Increased gastric mucosal perfusion in cirrhotic patients with portal hypertensive gastropathy

Panés, Julián; Bordas, Josep M.; Piqué, Josep M.; Bosch, Jaume; García-Pagán, J.C.; Feu, Faust; Casadevall, María; Terés, Josep; Rodés, Joan

doi:10.1016/0016-5085(92)91447-c

Cited by 107 publications

(55 citation statements)

References 23 publications

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“…Portal hypertension, and not cirrhosis, is the main factor, because PHG has been described in patients with and without liver disease [7]. There is, however, no good correlation between the endoscopic findings and portal pressure [8], and gastric blood flow studies showed both increased and reduced gastric perfusion [9,10].…”

Section: Introductionmentioning

confidence: 99%

Effect of Portal Hypertension in the Small Bowel: An Endoscopic Approach

et al. 2007

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Background and aim The effects of portal hypertension in the small bowel are largely unknown. The aim of the study was to prospectively assess portal hypertension manifestations in the small bowel. Methods We compared, by performing enteroscopy with capsule endoscopy, the endoscopic findings of 36 patients with portal hypertension, 25 cirrhotic and 11 non-cirrhotic, with 30 controls. Results Varices, defined as distended, tortuous, or saccular veins, and areas of mucosa with a reticulate pattern were significantly more frequent in patients with PTH. These two findings were detected in 26 of the 66 patients (39%), 25 from the group with PTH (69%) and one from the control group (3%) (P \ 0.0001). Among the 25 patients with PTH exhibiting these patterns, 17 were cirrhotic and 8 were non-cirrhotic (P = 0.551). The presence of these endoscopic changes was not related to age, gender, presence of cirrhosis, esophageal or gastric varices, portal hypertensive gastropathy, portal hypertensive colopathy, prior esophageal endoscopic treatment, current administration of beta-blockers, or Child-Pugh Class C. More patients with these endoscopic patterns had a previous history of acute digestive bleeding (72% vs. 36%) (P = 0.05). Active bleeding was found in two patients (5.5%). Conclusions The presence of varices or areas of mucosa with a reticulate pattern are manifestations of portal hypertension in the small bowel, found in both cirrhotic and non-cirrhotic patients. The clinical implications of these findings, as regards digestive bleeding, are uncertain, although we documented acute bleeding from the small bowel in two patients (5.5%).

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Section: Introductionmentioning

confidence: 99%

Effect of Portal Hypertension in the Small Bowel: An Endoscopic Approach

et al. 2007

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“…The study concluded that PHG was associated with severity of portal hypertension and prognosis in patients with cirrhosis. However, other studies have been unable to demonstrate a correlation between the severity of portal hypertension and that of PHG [21][22][23].…”

Section: Pathophysiologymentioning

confidence: 91%

Gastric Antral Vascular Ectasia and Portal Hypertensive Gastropathy

Ramai¹,

Linn²,

Reddy³

2018

Stomach Disorders

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Gastric antral vascular ectasia (GAVE) and portal hypertensive gastropathy (PHG) are mucosal lesions that can cause chronic gastrointestinal bleeding in the patients with cirrhosis. While PHG occurs exclusively in patients with liver cirrhosis, GAVE can also present in patients with systemic and autoimmune conditions. The need to accurately characterize these two conditions is dependent on clinical, endoscopic, and histological parameters. The management of GAVE utilizes endoscopic ablation techniques, while medical therapy is directed toward stabilizing portal pressure in patients with PHG. Herein, we review the epidemiology, diagnosis, pathophysiology, and medical, endoscopic, and surgical management of GAVE and PHG.

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“…The laser Doppler technique has been widely used to estimate gastrointestinal mucosal perfusion [7, 19, 20, 21, 22]. After the patient fasted overnight, we performed a routine endoscopic examination and measured the gastric mucosal blood flow (GMBF) by passing the endoscopic probe (PF-309; Perimed, Stockholm, Sweden) of the laser Doppler flowmeter (Periflux PF-3; Perimed) through the biopsy channel of the fiberscope.…”

Section: Methodsmentioning

confidence: 99%

“…Blood flow measurements were performed with a bandwidth of 12 kHz and a time constant of 0.2 s, without using the movement artifact filter. During the procedure, contact pressure between the gastric mucosa and the probe was kept slight, and air insufflation was kept minimal to avoid any possible changes in the gastric mucosal blood flow caused by high intragastric pressure [19, 23]. The output signal from the flowmeter was continuously printed on a recorder (SS-100F; Sekomic Ltd., Tokyo, Japan; chart speed, 2.5 mm/s).…”

Section: Methodsmentioning

confidence: 99%

“…The findings of various hemodynamic studies on PHG remain controversial [3, 4, 5, 6, 7]. Some studies have reported that the gastric mucosal blood flow increases in patients with PHG [3, 4, 5, 6]while others have reported that it decreases [7]. Morphological studies have shown PHG to be characterized by marked dilatation of the mucosal and submucosal vessels without any inflammation [1, 8].…”

Section: Introductionmentioning

confidence: 99%

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Role of Vascular Endothelial Growth Factor in Portal Hypertensive Gastropathy

Tsugawa¹,

Hashizume

Migou³

et al. 2000

Digestion

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Background and Aims: Portal hypertensive gastropathy (PHG) is now recognized as a distinct entity; however, the angiogenesis in the portal hypertensive gastric mucosa has yet to be elucidated. Vascular endothelial growth factor (VEGF) is a potent angiogenic factor involved in both physiological and pathological angiogenesis. The aim of this study was thus to examine the function of VEGF in the portal hypertensive and non-portal hypertensive gastric mucosa. Method: Forty-five cirrhotic patients were divided into 3 groups as follows. Group I included 15 patients without PHG who were treated with 1.5 g teprenone/day for 8 weeks: PHG(–)-t. Group II included 15 patients with PHG who were not treated with teprenone: PHG(+)-n. Group III included 15 patients with PHG who were treated with teprenone for 8 weeks: PGH(+)-t. The gastric mucosal blood flow (GMBF), the concentration of gastric mucosal VEGF and hexosamine and the endoscopic findings were studied both before and after medication. Results: Before teprenone treatment, the GMBF in the antrum, fundus, fornix were significantly higher in PHG(+)-n than PHG(–)-t. After treatment, the GMBF in the fundus and fornix significantly decreased more than before treatment in the PHG(+)-t. After treatment, the GMBF in the antrum increased significantly more than before treatment in PHG(–)-t. The gastric VEGF and hexoxamine concentration in the antrum were significantly higher in PHG(+)-n than in PHG(–)-t. After treatment, the gastric VEGF and hexosamine concentration in the antrum significantly decreased in PHG(+)-t while no change in concentration was recognized in PHG(+)-n. In the endoscopic findings, a decrease in the PHG score was recognized in 2 patients in PHG(+)-t. Conclusion: Portal hypertensive gastric mucosal change was thus found to trigger a high concentration of VEGF and hexosamine. Such increased activity of VEGF and hexosamine may thus account for the presence of active congestion in PHG.

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Increased gastric mucosal perfusion in cirrhotic patients with portal hypertensive gastropathy

Cited by 107 publications

References 23 publications

Effect of Portal Hypertension in the Small Bowel: An Endoscopic Approach

Effect of Portal Hypertension in the Small Bowel: An Endoscopic Approach

Gastric Antral Vascular Ectasia and Portal Hypertensive Gastropathy

Role of Vascular Endothelial Growth Factor in Portal Hypertensive Gastropathy

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