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Reduced gastric mucosal blood flow in patients with portal‐hypertensive gastropathy
Author(s) -
Iwao Tadashi,
Toyonaga Atsushi,
Ikegami Motoki,
Oho Kazuhiko,
Sumino Michihiro,
Harada Hiroshi,
Sakaki Munenori,
Shigemori Hiroyuki,
Aoki Toshichika,
Tanikawa Kyuichi
Publication year - 1993
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840180107
Subject(s) - portal hypertensive gastropathy , medicine , gastroenterology , portal hypertension , blood flow , cirrhosis , esophageal varices
Abstract 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 (0.91 ± 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. (H EPATOLOGY 1993;18:36–40).