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Kang Hyun Choi  (Choi KH) 3 Articles
A Case of Necrobiosis Lipoidica at the Insulin Injection Site in a Patient with Type 2 Diabetes Mellitus.
Woo Tae Kim, Tae Hoon Kim, Se Min Lee, Kang Hyun Choi, Seung Hyun Ko, Yu Bai Ahn, Ki Ho Song, Ho Young Son, Kyung Moon Kim, Si Young Kim
Korean Diabetes J. 2004;28(5):452-457.   Published online October 1, 2004
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AbstractAbstract PDF
Nearly one third of patients with diabetes mellitus have some kinds of dermatologic complication. Necrobiosis lipoidica (NL) is a rare degenerative disease of the collagen in the dermis occurring in 0.3~0.7% of the diabetic population. This is a dermatologic condition presenting plaques that have an erythematous, violaceous border and yellowish atrophic center with telangiectasis on its surface. One third of these lesions may progress to ulcer if exposed to any trauma. There is some controversy regarding the degree of association between NL and diabetes mellitus. Necrobiosis lipoidica is commonly seen in patients with type 1 diabetes, but 7~30% of diabetic patients with NL have type 2 diabetes. We report a case of 54 year-old woman with 25 years of diabetic history. Her skin lesion was oval or irregular indurated plaques with central atrophy occurring both arm, lower abdomen and both anterior thigh, especially at insulin injecton site. We focused glycemic control as a treatment and used antiplatelet agents such as aspirin and cilostazol on the basis of microangiopathic athophysiology, combined with antibiotics. We need to inspect more closely any of skin lesions in diabetic patients, thus misdiagnosis and improper treatment should be reduced.
Relative Hyperglucagonemia and Its Related Factors in Patients with Type 2 Diabetes.
Kang Hyun Choi, Ki Ho Song, Sang Hoon Lee, Seong Hoon Chung, Eun Jung Kim, Seung Hyun Ko, Hyuk Sang Kwon, Yu Bae Ahn, Kun Ho Yoon, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang
Korean Diabetes J. 2004;28(4):338-345.   Published online August 1, 2004
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AbstractAbstract PDF
BACKGROUND
Excessive secretion of glucagon contributes to metabolic disturbance in type 2 diabetes. A hyperglucagonemic state is likely to be involved in increased hepatic glucose output resulting from both gluconeogenesis and glycogenolysis. The mechanism of hyperglucagonemia, though still unclear, is explained, in part, by the decreased sensitivity of cells to insulin or glucose and disturbances of the normal oscillatory secretory pattern of insulin. The aim of the study was to determine the extent of glucagon excess and its related factors in Korean patients with type 2 diabetes. METHODS: The subjects of this study were 21 controls and 102 type 2 diabetic patients. The blood glucose, glucagon and insulin concentrations were measured at 0, 30, 60, 90 and 120 min after ingestion of 75 g of glucose, and the areas under the curve (AUC) calculated. RESULTS: The AUC of plasma glucose (AUCgc) was significantly higher in the type 2 diabetic patients than in the controls (2,026.1585.8 vs. 854.8190.3 mmol/min, P<0.01), but there was no difference in the AUC of plasma glucagon (AUCgn) between the two groups. The AUCgn in the type 2 diabetic patients was positively correlated with the duration of diabetes (r=0.202, P<0.05) or HbA1c (r=0.208, P<0.05). The AUC of serum insulin (AUCin) was negatively correlated with the duration of diabetes (r=-0.291, P<001). AUCgn, AUCgc and HbA1c in long-term diabetic patients (duration of diabetes 10 years, n=32) were significantly higher compared with recently diagnosed patients (duration of diabetes <1 year, n=38) (11,362.35,981.9 vs. 9,097. 22,990.4 ng/min; 2,119.9519.0 vs. 1,832.2477.6 mmol/min; 9.52.0 vs. 8.32.1%, P<0.05). In addition, the AUCin and insulinogenic index in long-term patients were significantly lower compared with recently diagnosed patients. (Eds note: the highlighted figures are confusing, due to your various uses of commas and period marks, olease clarify?) CONCLUSIONS: Our results suggest that duration of diabetes and poor glycemic control might be closely associated with relative hyperglucagonemia in Korean type 2 diabetic paticnts.
A Case of MELAS(Mitochondrial Encephalomyopathy, Lactic Acidosis, Stroke-like Episodes) Syndrome Manifested by Diabetic Ketoacidosis.
Sung Hoon Jung, Eun Jung Kim, So Hi Im, Kang Ju, Kang hyun Choi, Seung Hyun Ko, Yu Bae Ahn, Ki Ho Song, Ho Young Son, Sung Kyung Park, Jeong Su Jun
Korean Diabetes J. 2004;28(3):231-237.   Published online June 1, 2004
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AbstractAbstract PDF
MELAS(mitochondrial encephalomyopathy, lactic acidosis, stroke-like episodes) syndrome is a rare cause of mitochondrial encephalomyopathy, with variable clinical features, such as encephalomyopathy, lactic acidosis, stroke, diabetes, short stature, sensorineural hearing loss and basal ganglia calci-fication, etc. It can be confirmed by molecular genetic analysis that reveals the mitochondrial A3243G point mutation. Among the clinical manifestations in MELAS syndrome, diabetes mellitus is associated with impaired insulin secretion and often misdiagnosed type 1 diabetes. Herein, a rare case for the MELAS syndrome, with diabetes mellitus that came from ketoacidosis, is introduced. A 21-year-old woman, carried to the emergency department had a stuporous mentality. She was thin(BMI 16.1kg/m(2)), and had difficulty with her hearing capacity. According to the initial laboratory results, she showed the metabolic acidosis, hyperglycemia, ketonemia, and ketonuria. She was diagnosed as diabetic ketoacidosis and treated with insulin and hydration. Brain imaging from MRI, and a CT scan showed basal ganglia calcification, hemorrhagic infarction and diffuse brain atrophy. The markers for beta-cell autoimmunity were negative. Her electromyography suggested proximal myopathy. In addition, a molecular genetic analysis identified A3243G point mutation in the peripheral blood leukocytes from her, her mother and her sister.

Diabetes Metab J : Diabetes & Metabolism Journal