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포스터 전시 : 간 15 ; 만성 간질환에서 혈중 gelatinase (Matrix metalloproteinase-2와 9)의 측정 의의
권오상 ( Oh Sang Kwon ),정혁상 ( Hyuk Sang Chung ),주기탁 ( Ki Tak Ju ),정문기 ( Moon Gi Chung ),박동균 ( Dong Kyun Park ),김선숙 ( Sun Suk Kim ),김연석 ( Yeon Suk Kim ),구양서 ( Yang Suh Koo ),김유경 ( Yu Kyung Kim ),최덕주 ( Duc 대한소화기학회 2002 대한소화기학회 추계학술대회 Vol.2002 No.-
문인성 ( In Sung Moon ),권오상 ( Oh Sang Kwon ),정혁상 ( Hyuk Sang Jung ),김영남 ( Young Nam Kim ),설원종 ( Won Jong Seol ),정승기 ( Seung Ki Jeong ),주기탁 ( Ki Tak Ju ),김선숙 ( Sun Suk Kim ),서태석 ( Tae Seok Seo ),양달모 ( Dal 대한소화기학회 2003 대한소화기학회지 Vol.41 No.6
Chronic mesenteric ischemia is characterized by postprandial pain and marked weight loss. It is provoked by inadequate intestinal blood flow and the increased metabolic demands associated with digestion. Diagnosis must be based on clinical symptoms, arteriographic demonstration of an occlusive process of the splanchnic vessels, exclusion of other gastrointestinal disorders, and the response to revascularization. Specially, angiography is indicated to confirm the diagnosis, to assess disease severity, and to plan revascularization. It can be treated by either surgical reconstruction of an artery or percutaneous transluminal balloon angioplasty with or without stenting. We had experienced a 63-year-old man who presented with postprandial abdominal pain and weight loss unexplained by conventional diagnostic studies. The aortography revealed about 80% of stenotic lesion in the superior mesenteric artery. After percutaneous transluminal angioplasty, postprandial abdominal pain was completely relieved. We report a case of chronic mesenteric ischemia with a review of relevant literature. (Korean J Gastroenterol 2003;41:499-503)
급성 골수성 백혈병에서 AML1 / ETO 융합유전자와 예후
조은경(Eun Kyung Cho),정은경(Eun Kyung Jung),안정렬(Jeong Yeal Ahn),임도윤(Do Yoon Lim),경선영(Sun Young Kyung),주기탁(Ki Tak Ju),방수미(Soo Mee Bang),서일혜(Yiel Hea Seo),신동복(Dong Bok Shin),이재훈(Jae Hoon Lee) 대한내과학회 2001 대한내과학회지 Vol.61 No.6
Background: The t (8;21) (q22;q22), which produces the fusion gene AML1/ETO, is associated with relatively good prognosis and, in particular, with a good response to cytosine arabinoside. Analysis of t (8;21) positive leukemic blasts has shown characteristic morphological and immunological features. We performed this study to investigate the incidence of AML1/ETO rearrangement in adult AML, especially in M2 subtype, to make a comparison of morphologic, immunophenotypic and clinical characteristics between AML1/ETO rearrangement positive and negative group in patient with AML and to analyze the correlation with other biological parameters. Methods: From May 1995 to Sep. 2000, fifty-nine patients with AML including twenty-nine AML-M2 were studied. RNAs were extracted from leukemic cells and reverse transcriptase mediated polymerase chain reaction (RT-PCR) for AML1/ETO fusion transcript was done. Chromosome study, immunophenotypic, and clinical characteristics were analysed and statistical analysis was done. Results: The male to female ratio was 32:27 in AML and 17:12 in AML-M2. The median age was 43 years (range 14-86) in AML and 43 