serum glucose level, 62.5 mg/dL), whereas, there were no statistically significant differences in the other hormone responses between the two groups. In contrast, in the patients with insulin autoimmune syndrome (median serum glucose level, 34.5 mg/dL), plasma glucagon levels (median, 73.7 vs. 76.2 pg/mL, respectively) were lower than those in the control subjects, but there was no statistically significant difference between the two groups. There were no statistically significant differences in counterregulatory hormone responses during spontaneous hypoglycemia between patients with insulinoma and patients with insulin autoimmune syndrome. CONCLUSION: Our results suggest that defective glucagon secretion in patients with insulinoma rather than insulin autoimmune syndrome may contribute to hypoglycemia in addition to hyperinsulinemia.
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Glycogenic hepatopathy in a Korean girl with poorly controlled type 1 diabetes mellitus Hwal Rim Jeong, Young Seok Shim, Young Bae Kim, Hae Sang Lee, Jin Soon Hwang Annals of Pediatric Endocrinology & Metabolism.2014; 19(1): 49. CrossRef
Glucose Counterregulatory Hormone Response During Hypoglycemia due to Endogenous Hyperinsulinemia Jung Guk Kim Journal of Korean Endocrine Society.2009; 24(3): 162. CrossRef
BACKGROUND The present study investigated the rates and the potential predictors of either new pituitary loss or recovery of hormonal function after transsphenoidal removal of a non-functioning pituitary adenoma. METHODS: Patients who underwent transsphenoidal removal of a non-functioning pituitary adenoma from January 2003 to December 2007 at Ajou University Medical Center were included in this retrospective analysis. Patients were excluded if they had a history of previous pituitary tumor surgery, or did not have preoperative pituitary hormonal data. RESULTS: Of 42 patients included in the analysis, 36 patients had hypopituitarism, 21 patients had "stalk compression" hyperprolactinemia, and 2 patients had normal pituitary function. At long term follow-up (longer than 6 months), 13 patients showed postoperative pituitary hormonal recovery in at least 1 hormonal axis, while 6 patients had developed postoperative hormonal loss in at least 1 hormonal axis. On analysis, neither preoperative serum prolactin level nor tumor size was related to postoperative pituitary hormonal changes. CONCLUSION: More than 1/3 of patients who underwent transsphenoidal surgery showed postoperative pituitary hormonal recovery.
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Childhood Onset Pituitary Adenoma: Clinical Presentations and Outcomes of 24 Cases Hwa Young Kim, Hae Woon Jung, Jieun Lee, Ju Young Yoon, Young Ah Lee, Choong Ho Shin, Sei Won Yang Annals of Pediatric Endocrinology & Metabolism.2012; 17(2): 82. CrossRef
Se Kyung Park, Duk Su Kim, Mi Oh Roh, Min Soo Song, Chan Hee Jung, Jung Hwa Jung, Hyeong Kyu Park, Yeo Ju Kim, Ji Oh Mok, Sang Jin Kim, Chul Hee Kim, Dong Won Kim, Dong Won Byun, Kyo Il Suh, Myung Hi Yoo
J Korean Endocr Soc. 2009;24(3):189-194. Published online September 1, 2009
Pheochromocytoma not only decreases insulin secretion but also increases insulin resistance. One third of patients with pheochromocytoma have diabetes mellitus and their clinical prognosis showed improvement after surgery. Until now, those patients whose prognosis for diabetes mellitus improved after the operation of pheochromocytoma had typical characteristics such as hypertension, palpitation, headache and elevated hormones such as Vanillylmandelic acid, metanephrine, epinephrine and norepinephrine. We present the case of a 75-year-old woman with asymptomatic adrenal incidentaloma identified as pheochromocytoma which exhibited normal biochemical test results, and after removal of the abdominal mass, her severe hyperglycemia improved.
