• Title/Summary/Keyword: 헬리코박터

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Medi focus - 헬리코박터균은 무엇일까?

  • Lee, Haeng-Rim
    • 건강소식
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    • v.39 no.9
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    • pp.24-25
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    • 2015
  • 한 조사에 따르면 헬리코박터균은 우리나라에 비교적 높은 빈도로 분포하고 있으며, 어린이의 20%, 중년충의 70%, 노년층의 90%가 감염되어 있다고 한다. 헬리코박터균의 정체가 새삼 궁금해지는 대목이다.

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Plumbagin Inhibits Expression of Virulence Factors and Growth of Helicobacter pylori (Plumbagin에 의한 헬리코박터 파이로리균의 성장 및 병원성 인자 발현 억제효과)

  • Lee, Min Ho;Woo, Hyun Jun;Park, Min;Moon, Cheol;Eom, Yong-Bin;Kim, Sa-Hyun;Kim, Jong-Bae
    • Microbiology and Biotechnology Letters
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    • v.44 no.2
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    • pp.218-226
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    • 2016
  • Helicobacter pylori primarily colonizes the human stomach. Infection by this bacterium is associated with various gastric diseases, including inflammation, peptic ulcer, and gastric cancer. Although there are antibiotic regimens for the eradication of H. pylori, the resistance of this species against antibiotics has been continuously increasing. The natural compound plumbagin has been reported as an antimicrobial and anticancer molecule. In this study, we analyzed the inhibitory effect of plumbagin on H. pylori strain ATCC 49503 as well as the expression of various molecules associated with H. pylori growth or virulence by immunoblotting and reverse transcription polymerase chain reaction (RT-PCR) analyses. We demonstrated the minimal inhibitory concentration of plumbagin on H. pylori through the agar dilution and broth dilution methods. Furthermore, we investigated the effect of plumbagin treatment on the expression of the RNA polymerase subunits and various virulence factors of H. pylori. Plumbagin treatment decreased the expression of RNA polymerase subunit alpha (rpoA), which is closely associated with bacterial survival. Moreover, the mRNA and protein levels of the major CagA and VacA toxins were decreased in plumbagintreated H. pylori cells. Likewise, the expression levels of urease subunit alpha (ureA) and an adhesin (alpA) were decreased by plumbagin treatment. Collectively, these results suggest that plumbagin may inhibit the growth, colonization, and pathogenesis of H. pylori by the mechanism demonstrated in this study.

모든 병의 타깃, 만성질환 - 만성위장질환의 대표적인 원인, 위나선균과 관련된 소화기계 질환

  • Kim, Jae-Gyu
    • 건강소식
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    • v.34 no.6
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    • pp.18-19
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    • 2010
  • 한 유제품 CF로 인해 누구나 한 번쯤은 들어보았을 헬리코박터 파이로리(Helicobacter Pylori). 헬리코박터 파이로리균은 위 점막에 기생하는 나선균으로 위나선균으로도 불린다. 이 세균은 환자에게서 분리된 균주마다 서로 다른 유전체 구조를 가진 특이한 세균집단으로 만성 전정부 위염, 소화성궤양, 위 MALT(점막연관림프조직형) 림프종, 위암 등의 원인이다.

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Helicobacter pylori Eradication and Risks of Metachronous Recurrence after Endoscopic Resection of Gastric Adenoma: A Systematic Review and Meta-Analysis (위선종의 내시경 절제 후 이시성 재발의 예방을 위한 헬리코박터 제균 치료: 체계적 문헌분석 및 메타분석)

  • Kim, Jie-Hyun;Nam, Su Youn;Chun, Jaeyoung;Youn, Young Hoon;Park, Hyojin
    • Journal of Digestive Cancer Reports
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    • v.8 no.2
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    • pp.91-96
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    • 2020
  • The effect of Helicobacter pylori (H. pylori) eradication on the development of metachronous recurrence after endoscopic resection (ER) of gastric adenoma is not well defined. The aim of this study was to assess the efficacy of H. pylori eradication after ER of gastric adenoma for the prevention of metachronous recurrence. A systematic literature review and meta-analysis were conducted using the databases Ovid-MEDLINE, EMBASE, Cochrane Library, KoreaMed, and KMBASE. Thus, a systematic review and meta-analysis was performed to investigate this relationship. Pooled risk ratio for metachronous gastric lesions with regard to H. pylori eradication was calculated, and heterogeneity was also measured. Five eligible studies were finally identified in systematic review, and included in meta-analysis. H. pylori eradication was associated with overall 55% lower odds of metachronous events (RR=0.55; 95 % CI 0.34-0.92). Based on the best available evidence, eradication of H. pylori can also provide protection against metachronous recurrence after ER of gastric adenoma.