years (range 14-77) in AML-M2. The incidence of AML1/ETO fusion transcripts was 22.0% in AML and 44.8% in AML-M2. The morphologic finding of bone marrow in AML-M2 showed higher incidence of Auer rods, large blast with prominent golgi and abnormal granules in AML1/ETO positive patients. There was no significant difference of immunophenotype. AML patients with AML1/ETO rearrangement had a tendency of higher complete remission rate (81.8% vs 56.6%, p=0.13). The overall survival (median 82.2 weeks vs 34.4 weeks, p=0.02) and progression free survival (median 50.9 weeks vs 20.4 weeks, p=0.02) of AML1/ETO positive group were longer than those of negative group in AML. AML-M2 patients with AML1/ETO rearrangement had also a tendency of longer overall survival and progression free survival, although there was no significant difference between both group (median OS 82.4 weeks vs 15.6 weeks, p=0.07, median PFS 50.9 weeks vs 16.0 weeks, p=0.09). Conclusion: Our data suggest that AML1/ETO rearrangement is detected frequently in AML, especially M2, and is a favorable prognostic factor. Thus, molecular diagnostic approaches should be used routinely to identify patients with this genetic subtype of AML.(Korean J Med 61:650-659, 2001)
만성 B형 간질환에서 라미부딘 내성의 임상적, 바이러스적 특성
김선숙,정문기,주기탁,박동균,권오상,구양서,김유경,최덕주,황유진,김주현 대한간학회 2002 Clinical and Molecular Hepatology(대한간학회지) Vol.8 No.4
목적: B형 간염 바이러스의 증식을 억제하는 라미부딘은 초기 치료효과는 좋으나 장기간 사용시 내성으로 인한 간염의 재발이 문제이다. 본 연구는 라미부딘 치료 중인 만성 B형 간질환자에서 라미부딘 내성의 발생률, 예측인자, 임상 경과 및 약제 내성에 관여한다고 알려진 polymerase 유전자의 변이 양상에 대하여 알아보고자 하였다. 대상과 방법: 라미부딘을 1일 100 mg씩 12 개월 이상(평균 15.4개 월) 투여한 만성 B형 간질환자 170명(남녀비 3.6:1, 평균연령 38.6세)을 대상으로 하였다. 라미부딘 투여중 DNA breakthrough가 관찰된 군(이하 내성군)과 DNA breakthrough가 관찰되지 않은 군(이하 비내성군)으로 분류하여, 임상적, 생화학적, 바이러스적 특징과 임상적 경과를 비교하였으며 내성군 중 혈청 보관이 가능했던 26예는 치료 전과 내성 발생후 혈청에서 직접 염기순서분석법과 RFLP을 시행하여 YMDD motif를 포함한 polymerase유전자의 변이양상을 분석하였다. 결과: 1) 라미부딘 약제 내성은 총 170예 중 32예(19%)에서 발생하였고 누적발생률은 12개월에 11%, 24개월에 34%였다. 2) 내성군의 평균연령이 35.6±9.4세로 비내성군의 39.4±9.4세에 비하여 유의하게 낮았다(P<0.05). 평 균 투여기간은 내성군이 17.8±3.5개월로 비내성군 의 14.93.6개월에 비하여 긴 경향을 보였고 성별, 치료 전 ALT, HBV-DNA치, 알부민, 혈소판치는 두 군간의 유의한 차이가 없었다. 치료 전 HBeAg이 양성인 148예 중 32예(22%)에서 내성이 발생하였으나 치료 전 HBeAg이 음성인 경우에는 내성 발생이 한 예도 없었다(p<0.05). 치료 중 HBeAg이 음전된 47예 중 2예(4%)에서 내성이 발생하였으나 치료 중 HBeAg이 음전되지 않은 101예 중 30예(30%)에서 내성이 발생하여 유의한 차이가 있었다.(p<0.05). 3) 약제내성과 관련된 예측인자를 알아보기 위하여 다변량 분석을 시행하였는데 유의한 예측인자는 없었다(p>0.05). 4) 라미부딘 내성 발생까지의 평균 투 여기간은 12.4±3.7개월이었고 내성 발생 후 평균 투여기간은 5.9±3.5개월이었다. 5) 내성군의 임상경과는 ALT치가 치료전보다 높게 상승한 예는 17예 (53%)였고 낮게 상승한 예는 13예(41%)였으며 2예 (6%)는 ALT의 변화가 없었다. 내성 발생 후 ALT 치, HBV DNA치의 변화는 다양하였지만 황달이나 복수 등 비대상성 악화는 관찰되지 않았고 1예에서 라미부딘 내성과 함께 HBeAg이 음전되었다. 6) Polymerase 유전자의 YMDD motif 변이는 26예 중 19예(73%)에서 관찰되었는데 M552I가 13예, M552V + L528M가 2예, 야생형과의 혼재한 경우가 4예였고 이들은 치료 전 혈청에서는 관찰되지 않았다. YMDD motif외의 다른 부위에서 L547V, I572V, L577W, E611D, V614I, L615Q, I617L등의 변이가 관찰되었는데 이들은 치료 전 혈청에서도 관찰되었다. 