The term pseudohypoparathyroidism describes a rare disorder characterized by resistance to the action of immunoreactive parathyroid hormone (PTH) in peripheral tissue rather than a deficiency of PTH. Patients present with tetany, spasm, hypocalcemia, hyperphosphatemia, and Albright's hereditary osteodystrophy (AHO). We present a case of symptomatic hypocalcemia due to pseudohypoparathyroidism aggravated by rhabdomyolysis. A 21-year-old man presented with tetany, AHO phenotypes and an ankle infection. Rhabdomyolysis was confirmed by marked elevation of serum creatine phosphokinase, more than 10 times above normal. Spasm was observed and the serum value of total calcium was as low as 3.7 mg/dL and that of phosphate was as high as 7.0 mg/dL, and the peak level of PTH was at 80.4 pg/mL. Although not surveyed by Ellsworth-Howard test and molecular study, it was classified as pseudohypoparathyroidism type 1a or 1c. The clinical and laboratory abnormalities were corrected by vitamin D in addition to calcium. The patient's mother, sister, and grandmother had AHO phenotypes without clinical and biochemical manifestations. To the best of our knowledge, this is the first case by maternal inheritance that AHO phenotypes appear for three generations of a family in Korea.
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A Case of Pseudohypoparathyroidism with Graves' Disease Gil Woo Lee, Jae Hoon Kim, Kang Won Lee, Sa Il Kim, Sang Mo Hong, Dong Sun Kim, Woong Hwan Choi, You Hern Ahn, Tae Wha Kim Endocrinology and Metabolism.2010; 25(3): 221. CrossRef
Primary aldosteronism is a syndrome characterized by various clinical features that are due to excessive autonomous aldosterone secretion not sustained by the activation of the renin-angiotensin system. Aldosterone-producing adrenal adenoma is found in approximately 35% of the patients who suffer with primary aldosteronism. Laparoscopic adrenalectomy is the standard treatment for aldosterone-producing adrenal adenoma, and the result of this operation is normalization of the serum potassium and plasma aldosterone concentrations, as well as correcting the plasma renin activity in most cases. However, it is known that some of the patients with aldosterone-producing adrenal adenoma show transient hyperkalemia postoperatively due to the reversible suppression of the renin-aldosterone axis. We recently experienced the case of a 54-year-old woman with an aldosterone-producing adrenal adenoma, and she presented with severe hyperkalemia after unilateral adrenalectomy. Compared with the previously reported cases that showed transient suppression of the rennin-aldosterone axis for less than 7 months, our patient revealed a prolonged episode of hyperkalemia for 8 months postoperatively, and this required continuous mineralocorticoid replacement.
Here we describe a male patient who attained normal height despite combined hypopituitarism with an abnormal growth hormone-insulin-like growth factor (IGF)-I axis. When he was an 18-year-old, he presented with a short stature and underdeveloped external genitalia. The patient had not undergone normal pubertal development and he displayed a height below the fifth percentile. Hormonal and radiological studies revealed the findings of severe anterior pituitary hormone deficiency and an atrophic pituitary gland. There had been no recent follow-ups with the patient or medical treatment since that time. In the current presentation, the patient, now 22 years of age, had attained normal height, yet he remained prepubertal and showed manifestations of delayed bone age and combined hypopituitarism. In addition, the patient's IGF-II levels were increased for his age.
Many studies have shown that patients taking antiepileptic drugs are at an increased risk for metabolic bone disease and low bone mineral density. Traditionally, this has been attributed to alterations in vitamin D metabolism by antiepileptic drugs which induce hepatic microsomal cytochrome P450 enzyme. However, there appear to be multiple mechanisms for antiepileptic drug-induced bone loss including lack of physical activity, reduced sunlight exposure, increased propensity for falling, and fractures associated with seizures or loss of consciousness. We experienced a case of antiepileptic drug-induced osteomalacia in a 63-year-old woman who had been on phenytoin for 8 years and was admitted with hypocalcemic seizures and multiple pathological fractures. This patient also had other risk factors for osteomalacia including reduced sunlight exposure, prolonged immobilization, and decreased dietary vitamin D intake. We discontinued phenytoin, and started calcium and vitamin D replacement. The patient's serum calcium and vitamin D level were normalized after treatment. Metabolic bone disease including osteomalacia should be considered in patients who are taking antiepileptic drugs especially those who are exposed to other risk factors.
Intramural hematoma of the aorta is a variant of aortic dissection characterized by the absence of direct communication between the false lumen and the true lumen of the aorta. Primary aldosteronism, which is an uncommon cause of hypertension, may direct alter arterial structure through the pleiotropic effects of aldosterone as well as pressure-mediated indirect alterations. There have been several reported cases of aortic dissection in patients with primary aldosteronism, which suggests a causal relationship between the two diagnostic entities. However, intramural hematoma has not been described in a patient with primary aldosteronism. We describe a case of aortic intramural hematoma in a patient with primary aldosteronism and speculate about the causal relationship between these two entities.