급성 출혈성 직장 궤양에 의한 직장 출혈

출혈성 직장 궤양 증후군은 하부 위장관 출혈의 매우 드 문 원인이다. 그러나 심각한 전신 질환을 동반한 노인에게서 복통 없이 갑작스러운 대량의 선홍색 혈변을 보일 때 혈변의 원인으로 급성 출혈성 직장 궤양을 고려해보는 것은 중요하다. 출혈성 직장 궤양을 인식하고 있다면 불필요한검사를 피하고 조기에 정확한 진단을 함으로서 환자의 예후 도 향상시킬 수 있을 것이다. 저자는 하부 위장관 출혈의 원인으로 알려져 있으나 인지되지 않아 아직까지 국내에서 보고되지 않은 것으로 생각되는 급성 출혈성 직장 궤양 증후군 환자를 경험하였기에 문헌고찰과 함께 보고하는 바이다.Acute hemorrhagic rectal ulcer syndrome (AHRUS) is characterized by the sudden onset of painless, massive, fresh rectal bleeding in elderly or bedridden patients with serious underlying illnesses. With increasing elderly populations, and improved survival in critically ill patients, the incidence of AHRUS has increased in Japanand Western countries in recent years. However, AHRUS remains a controversial disease entity and has not yet been documented in Korea. Here, we present a case of AHRUS to highlight this uncommon disease entity as a potential etiology of massive rectal bleeding in critically ill patients

종격동 농양이 동반된 자발성 점막하 식도 박리 1예

Spontaneous submucosal dissection of the esophagus (SDE) is a rare disease, in which spontaneous submucosal spot bleeding or intramural hematoma leads to the tearing of the layers between submucosa and muscle of the esophageal wall without any definitive cause, and the pathogenesis of SDE has not been well documented yet. Typical symptoms of SDE are chest pain, hematemesis, dysphagia, and odynophagia. The laboratory tests are usually normal and symptoms could be mild and ambiguous, so the diagnosis of SDE is conducted with endoscopy or esophagogram in most cases. The prognosis of SDE is usually very good with just conservative cares such as fasting and fluid therapy. Esophageal perforation complicated by SDE is very rare because symptoms od SDE usually bring the patients to hospital before perforation. Recently, we experienced a case of a 54 year-old male showing the endoscopic findings of SDE and complicated mediastinal abscess probably following esophageal perforation. The patient had social history of chronic heavy alcoholic ingestion and had symptoms of substernal pain, dysphagia, and odynophagia. The patient recovered after partial esophagectomy, abscess drainage and antibiotic therapy. (Korean J Gastrointest Endosc 2005;31:97-101

간문맥 혈전이 동반된 진행성 간세포암에서 간동맥내 항암제 주입요법

Background: Advanced hepatocellular carcinoma (HCC) with portal vein thrombosis has a poor prognosis and has little hope for meaningful therapy. Transarterial chemoembolization has been performed as a treatment for advanced HCC, but some patients die from progressive liver failure after therapy. This study was undertaken to evaluate the therapeutic effects of intra-arterial infusion chemotherapy in advanced HCC with portal vein thrombosis, and to compare with those of systemic chemotherapy, and to identify prognostic factors that could affect survival. Methods: Between January 1995 and January 2001, a total of 102 patients with advanced HCC having portal vein thrombosis (TNM stage IVa) were enrolled and divided into 3 groups; Group 1 (n=24) was managed with only conservative treatment, group 2 (n=25) received systemic combination chemotherapy consisting of 5-fluorouracil (FU) + Adriamycin + Mitomycin C, or 5-FU + Etoposide Cisplatin, and group 3 (n=52) received intra-arterial infusion chemotherapy with 5-FU (250 mg for 5 days) + cisplatin (10 mg for 5 days) via implanted chemoport. Results: One-year survival rates were 0%, 4%, 21%, and median survivals were 2-, 4-, 6 months in group 1, group 2, group 3, respectively (p=0.003). When we divide group 3 patients into long term survivors (more than 8 months) or short term survivors (less than 8 months), former had significantly lower level of serum AST (p=0.032) and alkaline phosphatase (p=0.033). Especially, all female patients (n=9) survived more than 8 months, and had a longer survival than male patients (p=0.000). Other favorable prognostic factors for survival were cirrhosis of Child-Pugh class A (p=0.003), only one major branch involvement of the portal vein by tumor (p=0.005), presence of enhancement of tumor portion in arterial phase of CT scan (p=0.044), presence of enhancement of non-tumor portion in portal phase of CT scan (p=0.029). Conclusion: Intra-arterial infusion chemotherapy achieved favorable results in advanced HCC with portal vein thrombosis and showed better survival in selected patients. This therapy can be tried as a treatment option for the management of advanced HCC

