Controversy exists as to the nature of gastric perfusion in portal-hypertensive gastropathy. To investigate portal hemodynamics and gastric mucosal perfusion in cirrhotic patients with and without portalhypertensive gastropathy, we subjected 56 cirrhotic patients with portal hypertension to portal v
Reduced gastric mucosal blood flow in patients with portal-hypertensive gastropathy
✍ Scribed by Tadashi Iwao; Atsushi Toyonaga; Motoki Ikegami; Kazuhiko Oho; Michihiro Sumino; Hiroshi Harada; Munenori Sakaki; Hiroyuki Shigemori; Toshichika Aoki; Kyuichi Tanikawa
- Publisher
- John Wiley and Sons
- Year
- 1993
- Tongue
- English
- Weight
- 554 KB
- Volume
- 18
- Category
- Article
- ISSN
- 0270-9139
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✦ Synopsis
Although congestive gastric mucosal circulation has been suggested in patients with portal-hypertensive gastropathy, whether it is due to "active" (overflow) or "passive" (stasis) congestion is not known. To answer this question, we assessed regional gastric mucosal blood flow with laser Doppler flowmetry in 57 patients with portal hypertension and 30 controls. Twelve patients had portal-hypertensive gastropathy of the antrum: in eight it was mild and in four it was severe. Portal-hypertensive gastropathy of the corpus was seen in 32 patients: it was mild in 24 and severe in 8. Thus prevalence of portal-hypertensive gastropathy was higher in the corpus than in the antrum (p < 0.01). In the antrum, gastric mucosal blood flow was significantly lower (p < 0.05) in patients with severe portalhypertensive gastropathy (0.54 & 0.27 V) than in controls (1.12 * 0.44 V), whereas the values in patients without portal-hypertensive gastropathy (0.90 * 0.35 V) and with mild portal-hypertensive gastropathy (0.9 1 f 0.31 V) were not significantly different from the values in controls (p < 0.05 on one-way analysis of variance). In the corpus, gastric mucosal blood flow was significantly lower in patients with mild (0.75 0.25 V) or severe portal-hypertensive gastropathy (0.42 ? 0.22 V) than in controls (1.16 ? 0.37 V) (p < 0.01 and p < 0.01, respectively) whereas the value in patients without portal-hypertensive gastropathy (0.99 * 0.37 V) was not significantly different from values in controls (p < 0.01 on one-way analysis of variance). We conclude that the gastric mucosa in patients with portal-hypertensive gastropathy (in particular, severe portal-hypertensive gastropathy) is poorly perfused. This is probably due to "passive" congestion. This information may have important clinical implications in patients with portal-hypertensive gastropathy. (HEPATOLOGY 1993;18:36-40.)
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