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1. |
Helicobacter pylori:Causal agent in peptic ulcer disease? A Working Team Report. Introduction |
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Journal of Gastroenterology and Hepatology,
Volume 6,
Issue 2,
1991,
Page 103-103
G. N. J. TYTGAT,
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ISSN:0815-9319
DOI:10.1111/j.1440-1746.1991.tb01447.x
出版商:Blackwell Publishing Ltd
年代:1991
数据来源: WILEY
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2. |
I.Helicobacter pylori: Its epidemiology and its role in duodenal ulcer disease |
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Journal of Gastroenterology and Hepatology,
Volume 6,
Issue 2,
1991,
Page 105-113
DAVID Y. GRAHAM,
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ISSN:0815-9319
DOI:10.1111/j.1440-1746.1991.tb01448.x
出版商:Blackwell Publishing Ltd
年代:1991
数据来源: WILEY
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3. |
II.Helicobacter pylori: Causal agent in peptic ulcer. Microbiological aspects |
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Journal of Gastroenterology and Hepatology,
Volume 6,
Issue 2,
1991,
Page 115-120
ADRIAN LEE,
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ISSN:0815-9319
DOI:10.1111/j.1440-1746.1991.tb01449.x
出版商:Blackwell Publishing Ltd
年代:1991
数据来源: WILEY
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4. |
III. Virulence and pathogenicity ofHelicobacter pylori |
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Journal of Gastroenterology and Hepatology,
Volume 6,
Issue 2,
1991,
Page 121-124
BARRY J. MARSHALL,
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摘要:
AbstractH. pyloriis a highly virulent organism as evidenced by its low infective dose and widespread high prevalence in human populations. Its virulence is achieved through its ability to survive in a moist environment and its massive urease production which allows it to survive in the acidic gastric juice long enough to colonize the gastric mucus.Gastric colonization is facilitated by cell wall associated lectins which permit the bacterium to bind to gastric mucus and the gastric epithelial cell. Once in this location,H. pyloriproduces several enzymes which may harm the gastric epithelium, particularly urease (through ammonia generation) and phospholipases A andC. H. pylorialso weakens the gastric mucous layer by digesting its glycoproteins and lipids, making the mucus less hydrophobic and more water soluble.Helicobacter pyloriattracts phagocytic cells, inducing both acute and chronic inflammation as well as an antibody response. Persistence ofH. pyloriin the mucosa may be enhanced by its cytotoxin and catalase production, by which it survives after phagocytosis by neutrophils.
ISSN:0815-9319
DOI:10.1111/j.1440-1746.1991.tb01450.x
出版商:Blackwell Publishing Ltd
年代:1991
数据来源: WILEY
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5. |
IV.Helicobacter pyloriand peptic ulceration: Histopathological aspects |
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Journal of Gastroenterology and Hepatology,
Volume 6,
Issue 2,
1991,
Page 125-130
MICHAEL F. DIXON,
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ISSN:0815-9319
DOI:10.1111/j.1440-1746.1991.tb01451.x
出版商:Blackwell Publishing Ltd
年代:1991
数据来源: WILEY
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6. |
V.Helicobacter pyloritherapy: Effect on peptic ulcer disease |
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Journal of Gastroenterology and Hepatology,
Volume 6,
Issue 2,
1991,
Page 131-137
A. T. R. AXON,
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ISSN:0815-9319
DOI:10.1111/j.1440-1746.1991.tb01452.x
出版商:Blackwell Publishing Ltd
年代:1991
数据来源: WILEY
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7. |
Helicobacter pylori: Causal agent in peptic ulcer disease? Conclusion |
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Journal of Gastroenterology and Hepatology,
Volume 6,
Issue 2,
1991,
Page 139-140
G. N. J. TYTGAT,
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ISSN:0815-9319
DOI:10.1111/j.1440-1746.1991.tb01453.x
出版商:Blackwell Publishing Ltd
年代:1991
数据来源: WILEY
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8. |
Medical treatment of duodenal ulcer: Acid inhibition orHelicobacter pylorieradication? |
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Journal of Gastroenterology and Hepatology,
Volume 6,
Issue 2,
1991,
Page 141-144
KWOK‐HUNG LAI,
FULL‐YOUNG CHANG,
SHYH‐HAW TSAY,
