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인슐린 비의존형 당뇨병환자에서 중식성 망막증 발생에 관한 종적연구
조구영(Goo Yeong Cho),김상욱(Sang Wook Kim),이미화(Mee Wha Lee),박중열(Joong Yeol Park),제수정(Soo Jung Je),이기업(Ki Up Lee),김기수(Ghi Su Kim) 대한내과학회 1994 대한내과학회지 Vol.47 No.4
N/A Background: Proliferative diabetic retinopathy (PDR), a late stage of diabetic retinopathy, is the com- monest cause of acquired blindness in adults. Despite many previous studies, the risk factors for the development of PDR in Korean NIDDM patients have not been precisely defined yet. The aims of the present study were to evaluate the incidence and the risk factors of PDR. Method: From April to June 1993, we retrospectively studied 243 NIDDM outpatients (duration of diabetes 7.9±7.1, age 54.5±10.8, male 110 and fema1e 133) who had undertaken fundoscopic examination for diabetic retinopathy before April 1991. At the time of the examination, 70 patients had nonproliferative diabetic retinopathy (NPDR). Of those, 12 patients progressed to PDR and 58 patients did not. Clinical characteristics and laboratory findings of progressed group were compared with non-progressed group. Results: Of the 162 patients who were free of diabetic retinopathy at the initial examination, 18 patients progressed to diabetic retinopathy; the incidence rate of diabetic retinopathy was 34.9/1,000 person-yr. Of these, 1 patients had PDR (1.9/1,000 person-yr). After 2.6 years of mean follow-up, 12 out of 70 patients with initial NPDR progressed to PDR. The incidence rate of PDR in the patients with NPDR was 63.2/1,000 person-yr. Microalbuminuria, more severe weight loss, lower level of C-peptide and insulin therapy were associated with an increased 2.6-year risk of developing PDR. However, sex, smoking, use of antihypertensive drugs or aspirin, age, duration of diabetes and the mean fasting serum glucose, hemoglobin Al, cholesterol, systolic or diastolic blood pressure levels during the follow-up period were not associated with the progression to PDR. Forward stepwise multiple logistic regression analysis revealed that initial microalbuminuria and delta BMI are significant independent predictor for the progression to PDR. Conclusion: Microalbuminuria can be used as a predictor for progression to PDR. Lower level of C-peptide, more severe weight loss and current insulin use may be also the risk factors for progression to PDR in Korean NIDDM patients with nonproliferative retinopathy. However, long-term prospective study is warranted to answer the question more properly.
부신피질 호르몬이 사람골수기질세포의 Apoptosis에 미치는 영향
김하영,김덕재,이시열,홍정수,김동관,김기수 대한내분비학회 2002 Endocrinology and metabolism Vol.17 No.1
Background: Osteoporosis is one of the most serious side effects of long-term glucocorticoid therapy, but the mechanism of glucocorticoid-induced bone loss remains poorly defined. Glucocorticoid induces decreased bone formation and death of isolated segments of bone (osteonecrosis) suggesting that glucocorticoid excess may affect the birth or death rate of bone cells and thereby reduce their numbers. It has been known that reduction in bone formation is due to reduced proliferation in osteoblast precursor cells and reduced matrix synthesis in mature osteoblast. Here, we present evidence for dexamethasone-induced apoptosis on human bone marrow stromal cells (hBMSC). To understand the mechanism of glucocorticoid-induced osteoporosis, we investigated the effects of glucocorticoid on primary cultured hBMSC. Methods: Treatment with dexamethasone at the concentration of 10^-9 M for 3∼5 days significantly decreased cleavage tetrazolium salt WST-1 level/concentration by mitochondrial dehydrogenase in viable cells. Greater decrease was observed with higher concentration of dexamethasone (10^-7 M, and 10^-5 M). Apoptosis was measured by annexin V binding/propidium iodide using fluorescence-activated cell sorter (FACS) analysis and nuclear morphology stained with the fluorescence dye, Hoechst 33342. Results: The level/concentration of apoptotic hBMSC (annexin V positive / PI negative) was increased with 10^-9 M dexamethasone (1.2% to 5.3%) and further increased with 10^-7 M, and 10^-5 M concentration (11.7% and 12.5%, respectively). The same result was observed with Hoechst 33342 staining. Conclusion: These results indicate that glucocorticoid induces apoptosis on osteoblast precursor cell, hBMSC, and may contribute to decrease bone formation