Gastric antral vascular ectasia: the evolution of therapeutic modalities

Naidu, Harini; Huang, Qin; Mashimo, Hiroshi

doi:10.1055/s-0034-1365525

Cited by 18 publications

(20 citation statements)

References 58 publications

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“…Marked dilation of capillaries and venules in gastric mucosa and submucosa with areas of intimal thickening, fibrin thrombi, fibromuscular hyperplasia and spindle cell proliferation [72,191,196,197] Clinical presentation/ complications…”

Section: Strong Associationmentioning

confidence: 99%

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Gjeorgjievski¹

2016

WJH

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AIM:To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy (PHG) based on a systematic literature review. METHODS:Computerized search of the literature was performed via PubMed using the following medical subject headings or keywords: "portal" and "gastropathy"; or "portal" and "hypertensive"; or "congestive" and "gastropathy"; or "congestive" and "gastroenteropathy". The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS:PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG. Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt and liver transplantation are highly successful ultimate therapies because they reduce the underlying portal hypertension. SYSTEMA...

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Section: Strong Associationmentioning

confidence: 99%

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Gjeorgjievski¹

2016

WJH

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“…an attempt to limit the recurrence of gastric antral vascular ectasia (GAVE), which has been described after standard APC or radiofrequency ablation because of the persistence of the deeper vascular network [13].…”

Section: Videomentioning

confidence: 99%

Thulium laser in interventional endoscopy: animal and human studies

et al. 2017

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The thulium laser system (TLS) is an emerging surgical tool. The 2-μm wavelength provides a confined coagulation depth (0.2 - 0.4 mm) to reduce the potential for inadvertent injuries. For the first time ever, we assessed TLS feasibility for endoscopic hemostasis ex vivo in pigs. In addition, we performed the first in vivo hemostatic treatments in humans. Tissue damage induced by TLS using different settings and optical fibers was compared to that from argon plasma coagulation (APC) in established ex vivo animal models. Three consecutive patients with complex nonvariceal upper gastrointestinal bleedings were treated and followed up. No deep submucosal injury was observed in animal models. The TLS showed a progressive penetration depth with increased power outputs and tissue exposures but very limited vertical tissue injury (0.1 - 2.0 mm) and lateral spreading damage (0.1 - 0.3 mm and 0.2 - 0.7 mm using the 365-µm and 550-µm fibers, respectively). In vivo, endoscopic hemostasis with TLS was always successful without complications. The TLS has proven to be very precise and easy to use. This novel technique appears to be a promising tool for advanced interventional endoscopy.

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“…Over the past several years, treatment for GAVE has continued to evolve as the number of available effective therapeutic interventions has increased. These included: YAG laser, APC, EBL, cryotherapy and surgical anterectomy (Figure 5 )[ 10 , 13 - 15 ]. APC is most commonly used but has been associated with sepsis, post-APC bleeding, gastric outlet obstruction and increased incidence of hyperplastic polyps[ 16 - 18 ].…”

Section: Discussionmentioning

confidence: 99%

Case series on multimodal endoscopic therapy for gastric antral vascular ectasia, a tertiary center experience

Matin

Naseemuddin

Shoreibah

et al. 2018

WJGE

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AIMTo study and describe patients who underwent treatment for gastric antral vascular ectasia (GAVE) with different endoscopic treatment modalities.METHODSWe reviewed patients with GAVE who underwent treatment at University of Alabama at Birmingham between March 1, 2012 and December 31, 2016. Included patients had an endoscopic diagnosis of GAVE with associated upper gastrointestinal bleeding or iron deficiency anemia.RESULTSSeven out of 15 patients had classic watermelon description for GAVE, 1/15 with diffuse/honeycomb pattern and 6/15 with nodular GAVE per EGD description. Seven out of 15 patients required multimodal treatment. Four out of six of patients with endoscopically nodular GAVE required multimodal therapy. Overall, mean pre- and post-treatment hemoglobin (Hb) values were 8.2 ± 0.8 g/dL and 9.7 ± 1.6 g/dL, respectively (P ≤ 0.05). Mean number of packed red blood cells transfusions before and after treatment was 3.8 ± 4.3 and 1.2 ± 1.7 (P ≤ 0.05), respectively.CONCLUSIONPatients with nodular variant GAVE required multimodal approach more frequently than non-nodular variants. Patients responded well to multimodal therapy and saw decrease in transfusion rates and increase in Hb concentrations. Our findings suggest a multimodal approach may be beneficial in nodular variant GAVE.

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Gastric antral vascular ectasia: the evolution of therapeutic modalities

Cited by 18 publications

References 58 publications

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Thulium laser in interventional endoscopy: animal and human studies

Case series on multimodal endoscopic therapy for gastric antral vascular ectasia, a tertiary center experience

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