LEE‐CHENG LU,
JIUNN‐TARNG CHENG,
SHENG‐SHONG JENG,
TZEE‐CHUNG WU,
WAI‐WAH NG,
JIN‐SHIUNG JENG,
SHOU‐DONG LEE,
YANG‐TE TSAI,
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摘要:
AbstractTo ascertain whether acid inhibition orHelicobacter pylori(HP) colonization is the decisive factor in the healing of duodenal ulcer, we treated 54 patients with famotidine and carried out long‐term follow‐up.Helicobacter pyloricolonization was found in 70.4% of patients before treatment. There were no differences in the pre‐treatment characteristics between patients with HP positive or HP negative ulcers. The 4‐week and 8‐week healing rates after famotidine treatment were 72.5% and 82.4% respectively. No difference in HP colonization was found between patients with ulcer healed and those with ulcer not healed (78.4%vs64.3% at 4th week and 77.3%vs71.4% at 8th week,P>0.05). In patients with ulcer healed at 4th week, the intragastric pH was raised significantly and the antral acute inflammation was less severe than those with ulcer not healed. Ulcer recurrence was found in 76.9% of patients within 1 year, but there was no difference in ulcer recurrence between the patients with positive or negative HP colonization at the time of ulcer healing. Our results suggest that duodenal ulcer healing and recurrence are closely related to acid inhibition rather than to HP col
ISSN:0815-9319
DOI:10.1111/j.1440-1746.1991.tb01454.x
出版商:Blackwell Publishing Ltd
年代:1991
数据来源: WILEY
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9. |
Snake skin pattern gastropathy in cirrhotic patients |
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Journal of Gastroenterology and Hepatology,
Volume 6,
Issue 2,
1991,
Page 145-149
WEN‐JEH LIN,
FA‐YAUH LEE,
HAN‐CHIEH LIN,
YANG‐TE TSAI,
SHOU‐DONG LEE,
KWOK‐HUNG LAI,
HSIAO‐CHUNG HSIA,
SUN‐SANG WANG,
KWANG‐JUEI LO,
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摘要:
AbstractGastric mucosal lesions are common in patients with cirrhosis. Among them, snake skin pattern gastropathy (SSPG) is the most distinguishing one. A prospective study was conducted to investigate the incidence of SSPG in cirrhotic patients, the relationship between the degree of portal pressure and SSPG, and the possible association of SSPG with serum levels of gastrin and pepsinogen I. SSPG was found to be significantly more common in 100 cirrhotic patients than in 100 age‐ and sex‐matched healthy controls (41%vs0%,P0.05) in cirrhotic patients with or without SSPG. In conclusion, SSPG is common in cirrhotic patients. Portal pressureper semay not be the only factor causing SSPG—other aggressive factors may be needed together to cause the gastropathy. There is no evidence of correlation between serum gastrin or pepsinogen I lev
ISSN:0815-9319
DOI:10.1111/j.1440-1746.1991.tb01455.x
出版商:Blackwell Publishing Ltd
年代:1991
数据来源: WILEY
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10. |
Significance of blood flow in the inferior and superior mesenteric veins for the formation of oesophageal varices |
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Journal of Gastroenterology and Hepatology,
Volume 6,
Issue 2,
1991,
Page 151-154
SUSUMU SHIOMI,
TETSUO KUROKI,
TADASHI UEDA,
NAOKO IKEOKA,
SHUHEI NISHIGUCHI,
SHINYA NAKAJIMA,
KENZO KOBAYASHI,
TAKEYUKI MONNA,
HIRONOBU OCHI,
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摘要:
AbstractThe degree of involvement of blood flow in the superior mesenteric vein and inferior mesenteric vein in the formation of oesophageal varices is not known. We have developed a method by which the contributions of these veins to portal blood flow can be evaluated simultaneously in a relatively non‐invasive way. An enteric‐coated capsule containing [123I]iodoamphetamine (IMP) is given by mouth and 3 h later [123I]IMP is instilled into the rectum. The data obtained are treated by computer to calculate the portal shunt index via the inferior and superior mesenteric veins. In chronic hepatitis and cirrhosis, when varices were absent, the difference in these indices was not significant. In the presence of varices, the portal shunt index via the inferior mesenteric vein was significantly higher than that via the superior mesenteric vein. It was suggested that the contribution of blood flow in the inferior mesenteric vein the portal/splenic axis is important in the formation of vari
ISSN:0815-9319
DOI:10.1111/j.1440-1746.1991.tb01456.x
出版商:Blackwell Publishing Ltd
年代:1991
数据来源: WILEY
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