내시경적 지혈술로 치료된 결절성 다발 동맥염에 의한 공장 출혈 1예

Polyarteritis nodosa is a necrotizing vasculitis of the small and medium-sized arteries of multiple organ systems. The common symptoms of gastrointestinal involvement are abdominal pain, nausea, and vomiting. However, the symptoms at presentation are sometimes non-specific and vague. The well-known complications of gastrointestinal involvement are mucosal ulceration, bowel infarction, perforation, cholecystitis and hepatitis. We describe a case of a 6-year-old male with jejunal bleeding who was diagnosed with polyarteritis nodosa by angiography. After controlling the systemic symptoms with immunosuppressants and steroids, jejunal bleeding occurred. The jejunal bleeding was treated endoscopically with a hemoclip and increasing the immunosuppressant dose. Generally, massive gastrointestinal bleeding in a patient with polyarteritis nodosa is treated surgically. In this case, the jejunal bleeding was controlled with an endoscope because the bleeding site was located within reach of the endoscope, and systemic symptoms subsided with medication. There is no report of gastrointestinal bleeding from the polyarteritis nodosa in a child in Korea. Therefore, we report this case with a review of the relevant literature

PRECEDE-PROCEED 모델의 개념틀을 이용한 제조업 노동자의 건강행동에 영향을 미치는 요인에 대한 다수준 분석

학위논문(석사)--서울대학교 보건대학원 :환경보건학과 환경보건학전공,2004.Maste

위계적 질환군(HCC) 위험조정모델 기반 의료비용 예측

연구목적 많은 OECD 국가들에서 의료비용 증가는 건강보험 지속성을 위협하는 심각한 문제로 인식되고 있으며, 소비자 선택권 보장과 공급자 경쟁을 통해 건강보험을 개혁하고 있다. 전문가들은 위험조정모델을 건강보험 개혁의 핵심으로 꼽고 있다. 본 연구에서는 건강보험 표본코호트를 활용하여 미국 메디케어의 위계적 질환군 (HCC, Hierarchical Condition Category) 위험조정모델을 기초로 한국의 투약자료와 이전 의료이용 변수를 추가한 위험모델을 구축하고, 의료비용을 예측하고자 한다. 연구방법 건강보험공단에서 구축한 표본코호트 DB 2009년 자료를 이용하여 회귀모델을 구축하고, 변수별 회귀계수를 산출하였다. 2010년 자료를 바탕으로 2011년 개인별 의료비용을 예측하고, 2011년 실제 의료비용과 비교하였다. 의료비용 예측을 위해 4개의 모델을 이용하였다: model 1 (demographics), model 2 (HCCs & demographics), model 3 (bed-days, HCCs, & demographics), model 4 (medication-days, bed-days, HCCs & demographics). 개인 수준에서 모델을 평가하기 위해 R2를 이용하였고, 상위 5% 고의료비용 환자에 대해서는 양성예측도 (PPV, predictive positive value)를 이용하여 평가하였으며, 특정집단에 대한 의료비용 예측 비교는 예측비 (PR, predictive ratio)를 이용하였다. 결과 이전 입원일수 (bed-days), 이전 투약일수 (medication-days)를 포함하는 모델의 의료비용 예측력이 더 높았다. model 1, model 2, model 3, model 4 각각의 R2 값은 8%, 38%, 58%, 59%였다. 의료비용 상위 0.5% 극단값을 절단한 후 분석한 R2 값은 4개 모델에서 모두 증가했다. 가장 높은 의료비용 집단에서는 총의료비용이 과소예측되었고, 나머지 4개 집단에서는 과대예측 되었다. 나이가 젊은 집단에서 고령 집단으로 갈수록 남자, 여자 모두에서 예측비가 낮아지는 경향을 보였다. 결론 위험조정모델은 보험사 급여지급, 의료서비스 보상체계, 프로파일링, 연구 등 다방면에서 중요성이 높아졌다. 기존의 진단자료와 이전 의료이용 자료를 조합한 위험조정모델이 높은 의료비용 예측력을 보여주었고, 고의료비용 환자들을 비교함에 있어서 어느정도 정확성을 보여주었다. 향후 질병의 시간 흐름에 따른 변화와 한국 의료환경의 특성을 반영할 수 있는 모델에 대한 연구와 평가가 필요하다.Ⅰ. 서론 01 A. 연구배경 및 필요성 01 B. 연구목적 07 C. 이론적 배경 08 1. 한국의 국민건강보험 08 2. 건강보험 개혁의 새로운 흐름 09 3. 위험조정 16 4. 위계적 질환군 (HCC) 위험조정모델 25 5. 용어 정리 41 Ⅱ. 연구대상 및 방법 43 A. 연구모형 43 B. 연구대상 및 자료 45 1. 연구대상 자료 45 C. 변수의 정의 46 1. 결과변수 46 2. 설명변수 46 D. 분석방법 51 1. 모델분석 51 2. 모델평가 51 Ⅲ. 연구결과 54 A. 개인 의료비용에 대한 모델의 설명력 54 B. 2010년 실제 고의료비용 환자와 2011년 예상 고의료비용 환자의위험요인과의 연관성 55 C. 2011년 예상 의료비용과 실제 의료비용의 비교 57 1. 나이/성별 기준 57 2. 의료비용 5분위 기준 57 3. 만성질환 기준 57 D. 의료비용 상위 5%의 양성예측도 59 Ⅳ. 고찰 60 Ⅴ. 결론 65 참고문헌 66 부록 72 ABSTRACT 81Docto

