Neuroendocrine cell proliferations in gastric antral vascular ectasia

Lowes, J.R.; Rode, J.

doi:10.1016/0016-5085(89)91437-6

Cited by 72 publications

(49 citation statements)

References 27 publications

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“…This draws mucosa into accentuated longitudinal folds and induces fibromuscular hyperplasia of the antrum and formation of ectatic vessels as a secondary reaction. Lowes and Rode [21] support the theory of mechanical stress as they found no other explanation for the typical pattern of distribution of GAVE lesions.…”

Section: Pathophysiologymentioning

confidence: 62%

“…Two studies suggest a role for abnormal antral motility and physical stress on the mucosa [18, 21]. The evidence for all 4 of the above theories remains patchy and unconvincing.…”

Section: Discussionmentioning

confidence: 99%

“…Only 1 study found raised Prostaglandin E 2 levels [20]. Based on a single case, proliferations of neuroendocrine cells producing 5-hydroxytryptamine and vasoactive inhibitory peptide have been postulated as a causal factor [21]. …”

Section: Discussionmentioning

confidence: 99%

“…A histological study by Lowes and Rode [21] on a single patient with GAVE found extra-epithelial and intra-epithelial proliferations of neuroendocrine cells in close proximity to ectatic blood vessels. A majority of these showed immunoreactivity for 5-hydroxytryptamine and vasoactive inhibitory peptide.…”

Section: Pathophysiologymentioning

confidence: 99%

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Gastric Antral Vascular Ectasia (GAVE): An Update on Clinical Presentation, Pathophysiology and Treatment

2008

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Gastric antral vascular ectasia (GAVE), though a rare disorder, causes up to 4% of non-variceal upper GI bleeding. This paper gives an overview of studies examining clinical presentation and pathophysiology, and reviews the current evidence for invasive and non-invasive treatments. GAVE is often associated with systemic illnesses, such as cirrhosis of the liver, autoimmune connective tissue disorders, bone marrow transplantation and chronic renal failure. The pathophysiological changes leading to GAVE have not been fully explained and remain controversial. Patient presentation varies from chronic iron-deficiency anaemia to heavy acute gastrointestinal bleeding. It is important to differentiate GAVE from portal hypertensive gastropathy as GAVE does not respond to measures reducing portal pressures. Endoscopic ablation (Nd:YAG-laser or argon plasma coagulation) is the first-line treatment of choice. As evidence for pharmacological therapy with oestrogen (and/or progesterone), tranexamic acid or thalidomide stems from case reports only, these should be used if endoscopic measures have failed to stop chronic blood loss. Surgical antrectomy should be reserved for unresponsive cases as it is associated with a high mortality. Ultimately, treatment of the underlying medical co-morbidities may lead to resolution of GAVE.

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Section: Pathophysiologymentioning

confidence: 62%

“…Two studies suggest a role for abnormal antral motility and physical stress on the mucosa [18, 21]. The evidence for all 4 of the above theories remains patchy and unconvincing.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Pathophysiologymentioning

confidence: 99%

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Gastric Antral Vascular Ectasia (GAVE): An Update on Clinical Presentation, Pathophysiology and Treatment

2008

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“…hormone, which was hypothesised to induce spindle cell proliferation, hyperplasia, prolonged sphincter relaxation and also capillary and venous dilatation. A possible role of both VIP and 5-hydroxytryptamine has been proposed after the evidence of the presence of actively proliferating neuroendocrine cells surrounding the ectasic vessels in the lamina propria of patients with GAVE [30] . The release of these substances seems to be responsible for the local vasodilatation and the tendency to bleed.…”

Section: Medical Therapymentioning

confidence: 99%

Diagnosis and management of gastric antral vascular ectasia

Fuccio¹

2013

WJGE

125

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Gastric antral vascular ectasia (GAVE) is an uncommon but often severe cause of upper gastrointestinal (GI) bleeding, responsible of about 4% of non-variceal upper GI haemorrhage. The diagnosis is mainly based on endoscopic pattern and, for uncertain cases, on histology. GAVE is characterized by a pathognomonic endoscopic pattern, mainly represented by red spots either organized in stripes radially departing from pylorus, defined as watermelon stomach, or arranged in a diffused-way, the so called honeycomb stomach. The histological pattern, although not pathognomonic, is characterized by four alterations: vascular ectasia of mucosal capillaries, focal thrombosis, spindle cell proliferation and fibrohyalinosis, which consist of homogeneous substance around the ectatic capillaries of the lamina propria. The main differential diagnosis is with Portal Hypertensive Gastropathy, that can frequently co-exists, since about 30% of patients with GAVE co-present a liver cirrhosis. Autoimmune disorders, mainly represented by Reynaud's phenomenon and sclerodactyly, are co-present in about 60% of patients with GAVE; other autoimmune and connective tissue disorders are occasionally reported such as Sjogren's syndrome, systemic lupus erythematosus, primary biliary cirrhosis and systemic sclerosis. In the remaining cases, GAVE syndrome has been described in patients with chronic renal failure, bone marrow transplantation and cardiac diseases. The pathogenesis of GAVE is still obscure and many hypotheses have been proposed such as mechanical stress, humoural and autoimmune factors and hemodynamic alterations. In the last two decades, many therapeutic options have been proposed including surgical, endoscopic and medical choices. Medical therapy has not clearly shown satisfactory results and surgery should only be considered for refractory severe cases, since this approach has significant mortality and morbidity risks, especially in the setting of portal hypertension and liver cirrhosis. Endoscopic therapy, particularly treatment with Argon Plasma Coagulation, has shown to be as effective and also safer than surgery, and should be considered the first-line treatment for patients with GAVE-related bleeding.

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Gastrointestinal Vascular Malformations and Neoplasms: Arterial, Venous, Arteriovenous, and Capillary

Travis

Korzenik

2015

Yamada' S Textbook of Gastroenterology

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Neuroendocrine cell proliferations in gastric antral vascular ectasia

Cited by 72 publications

References 27 publications

Gastric Antral Vascular Ectasia (GAVE): An Update on Clinical Presentation, Pathophysiology and Treatment

Gastric Antral Vascular Ectasia (GAVE): An Update on Clinical Presentation, Pathophysiology and Treatment

Diagnosis and management of gastric antral vascular ectasia

Gastrointestinal Vascular Malformations and Neoplasms: Arterial, Venous, Arteriovenous, and Capillary

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