결론: 1) 라미부딘 내성의 누적발생율은 12개월 에 11%, 24개월에 34%였다. 2) 약제내성과 관련된 유의한 예측인자는 없었다. 3) 내성 발생 후 간염의 경과는 다양하였지만 황달이나 복수 등 비대상성 악화는 관찰되지 않았다. 4) 라미부딘 내성 시 YMDD motif 변이는 약 73%에서 관찰되었으며, 내성에 관여하는 요인에 대한 연구 및 장기 추적연구가 있어야 할 것이다. Background/Aims: Lamivudine therapy in chronic hepatitis B has been shown to be effective in inhibiting HBV replication. However, lamivudine resistance has been developed with prolonged use. We studied to determine the prevalence, predictive factors, and clinical outcomes of lamivudine resistance. Mutations in YMDD motif of HBV polymerase, which have been associated with lamivudine resistance, were also assessed. Methods: 170 patients with HBV-associated chronic liver disease who have received lamivudine for at least one year, were studied. The clinical, biochemical, and virologic characteristics were analyzed and compared according to presence (resistance group) or absence (non-resistance group) of DNA breakthrough. Their clinical outcomes were regularly followed. Stored sera before treatment and after DNA breakthrough were examined for detection of HBV polymerase mutation by direct sequencing and/or RFLP. Results: Cumulative rates of lamivudine resistance after one and two years of treatment were 11% and 34%, respectively. In the resistance group, as compared to the non-resistance group, age, the presence of HBeAg before treatment, and disappearance of HBeAg during treatment, were significantly different. The predictive factors associated with lamivudine resistance were not found. ALT and HBV-DNA level after lamivudine resistance was variable, but jaundice or hepatic failure was absent. Mutation in YMDD motif was detected in 73% and other variable mutations were detected before treatment and after DNA breakthrough. Conclusions: Lamivudine resistance increases the longer the duration of treatment and clinical outcomes are variable. The mutation in YMDD motif was found in about 2/3 of cases. Other causes for lamivudine resistance may be considered.(Korean J Hepatol 2002;8:405-417)
임신 후반기에 진단된 쿠싱 증후근 산모에서 미숙아 분만후 부신적출술을 경험한 1 예
송광식,이기영,송석호,양달모,강문호,김홍규,황재경,주기탁,이항진,서찬종,박혜영,오영하 대한내분비학회 2001 Endocrinology and metabolism Vol.16 No.1
We experienced a case of Cushing's syndrome due to adrenocortical adenoma associated with 3lth week (third trimester) pregnancy in a 29 year-old female patient. The patient complained of generalized weakness, fatigue, and febrile sensation. On physical examinations, hypertension, moon face, plethoric face, abdominal striae, and scattered petechiae were found. Laboratory findings showed increased serum cortisol (AM 8:00.8 pg/dL, PM 1l:0054.9 pg/dL), increased 24 hours-urinary free cortisol (1,598 pg/day), and decreased plasma ACTH (AM 8:00.41 pg/mL, PM 11:005.66 pg/mL) and not suppressed high dose dexamethasone suppression test. Abdominal MRI demonstrated 3?4 cm sized well marginated and round shaped left adrenal mass. At the 31th week of pregnancy, unexpectedly ruptured membrane was developed. She delivered baby weigting 1.3 kg through induction vaginal delivery. Unilateral adrenalectomy was performed after delivery and the mass was canfirmed to be benign adrenal adenoma. Steroid replacement therapy was contnued with 5mg prednisolone after left adrenalectomy. After unilateral adrenalectomy and conservative management, her symptoms was improved gradually (J Kor Soc Endocrinol 16:134-139, 2001).