Helicobacter 위염에서 TLR-4 신호전달을 매개로 한 Epigallocatechin-3-gallate의 위점막 보호 효과

Helicobacter pylori infection leads to gastric mucosal damage by several mechanisms including the direct effect of virulence factors produced by H. pylori, propagation of inflammation, oxidative stress, DNA damage, and induction of apoptosis. (-)-Epigallocatechin-3-gallate (EGCG), one of green tea catechins, is known to suppress H. pylori-induced gastritis through its antioxidative and anti-bacterial actions. In this study, we evaluated protective mechanism of EGCG against H. pylori-induced cytotoxicity in gastric epithelial cells. For analyzing EGCG effect on viability of gastric epithelial cells, MTT assay and dye exclusion assay were performed. The degree of DNA damage was evaluated by Comet assay and apoptotic DNA fragmentation assay. To investigate EGCG effect on H. pylori-induced the toll-like receptors 4 (TLR-4) signaling, RT-PCR and western blot analysis corresponding to glycosylated TLR-4 was done. LOX metabolites were measured with RP-HPLC. EGCG pretreatment effectively rescued gastric mucosal cells from the H. pylori-induced apoptotic cell death and DNA damage, and administration of this catechin enhanced gastric epithelial cell proliferation. H. pylori infection stimulated the glycosylation of TLR-4 which initiates intracellular signaling of infected host cell, and then pretreatment of EGCG completely blocked its glycosylation. The blockage of TLR-4 activation by EGCG resulted in inactivation of ERK1/2 and NF-kB as downstream molecules of TLR-4 signaling induced by H. pylori. This disturbance of H. pylori-induced host cell signaling by EGCG attenuated the synthesis of proinflammatory mediators, HETEs. EGCG pretreatment showed significant cytoprotective effects against H. pylori-induced gastric cytotoxicity via interference of TLR-4 signaling induced by H. pylori. Thus, our result implies that continuous intakes of green tea could prevent the deleterious consequences of H. pylori infection.Helicobacter pylori (HP)가 위점막에 감염되면 염증성 사이토카인를 분비하여 염증 세포를 유인하고, 산화적 스트레스를 가하여 DNA의 손상 및 세포 사멸을 유발하여 위점막 손상을 일으킨다. 