Inhibitory Mechanism of Daidzein on Helicobacter pylori Growth (Helicobacter pylori 의 생육에 대한 Daidzein의 저해 특성)

  • Bae, Kyung-Mi;Lee, Ju-Youn;Lee, Hee-Seob
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.39 no.7
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    • pp.1083-1086
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    • 2010
  • This study was conducted to investigate the inhibitory effects of daidzein against H. pylori and its cholesterol $\alpha$-glucosyltransferase ($CHL{\alpha}GcT$). $CHL{\alpha}GcT$ is responsible for the production of $\alpha$-glucosyl cholesterol which constitutes more than 25% of cell wall lipids in H. pylori, and it has been suggested that it is essential for H. pylori viability. $CHL{\alpha}GcT$ was inhibited by daidzein, in a dose-dependant manner, of which $IC_{50}$ value was $128.5\;{\mu}M$. Daidzein also showed the inhibitory effect toward H. pylori growth by paper disc diffusion assay. Therefore, it is thought that the inhibition of daidzein on $CHL{\alpha}GcT$ was related to its anti-Helicobacter activity.

Do We Have to Treat Helicobacter pylori for Elderly Patients to Prevent Gastric Cancer? (고령 환자에서 위암 발병 감소를 위해 헬리코박터 제균 치료를 해야 하는가?)

  • Park, Seon-Young
    • The Korean journal of helicobacter and upper gastrointestinal research
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    • v.18 no.3
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    • pp.215-216
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    • 2018
  • 위암의 발병률이 감소하고 있기는 하지만 전 세계적으로 여전히 연 100만 명 이상이 새롭게 위암으로 진단되고 있으며, 앞으로 향후 몇십 년 동안은 인구의 고령화로 인하여 위암에 대한 사회적 경제적 부담이 줄어들지 않을 것으로 추측된다. 최근 메타분석에서 Helicobacter pylori 제균 치료가 위암발병을 33~47% 감소시킨다고 보고하였으나, 중국에서 시행된 무작위 대조 연구에서는 제균 치료가 위암의 전구 병변 감소에 도움이 되지 않았다고 보고하고 있어 위축성 위염이나 장상피화생을 동반한 경우 제균 치료가 위암 예방에 큰 도움이 되지 않을 수 있음을 제시하고 있다. 그렇다면 위축성 위염이 있는 경우가 많은 고령 환자에서는 과연 헬리코박터 제균 치료가 도움이 될 것인가? 저자들은 빅데이터 분석을 통해 헬리코박터 제균 치료가 위암 발병에 미치는 영향을 성별과 연령에 따라 분석하였다. 2003년부터 2012년까지 'Hospital Authority'에 등록된 clarithromycin 포함 3제 요법을 받은 환자들에서의 위암 발생률과 2003년부터 2013년까지 'Hong Kong Cancer Registry'에 등록된 성별과 연령이 일치된 대조군에서의 위암기대 발생률(expected incidence)을 비교하였다. 3제 요법을 받은 73,237명의 환자들을 확인하였을 때, 평균 7.6년의 추적기간 중 200명(0.27%)에서 위암이 발생하였다. 연령에 따라 40세 미만, 40~59세, 60세 이상의 그룹으로 나누어 각각 위암발생률을 대조군과 비교한 결과 60세 이상 환자군에서만 standardized incidence ratio (SIR)가 0.82로 감소하였다. 치료 성공여부에 따라 위암 발생률을 분석하였을 때, 제균 치료에 성공한 60세 이상 군에서 SIR이 0.78로 감소하였으나 재 치료를 받은 40~59세 군에서는 SIR이 2.43으로 증가하였다. 제균 치료시점이 위암 발생률에 미치는 영향으로는 제균 치료 후 10년 미만에서의 위암 발생률에는 큰 영향이 없었으나 10년 이상 경과한 경우 60세 이상 군과 40~59세 군에서의 위암 발병률이 대조군의 위암 예측 발병률보다 낮았다.

Diagnosis and Treatment of Gastric MALT Lymphoma (위 MALT 림프종의 진단 및 치료에 대한 고찰)

  • Tae Ho Kim
    • Journal of Digestive Cancer Research
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    • v.3 no.2
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    • pp.82-88
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    • 2015
  • Gastric lymphoma comprises 1-6% of all gastric malignant neoplasms and among them 50% is gastric MALT lymphoma. The 60-70% of MALT lymphomas is diagnosed at early, localized diseased state. Gastric MALT lymphoma is assumed that it progress slowly with indolent course. It presents nonspecific symptoms such as epigastric pain, dyspepsia, nausea and vomiting. It is rarely associated with serious complication such as gastrointestinal bleeding or perforation. The definite diagnosis of gastric MALT lymphoma should be made with histopathologically. Wotherspoon score is used to differential diagnosis with Helicobacter pylori associated gastric inflammatory change. Gastric MALT lymphoma is associated with Helicobacter pylori infection with supported by epidemiologic and histopathologic studies. Gastric MALT lymphoma is characterized with genetic aberrations such as trisomy 3, trisomy 18, chromosomal translocations t(11;18), t(1;14), t(14;18), t(3;14). Appropriate clinical staging is essential to determine the optimal treatment strategy for gastric MALT lymphoma. Lugano International Conference classification has been applied widely. Helicobacter pylori eradication is used as the first line treatment for gastric MALT lymphoma independent of the stage. The complete remission has been achieved in 60-90% of the stage I/II1 patients with Helicobacter pylori eradication only. The treatment options for the patients with refractory to eradication are radiotherapy, chemotherapy and/or immunotherapy with the complete remission rate of 75% to 100%. The incidence of gastric MALT lymphoma can be expected to down by virtue of the decrease of Helicobacter pylori infection rate. Further basic and clinical research is necessary to advance in determine the pathogenesis and management.

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