- A Case of Myxedema Coma with Severe Hypoventilation.
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Jin Young Shim, Seung Won Lee, Hyun Woo Lee, Joon Hyuck Choi, Young Jun Song, Hyoung Suk Lee, Yoon Sok Chung, Kwan Woo Lee
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J Korean Endocr Soc. 2004;19(2):203-208. Published online April 1, 2004
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- A myxedema coma, representing the extreme feature of hypothyroidism is rare. Despite early vigorous treatment, a myxedema coma is associated with a mortality rate as high as 60%. Herein, a case of a myxedema coma, with severe hypoventilation, is described. When the patient arrived at the emergency room, she complained of dyspnea and general weakness, and was of a drowsy mental status. 7 days after admission, she was more confused and disoriented, and respiratory insufficiency had developed. Although levothyroxine was continued and her respiration improved, she still had a confused mentality and seizure developed. Despite medication her consciousness did not improve, so was discharged in despair by her family members. The respiratory abnormality with a myxedema coma is a depressed ventilatory response to hypercapnea, resulting in a decrease in alveolar ventilation, with progressive CO2 retention. An upper airway obstruction, especially during sleep, and neuromuscular dysfunction in breathing may be shown in hypothyroidism. Therefore, a myxedema coma, accompanied by severe hypoventilation, should be intensively treated with thyroid hormone replacement therapy and mechanical ventilatory support
- Clinical Characteristics of 10 Cases of Korean Osteogenesis Imperfecta.
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Hyoung Suk Lee, Hyon J Kim, Jae Hyun Cho, Seong Won Lee, Hyun A Kim, Joon Hyuck Choi, Young Jun Song, Dae Jung Kim, Kwan Woo Lee, Yoon Sok Chung
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J Korean Endocr Soc. 2003;18(5):496-503. Published online October 1, 2003
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- Osteogenesis Imperfecta (OI) is a relatively rare hereditary disease, which is characterized by multiple bone fractures and spine scoliosis, due to the fragility of bone, and is often associated with blue sclerae, deafness and dentinogenesis imperfecta. Four types of OI can be distinguished, according to the clinical findings. Although mutations affecting type I collagen are responsible for the disease in most patients, the mechanism by which the genetic defects cause abnormal bone development remains to be fully understood. Here, the clinical characteristics of 10 OI patient cases are reported, with a review of the literature. All the cases, including 4 type I, 4 type III and 2 type IV, inherited OI as an autosomal dominant trait. All the subjects had multiple old fractures and decreased bone densities. In this study, the biochemical marker of bone formation, serum alkaline phosphatase, was found to be increased only in the pediatric OI patients, while the biochemical marker of bone resorption, urinary deoxypyridinoline, was increased in all cases. The mobility score was found to correlate with the severity of the type on diagnosis.
- Impaired Metabolic Signal Transduction Networks in Isolated Skeletal Muscle in Korean type 2 Diabetic Patients.
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Joon Hyuck Choi, Kwan Woo Lee, Hyo Jeong Kim, Dong Hun Lee, Jong Woo Lee, Jung Eun Kim, Hyun Chae Yim, Kyung Mi Kim, Sung Yi Choi, Yoon Sok Chung, Hyeon Man Kim
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J Korean Endocr Soc. 2002;17(5):685-697. Published online October 1, 2002
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- BACKGROUND
The glucose uptake rate is the limiting step in glucose utilization and storage. The failure of insulin to stimulate glucose uptake in muscle appears to be a primary defect of insulin resistance. This study was undertaken to examine the effect of physiological hyperinsulinemia on the phosphorylation of the insulin receptor (IR-beta), insulin receptor substrate (IRS), Akt kinase and GSK-3 in isolated skeletal muscle, in people with type 2 diabetes (n=9) and control subjects (n=11). METHODS: 75g OGTT and euglycemic hyperinsulinemic clamp test were done. And vastus lateralis muscle was obtained before and 30 min into the euglycemic clamp. Western blots were performed for tyrosine phosphorylation of insulin receptor substrate (IRS) and phosphorylation of the insulin receptor(IR-beta), Akt and GSK-3. RESULT: There were no statistical differences in the mean age, BMI and body fat between the control subjects and diabetic patients. The fasting blood sugar and HbA1c in controls and diabetic patients were 98.+/-1.3 and 208.1+/-16.5 ng/dl, and 5.4+/-0.5 and 9.2+/-0.6%, and 1.4+/-0.2 in the control subjects, and 72.2+/-52.3% (p<0.01) and 10.2+/-6.3 (p<0.01) in the diabetic patients, respectively. The insulin resistance from the euglycemic hyperinsulinemic clamp tests were 8.2+/-0.6 mg/kg/min and 3.7+/-1.1 ng/kg/min in the control subjects and in the diabetic patients, respectively (p<0.01). Compared with the normal controls, insulin-stimulated IR phosphorylation was no different to that in the diabetic patients. However, insulin-stimulated IRS phosphorylation, insulin-stimulated Akt phosphorylation and insulin-stimulated GSK-3 phosphorylation were reduced in the diabetic patients compared with the normal controls by 24, 43 and 25%, respectively (p<0.05). CONCLUSION: In korean type 2 diabetic patients, the insulin resistance may be due to the impairment of the upstream insulin signal molecular network. Further studies will focus on determining whether these signaling defects are the cause of the development of insulin resistance, or secondary to the altered metabolic state, associated with type 2 diabetes mellitus
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