녹차 catechin의 일종인 Epigallocatechin-3-gallate (EGCG)는 과거부터 항염증 및 항균 작용이 있다고 알려져 있고 최근 HP에 의한 위점막 손상을 감소시키는 효과가 있다고 보고 되었으나 구체적으로 어떤 기전으로 위점막 손상을 감소시키는지 알려져 있지 않아 그 기전을 규명하고자 본 연구를 시작하였다. 재료 및 방법: EGCG가 HP 감염된 위상피 세포의 생존에 미치는 영향을 알기 위하여 MTT법과 dye exclusion법을, DNA 손상에 대한 효과를 알기 위하여 Comet법과 DNA fragmentation 분석법을, toll-liker receptors 4 (TLR-4)에 대한 영향을 알기 위하여 RT-PCR법과 glycosylated TLR-4에 대한 western blot법을, lipooxygenase(LOX) 대사 산물의 변화를 알기 위하여 reverse phase-high performance liquid chromatography(RP-HPLC)법을 각각 이용하였다. 결과: EGCG를 전처치하였을 때 HP 감염에 의한 세포 사멸과 DNA 손상이 현저히 감소하였고 위상피 세포의 증식이 증가하였다. HP의 감염은 세균 감염에 대한 세포내 신호 전달을 담당하는 TLR-4의 glycosylation을 증가시키고 NF-κB와 ERK1/2의 발현을 증가시켰으나 EGCG로 전처치할 경우 TLR-4의 glycosylation을 완전히 억제시켰고 NF-κB와 ERK1/2의 발현을 억제시켰다. EGCG를 전처치할 경우 HP 감염에 의한 염증 매개 물질 및 hydroxyeicosatetraneoci acid(HETE)의 발현 증가를 현저히 감소시켰다. 결론: EGCG의 전처치는 TLR-4의 발현 억제릉 통하여 HP 감염에 의한 위점막 손상을 감소시켰고, HP가 감염된 경우 지속적으로 녹차를 음용할 HP에 의한 위점막 손상을 예방할 수 있으리라 생각된다."TABLE OF CONTENTS ABSTRACT = ⅰ TABLE OF CONTENTS = ⅲ LIST OF FIGURES = ⅴ ABBREVIATION = ⅵ Ⅰ. INTRODUCTION = 1 Ⅱ. MATERIALS AND METHODS = 4 A. MATERIALS = 4 1. Chemicals and reagents = 4 2. Cells, Bacterial strains, and Growth conditions = 4 B. METHODS = 5 1. MTT assay and cell growth = 5 2. Comet assay = 6 3. DNA fragmentation method = 6 4. Western blot assay = 6 5. RT-PCR = 7 6. Electrophoretic mobility shift assay (EMSA) = 7 7. RP-HPLC for identification of LOX metabolites = 8 8. Statistical analysis = 8 Ⅲ. RESULTS = 9 1. Prevention of H. pylori-induced gastric mucosal cytotoxicity with EGCG pretreatment = 9 2. DNA damage by H. pylori infection, and its attenuation by EGCG = 10 3. Blockage of H. pylori-induced TLR-4 glycosylation by EGCG = 17 4. Inactivation of MAPK ERK1/2 and NF-kB by EGCG = 20 5. EGCG inhibits the synthesis of 5S-HETE induced by H. pylori infection = 20 Ⅳ. DISCUSSION = 27 Ⅴ. CONCLUSION = 32 REFERENCES = 33 국문요약 = 42"Docto

내시경적 절제술로 치료된 위장의 고위험성 위장관 기질 종양 3예

Gastrointestinal stromal tumors (GISTs) are the most common subepithelial tumor of the gastrointestinal tract. They originate from mesenchymal tissue. Because of difficulties in discriminating between benign and malignant GISTs, the treatment modality is selected on the base of tumor size, mitosis count, location, originating layer, and the presence of complications. Regular follow-up, open resection, or laparoscopic operation were considered main treatments for GISTs. Surgical resection is standard treatment for a huge GIST. However, the treatment method is not determined for GISTs of less than 3 cm that show a benign clinical course. Recently, endoscopic treatment was attempted because of recent endoscope developments and associated devices. We report three cases of gastric GISTs with a high risk of aggressive behavior that were successfully treated by endoscopic resection.GIST는 위장관의 간엽 조직에서 발생하고, 상피하병변에서 가장 흔한 종양성 병변 중 하나이다. GIST는 양성과 악성의 경계가 불분명하여 종양의 크기, 유사분열 수, 위치, 기원한 층, 합병증의 유무 등을 종합적으로 고려하여 치료 전략을 결정하지만 현재까지는 주기적인 경과 관찰, 개복 혹은 복강경을 통한 절제수술 등이 치료의 주류를 이루어 왔다. GIST 중 크기가 큰 경우는 악성화 위험도가 높아서 수술적 절제가 표준치료이고, 직경 3 cm 미만의 종양의 경우는 대개 양성의 임상경과를 보여 수술을 할지 혹은 경과 관찰할 지에 대한 정립된 치료방침이 없으나 최근 내시경 기구의 발달로 위장관 상피하종양을 내시경적 방법으로 절제하는 시도가 늘고 있다. 저자들은 위장에서 발생한 GIST를 내시경적 방법으로 절제하였고 조직 검사상 고위험군에 해당되었던 3예를 경험하였기에 이를 보고한다

서비스양을 고려한 수가 결정모형에 의한 추정 환산지수와 실제 환산지수의 비교

Background: Price control alone may not successfully restrain growth in health expenditures. This study aimed to propose fee adjustment model suitable for Korea reflecting health service volume and to clarify applicability of the model by comparing actual conversion factor with estimated conversion factor from simulation of this model. Methods: Fee adjustment model was developed based on Alberta’s fee adjustment formula in Canada and 7 alternatives were assessed according to diversely applied parameters of the model. Results: Estimated conversion factors of the tertiary care hospital and the hospital were lower than actual conversion factors, since the utilization of heath service has been increased. However, there was no big difference between estimated conversion factors and actual conversion factors of the general hospital and the clinic. Eventually this fee adjustment model could estimate proper conversion factor reflecting health service volume. Conclusion: This model may be applicable to the mechanism as determining conversion factor between insurer and provider via negotiation and controling growth in health expenditures

Helicobacter pylori 감염 실험 동물모델

The establishment of laboratory animal models persistently infected with Helicobacter pylori (H. pylori) has been difficult, but strongly required to document the causative role of H. pylori on ensuing gastritis, peptic ulcer disease and even gastric cancer. Although H. pylori are generally regarded as the most important etiologic agent of chronic active gastritis, peptic ulcer diseases, primary gastric marginal zone lymphoma, and gastric cancer, the detailed pathogenic mechanisms are not resolved. In an effort to develop an animal model that could show the same course of the infection that occurs in the human host, diverse kinds of animal model have been proposed. This review attempted to highlight salient features of H. pylori-infected animal models